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by Kayla Sheehan (@kksheehan)

October TW, Dizon ZB, Arnold RM, Rosenberg AR. Characteristics of Physician Empathetic Statements During Pediatric Intensive Care Conferences With Family Members: A Qualitative Study. JAMA Network Open. 2018;1(3):e180351. doi:10.1001/jamanetworkopen.2018.0351

Ask any patient what qualities they desire in a physician, and empathy will almost always make the list. A physician’s ability to demonstrate empathy has been shown to significantly impact patient outcomes¹, increase patient satisfaction², and raise physician “compassion satisfaction,” which may hinder burnout (3). Though much debate surrounds empathy’s teachability, learning how and when to make empathetic statements is a crucial aspect of physician training. Many of us struggle with finding the right thing to say, but a recent open access study published in JAMA Network Open shows there may be more power in pauses made after empathetic statements than in the words themselves.

The study recorded 68 pediatric intensive care unit conferences over four years. Transcripts of every meeting were made, and empathetic statements were noted using the infamous NURSE criteria (naming, understanding, respecting, supporting, exploring). “Missed opportunities” to express empathy were noted as well. Empathetic statements were placed into two categories, “buried” and “unburied.” A buried statement was one in which the physician expressed empathy, but did not allow time for the family to respond. This most commonly occurred with the physician immediately segueing into clinical jargon, but was also counted as buried if another member of the team interrupted, or if the physician finished the statement with a closed-ended question.



Transcript analysis showed that physicians are fairly good at identifying when to express empathy, taking advantage of 74% of the opportunities analyzers identified. However, almost 40% of these statements were buried, and “medical talk” accounted for the vast majority of buried statements (95%). Interestingly, non-physician team members (typically a social worker or nurse) spoke only 5% of the time, but when they offered empathy, they did so unburied 87% of the time, further demonstrating the importance of a multi-disciplinary team in fully supporting patients and their families.



Physicians have a wealth of medical knowledge to share, but timing is paramount, and tacking jargon onto the end of a well-intentioned empathetic statement may prevent patients and families from even recognizing the empathetic effort at all. In October’s study, when physicians made unburied empathetic statements, families were 18 times more likely to respond with additional information, to express their fears, and to discuss their goals. Clear communication is an obvious cornerstone of the physician-family relationship, and while buried empathetic statements may be better than no expressions of empathy at all, they may leave families with a feeling of being unheard and ignored.



Though a busy clinician may not feel they have the time to open the Pandora’s box of family concerns and fears, investing time in “a pause” may pay dividends for all parties involved. For physicians, better communication skills have been shown to decrease instances of burnout, lower rates malpractice suits, and raise patient satisfaction scores⁴. Meanwhile, the family leaves these conversations feeling heard and understood, and the patient receives care tailored to them, with every fear, concern, and hope kept in mind.

If, as cellist Yo-Yo Ma would assert, “music happens between the notes,” perhaps the heart of medicine lives in the pause.

More Pallimed posts from Kayla Sheehan can be found here. More journal article reviews can be found here. More posts on communication can be found here.


Kayla Sheehan is a third-year medical student at California Northstate University. She enjoys singing, sharp cheddar, and long walks with her Australian Shepherd, Posey.

References:

1) Kim SS, Kaplowitz S, Johnston MV. The effects of physician empathy on patient satisfaction and compliance. Eval Health Prof. 2004 Sep;27(3):237-51. PubMed PMID: 15312283.

2) Pollak KI, Alexander SC, Tulsky JA, Lyna P, Coffman CJ, Dolor RJ, Gulbrandsen P, Ostbye T. Physician empathy and listening: associations with patient satisfaction and autonomy. J Am Board Fam Med. 2011 Nov-Dec;24(6):665-72. doi:10.3122/jabfm.2011.06.110025. PubMed PMID: 22086809;

3) Gleichgerrcht E, Decety J (2013) Empathy in Clinical Practice: How Individual Dispositions, Gender, and Experience Moderate Empathic Concern, Burnout, and Emotional Distress in Physicians. PLoS ONE 8(4): e61526. https://doi.org/10.1371/journal.pone.0061526

4) Boissy, A., Windover, A.K., Bokar, D. et al. Communication Skills Training for Physicians Improves Patient Satisfaction. J Gen Intern Med (2016) 31: 755. https://doi.org/10.1007/s11606-016-3597-2

Altmetric for this study: October TW, Dizon ZB, Arnold RM, Rosenberg AR. Characteristics of Physician Empathetic Statements During Pediatric Intensive Care Conferences With Family Members: A Qualitative Study. JAMA Network Open. 2018;1(3):e180351. doi:10.1001/jamanetworkopen.2018.0351

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by Denise Hess

An American pastor recently visited Australia and encountered a curious practice. At the start of meetings, any kind of meeting not just religious ones, she found it is common practice to begin with what is called an “acknowledgment of country.” According to reconciliation.org.au:

An Acknowledgement of Country is an opportunity for anyone to show respect for Traditional Owners and the continuing connection of Aboriginal and Torres Strait Islander peoples to Country. It can be given by both non-Indigenous people and Aboriginal and Torres Strait Islander people.

And it goes something like this:

“I’d like to begin by acknowledging the Traditional Owners of the land on which we meet today. I would also like to pay my respects to Elders past and present.”

I happened to hear this story from that American pastor the same week of the Charlottesville protests and counter protests, and the same week I watched the HBO adaptation of The Immortal Life of Henrietta Lacks. These events made me think again about the role of race in palliative care.

In over a decade of working in palliative care, I can say with confidence that I have never met an all-out “racist” palliative care physician, nurse, social worker, or chaplain. However, everyone of us has biases, prejudices, preconceived ideas of how people “should” act and what they “ought” to do, and we carry these biases with us wherever we go. Awareness helps, efforts to counter bias help, but we cannot rid ourselves of bias.

For example, I don’t think I am alone in noticing that I have pre-conceived ideas and expectations about how a patient or their loved ones will respond to palliative care interventions based on their cultural and ethnic background. This is bias. We are all infected with it.

Also, many of us have been given an unearned advantage, by accident of birth, called privilege, that
opens doors we didn’t even realize were closed to others. Privilege is as invisible as air unless you don’t have it and want to breathe. For example, whites and people of color are likely to have vastly different experiences of serious illness and palliative care. As has been well documented by bright minds among us¹, people of color tend to receive a lesser-quality version of palliative care² after receiving less preventative care, later diagnosis, and more challenging access to curative care in the first place.³

As a white woman, if I were diagnosed with a serious illness, I would likely receive high quality palliative care, assistance with advance care planning, excellent pain and symptom management, and help to die in the place of my choice. As a person of color, I may not receive any of the above.

