Contact hours awarded: 30
Step 1: Read and learn the course content.
2019 Comprehensive Nursing Update
This 30 hour course is a complication of 11 different topics. There is an evaluation at the end of the module (not after each individual section). Please refer to the above instructions if you have any difficulty proceeding.
1.Issues Faced By Modern Day Nurses
Nurses have been treating patients for as long as illness has been afflicting humans. The history of nursing is a long and at times, difficult story that most of us can sympathize deeply with. What other profession has both relieved the burden of disease while also carrying a portion of the burden themselves? Every nurse knows that bond forged between a patient and nurse is sacred and highly unique. The nurse allows the patient to cast his or her pain, suffering, and worries upon them. They do so willingly and return to them comfort, peace, and care.
Nurses also hold a unique position within healthcare. What other profession does so much and has such an impact on patient care? Bedside nurses deliver the vast majority of treatments, perform the majority of assessment and in today’s profession they are becoming increasingly responsible for treatment decisions. Bedside nurses are no long handmaidens and water fetchers. Today’s bedside nurses is a highly competent, trained professional with an expansive knowledge base. It is not uncommon to see experienced nurses training residents, fellows, and at times attending physicians. The line between nursing and medicine is becoming blurred as nurses continue to advance and grow as a profession. On a given day you may see Nurse Practitioners and Nurse Anesthetists performing highly complex procedures such as endotracheal intubation, central line placement, chest tube placement, and even diagnostic cardiac catherization in some facilities!
However, this growth has not came without it’s own growing pains. In this lesson we will discuss some challenges and issues that are unique to modern day nurses and potential solutions.
1.) Nursing Burnout
From ambulatory facilities to ICUs everyone is working longer hours. As budgets become thin nursing workloads become more and more stretched. The acuity of patients is higher than ever thanks to advanced medical care. It seems our profession has not kept pace with the demands of today’s patients, or rather it has not acclimated to provide an environment which fosters high level care from nurses. Indeed many studies (1) have linked increasing levels of nursing burnout to decreased patient safety. Another study (2) found that higher levels of burnout correlated with worse patient satisfaction.
Most nurses would not be surprised by this. It is safe to say that most nurses have experienced some degree of burnout. One study (3) found that up to 35% of nurses experience signs of burnout their roles. So what are the risk factors and protective factors for nursing burnout?
- Inpatient (hospital) work setting
- Increasing or unreasonable workloads, which impair or impede nurses’ abilities to perform their jobs correctly
- Increase patient:nurse ratios
- Negative physician-nurse relationships
- Unsupported management
- Supportive management and environments
- Positive physician-nurse relationships
- Being involved in decisions affecting nursing and patient care
- Being able to discuss new ideas openly
*Based on data from studies (1-4)
This list is by no means all-inclusive and as you can see many of the factors listed are unfortunately not uncommon. We have demonstrated it is bad for patient and it is obviously detrimental to nurses. Furthermore it is in fact a threat to the entire profession. One in six nurses (5) frequently considers leaving the profession. This is no surprise to those practicing in areas at high risk for burnout. It seems that nurses leave the profession or advance their degree in order to avoid the stress of bedside nursing.
So how do we combat this issue? The first step is acknowledgement. Though the term has created quite a buzz in the healthcare world there is little action being taken to prevent burnout. It is difficult to blame anyone given the amount of pressure healthcare systems are under as they adapt to ever-changing regulations and legislation with increasingly meager budgets. However, the author believes that without proper resource allocation the burnout epidemic will continue to grow, which will affect patients and nurses alike.
The answer is not simple. Interventions must be multi-faceted and be aimed at several levels.
Nurses Coping Mechanism
We teach pilots how to deal with stressful situations as a basic aspect of their training. We have seen the effects of unchecked stress in our war veterans as the nations reels in a PTSD epidemic that is seemingly impossible to control. The nursing profession would be wise to intervene earlier. This can start with teaching nurses appropriate coping mechanism and preparing them for the stresses they will inevitably face. A BREATHE technique (6) was developed and tested with positive results. Nurses who utilized this program and the techniques reported lower stress levels than controls. The key aspects of this course were: 1.) Assessing stress 2.) Identifying stressors 3.) Managing stress 4.) Avoiding negative coping 5.)recognizing when professional mental healthcare is necessary.
