Welcome, to all new and returning Acute and Critical Care SIG members! We had a very nice meeting at the ONS Congress this year and met some dynamic members. If you attended and haven't received an e-mail from me, please contact me so I can follow up with everyone. Please stop by our meeting at next year's ONS Congress in San Antonio, TX.

If you wish to ask a question, make a comment, reply to a
question, etc., please go to our Discussion Forum on the SIG virtual community. We would like to see far more posts but are happy for the ones that we do get. This is a place where you can get some of your questions answered, so take advantage of it! Please click here to visit our virtual community, and then click on Discussion at the top right of the page.

I will be the Chairman of the SIG Leadership Council in 2009, so feel free to contact me even after Patti Woods, RN, OCN^®, takes over as SIG Coordinator at the ONS Congress in 2009. Because I still will be involved with the ONS leadership, I can pass your ideas along. You can reach me directly at cyndi@RealNurseEd.com.

The Acute and Critical Care SIG has offered multiple presentations at ONS conferences that we hope are of interest to our members. In Philadelphia, PA, we did a presentation on structural oncology emergencies. I hope some of you were able to attend.

We are very excited that we will be presenting a full day pre-Congress session at the 2009 ONS Congress called "Oncology Emergencies: A Case Based Approach." We think this is an important topic for our members and have wanted to be able to do this for quite some time. I will be presenting along with three other members, including Brenda Shelton, RN, MS, CCRN, AOCN^®, Cathy Sargent, MS, RN, BC, AOCN^®, and Linda Johnson, RN, OCN^®. Come up and introduce yourself if you are able to attend!

I want to stress that this SIG is all about you! But, we need your feedback so we can try to meet your needs. Please let me know if we could do anything for you that we are not accomplishing. We are a small leadership group, which limits some of what we can offer you, but that means  limitless opportunities exist for you to get involved!

If you would like to write an article for the newsletter, join our Discussion Forum, submit a topic (presentation or poster) for an ONS conference sponsored by the SIG, share your ideas with the leadership, run for coordinator, etc., the opportunities exist, and we warmly welcome you!

Article Review
Pulmonary Complications of Novel Antineoplastic Agents in Solid Tumors

Brenda K. Shelton, MS, RN, CCRN, AOCN^®
Finksburg, MD
sheltbr@jhmi.edu

Vahid, B., & Marik, P.E. (2008). Pulmonary complications of novel antineoplastic agents in solid tumors. Chest, 133(2), 528–538.

Pulmonary toxicities of antineoplastic therapies, while rare, are significant etiologies of respiratory failure in the patient with cancer. Newer therapies that inhibit tyrosine kinase or older agents such as thalidomide with more widespread use are bringing awareness of newer and unique pulmonary toxicities to the forefront. Because many patients who develop pulmonary drug toxicities have risk factors for other pulmonary complications such as pneumonia, pulmonary embolism, cardiogenic pulmonary edema, alveolar hemorrhage, and graft versus host disease, it becomes essential for specialty clinicians to recognize risk factors and diagnostic tests necessary to identify pulmonary toxicities. This article targets critical care clinicians who care for patients with cancer. It emphasizes the importance of early consideration and diagnostic evaluation for drug toxicity. The discontinuation of potential causitive chemotherapeutic agents and treatment with high-dose systemic corticosteroids may result in improved outcomes for these patients.
This article provides the reader with an overview of the different clinical findings of anti-neoplastic therapy-induced pulmonary toxicity and a comprehensive description of the findings associated with newer agents such as bevacizumab, imatinib, and oxaliplatin. A summary of a few of these key findings are listed in Table 1.

Although each agent creates a unique profile of pulmonary and systemic symptoms, the authors recommend a logical process for assessment of patients. This is summarized in the literature review in Figure 1.