The excellent health insurance I have is the result of the job I have, which is the result of the education I have, which is the result of the family I have, which is the result of the access they had to jobs, education, and opportunities, which is the result in large part of where they were born, when they were born, the color of their skin, the color of their eyes, the texture of their hair. Without those things, I could be without quality health insurance, showing up in the emergency room for primary care. Chance of birth is the source of my privilege.

To add to that, we are all part of health care systems that have institutionalized, operationalized, and standardized racism as part and parcel of their business models. Racism is embedded within the very fiber of organizations and shows up as disparities, lack of access, uneven quality, poor care coordination, and lower patient safety outcomes.

So how to respond? White guilt is not the answer. White guilt makes me the subject and people of color the object once again. White guilt only changes optics, not practices, and definitely not institutions or systems. However, using privilege for the benefit of others can help. Using our voices and our influence over organizations on behalf of those who have been shut out or excluded from various tables of influence can effect change. But even better, using our privilege to lift up the voices of people of color is an excellent step in the right direction.

“But,” I hear you say, “I am a busy (fill-in-the-blank-doctor-nurse-social worker-chaplain), I don’t have time to use my voice to change the system. I’m just trying to finish my documentation!” Fair enough. Yet, spending the currency in our bank of privilege on behalf of others does not have to (but absolutely can) include protest marches, trips to Washington DC, or even visits to the C suites. We can spread our wealth of privilege in simple yet powerful acts like our friends’ in Australia “acknowledgment of country.” Here are a few palliative care possibilities:

1. Include a person of color in a case presentation as a “positive” example, e.g. not “noncompliant,” “resistant to palliative care,” “opposed to advance care planning.”
2. Increase your cultural curiosity and competence through relationships with those outside your cultural group.
3. Read Between the World and Me by Ta-Nehisi Coates, The New Jim Crow by Michelle Alexander (as a start) or watch the film 13th, or I Am Not Your Negro and discuss as a team.
4. Assess your team’s cultural reach. What groups are over/underrepresented in your patient census based on your local demographics?
5. Inventory your language. Notice where and when you use terms such as “difficult” patient or, “resistant” family, or when you go into a family meeting with the expectation that the family will "want everything done.”
6. Watch for “acknowledgment of country” moments when meeting with patients and their loved ones. Are there opportunities to name the ways disparities may be impacting a patient’s situation? Was care difficult to access? Was quality of care poor? Talk about it.

These micro-non-aggressions and micro-extensions of our own privilege on behalf of others are not insignificant. We do not need to be the “white saviors.” We do not need to lead the charge to eradicate racism from our institutions. That would be appropriation. We need to be allies, learning from the experiences of persons of color, always stepping aside to make room for the neglected voices that need to be heard and honored.

Denise Hess MDiv, BCC-HPCC, LMFT is a palliative care chaplain and marriage and family therapist who currently serves as the Executive Director of the Supportive Care Coalition. She is currently on a quest to try all the donuts in Portland, Oregon.

References
1 Johnson KS. Racial and ethnic disparities in palliative care. J of Palliat Med 2013;16(11). Open Access PDF
2 Welch LC, Teno JM, Mor V. End-of-life care in black and white: race matters for medical care of dying patients and their families. J Am Geriatr Soc. 2005 53(7).
3 2016 National Healthcare Quality and Disparities Report. Rockville, MD: Agency for Healthcare Research and Quality; July 2017.

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by Drew Rosielle

In neuro-critical care, prediction of outcomes is often tricky because of the wide variability in the ability of the brain to recover and the usual long periods needed before seeing what is the limit of recovery. Most people are familiar with the Glasgow Coma Scale, but back in 2009 Mayo Clinic Proceedings published a study of the FOUR score), which presents some prognostic data for ICU patients. FOUR = 'Full Outline of UnResponsiveness.' (It is also written as 4S. - Ed.)

This was a single institution study (Mayo Rochester) primarily designed to investigate whether the FOUR score is a reliable coma scale when applied in ICUs by non-neuroscience types (it has been studied before in neuro ICUs - this study involved non-neuroscience trained nurses, consulting docs, fellows, and intensivists in several ICUs at Mayo). Part of the context for the score is that the Glasgow Coma Scale, the most commonly used coma scale, measures verbal responsiveness - something which is difficult to do on intubated patients. The 4S measures eye response, motor response, brainstem reflexes, and respiratory pattern and assigns 0-4 ratings to each category (see graphic below). All ICU patients (not all intubated) over a 1 year time frame who had 'abnormal consciousness' and who weren't receiving pharmacologic sedation or paralysis were included for the study. Basically different ICU team members were assigned to do 4S evaluations on these patients, and interrater reliability, etc. was measured.

100 patients were evaluated - 45% intubated - with a broad range of illnesses (at least 40% had some primary CNS pathology such as strokes, 'craniotomy,' etc.). Despite the fact that they noted an inclusion criteria of 'abnormal consciousness,' about a 3rd of the patients were described as 'alert': basically all the non-alert patients either had a primary CNS pathology or anoxic or metabolic encephalopathy (as expected; those patients without those issues would be expected to either be alert or pharmacologically sedated). 33% of the patients died - all of them either by neurologic criteria or after life-prolonging treatments were withdrawn due to poor prognosis.

Basically, the 4S looked good from an interreliability, etc. standpoint, and compared favorably with the GCS. As expected, lower (worse) summative 4S scores were associated with worse outcomes including in-hospital death (e.g. every 1 point decrease in the 4S was associated with a 15% improvement in the odds of in-hospital survival). (Note that is odds not rates - most of the outcomes are presented as odds ratios and not actual event-rates.) The only rates presented are for those 9 patients with the lowest 4S scores (presumably zero): 89% died in-hospital, and one assumes that 6 of these were the ones declared dead by neurologic criteria. Notably, the in-hospital mortality for those with the lowest GCS score (3) was 71%, suggesting perhaps the 4S (as it measures more characteristics than the GCS) can more precisely characterize the very sickest.

That said, from a clinical standpoint one isn't particularly helped by new data that a patient with no signs of consciousness, withdrawal to pain, brainstem reflexes, or spontaneous respirations, without the help of sedating drugs (ie a 4S of 0), is highly likely to die. We knew that already, and of course this paper wasn't intended to really demonstrate anything other than the 4S is a reliable way to measure/stratify degrees of unresponsiveness/coma. It is a reminder to me as a reader of this research how my interests in what data I want presented (in this case gross in-hospital mortality rates for each 4S rank) as I naively hope for answers/clinically-relevant information is not what others find important, even though they have the data. The 4S seems to be a straight-forward and easy to measure coma scale, and perhaps we'll be seeing more of it, including frank outcome data.