Though these techniques cannot change the work environment or other factors, they can potentially render nurses more resistant to the effects.
As we have discussed, the work environment is a major factor in nursing burnout development. In order to minimize the effects of burnout it is required that healthcare institutions identify the contributing factors and make burnout reduction a priority. This includes: improving nurse:patient ratios, improving nurse-physician communication/interactions,
Nursing leaders have been traditionally chosen based on experience and performance at other roles, such as bedside nursing. However, this does not directly correlate with management/leadership aptitude. It has been demonstrated that effective leadership and management (2) can reduce the burden of nursing burnout. Choosing and training effective leaders is a must for the profession of nursing.
Burnout is without a doubt one of the great challenges of our generation of nurses. It remains under-studied and under-addressed. By educating and empowering nurses we hope to raise awareness of the issue, which is pivotal to the future of our profession and for quality patient care.
Other useful resources:
2.) Social Media
As our world evolves social media has become a highly personal yet public aspect of all lives, including nurses and patients. Traditional nurse-patient relationship boundaries can be blurred by social media. Most nurses have read or heard stories about nurses losing their jobs or license due to an issue stemming from social media. So what is best practice for nurses when it come to social media?
- Avoid posting any negative materials concerning patients, healthcare facilities or the profession in general on social media.
- Avoid posting any material that may violate HIPAA, ethical standard, or any institutional policies.
- Approach social media relationships between yourself and patients with a great deal of caution. Always consult with your state board of nursing, leadership, and institutional guidelines on this matter. An initiation of contact (friend request or message) by a patient does not make the action permissible.
- Avoiding taking any pictures at work that reveal patient information or that may breach any institutional policies.
- Never discuss protected information with a patient over social media, even if you intend on disclosing this information via another route (in-person visit, phone call, etc.)
3.) Acts of violence against nurses and healthcare personnel
Reports of violence leading to serious harm and even death have increased in the healthcare world. Factors leading to patient agitation / violence include: 1.)Staff behavior 2.) Patient behavior 3.) care settings 4.) and waiting times. The most common reasons reported for an eruption of violence were 1.)Dissatisfaction with the perceived quality of care 2.) an unacceptable comment by a staff member 3.) lack of staff professionalism (6)
We know that when violence erupts, both patients and staff report having felt fear, frustration, loss of control, and pressure (7). The outcome of a violent event is not beneficial to either party. Patients may be subject to civil justice and potentially a reduced quality of care. Nurses who are attacked may suffer severe mental and physical damage both short and log-term (7).
It is evident that avoiding healthcare violence is in the best interest of all parties. However, the factors that lead to these situations are multi-factorial and cannot be reduced by a single measure. Let’s explore the factors surrounding violent episodes a bit more closely. Below are the results from a survey of patients who were violent with hospital staff detailing their specific complaint/trigger:
1.) Staff behaviors: dismissive, arrogant, superiority, blunt tone, mismanaged patient expectations, and poor guidance provided by healthcare staff.
2.) Patient factors: violent tendencies, feelings of sickness, anxiety, having underlying psychiatric disease, and feeling fearful.
3.) Disturbing hospital settings: Uncomfortable accommodations (physically), lack of adequate staffing, lack of transparency.
*Based on data from (7).
So how do nurses and healthcare staff go about reducing violence? The organisational factors (uncomfortable accommodations, lack of staff, etc.) will continue to agitate and provoke patients. Healthcare workers must take a position of de-escalation when tensions rise. This includes managing expectations, maintaining a respectful and professional nature despite patient behaviors, and maintaining transparency with patients. Behaviors to be avoided include: harsh mannerisms and tone, condescending comments (7), and focusing on de-escalation rather than confrontation when patients become upset. Early and judicious use of security staff is also imperative in preventing serious physical harm.