Figure 1

Clinical symptoms—fever, cough, hypoxemia, pulmonary infiltrates on chest x-ray

Consider risk factors for common pulmonary disorders—infection, pulmonary edema, alveolar hemorrhage, chemotherapy-induced pulmonary toxicity

Symptoms and temporal relationship to administration of a pulmonary toxic chemotherapy agent—

• Chest CT scan shows diffuse or patchy unilateral or bilateral, ground-glass or consolidated pulmonary infiltrates
• Pulmonary function tests—Decreases in the following tests
  • Forced vital capacity [FVC],
  • Forced expiratory volume in 1 minute [FEV1], and Diffusing lung capacity for Carbon monoxide (DLCO)

Check complete blood count with total and differential of white blood cells.

Continued suspicion—check nonspecific indicators of inflammation (e.g., erythrocyte sedimentation rate (ESR), C-reactive protein, rule out cardiogenic pulmonary edema with an echocardiogram
Consider bronchoalveolar lavage for elevated neutrophils, lymphocytosis, eosinophilia. Check for hemosiderin-laden macrophages indicative of alveolar hemorrhage, and culture for common infecting organisms.

• Check BAL fluid cytology for malignant infiltration
• Serum levels of  Krebs von den Lunge-6 (KL-6) > 500 units/mL have been found with some types of drug toxicity and are rarely found with bacterial or fungal pneumonia, chronic lung disease, or pulmonary embolism

Pulmonary Toxicity of Cyclophosphamide

Brenda K. Shelton, MS, RN, CCRN, AOCN^®
Finksburg, MD
sheltbr@jhmi.edu

Cyclophosphamide (Cytoxan) is a significant antineoplastic agent used to treat a variety of cancers and autoimmune disorders. The difficulty in diagnosing and treating pulmonary toxicity related to cyclophosphamide largely comes from the presence of other potential etiologies, such as other infectious diseases, diffuse pulmonary malignancies, other medications, or oxygen toxicity (Malik, Myers, DeRemee, & Specks, 1996). Early management of pulmonary toxicities of this agent is paramount for best patient outcomes. This article provides a summary of information on pulmonary toxicity of cyclophosphamide.

The primary mechanism of pulmonary toxicity is thought to be related to accumulation of alkylating metabolites and acrolein (Patel, 1990). Acrolein produces microsomal lipid peroxidation normally cleared by pulmonary antioxidant defense mechanisms. When these metabolites accumulate they erode the lipid layer and cause microvascular damage (Patel, 1990; Specks, 2008).

Two distinct forms of cyclophosphamide pulmonary toxicity exist and are referred to as early onset or delayed onset. Early onset pulmonary toxicity occurring within the first 48 days (+/- 14 days) is characterized by alveolar hemorrhage and may occur idiosyncratically at any dose, although it has been reported most commonly when cyclophosphamide doses exceed approximately 16000 mg (roughly 200 mg/kg or 1800 mg/m2) (Hamada, Nagal, Kitaichi, et al., 2003; Patel, 1990; Specks, 2008). Hyperoxic lung conditions such as are found with poor oxygen extraction (methemoglobinemia, lactic acidosis), inadequate oxygen transport (lactic acidosis, anemia), or excess oxygen delivery with oxygen toxicity (paO2 > 160 mm Hg) are known to enhance this lipid layer destruction (Wikipedia, 2008). Oxygen toxic changes most often occur when exposure to inspired oxygen greater than 60% exceeds 16–18 hours (Wikipedia, 2008).

Chronic pulmonary changes involve progressive interstitial fibrosis with pleural thickening. This syndrome begins 15–18 weeks after exposure but also has been reported up to six years after discontinuation of the agent (Hamada, Nagai, Kitaichi, Jin, Shigermatsu, Nagao, et al., 2003). This disorder is progressive, occurs over several months to years, and is pathologically different than other drug-induced interstitial lung diseases (Specks, 2008). In cyclophosphamide fibrosis, crackles are lacking and nodular opacities do not have the bibasilar distribution usually seen with drug-induced fibrosis (Specks, 2008). In evaluation of potential cofactors exacerbating cyclophosphamide pulmonary toxicity, a lack of evidence exists associating it with tobacco use, age, or baseline pulmonary function (Fassas, Gojo, Rapaport, Cottler-Fox, Meisenberg, Papadimitriou, & Tricot, 2001).