Drew Rosielle, MD is a palliative care physician at University of Minnesota Health in Minnesota. He founded Pallimed in 2005. For more Pallimed posts by Drew click here. 

References:
Iyer VN, Mandrekar JN, Danielson RD, Zubkov AY, Elmer JL, Wijdicks EFM. Validity of the FOUR score coma scale in the medical intensive care unit. Mayo Clin Proc. 2009;84(8):694-701. doi:10.1016/S0025-6196(11)60519-3. Open Access PDF

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by Jordan Keen

Case:
SM is a 25-year-old female with progressively worsening rhabdomyosarcoma despite multiple rounds of chemotherapy and surgery. She presented to the emergency department with worsening of her chronic tumor-related abdominal pain and new, diffuse pain of the muscles and joints. Family reported she had been experiencing episodes of confusion and hallucinations over the past week. Her home pain regimen of long-acting morphine and as needed oxycodone had been titrated aggressively over the past month in an attempt to control her pain (600mg total daily oral morphine equivalents).

When first evaluated by the palliative care consult service, she was in severe distress. She described severe, 10/10, diffuse pain. On exam there was generalized tenderness of the abdomen, as well as her shoulders, upper legs, and lower back. She was exhibiting myoclonic jerks of her upper extremities every 3-4 seconds. Although she was alert and oriented, she was easily distracted during the exam and required frequent redirection.

Our palliative care team was concerned about opioid-induced hyperalgesia (OIH). Suspicion was high given the paradoxical worsening of her pain despite high doses of opioids and the neuroexcitatory signs and symptoms (myoclonus, confusion, and hallucinations) she was exhibiting. Therefore, it was decided to lower the overall dosage and switch her opioid regimen in an attempt to reverse OIH. Her long-acting morphine was discontinued and replaced with methadone 5mg three times per day. Her as-needed oxycodone dose was reduced from 30mg to 5mg every 4 hours. To control the myoclonus, low dose lorazepam was administered three times per day.

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Discussion:
Opioid-induced hyperalgesia (OIH) is a rare syndrome of increasing pain, often accompanied by neuroexcitatory effects, in the setting of increasing opioid therapy. Clinicians should consider OIH in patients on high dose opioids or during a period of rapid opioid escalation. While case reports show a wide range of dosages can provoke this syndrome, the majority of patients are on very high doses, often greater than 1000mg oral morphine equivalents per day and typically via parenteral routes (IV and intrathecal). Morphine is by far the most common opiate implicated in OIH. Hydromorphone and oxycodone, members of the same class of opiate as morphine (phenanthrenes), can also cause OIH, but oxymorphone has not yet been reported to cause it. Methadone, a synthetic opioid in the class of diphenylheptanes, and fentanyl, a synthetic opioid in the class of phenylpiperidine, are considered less likely to precipitate OIH.

Existing data suggests that OIH is caused by multiple opioid-induced changes to the central nervous system including:

• Activation of N-methyl-D-aspartate (NMDA) receptors
• Inhibition of the glutamate transporter system
• Increased levels of the pro-nociceptive peptides within the dorsal root ganglia
• Activation of descending pain facilitation from the rostral ventromedial medulla
• Neuroexcitatory effects provoked by metabolites of morphine and hydromorphone

OIH can be confused with tolerance as in both cases patients report increased pain on opioids. The two conditions can be differentiated based on the patient’s response to opioids. In tolerance, the patient’s pain will improve with dose escalation. In OIH, pain will worsen with opioid administration. This paradoxical effect is one of the hallmarks of the syndrome. On physical exam, patients are grimacing in pain with moderate-to-severe distress, myoclonus, altered mental status or delirium and often allodynia (pain due to non-painful stimuli, such as light touch).

Typically, if you suspect OIH, you should get a pain or palliative care consultation because it will seem wrong to decrease opiates in a patient in severe pain. Opiate dose reduction and rotation to a synthetic opioid such as fentanyl or methadone is recommended. Methadone has the additional benefit of NMDA antagonism. It is not surprising that methadone has been shown to improve or resolve OIH given the role NMDA activation plays in causing OIH. Adjuvant therapies, such as acetaminophen or neuropathic pain medications, should be considered as they may decrease the need for opioids. Benzodiazepines may be a temporary addition to manage myoclonus as the OIH resolves.

Symptoms of OIH do resolve when patients are treated with the above strategies. However, it can be long and difficult to wean some patients to a low enough level of opioids to stop OIH. Existing literature does not address any long-term consequences of OIH. We hope to see more research on this subject.

Over the next 48 hours in the hospital, her myoclonus improved. Her pain and mental status improved more slowly. It took a week to re-establish control of her pain. At the time of discharge, she rated her pain as 3/10. Her new pain regimen consisted of methadone 10mg three times a day and oxycodone 5mg every 4 hours as needed.

References:
1. Chu, L. Opioid-induced Hyperalgesia in Humans: Molecular Mechanisms and Clinical Considerations. The Clinical Journal of Pain Issue: Volume 24(6), pp 479-496. 2008.

2. Smith, M. Neuroexcitatory Effects Of Morphine And Hydromorphone: Evidence Implicating The 3-GlucuronideMetabolites. Clinical and Experimental Pharmacology and Physiology, 27, pp 524–528. doi: 10.1046/j.1440-1681.2000.03290. 2000.

3. Mao, J. Opioid-induced abnormal pain sensitivity. Current Pain and Headache Reports. Volume 10, Issue 1, pp 67-70. 2006

4. Lee, M et al. A Comprehensive Review of Opioid-Induced Hyperalgesia. Pain Physician 2011; 14:145-161. ISSN 1533- 3159. Open Access PDF

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by Christian Sinclair

In palliative care, the symptoms we frequently encounter (fatigue, pain, nausea, dyspnea, depression, anxiety) have unique challenges, yet many of us have a comfort and confidence in the availability of therapies and the understanding of the symptom. Recently, I have seen two uncommon symptoms, prolonged isolation and fear as a result of a weak immune system. Frankly I don’t quite have a confident construct to understand and treat these two novel issues. It is not any single case that has stood out, but as I work more in outpatient palliative care in an academic cancer center, these themes of fear and isolation are pronounced and different than the fear and isolation that we may see in patients who are in their last days of life.

For many people undergoing chemotherapy or transplants with anti-rejection medications, they find themselves with prolonged periods of weakened immune systems. Obviously there are more dangerous periods with severe neutropenia (low white blood cells), but it is a new situation (to me, at least) when the immunocompromised state is more chronic, more permanent. I understand the biomedical and infectious issues fine. It is the psyschosocial aspects which have piqued my interest.