Despite the best intentions by nursing staff, violent events will continue to occur. The role of the patient has changed significantly in recent years and some hypothesize this is partially to blame for this epidemic. The role of the patient has went from “passive” and “a receiver of care” to a “empowered, knowledgeable participant in care”. However, patients often do not have the requisite knowledge to assume this role, which may lead to feelings of frustration, fear, and misunderstanding. Working collegiality with patients and attempting to educate them at each juncture of care may help reduce these feelings.
1.)Hall, L. H., Johnson, J., Watt, I., Tsipa, A., & O’Connor, D. B. (2016). Healthcare Staff Wellbeing, Burnout, and Patient Safety: A Systematic Review. PloS one, 11(7), e0159015. doi:10.1371/journal.pone.0159015
2.)Vahey, D. C., Aiken, L. H., Sloane, D. M., Clarke, S. P., & Vargas, D. (2004). Nurse burnout and patient satisfaction. Medical care, 42(2 Suppl), II57–II66. doi:10.1097/01.mlr.0000109126.50398.5a
3.)McHugh, M. D., Kutney-Lee, A., Cimiotti, J. P., Sloane, D. M., & Aiken, L. H. (2011). Nurses’ widespread job dissatisfaction, burnout, and frustration with health benefits signal problems for patient care. Health affairs (Project Hope), 30(2), 202–210. doi:10.1377/hlthaff.2010.0100
4.)Sillero, A., & Zabalegui, A. (2018). Organizational Factors and Burnout of Perioperative Nurses. Clinical practice and epidemiology in mental health : CP & EMH, 14, 132–142. doi:10.2174/1745017901814010132
5.)Hämmig O. (2018). Explaining burnout and the intention to leave the profession among health professionals – a cross-sectional study in a hospital setting in Switzerland. BMC health services research, 18(1), 785. doi:10.1186/s12913-018-3556-1
6.)Hersch, R. K., Cook, R. F., Deitz, D. K., Kaplan, S., Hughes, D., Friesen, M. A., & Vezina, M. (2016). Reducing nurses’ stress: A randomized controlled trial of a web-based stress management program for nurses. Applied nursing research : ANR, 32, 18–25. doi:10.1016/j.apnr.2016.04.003
6.)Shafran-Tikva, S., Chinitz, D., Stern, Z., & Feder-Bubis, P. (2017). Violence against physicians and nurses in a hospital: How does it happen? A mixed-methods study. Israel journal of health policy research, 6(1), 59. doi:10.1186/s13584-017-0183-y
2.Nursing Documentation 101: How to Guard Your License
“I just love charting,” said no nurse, ever. If you ask most people why they want a career in healthcare, their response is that they wanted to help people. They did not want to spend hours in front of a computer clicking boxes. This time-consuming task of documenting in the medical record, or charting, is dull, repetitive, and sometimes disconcerting. It takes time away from being able to provide care for the patient. Yet documentation in the medical record is truly a vital part of patient care.
Nursing documentation fills a significant portion of the medical record. Nurses need make sure what they are adding is accurate and complies with the guidelines set by their facility and the state board. This principle is the same, even though there are differences to be aware of now that the electronic medical record has become the standard.
The Who, What, When, Where, Why and How
There are approximately 2.9 million working RNs in the United states, with about 1.6 million working in hospitals (1). Nurses on a med-surg unit typically spend about one-third of their total working hours documenting (2). Considering a nurse on a med-surg floor spends about 2.5 hours per shift charting, that roughly translates into 7 billion hours spent charting each year. And that is only for the nurses!