A single case of pulmonary toxicity has been reported after one dose of cyclophosphamide (Gupta, 2007) in a patient who also had received long-term amiodarone, a known etiology of pulmonary fibrosis. Use of methotrexate and the presence of chronic graft versus host disease also have been associated with increased incidence of pulmonary toxicity (Hamada et al., 2003).

The most common presenting symptoms of cyclophosphamide-induced pulmonary toxicity are dyspnea, cough, and fever (Hamada et al., 2003; Malik et al., 1996; Wikipedia, 2008). Substernal pain also has been reported (Wikipedia, 2008). One clinical change in pulmonary function tests that has proven significantly predictive for cyclophosphamide pulmonary toxicity is reduction of the diffusing lung capacity for carbon monoxide (DLCO). The role of prior chemotherapy to incidence of pulmonary toxicity with cyclophosphamide is little studied but a reasonable concern to clinicians. In one study, patients with breast cancer treated previously with cyclophosphamide, adriamycin, and fluorouracil (CAF) prior to HSCT showed a 12.6% decrease in DLCO for every chemotherapy cycle after the third. (Bhalla, Wilczynski, Abushamaa, Petros, McDonald, Loftis, et al., 2000). It is considered prudent practice to obtain baseline pulmonary function tests as a screening tool to determine transplant candidacy or choice of the preparative regimen. Open lung biopsy has not proven useful in diagnosis of cyclophosphamide pulmonary toxicity (Specks, 2008).

Early onset pneumonitis (one to four months after exposure) is usually reversible and responsive to corticosterids (Fassas et al., 2001; Specks, 2008). Delayed onset interstitial fibrosis with pleural thickening is less responsive to corticosteroids (Hamada et al., 2003).

References

Bhagat, R., Spor, T.A., Long, G.D., & Folz, R.J. (2001). Amiodarone and cyclophospamide: Potential for enhanced lung toxicity. Bone Marrow Transplantation, 27, 1109–1111.

Bhalla, K.S., Wilczynski, S.W., Abushamaa, A.M., Petros, W.P., McDonald, C.S., Loftis, J.S., et al. (2000). Pulmonary toxicity of induction chemotherapy prior to standard or high-dose chemotherapy prior to autologous hematopoietic support. American Journal of Respiratory Disease and Critical Care Medicine, 161(1), 17–25.

Fassas, A., Gojo, I., Rapaport, A., Cottler-Fox, M., Meisenberg, B., Papadimitriou, J.C., et al. (2001). Pulmonary toxicity syndrome following CDEP (cyclophosphamide, dexamethasone, etoposide, cisplatin) chemotherapy. Bone Marrow Transplantation, 28(4), 399–403.

Gupta, S., & Mahipal, A. (2007). Fatal pulmonary toxicity after a single dose of cyclophosphamide. Pharmocotherapy, 27(4), 616–618.

Hamada, K., Nagai, S., Kitaichi, M., Jin, G., Shigermatsu, M., Nagao, T., et. al. (2003). Cyclophosphamide-induced late-onset lung disease. Internal Medicine, 42(1), 82–87.

Kachel, D.L., & Martin, W.J. (1994). Cyclophosphamide-induced lung toxicity: Mechanism of endothelial cell injury. Pharmacology, 268(1), 42–46.
 
Malik, S.W., Myers, J.L., DeRemee, R.A., & Specks, U. (1996). Lung toxicity associated with cyclophosphamide use. Two distinct patterns. American Journal Respiratory and Critical Care Medicine, 154(6 pt 1), 1851–1856.

Patel, J.M. (1990). Metabolism and pulmonary toxicity of cyclophosphamide. Pharmacologic Therapy, 47(1), 137–146.

Segura, A., Yuste, A., Cercos, A., et al. (2001). Pulmonary fibrosis induced by cyclophosphamide. Annals of Pharmaotherapy, 35, 594–897.

Specks, U. (2008). Cyclophosphamide pulmonary toxicity. Up-to-Date. Retrieved July 26, 2008, from http://www.uptodate.com/patients/content/topic.do?topicKey=int_lung/24001

Wikipedia. (2008). Retrieved July 26, 2008, from http://en.wikipedia.org/wiki/Oxygen_toxicity

Wooley, I., Collett, J., & Goldstein, D. (2008). Diffuse alveolar damage following a single administration of cyclophosphamide containing chemotherapy regimen. Internal Medicine Journal, 27(5), 605–606.