It is not uncommon to hear patients say that have cut out their favorite outdoor hobbies, or describe themselves as newly minted introverts. “Church? I’d love to go to church, but it isn’t good for me to be around that many people. I could get sick.” “We had a family reunion, but I only stopped by for a few minutes to say hi to everyone. There were a lot of young kids there with germs.” These are real injuries to quality of life, and there is no medicine that can fix that.

Now of course, not everyone who is chronically immunocompromised feels this way, but I am seeing a new trend for my clinical experience. If I want to do a stand-up job for patients, I feel I need a better understanding about the psychological aspects of infection control. And when I don’t know what to do, I go to the literature!

Looking around PubMed there is not too much about the long-term psychosocial impact of infection precautions. Most papers are focused on hospital based isolation (easier to study probably) compared to long-term self-imposed isolation as a result of being chronically immunocompromised. But let’s see what we can learn.

Prototype for isolation gowns?

As you may have already guessed, people who were placed in isolation in hospitals have been found to have (over multiple studies): lower self-esteem, more anxiety, more depression, more fear, more isolation, less nurse and doctor visits, less time when those clinicians were there, more adverse events, less satisfied with their care. Patients and families also do not understand the reasons for isolation in the hospital setting. (Perhaps we send mixed signals, or do not inform well?). Although in chronic immunosuppression, the reason for isolation is most likely the patient’s own fear of getting any infection.

Otherwise there really is not much published on the psychosocial risk and impacts of chronic immunosuppression. I also looked at some of the HIV/AIDS literature, but much of the psychosocial studies were not about the issue of isolation secondary to being immunocompromised. Even long term quality of life studies for people who have received transplants, focus on the frequency of infections and related hospitalizations when discussion of immunosuppression, not the risks of fear or isolation.

I have many more questions now on this topic, all without great (published) answers. How effective are the various ‘germ-free’ strategies? Do we sometimes go overboard to the detriment of patients? Is contact with other people potentially of more benefit than the risk of an infection? How do we help build resilience and support for people who are feel so isolated (meditation, prayer, FaceTime, Skype, and Frankl’s “Man Search for Meaning” are some ideas)? Does it help to let them see your face at least once before you put on the mask?

So without a lot of good published evidence, I still don’t quite have a good context in which to understand these trends. Hopefully, the patients and families I meet will teach me something. I’m really interested to see if any other palliative care clinicians, oncologists, BMT docs and nurses, or transplant professionals have any good tips or evidence. Also if you are a patient or family member, it would be great to hear your experience dealing with chronic immunosuppression.

References:

• Abad, C., Fearday, A., Safdar, N. (2010). Adverse effects of isolation in hospitalised patients: a systematic review. The Journal of Hospital Infection, 76(2), 97–102. doi:10.1016/j.jhin.2010.04.027 (OPEN ACCESS PDF)
• Day, H. R., Perencevich, E. N., Harris, A. D., Himelhoch, S. S., Brown, C. H., Gruber-Baldini, A. L., Morgan, D. J. (2011). Do contact precautions cause depression? A two-year study at a tertiary care medical centre. The Journal of Hospital Infection, 79(2), 103–7. doi:10.1016/j.jhin.2011.03.026 (OPEN ACCESS PDF)
• Radtke et al. Determining the Psychological Impact of Isolation Precautions on Families of ICU Patients. Retrieved June 13, 2015, from http://nursing.jhu.edu/admissions/financial-aid/fellowships/fuld/documents/cohort 3/Posters/Radtke_Fuld_Poster_Final.pdf (OPEN ACCESS PDF)
• Yokoe D et al. Infection prevention and control in health-care facilities in which hematopoietic cell transplant recipients are treated. Bone Marrow Transplantation. 2009 44: 495-507. doi:10.1038/bmt.2009.261 (OPEN ACCESS PDF)

Christian Sinclair, MD, FAAHPM is a palliative care physician at the University of Kansas Medical Center in Kansas City, KS and editor of Pallimed. In his free time, he enjoys coming up with nicknames for the new family dog, Spud.

Photo Credit: "Splendid Isolation" by Colin Smith, licensed via Creative Commons
Photo Credit: "Betty Ford's lemon yellow polka dot gown" by Wikimedia Commons, licensed via Public Domain

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by Yael Schenker, MD, MAS

Case:
A 58-year old man receives a left ventricular assist device (LVAD) for chronic end-stage heart failure in 2010. His LVAD is initially placed as a bridge to transplant. However his post-operative course is complicated by persistent chronic infection, multiple embolic strokes and prolonged hospitalization. He is taken off the transplant list. In 2012 he is readmitted to the hospital from a long-term acute care facility for aortic valvuloplasty and LVAD weaning studies. This hospitalization is complicated by a hematoma causing nerve compression in his right leg and he is no longer able to walk. He tells the cardiothoracic surgery team that he wants his LVAD to be turned off and the team calls a palliative care consult.

Discussion:
The left ventricular assist device (LVAD) was initially designed as a bridge to heart transplant. Open-heart surgery is required to implant an LVAD, which is attached to the left ventricle and the aorta in parallel with the patient’s native cardiovascular system. A small pump is placed in the patient’s abdominal cavity and connected to external battery controlled system that can be worn over or under clothing. (1)

In 2003, the LVAD was approved as destination therapy (LVAD-DT) for patients with chronic end-stage heart failure who are not candidates for a heart transplant. This decision arose from a prospective randomized controlled trial conducted between 1998 and 2001 comparing LVAD-DT to optimal medical management (OMM) for chronic endstage heart failure, in which patients receiving LVADDT showed improved survival over patient receiving OMM at 1-year (52% vs. 25%, p = 0.002) and 2-years (23% vs. 8%, p = 0.09). (2) Improved survival rates with LVADs are coupled with frequent and disabling complications including serious infections and strokes. (1)

Increasing numbers of patients living longer with LVADs has led to growing recognition of an important role for palliative care that may begin before implantation of an LVAD and continue through the end of life. (3) A palliative care clinician may be asked to assess whether LVAD implantation is consistent with a patient’s goals and/or to assist with a transition to comfort-oriented treatment if the decision is made not to implant a device. Palliative care clinicians may help patients and families to complete advance directives that name a surrogate decision maker and describe the circumstances under which withdrawal of the LVAD device would be desired. Palliative care clinicians may also help to assess physical, psychological and spiritual needs that arise with LVAD use and refer patients and families to appropriate resources. Transitions in care, such as the determination that a patient with an LVAD is no longer a candidate for heart transplant, are important opportunities for palliative care clinicians to acknowledge emotions and provide support. A recent article by Goldstein et al provides sample communication techniques for each of these time points. (3)

Most commonly, palliative care clinicians are called to assist with the decision about whether to discontinue a LVAD, as occurred in this case of the month. At this advanced disease stage, not all patients will be able to communicate or have capacity to make decisions. However, conversations should include patients if they are able to participate and want to be involved. A first step is to assess what the patient and/or family understand about heart failure and the LVAD. Opening with a simple question such as “tell me what you understand about your disease” or “tell me what the doctors have talked with you about so far” can offer significant insights.