Every discipline of the healthcare team contributes to the patient’s medical record. These different clinicians may not have the opportunity to report off to one another, and they must refer to the medical record to gather the information they need in order to care for the patient. Even kitchen staff responsible for preparing meals for patients must be able to see the dietary order for the patient. The following are a few examples of the clinicians who contribute to or review the patient’s medical record:
- Medical Team: physicians, nurse practitioners, physician assistants, surgeons, specialists, residents
- Nurses and LPNs
- Medical Assistants, CNAs, patient care assistants or technicians
- Specialty technicians: radiology, anesthesia
- Therapists: physical, speech, occupational, respiratory
- Case managers or social workers
- Coding and billing specialists
The primary purpose of the medical record is to communicate data about the patient and care provided between different members of the healthcare team. The bulk of the medical record is a collection of assessment data obtained from the patient. Details concerning assessments and results from lab tests or radiology comprise a large portion of the data. Assessment data is usually collected on a flow sheet system. Progress notes are written by the medical team or therapists help to guide the intended plan of care for the patient. This is considered narrative charting. The medical record also includes orders for prescribed medications and treatments from the medical team. The following are typical components found in a patient’s medical record.
- Patient demographics: name, age, gender, contact information, language, insurance information.
- Past medical history: surgeries, chronic conditions, family history, allergies, home prescriptions.
- History and Physical (H&P): this can contain information about admitting diagnosis or chief complaint and narrative of the story leading to admission.
- Flowsheet of assessment data: vital signs, head-to-toe assessment, intake and output record
- Laboratory test results.
- Diagnostic test results: from radiology or procedures.
- Clinical notes: progress notes from the medical team, procedure notes, notes from consulting clinicians, education provided, discharge planning.
- Treatment Orders.
- Medication Administration Record (MAR).
The medical record should document every interaction the patient had with a member of the healthcare team. An encounter is created upon admission and everything occurring during a particular admission becomes part of the medical record. Phone calls made to patients and/or families may also become a part of the medical record.
Medical records are stored in various ways depending on their format and the facility. Paper records from small outpatient offices may be kept onsite. Records are now largely kept electronically. This is referred to as the electronic medical record (EMR) or electronic health record (EHR) and consists of Protected Health Information (PHI). They will be stored on a secure server, typically only accessible by authorized personnel.
The medical record is essential for several reasons. The primary reason for the medical record is that it allows members of the healthcare team the ability to review and analyze data in order to deliver appropriate care. It allows clinicians to keep track of all the care that has already been completed for the patient. It also provides the patient with a record of the treatment they received for as part of their lifetime medical history. The medical record is used for coding and creating a bill for the services the patient received. Medical records may also be used for process review and research. Ultimately, it is also a legal document and may be used in a court of law as applicable.
Medical records are in the final stages of evolution from a paper chart to an electronic medical record system (EMR). By 2017, 96% of acute care hospitals and over 80% of physician offices possessed certified health IT (3). This migration of medical records from paper to electronic format was made possible with advances in technology in the last 30 years. The EMR allows members of the healthcare team to access the medical record instantaneously and improves continuity of care. Utilization of the EMR ultimately reduces costs in healthcare (4) and increases efficiency.
While EMR does have some drawbacks, the benefits that it provides are substantial enough that the government has encouraged its adaptation. The Health Information Technology for Economic and Clinical Health (HITECH) Act was enacted in 2009. This program provided tens of billions of dollars in financial incentives for healthcare facilities to adopt an EMR system (5,6).
Privacy and Security
Since 1996, HIPAA, The Healthcare Information Portability and Accountability Act, has been the governing legislation that provides for the privacy protection of medical records. Compliance with HIPAA mandates that anyone who interacts with patients receives training that will ensure that they will maintain privacy for the patient. Part of the HIPAA legislation also allows the patient to request their medical records.
The patient also has the right to request to amend their medical record. Patient permission must be given prior to a third party’s access to their medical record (7). HIPAA legislation was introduced at the advent of EMR technology. A provision of HIPAA provided a framework to ensure privacy of electronic health records (8). However, breaches in security by hackers or cyberterrorists remains a potential threat.
Benefits of the EMR:
- Immediate data accessibility and communication of patient status.
- Clinicians can view records remotely, analyze the findings, and place orders immediately for faster patient treatment.
- Multiple clinicians can view the chart at one time.
- Records can be viewed from previous admission and/or outpatients visits easily.