Institutional Statistics and Support

Sherry Burrell, RN, MSN, CNE
Camden, NJ
sburrell14@comcast.net

Anne Delengowski, RN, MSN, AOCN^®
Philadelphia, PA
anne.delengowski@mail.tju.edu

Amy Callahan, MSN, RN, CNE, APRN, BC
Philadelphia, PA
Amy.Callahan@jeffersonhospital.org

Cindy Hanscome, RN
Philadelphia, PA
Cindy.Hansome@jeffersonhospital.org

In May of 2006, Thomas Jefferson University Hospital (TJUH) implemented a rapid response team (RRT). A RRT generally can be defined as a group of healthcare providers who bring critical care expertise to the bedside (or wherever it may be needed) to evaluate quickly and respond to changes in a patient’s condition before he or she goes into respiratory failure and/or cardiac arrest. Within minutes, the RRT joins the patient's nurse at the bedside in an attempt to reverse the patient's clinical instability. This proactive approach differs from the more reactive approach of the traditional code blue and emergency resuscitation team, which is called into action after patients’s hearts or lungs cease to function.

TJUH implemented a RRT in response to the current challenges in acute health care, such as the push to decrease length of hospital stays, the significant rise in levels of patient acuity, and the increasing complexity of medical treatments. These challenges result in a large number of patients being cared for in hospitals outside the critical care setting and whose condition may rapidly deteriorate. This especially is true for patients with cancer who often have co-morbid conditions and require multiple, concurrent treatment modalities to treat their cancer. In addition, patients with cancer require specialized nursing care to appropriately monitor and administer their complex cancer-fighting treatment regimens.  This results in physicians trying to keep these patients on specialized oncology nursing units as long as possible. TJUH sought to implement a hospital-wide RRT as a means to prevent “failure to rescue” situations; and moreover, to ensure good patient outcomes, despite these current challenges in the acute health care system.

At TJUH, the RRT consists of advanced cardiovascular life support (ACLS) trained healthcare professionals, which include a critical care nurse, a medical resident, a surgical resident, a pulmonary fellow, an anesthesiologist, and a respiratory therapist. All RRT members at TJUH have two-tier coverage allowing them to quickly respond to calls while still ensuring continuous care for their routine assignments. For example, the critical care nurse may have a client assignment, but the charge nurse for that particular unit would provide coverage during RRT calls. After first implementing the RRT in 2006, TJUH did not find a significant increase in workload for any of the RRT members and/or their colleagues; therefore, no additional staffing was indicated for continued RRT implementation. At TJUH, the total time required for RRT calls by team members, as measured by team member notification to return to their routine assignment, was on average 61 minutes. This includes time necessary to stabilize the patient, secure an appropriate bed, and transfer the patient.

TJUH’s RRT provides 24-hour coverage at this academic medical center with 957 inpatient beds. One RRT responds to all calls at TJUH based on a pre-established organization plan. The only variation in rapid response team members involves critical care nursing. The RRT’s critical care nurse is determined based on the patient’s clinical needs, which are broadly defined at TJUH as neonatal-pediatrics, obstetrics-gynecology, medical-respiratory, cardiac, general surgery, and neurology. Therefore, based on the clinical needs of the patient, the critical care nurse with the most expertise is simultaneously deployed to join the RRT physicians and respiratory therapist. For example, at TJUH, a patient with cancer requiring RRT intervention would benefit from the expertise of a critical care nurse from the medical-respiratory intensive care unit (MRICU).

All RRT calls at TJUH are fielded through a dedicated, high-priority, telephone line that is staffed by a trained hospital telephone operator. The TJUH telephone operator then notifies the RRT through designated rapid response beepers, which each member of the RRT wears at all times to ensure a prompt response to the patient’s needs. TJUH’s RRT response time, as measured by team member notification to team member arrival at the patient’s bedside, is on average 2.33 minutes.