Clinicians should follow up by asking what the patient and/or family want to know before offering additional information or clarifying misperceptions. The next step is to talk about overall goals of care. “Help me to understand what is important to you” is a good question to initiate this discussion. In this case, the patient described an acceptable quality of life as being able to walk and live independently. Once the patient’s goals have been articulated, the physician can help to develop a treatment plan that matches the patient’s values. (3) In this case, after multiple discussions, the patient made it clear that the burdens of the LVAD now outweighed its benefits for this patient.

Ethical guidelines and legal precedents support a patient’s right to request the withdrawal of any medical intervention, regardless of whether the patient is terminally ill and regardless of whether the intervention prolongs life. (4) If a patient lacks capacity, these rights extend to the appropriate surrogate decision maker. No ethical or legal distinction is made between different types of life-prolonging interventions (i.e., LVADs vs. feeding tubes vs. hemodialysis). Some clinicians have moral objections to turning off an LVAD. In such cases, the clinician should inform the patient of these objections without imposing his or her personal beliefs and help to find a colleague who can fulfill this role.

Turning off an LVAD requires a coordinated effort between physicians and nurses. The palliative care team can be helpful in answering questions and providing support for clinical staff as well as the patient and family. Most often when a LVAD is turned off the patient dies within minutes. However, if there is intrinsic heart function the patient may live for several days. Patients and families should be prepared for these outcomes. Medications such as opioids and benzodiazepines are used to ensure that the patient is comfortable. Premedication is important because most patients will have a significant decrease in cardiac output after the device is turned off.

Resolution:
The LVAD was turned off at the patient’s bedside. Morphine was given by both bolus and infusion to help control symptoms of dyspnea after the LVAD was turned off. He died comfortably approximately 48 hours later.

References:
1. Rizzieri AG, Verheijde JL, Rady MY, McGregor JL. Ethical challenges with the leftventricular assist device as a destinationtherapy. Philos Ethics Humanit Med. 2008;3:20. (OPEN ACCESS PDF)

2. Rose EA, Gelijns AC, Moskowitz AJ, Heitjan DF, Stevenson LW, Dembitsky W, et al. Long term use of a left ventricular assist device forend-stage heart failure. N Engl J Med. 2001;345(20):1435-43. (OPEN ACCESS PDF)

3. Goldstein NE, May CW, Meier DE. Comprehensive care for mechanical circulatorysupport: a new frontier for synergy withpalliative care. Circ Heart Fail. 2011;4(4):519- 27. (OPEN ACCESS PDF)

4. Lampert R, Hayes DL, Annas GJ, Farley MA, Goldstein NE, Hamilton RM, et al. HRS ExpertConsensus Statement on the Management ofCardiovascular Implantable Electronic Devices(CIEDs) in patients nearing end of life orrequesting withdrawal of therapy. Heart Rhythm. 2010;7(7):1008-26.


Pallimed Case Conference Disclaimer: This post is not intended to substitute good individualized clinical judgement or replace a physician-patient relationship. It is published as a means to illustrate important teaching points in healthcare. Patient details may have been changed by Pallimed editors to help with anonymity. Links and minor edits are made for clarity and Pallimed editorial standards.

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by Dr. Katherine Sleeman

On Tuesday 17th March from 3-4pm UK time (9-10am Central Standard Time) we will be holding the monthly Twitter Journal Club for hospice and palliative medicine: #hpmjc. The aim of the journal club is to provide an informal multidisciplinary forum for discussion of research findings, and we hope you will join us.

You can find some more information about the #hpmjc journal club here.

The paper for discussion this month is ‘High-flow oxygen and bilevel positive airway pressure for persistent dyspnea in patients with advanced cancer: a phase II randomized trial’. The paper was published in October 2013 in The Journal of Pain and Symptom Management, and is open access .

Lead author of the paper, Dr David Hui (@DrDavidHui) will lead this month’s journal club, and will be available to answer your questions on his study. Dr Hui is an assistant professor at the Department of Palliative Care & Rehabilitation Medicine and the Department of General Oncology, The University of Texas MD Anderson Cancer Center. His research interests include symptom management clinical trials, research methodology, prognostication, and integration of supportive/palliative care into oncology.

Background?

Breathlessness is one of the most distressing symptoms in cancer patients. Many patients continue to experience refractory breathlessness despite treatment with opioids, steroids and low flow supplemental oxygen. Novel strategies are needed to address this symptom.
This paper reports a randomised crossover trial of high flow oxygen and non-invasive ventilation. High flow oxygen is a novel gas delivery device that can deliver up to 40 L/min of humidified oxygen via nasal cannula. Bilevel positive airway pressure (BiPAP) provides not only oxygenation but also ventilation and thus respiratory muscle support.

What did the study find?

Among the 30 patients randomized, 13 completed 2 hours of HFO and 10 patients completed 2 hours of BiPAP. The total completion rate was 77%. In a before and after comparison, patients reported improvement in their breathlessness with high flow oxygen (mean change in numeric rating scale 1.9; P=0.02; mean change in modified Borg scale 2.1, P=0.007) and with BiPAP (mean change in numeric rating scale 3.2; P=0.004; mean change in modified Borg scale 1.5, P=0.13). Some physiologic parameters improved. No significant adverse effects were observed.

Questions for discussion:

• Do you have experience using high flow oxygen?
• What do you think about the study findings?
• What are the mechanisms in terms of how high flow oxygen and BiPAP relieve breathlessness?
• Is it ethical to provide non-invasive ventilation in the palliative care setting?
• What are some advantages and disadvantages of crossover designs?
• What are the implications of this research for your practice?

We look forward to discussing this on 17th March, and hope that you can join us. Just follow @hpmjc and use #hpmjc

Archive of past #hpmjc can be found here.

Katherine Sleeman is a clinician and academic in palliative medicine, Cicely Saunders Institute, King’s College London.