- Records can be instantly shared between facilities (in instances of shared systems).
- Reduction in errors.
- Errors due to misinterpretation of handwriting are eliminated.
- Allows for increased safety checks. The EMR can be set to flag missing components of information, tasks that were not yet completed or are overdue, recognize duplicates, and present warnings if documentation has not yet been validated or “signed.”
- Scanning medications is possible with EMR systems to reduce the risk of medication administration errors.
- Assists with appropriate billing by capturing charges of services provided to the patient.
- The EMR can provide reminders for necessity of certain preventative health screenings or vaccines.
- Automatic “signature” of data is completed simply by the user logging in with a unique ID and password. All entries are date and time stamped. If a correction is made, the original data can be accessed.
- Accessing patient EMR is tracked and can be audited to protect patient privacy from unnecessary viewing.
- It is expensive to convert records system to an electronic system
- The initial cost of the EMR software is very expensive.
- More workhours must be paid for staff training and coverage of patients during initial implementation of the program.
- Maintaining appropriate encryption and cybersecurity technology against viruses and hacking are also a costly component.
- Computer systems can be temporarily inaccessible, for example when updates and reboots are required. Paper charting is still necessary in the interim.
- Template charting has limitations (9)
- Templates may not exist for a specific problem and does not accurately reflect the patient’s condition. Atypical patients may have multiple problems or extensive interventions that must be documented in detail.
- Templates may also encourage cloned or copied documentation. It creates unnecessary redundancy and at times inaccurate information in the EHR. Some EHR systems are designed to facilitate cloning with such popular features as:
- “Make me the author” to assume the content of another person’s entry,
- “Demo recall” of “Duplicate Results” to copy forward vital signs or assessment data.
- “Smart phrases” pulls in specific identical data elements.
- Automated insertion of previous or outdated information through EHR tools, when not modified to be patient-specific and pertinent to the visit, may raise significant quality of care and compliance concerns.
Think about your current charting system.
How does your medical record system facilitate accurate charting?
Do you believe that your system is efficient?
What are some issues with your system that make it difficult to accurately and timely chart nursing care?
The Legal Requirements
If it wasn’t documented, it wasn’t done. Every healthcare practitioner has had this mantra ingrained in them from the very beginning of their career. Nurses are trained to document defensively, that is, if they are taught at all.
In a 2014 study, only 20% of new graduate nurses had received electronic medical record training as a part of their nursing school curriculum (6). It is not uncommon for clinicians to have the tendency to view the medical record as a defense tool against potential legal problems, rather than its more significant role as a communication tool for patient care.
Regardless, accurate and complete documentation is an essential. Your career, and more importantly, patient care, depends on it.
Did you receive proper training on documentation in your nursing program?
How can programs be improved to better prepare nurses?
When Documentation Becomes Your Defense
In the dreaded event of a legal problem, medical record will be scrutinized to every detail. It is usually the primary source of evidence for the case. A malpractice lawsuit requires four elements to be proven (10):
- That a medical professional assumed a duty to provide care for the patient.
- The clinician failed to provide appropriate care within their scope of practice for the patient.
- The failure in appropriate care caused an injury to the patient.
- The injury resulted in damage to the patient.
Potential legal problems that may arise include the following (11):
- Administrative liability – Professional licensure discipline, discharge (firing) from position.
- Civil Liability – Malpractice lawsuit, failure to provide necessary care.
- Criminal liability – Misdemeanor or felony charges for cases of gross negligence.
Fortunately, medical malpractice claims have begun to drop since 2001. In 2004, the medical practitioners involved, the defendants, won the case 83% of the time. The legal fees can still amount to $18,000 if the case is dropped, to as much as $93,000 even when the case is won (12,13).
In 2018, there were 8,718 malpractice cases that resulted in payments to injured patients (14). Of those events, 310 reports of malpractice suits that resulted in payments related to nursing care.
However, 180 of those, about 60% of those had payments to the injured patient that were over $50,000 (14). However, there were nearly 15,000 adverse action reports filed against nurses, which was more than the number combined filed against physicians, NPs, and PAs combined.