The RRT responds to calls with the necessary equipment to handle any patient situation, such as respiratory equipment, emergency medications, a code (crash) cart, and proper RRT documentation forms. The RRT physicians take control of the patient’s medical care and have the authority to order laboratory and diagnostic tests, medications, and any other interventions needed to stabilize the patient.

TJUH established clinical criteria for activating the RRT (which is listed in the accompanying box). The goal was to establish tangible criteria for activating the RRT for TJUH staff members. These specific guidelines are intended to empower staff members to call the RRT at the first sign of a patient’s decline whether because of objective or subjective criteria. TJUH chose to include objective criteria such as respiratory rate, oxygen saturation levels, and heart rate as well as subjective criteria such as “being concerned about your patient,” which allows staff members  to use their intuition (or gut feelings) to activate the RRT despite the lack of objective symptoms. At TJUH, the registered nursing staff utilized the RRT most often by placing greater than 90% of all RRT calls.

All hospital staff members were provided education on the RRT prior to its formal implementation, which began with a RRT “welcome packet.” This packet described the purpose of the team, identified team members, explained criteria for activating the RRT, and most importantly, stated how to contact the RRT. RRT flyers were also posted throughout the hospital to ensure that all staff members could glance quickly at the activating criteria and have easy access to the RRT’s phone number. In addition, all hospital staff members currently are required to complete a yearly computer learning tutorial that includes proper utilization of the RRT as part of the curriculum.

During the TJUH calendar year of 2007, 444 RRT calls were made (days=175, evenings=152, and nights=117). The nursing unit that utilized the RRT most was the oncology unit, which placed 10% of all RRT calls. Although the patients’s medical diagnoses and co-morbid conditions varied, the most reoccurring reason documented for the RRT calls was indicators of “respiratory compromise,” which accounted for 255 of all RRT calls. Of the RRT calls for “respiratory compromise” indicators, 25% of these patients required subsequent intubation. Of the total 444 RRT calls, 77% of patients required a higher level of care (telemetry, step-down, or full intensive care); of which a majority of these patients (67%) required full intensive care. Overall, the patient survival rate post-RRT call was 73% at the time of discharge to home (or other sub-acute care facility).

The greatest barrier that occurred during the implementation of the RRT at TJUH was the lack of knowledge about the RRT by the medical staff. Many house staff physicians resisted calling RRT to intervene for their patients, as they thought they could handle the situation without RRT expertise. Although this knowledge barrier still exists, TJUH created a RRT educational program lead by the chief medical resident and a critical care clinical nurse specialist to teach the house staff about the RRT. Each week these physicians are required to attend a RRT educational program which utilizes TJUH’s state-of-the-art simulation laboratory. The RRT simulations allow the house staff to learn firsthand the importance of early intervention on clinical deterioration; and moreover, how critical care expertise positively influences patient outcomes.

Empowering nurses to utilize the RRT has not been a barrier to RRT utilization at TJUH. The TJUH nursing staff shared that they believe that calling the RRT is the most efficient way to get patients the care they need such as cardiac monitoring and safe medication administration (i.e., critical care drugs) or even getting a physician to the bedside in a timely manner when warranted. The best example of this was when the oncology unit nurses called the RRT 45 times last year. On each of these occasions the patient required a higher level of care.

While the use of RRT is still in its infancy across the United States, many hospitals have adopted this measure as a way to improve patient outcomes and prevent “failure to rescue” situations. Though the Implementation of a RRT at TJUH has had a few bumps along the way, it has done exactly what it was intended to do: to ensure good patient outcomes over the past two years. If you are interested in implementing a RRT at your institution, the Institute for Healthcare Improvement offers guidelines on the internet.

Membership Information

SIG Membership Benefits

• Network with colleagues in an identified subspecialty area around the country.
• Contribute articles for your SIG’s newsletter.
• Participate in discussions with other SIG members.
• Contribute to the future path of the SIG.
• Share your expertise.
• Support and/or mentor a colleague.
• Receive information about the latest advancements in treatments, clinical trials, etc.
• Participate in ONS leadership by running for SIG coordinator-elect or join SIG work groups.
• Acquire information with a click of a mouse at http://ons.org/membership including
• Educational opportunities for your subspecialty
• Education material on practice
• Calls to action
• News impacting or affecting your specific SIG
• Newsletters
• Communiqués
• Meeting minutes.