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by Eric Widera, MD

In 2013, there were 43.8 million prescriptions for tramadol filled in the U.S. It has a slightly different method of action from many other pain medications, as tramadol is both a mu-opioid receptors agonist and a reuptake inhibitor of serotonin and norepinephrine. It is also thought that the opioid activity is due to both the parent compound and the more active O-desmethylated metabolite (which, like codeine is metabolized by CYP 2D6 and therefore gives the same big inter-individual differences in pharmacokinetics).

The overall efficacy as a pain medicine is comparable to that of other weak opioids. Most people know it is associated with serotonin syndrome as well as seizures especially when used with other medications that lower seizure threshold. A new study that came out in JAMA IM reveals a pretty robust association between tramadol use and hospitalizations for hypoglycemia, even in those without diabetes.

The Study

The authors of this study put together a large population-based cohort of patients from the UK who were either initiating tramadol or codeine therapy for non-cancer pain. They excluded those who were prescribed other opioids, as well as those with cancer and those previously hospitalized for hypoglycemia in the year before entry into the study.

The authors also did a whole bunch of different types of analysis to prove their point (nested case-control, cohort and case-crossover analyses) that would take me five blog posts to write about (if you are interested in the details, here is the article). They also controlled for a boatload (yes that is a technical term that I’m using) of potential confounders.

The Results

The analysis included 334,034 patients (28,110 taking tramadol and 305,924 taking codeine). Tramadol and codeine users were similar on nearly all baseline potential confounders. The authors found in this cohort:

• Tramadol use increased by more than 8 from 1999 to 2011
• Patients taking tramadol had a significantly higher risk of hospitalization for hypoglycemia (odds ratio 1.52)
• The risk of hospitalization for hypoglycemia was highest in the first 30 days of use (OR, 2.61) Patients NOT on a diabetic medication were at increased risk of developing hypoglycemia severe enough to be hospitalized compared to those those taking diabetic medications (adjusted odds ratio of 2.12 vs 1.11)

The Take Home Point

A lot of health care providers have the misconception that tramadol is a safer alternative to more traditional opioids like morphine. This study adds further evidence that this is just not true, and that we should add hypoglycemia as a risk, even in patients who do not have diabetes.

Eric Widera, MD is co-founder of GeriPal and fellowship director at UCSF. We are happy to have him post on Pallimed for the second of 3 posts owed to Pallimed from GeriPal for the World Series of Blogs wager of 2014.


Fournier JP, Azoulay L, Yin H, Montastruc JL, Suissa S (2014). Tramadol Use and the Risk of Hospitalization for Hypoglycemia in Patients With Noncancer Pain. JAMA Internal Medicine PMID: 25485799 (OPEN ACCESS!)

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It started with a Tweet. Back in October 2013, my Twitter friend and palliative care colleague Becky Baines tweeted from the Help the Hospices conference in the UK:

@Becbaines how about a twitter journal club for palliative care? Would there be enough people? #hospiceconf
— Katherine Sleeman (@kesleeman) October 22, 2013

I am happy to report: there were.

Four months and several emails and tweets later, #hpmJC was born on the 25th February 2014. For our first journal club, we chose this BMJ paper¹ on the safety of opioids and benzodiazepines in advanced COPD. Over thirty global participants (including palliative care and respiratory medicine specialists, research scientists, and data experts) from at least 3 continents contributed to the debate at #hpmJC, posting more than 200 tweets over the course of an hour.

As the chair of the inaugural #hpmJC, I was amazed by the enthusiasm, the depth of discussion, and the unexpected tangents that led from the main discussion. It was exhausting trying to keep track of all the threads but incredibly fun and rewarding.

We want #hpmJC to be of interest to #hpm practitioners and researcher globally. Therefore we will have a ‘pass the baton’ format for the chair and we are excited by the thought that the baton will be passed far and wide, with the times of #hpmJC varying accordingly. We only suggest that the paper discussed should be open access, and ideally it should be applicable not just to specialists in palliative care, but have messages for generalists delivering end of life care too.

All of the articles we have discussed so far as listed below.  Some higlights from past #hpmJC include: the Palliative Medicine paper² on the imminence of death amongst hospital inpatients. The study, carried out in 25 Scottish Hospitals, showed that almost 30% of hospital inpatients died during the subsequent year, and highlighted the need for end of life care in the acute hospital setting to be ‘everybody’s business’. The paper generated a huge amount of media interest, and we are thrilled that the first author of the paper, Prof David Clark (@dumfriesshire), joined us for the journal club. He has also written a blog about the paper here³. So, you never know if you join us to hear more about important research, you may get the rare opportunity to question the author directly.

Hope to see you at #hpmJC! The next one is scheduled for Nov 17th 7am NYC, 12n London, 11pm SYD on Identifying changes in the support networks of end-of-life carers using social network analysis!

Katherine Sleeman, BSc, MBBS, MRCP, PhD
Clinician and academic in palliative medicine, Cicely Saunders Institute, King’s College London

Follow @kesleeman
Follow @hpmjc
Tweet #hpmJC

1 http://www.bmj.com/content/348/bmj.g445.pdf%2Bhtml
2 http://pmj.sagepub.com/content/early/2014/03/17/0269216314526443.full.pdf+html
3 http://endoflifestudies.academicblogs.co.uk/how-many-people-in-hospital-today-will-die-within-a-year/

#hpmJC Events so far:

25th Feb led by Katherine Sleeman Follow @kesleeman
Safety of benzodiazepines and opioids in very severe respiratory disease: national prospective study http://www.bmj.com/content/348/bmj.g445

17th March led by Catherine Walshe Follow @cewalshe
Associations between palliative chemotherapy and adult cancer patients’ end of life care and place of death: prospective cohort study http://www.bmj.com/content/348/bmj.g1219.full.pdf+html

4th April led by Sarah Russell Follow @learnhospice (paper was made open access by Pallaitive Medicine for the journal club, and lead author @dumfriesshire joined in too Follow @dumfriesshire )
Imminence of death among hospital inpatients: Prevalent cohort study http://pmj.sagepub.com/content/28/6/474.long

5th May led by Elissa Campbell Follow @elissa_campbell
Interventions to encourage discussion of end-of-life preferences between members of the general population and the people closest to them - a systematic literature review http://www.biomedcentral.com/1472-684X/12/40

9th June led by Catherine Walshe Follow @cewalshe
Patients’, family caregivers’, and professionals’ perspectives on quality of palliative care: A qualitative study http://m.pmj.sagepub.com/content/early/2014/05/09/0269216314532154.abstract

29th September led by Ollie Minton Follow @drol007 (Pallimed post by Ollie Minton on this Journal Club)
Diagnosing dying: an integrative literature review http://spcare.bmj.com/content/4/3/263.full.pdf

17th November led by Libby Sallnow Follow @libby_sallnow and Publich Health and Palliative Care Intl Follow @PHP_care  - Facebook Event Reminder
Identifying changes in the support networks of end-of-life carers using social network analysis http://m.spcare.bmj.com/content/early/2013/11/19/bmjspcare-2012-000257.full?g=w_spcare_open_tab&fb_source=message

Image Credit: Animal Stock Photo

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by Ollie Minton Follow @drol007

Having come to the end of a medical education certificate I now know the value of reflection to consolidate the learning. However in the chaos of the real world and work and other things weeks go by without any chance to do so. One of the reasons I like using Twitter so much is the speed at which it moves and the diversity but it does not give you a chance to delve more deeply into any given theme. I am however committed and passionate about what I do as a consultant in palliative medicine both clinically, academically (when the chance arises) and through teaching (part of my day job).