The majority of medical malpractice cases primarily target the physician and the facility. However, anyone who made an entry into the patient’s medical record may be required to participate in legal proceedings.
Most common malpractice claims against nurses include failure to (15):
- Follow standard of care
- Follow safety protocols
- Perform procedures according to guidelines
- Use equipment properly
- Use or operate equipment within the manufacture’s details
- Failure to correctly document
- Communication with the provider
- The care you completed
- Follow assess and monitor
- Report a change in status of the physician
- Assess a patient with change in status
- Communicate pertinent data
- Provide appropriate discharge education and information
- Communicate properly and completely between shifts
Think about the last difficult shift you had. Did you properly document?
How would you prioritize documentation differently after reading this module?
What is Required for Nursing Documentation?
Necessary medical record documentation can vary significantly depending on the care area. For example, the documentation a circulating nurse in the operating room completes will be very different from what is documented on an emergency room patient. While the basic principles of documentation stay constant, the nurse needs to be familiar with the documentation requirements for that area based on requirements of the state board of nursing, the facility, and the unit.
There are standard requirements for medical record documentation that are applicable in all patient care settings, and in both paper and EMR systems. These standards include the following (16):
- Accurate: Clinicians must be careful to proofread documentation to make sure it is free from errors. A small typo can have serious repercussions, as it is more likely to be misinterpreted by others.
- Relevant, concise, organized and complete: It is important to keep the information concise and relevant so that other care providers can quickly find the pertinent information that they need. Assessment data should be entered in a systematic way. Complete documentation ensures all of the unit policies for documentation are addressed.
- Free of bias: Clinicians should only include information that is pertinent to the care of the patient and remain free from personal bias. Direction quotations should be utilized with proper context.
- Factual: Clinicians should not exaggerate or minimize findings. Charting is to be completed after completing a task, not before. Do not speculate data. Observations need to include exact times and measurements. Avoid approximations. Make sure to chart on the correct patient.
- Timely: What occurred during the shift should be documented during the shift. Documentation should be done as soon as possible after task completing. If something needs to be added in after the shift was completed, it should be denoted as a late entry with a reason as to why. Your facility likely has strict requirements regarding late entries.
- Legible/decipherable and clearly written: Paper documentation must be clearly legible. Writing must clearly convey meaning.
- Standardized: Clinicians must use appropriate medical terminology and approved acronyms and abbreviations.
- Labeled and Auditable: Paper documentation must be signed with credentials and must include date and time of the entry. When charting in the EMR, all entries and corrections are recorded and time stamped. Password sharing or having another clinician assist in documenting under incorrect username is fraudulent.
Do you currently incorporate all of the above principles in your documentation?
If not, how can you change your practice to improve your documentation?
Examples of Good and Bad Charting
The following will show some examples of these principles in action. These are based on the scenario of a patient admitted in the Emergency Department for chest pain.
|Example of good documentation||Example of poor documentation|
|Accuracy||Patient stated she took 800mg of Tylenol at 4pm, an hour after she began to feel chest pain.||Patient reports she took pain med for chest pain.|
|Relevant||Patient stated she has never experienced chest pain prior to this event, and does not have a history of cardiac problems.||Patient was a competitive athlete 20 years ago and used to be in great shape. Patient thinks she is still pretty healthy.|
|Concise||Vital signs taken, telemetry monitor applied, lab samples collected and PIV started per the chest pain protocol.||Patient was triaged and immediately brought to exam room. In accordance with the chest pain protocol, vital signs were taken first. Then the patient had a telemetry monitor applied. Next, the patient had blood samples drawn through the inserted PIV catheter.|
|Organized||Pt reports no allergies|
Prescriptions include hormone replacement therapy
Past medical history includes hysterectomy and foot surgery from a few years ago
Patient family history includes cardiovascular disease on her father’s side of the family
Pt denies smoking, illicit drug use, but does drink 3 times a week
Pt reports feeling fine until 1 hour after lunch when chest pain began.