Join a Virtual Community

A great way to stay connected to your SIG is to join its Virtual Community. It’s easy to do so. All you will need to do is

• Log on to the ONS Web site (http://www.ons.org/).
• Select "Membership" from the tabs above.
• Then, click on "ONS Chapters and Special Interest Groups."
• Scroll down to "Visit the ONS Special Interest Groups (SIG) Virtual Community" and click.
• Now, select "Find a SIG."
• Locate and click on the name of your SIG from the list of all ONS SIGs displayed.
• Once the front page of your SIG’s Virtual Community appears on screen, select "New User" from the top left. (This allows you to create log-in credentials.)
• Type the required information into the text fields as prompted.
• Click "Join Group" (at the bottom right of the text fields) when done.
  
  Special Notices
  
  
• If you already have log-in credentials generated from the ONS Web site, use this information instead of attempting to generate new information.
• If you created log-in credentials for the ONS Web site and wish to have different log-in information, you will not be able to use the same e-mail address to generate your new credentials. Instead, use an alternate e-mail address.

Subscribe to Your SIG’s Virtual Community Discussion Forum
Once you have your log-in credentials, you are ready to subscribe to your SIG’s Virtual Community discussion forum. To do so,

• Select "Log In," located next to "New User," and enter your information.
• Next, click on the "Discussion" tab on the top right of the title bar.
• Locate and select "Subscribe to Discussion"
• Enter e-mail address.
• Click "Finish."
• You are now ready to begin participating in your SIG’s discussion forum.

Participate in Your SIG’s Virtual Community Discussion Forum

• First, log in. (This allows others to identify you and enables you to receive notification [via e-mail] each time a response or new topic is posted.)
• Click on "Discussion" from the top title bar.
• Click on any posted topic to view contents and post responses.

Sign Up to Receive Your SIG’s Virtual Community Announcements
As an added feature, members also are able to register to receive their SIG’s announcements by e-mail.

• From your SIG’s Virtual Community page, locate the "Sign Up Here to Receive Your SIG’s Announcements" section.
• Select the "Click Here" feature, which will take you to a link to subscribe.
• Once the "For Announcement Subscription Only" page appears select how you wish to receive your announcements.
• As individual e-mails each time a new announcement is posted
• One e-mail per day comprised of all new daily announcements posted
• Opt-out, indicating that you will frequently browse your SIG’s Virtual Community page for new postings
• Enter your e-mail address.
• Click on "Next Page."
• Click "Finish"
• You are now subscribed to receive announcements.

Know someone who would like to receive a print copy of this newsletter?
To print a copy of this newsletter from your home or office computer, click here or on the printer icon located on the SIG Newsletter front page. Print copies of each online SIG newsletter also are available through the ONS National Office. To have a copy mailed to you or another SIG member, contact Membership/Leadership Administrative Assistant Carol DeMarco at cdemarco@ons.org or 866-257-4ONS, ext. 6230.

To view past newsletters, click here.

ONS Membership/Leadership Team Contact Information

Angie Stengel, MS, CAE, Director of Membership/Leadership
astengel@ons.org
412-859-6244

Diane Scheuring, MBA, CAE, CMP, Manager of Member Services
dscheuring@ons.org
412-859-6256

Carol DeMarco, Membership/Leadership Administrative Assistant
cdemarco@ons.org
412-859-6230

The Oncology Nursing Society (ONS) does not assume responsibility for the opinions expressed and information provided by authors or by Special Interest Groups (SIGs). Acceptance of advertising or corporate support does not indicate or imply endorsement of the company or its products by ONS or the SIG. Web sites listed in the SIG newsletters are provided for information only. Hosts are responsible for their own content and availability.

Oncology Nursing Society
125 Enterprise Dr.
Pittsburgh, PA 15275-1214
866-257-4ONS
412-859-6100
www.ons.org