I had the pleasure of being asked to host the September palliative medicine journal club (@hpmjc) run by Katherine Sleeman (@kesleeman) of the Cicely Saunders Institute London UK (@CSI_KCL). On this occasion, we had hijacked the very well established #hpmglobal slot hosted by Jim Cleary (@jfclearywisc). Despite printing off and yes actually reading in depth my chosen paper "Diagnosing Dying - an integrative literature review" – open access so everyone could read the full text – I felt suitably under-prepared.

"Piled Higher and Deeper" by Jorge Cham www.phdcomics.com

I had organised my day and ward round to be able to do this but knew I was relying on a National Health Service computer (not the most up to date in the world) and was denied access to Tweetdeck or any other service that would screen and automatically hashtag my tweets. My efforts to produce multiple drafts had also been defeated by a recent twitter software upgrade. Nevertheless I felt I could be in charge for the hour (or at least direct the flow).

I was really pleased to see the global nature of the chat rapidly develop. There were inputs from people I followed and know in real life but also so many others I could not have predicted from across the world. In addition, there were also contributions from relatives and patient groups.

The discussion focused on the complicated areas of diagnosing dying and highlighted some cultural differences. We all agreed on the more active dying phase but it was the preceding areas that were trickier to judge. There was no overall agreement other than the need to educate other professionals on illness trajectory, communicate clearly with everyone involved and acknowledge uncertainty. While we as palliative care professionals are familiar with that – involving others may not be straightforward. I think we all felt that the review did not offer specific guidance on how to move forward.

Afterwards I was exhausted – the level of concentration required, not being face to face and avoiding the temptation to be too school-master like - not that I had any tools to use beyond the obvious. While perhaps not surprisingly more questions than answers were generated and the ubiquitous “more research is needed” formed a part of the conclusions it was a great discussion. I felt the best conclusion I could ask for was in this tweet:

@drol007 Thanks for v interesting #Hpmjc with #Hpmglobal. input from Uk, USA, Australia, KSA, Rwanda, Burundi, Turkey. Did I miss others?
— jim cleary (@jfclearywisc) September 29, 2014

A complete summary of our chat is here hosted by Symplur.

No doubt there is another journal club planned –  "Identifying changes in the support networks of end-of-life carers using social network analysis." on Monday November 17th 12n GMT; 11p SYD; 7a NYC -  I will be taking part. I am just glad that is all I will be doing….

Dr Ollie Minton, PhD, FRCP is a locum consultant and honorary senior lecturer in palliative medicine. Outnumbered 3:1 by ladies at home and by a worse ratio at work I survive as a consultant in palliative medicine research cancer, survivorship, and fatigue

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Twitter accounts mentioned:
Follow @hpmjc
Follow @drol007
Follow @CSI_KCL
Follow @jfclearywisc
Follow @kesleeman
Tweet #hpmglobal

Image credit: Jorge Cham Reprinted with permission All rights reserved 

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Case:
Ms. Turner* is a 29-year-old woman with recently diagnosed ovarian cancer discovered after presenting to the ED with worsening abdominal pain. CT imaging showed a 4.8cm cystic mass extending from her right ovary, and the surgical pathology revealed ovarian adenocarcinoma. Two weeks post-operatively, she was hospitalized for initiation of chemotherapy, and the palliative care service was consulted for symptom management. Despite having received treatment with ondansetron (Zofran®), aprepitant (Emend®), dexamethasone (Decadron®), lorazepam (Ativan®), and haloperidol (Haldol®), she developed significant nausea and vomiting on the first day of chemotherapy infusion with symptoms worsening on her second day of chemotherapy. She described feeling utterly miserable and fearful about her next chemotherapy infusion, and she was continuing to experience nausea and repeated episodes of emesis overnight with minimal oral intake. Ms. Turner also described an underlying history of anxiety disorder predating her cancer diagnosis. At home she typically smoked marijuana on a daily basis to help manage her anxiety symptoms, which she reported did not interfere with her successful function at work and school. On review of systems, she noted abdominal discomfort for which she was taking low dose oxycodone and that she had not moved her bowels for several days.
Discussion:
Nausea and vomiting (NV) are commonly reported side effects with chemotherapy.¹ The primary pathway for NV involves the chemotherapy drugs directly stimulating the chemoreceptor trigger zone (CTZ), in the area postrema at the base of the fourth ventricle. Activated receptors in the CTZ transmit signals to the vomiting center in the brainstem to produce NV. Receptors in the CTZ include serotonergic receptor 5-hydroxytryptamine type 3 (5-HT3), dopaminergic (D2) and neurokinin type 1 (NK-1) receptors. In addition, chemotherapy can damage GI mucosa causing local release of 5-HT3 neurotransmitters by gut enterochromaffin cells, activating peripheral pathways along the vagus and splanchnic nerves and directly triggering the vomiting center. Finally, chemotherapy-associated anxiety may also stimulate the vomiting center through central cortical pathways. Whether transmitted via signals from the CTZ, the cortex, or peripheral inputs, the vomiting center has several different receptors involved in initiating the vomiting reflex: muscarinic acetylcholine (Achm), histamine type 1 (H1), and 5-hydroxytrypamine type 2 (5-HT2).¹

Given the pathways for chemotherapy-induced nausea and vomiting described above, 5-HT3 and NK-1 receptor antagonists such as ondansetron and aprepitant, in combination with dopamine antagonists such as haloperidol, are typically effective for treatment of NV. In some cases, however, patients may develop breakthrough nausea and vomiting despite adequate standard therapy requiring additional or alternative anti-emetic medications. According to guidelines from the American Society of Clinical Oncology and the National Comprehensive Cancer Network, there are several categories of second-line agents that may be useful in refractory cases.^2,3