|Patient was feeling fine until one hour after lunch, when she started to feel chest pain. Patient has no history of cardiac problems. However there is family history of cardiovascular disease on the father’s side. Patient had a hysterectomy and foot surgery a few years ago. Patient denies smoking and illicit drug use. Patient does take hormone replacement therapy prescription. Patient does not have any allergies. Patient reports drinking alcohol x3/week.|
|Complete||Patient complaining of 8/10 chest pain, described as “stabbing.” Pain has been experiencing this pain for three hours. She has taken Tylenol, but nothing is able to alleviate the pain.||Pt is complaining of chest pain.|
|Free of Bias||Education provided per chest pain protocol. Patient was instructed to call 911 immediately if experiencing chest pain in the future. Patient verbalized understanding.||Patient was given needed education about chest pain since she clearly didn’t understand that chest pain cannot wait 3 hours and she needs to call 911 right away because she can die of a heart attack.|
|Factual||Patient reports last meal was around 1300 which consisted of spicy foods. Her chest pain onset was 30 minutes after. She waited an additional three hours before seeking emergency care.||Patient presented to ER after lunch.|
|Legible/Decipherable||Patient was instructed to call for assistance with ambulation and how to utilize call light.||Patient cannot safe walk by she self. Call light assistance. Bathroom walk with me.|
|Standardized||Morphine Sulphate 2mg IV push, once PRN for 8/10 pain per chest pain protocol.||MSO4 2.0 mg, IV push, x1.|
|Timely||Documentation is completed in real-time, all documentation completed before transferring patient to telemetry.||Nurse documents three days later due to high volume of patients.|
Common Documentation Errors
- Falsification of a record. This can happen from charting an action was never done, or from charting information before the action was completed.
- Fraudulent charting is the act of knowingly making a false record. Criminal charges of forgery can result if the misrepresentation was done for personal gain. An example of this would be a nurse documenting administration of controlled substance but was instead diverting the medication.
- Inappropriate use of cloning features. Information “copied and pasted” from a different patient’s record or that was completed by another provider. Data copied from previous shift assessments that isn’t updated to reflect current status is also a false record (9).
- Fail to document communication. Notification of the medical team of a change in patient status or critical lab values should always been included. Clarification or confirmation of orders should also be documented (17). Include notification of other providers who assisted with patient are. This includes failure to document transfer of care to another nurse.
- Failing to document a reason why something wasn’t done. If a patient doesn’t receive a prescribed medication, the reason why the medication wasn’t given needs to be described. If you communicate with the provider, this should also be included.
Have you ever failed to document or failed to document a critical portion of care?
If you could alter your documentation, how would you better document in this situation?
Including all of the necessary information into each patient’s medical record is a daunting task. The nurse must make sure that they have included all of the relevant and accurate information that is required by their facility guidelines. It must usually be done in a loud environment and is frequently interrupted by actually having to provide care to the patients.
It is not only a tedious chore, but it also tends to cause a lot of apprehension. There is usually a worry of “did I chart enough?” or “did I chart everything I needed to?” This is due to the defensive practices and attitudes healthcare workers have adapted to protect against malpractice lawsuits. In this way, charting is a lot like paying taxes. No one likes it, but it still has to be done.
Perhaps a way to develop a healthy perspective toward charting is to change the focus back to its original purpose: to communicate care about the patient. The purpose of charting is to relay to the other healthcare team members what is going on with the patient. With this objective in mind, the nurse will inevitably cover all the necessary details. It may also be a bit more satisfying to know that even though they are in front of the computer, they are still doing something important for the patient.