The cannabinoids dronabinol (Marinol®) and nabilone (Cesamet®) are both FDA approved for refractory chemotherapy-induced nausea and vomiting.⁴ Unlike other anti-emetic medications which block receptor activity for their therapeutic effect, cannabinoid effect is exerted by agonist activity on the cannabinoid receptor in the brain CB1.⁵ Dronabinol is a Schedule 3 synthetic THC (delta-9 tetrahydrocannabinoid). Starting dose is typically 5mg 2 hours prior to chemotherapy and every 4 hours as needed, with a maximum dose of 15mg. Nabilone is a Schedule 2 drug with longer onset and duration of action, and is dosed 1-2 mg twice or three times daily as needed. Studies demonstrate that dronabinol and nabilone are effective for treatment of nausea and vomiting; however, their use is limited by their side effect profile including vertigo, xerostomia, hypotension, dysphoria, and hallucinations.^4,5

Olanzapine (Zyprexa®) is an atypical antipsychotic which antagonizes multiple neurotransmitters including dopamine at D1, D2, D3 and D4 brain receptors; acetylcholine at muscarinic receptors; serotonin at 5-HT2, 5-HT3, and 5-HT6 receptors; catecholamines at alpha-1 adrenergic receptors; and histamine at H1 receptors.⁶ Several studies have demonstrated its utility for treating chemotherapy-induced nausea and vomiting.⁶ No studies have specifically compared it to haloperidol or other atypical anti-psychotics for treatment of nausea, although several authors have argued that it is the multiplicity of olanzapine’s receptor activity which contributes to its effectiveness. The recommended dosing is 5mg orally daily starting 1-2 days before chemotherapy, then 5-10mg daily for days 1-4 of chemotherapy. Side effects include sedation, dry mouth, increased appetite, hyperglycemia and postural hypotension.^2,3

Metoclopramide (Reglan®) has central and peripheral anti-dopaminergic activity, and at high doses also exerts 5-HT3 antagonist effect which is thought to contribute to its anti-emetic effect.1,2 Because of its low therapeutic index, metoclopramide is typically reserved for patients who are intolerant or refractory to first line anti-serotonergic agents. Dosing is 10-40 mg IV 30 minutes prior to chemotherapy, then every 4 to 6 hours as needed.³ An alternate dosing strategy is 1-2 mg/kg 30 minutes before chemotherapy and then repeated 2 hours after chemotherapy for 2 doses, and then every 3 hours for 3 doses. Side effects include dystonia, akathisia, sedation, and esophageal spasm. Pretreatment with diphenhydramine (Benadryl®) will decrease risk of extrapyramidal reactions.²

Benzodiazepines are most useful in cases of anticipatory NV, which is thought to be a conditioned reflex as a result of prior poor control of emesis during chemotherapy treatment.³ The phenomenon involves the development of NV when a sensory stimulus (ie, the sights, sounds, or smells of chemotherapy clinic) becomes paired with the experience of symptomatic chemotherapy treatment. After a conditioning period (ie, repeated chemotherapy infusions in clinic), the sensory stimulus or anxiety from negative anticipation may trigger NV before the patient has even received the chemotherapy infusion.⁷ The mechanism involves signals along intracerebral projections in the cortex directly stimulating the vomiting center. Older studies had described the phenomenon in up to 25% of patients with poorly controlled symptoms by the fourth treatment cycle; however, the frequency appears to have decreased with the advent of more effective anti-emetic regimens. Patients with refractory NV are at higher risk of developing anticipatory NV. The intermediate-acting benzodiazepine lorazepam is helpful for treatment of anticipatory NV and as an adjunct in cases of refractory NV, with starting doses of 0.5-1mg oral or IV, and up to 2mg, every 6-8 hours as needed for anxiety and nausea.⁷

Resolution of the Case:
Based on her symptoms and previous history, Ms. Turner was started on dronabinol 5mg three times daily during her chemotherapy treatment while in the hospital, along with the scheduled ondansetron and haloperidol. A bowel regimen of senna (Senekot®) and polyethylene glycol 3350 (Miralax®) was also initiated, as opioid-induced constipation was likely contributing to her symptoms. Within 24 hours, she had resolution of emesis and improvement of her nausea, enabling her to resume oral intake.

Summary:
While standard anti-emetic therapies with 5-HT3 and dopamine antagonists are effective and well-tolerated in most cases of chemotherapy-induced nausea and vomiting, occasionally refractory symptoms necessitate addition of a second-line agent such as a cannabinoid, olanzapine, or metoclopramide. Patient characteristics such as age, previous experience with cannabinoids, and medical comorbidities will impact the choice of second-line agent. Dronabinol or nabilone may be most effective in younger patients and those with previous experience of tolerating cannabinoids. Olanzapine is preferable in elderly patients or populations for whom there may be a concern about the psychoactive properties of cannabinoids. Substitution of high dose IV metoclopramide for other dopaminergic and 5-HT3 medications could also be helpful in certain cases, especially if there are additional concerns about GI dysmotility or intolerance to standard 5-HT3 agents.

References:
1. Wood G, Shega J, Lynch B, Von Roenn J. Management of Intractable Nausea and Vomiting in Patients at the End of Life. JAMA 2007; 298(10): 1196-1207.
2. Basch E, Prestrud AA, Hesketh PJ. Antiemetics: American Society of Clinical Oncology clinical practice guideline update. J Clin Oncol 2011; 29:4189. Open Access PDF
3. Hesketh PJ. Chemotherapy-Induced Nausea and Vomiting. N Engl J Med 2008; 358(23):2482-94.
4. Wilner LS, Arnold R. Cannabinoids in the Treatment of Symptoms in Cancer and AIDS, 2nd edition. Fast Facts and Concepts. December 2007; 93.
5. Todaro B. Cannabinoids in the Treatment of Chemotherapy-Induced Nausea. J Natl Compr Canc Netw 2012; 10:487-492.
6. Nizukami N, Yamauchi M. Olanzapine for the Prevention of Chemotherapy-Induced Nausea and Vomiting in Patients Receiving Highly or Moderately Emetogenic Chemotherapy: A Randomized, Double-Blind, Placebo-Controlled Study. Journal of Pain and Symptom Management March 2014; 47 (3)542-550.
7. Roscoe J, Morrow G. Anticipatory Nausea and Vomiting. Support Care Cancer Oct 2011; 19 (10): 1533-1538. Open Access PDF


Pallimed Case Conference Disclaimer: This post is not intended to substitute good individualized clinical judgement or replace a physician-patient relationship. It is published as a means to illustrate important teaching points in healthcare. Patient details have been changed by Pallimed editors to help with anonymity. Links and small edits are made for clarity and to abide by Pallimed editorial standards.