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10. What is Malpractice? (n.d.). Retrieved from https://www.abpla.org/what-is-malpractice#medical
11. Cady, R. F., Esq. (2009). Criminal Prosecution for Nursing Errors. JONA’s Healthcare Law, Ethics, and Regulation,11(1), 10-16. Retrieved March 1, 2019, from https://www.nursingcenter.com/cearticle?an=00128488-200901000-00003&Journal_ID=260876&Issue_ID=848807
12. Kann, B. R., Beck, D. E., Margolin, D. A., Vargas, D., & Whitlow, C. B. (Eds.). (2018). Improving Outcomes in Colon & Rectal Surgery. Retrieved March 1, 2019, from https://books.google.com/books?id=O61vDwAAQBAJ&dq=Improving Outcomes in Colon & Rectal Surgery edited by Brian R. Kann, David E. Beck, David A. Margolin, H. David Vargas, Charles B. Whitlow&source=gbs_navlinks_s
13. Peters, P. G. (2008). Twenty Years of Evidence on the Outcomes of Malpractice Claims. Clinical Orthopaedics and Related Research, 467(2), 352-357. doi:10.1007/s11999-008-0631-7
14. Singh, H. (2018). National Practitioner Data Bank Generated Data Analysis Tool. Retrieved March 1, 2019, from https://www.npdb.hrsa.gov/analysistool/
15. Top 5 Malpractice Claims Made Against Nursing Professionals. (n.d.). Retrieved March 1, 2019, from https://www.proliability.com/portals/0/docs/nursemalpracticewhitepaper.pdf
16. American Nurses Association. (2010). ANA’s Principles for Nursing Documentation. Retrieved February 28, 2019, from https://www.nursingworld.org/~4af4f2/globalassets/docs/ana/ethics/principles-of-nursing-documentation.pdf
17. Lippincott Nursing Education. (2018, February 22). Lippincott Nursing Education Blog. Retrieved March 1, 2019, from http://nursingeducation.lww.com/blog.entry.html/2018/02/22/nursing_documentatio-S5hF.html
Other references include:
Reising, D. L., & Allen, P. N. (february 2007). Protecting yourself from malpractice claims. American Nurse Today,2(2). Retrieved March 1, 2019, from https://www.americannursetoday.com/protecting-yourself-from-malpractice-claims/.
Reising, D. L. (2012). Make your nursing care malpractice-proof. American Nurse Today,7(1). Retrieved March 1, 2019, from https://www.americannursetoday.com/make-your-nursing-care-malpractice-proof/
3.Influenza: Recognition, Treatment and Red Flags
Every year, ER waiting rooms, outpatient clinics, and inpatient hospital beds fill up with patients seeking treatment for the miserable symptoms brought on by the influenza virus. This illness does not discriminate and afflicts all ages, from young babies, to the elderly, and everyone in between. Symptoms can range in severity from several days of fever, chills, and cough in bed at home, to weeks of hospitalization, respiratory distress requiring mechanical ventilation, and even complications resulting in death.
Starting in October and often lasting well into spring, flu season tasks healthcare workers everywhere with promoting prevention, quickly and efficiently identifying those infected, and appropriately managing symptoms and any secondary complications that may arise.
An illness affecting the population on such a large scale requires healthcare professionals to stay up to date on disease trends, diagnosis and treatment protocols, and “red flags” of more serious cases in order to minimize the impact of flu season and keep complications and mortality as low as possible.
This course will review disease trends in recent years, common and more insidious symptoms to help identify flu infections, available testing methods and their accuracy, pharmacologic treatments and the importance of their timing, supportive treatments and symptom management, and the “red flags” of dangerous secondary infections and complications.
Upon completion of the course, the reader should be comfortable participating in prevention, identification, and management of the seasonal influenza virus.
Current Practice, Barriers and Need for Continued Education
Influenza is a serious global issue that has been affecting mankind since the beginning of recorded history. Despite medical advances in recent years, flu remains a major public health concern, with up to 20% of the US population being affected annually (13).
Over 200,000 people are hospitalized nationally each year, with around 36,000 deaths. This issue increases on a global level, with 3 to 5 million infections and over half a million deaths each year (14). Those most at risk are young children, those over age 65, and those with other chronic or underlying conditions such as asthma, diabetes, immunosuppression, etc.
Despite high rates of infection and risk of complications, the estimated annual vaccination rate amongst the general population remains fairly low, around 37.1% for adults (3) and 57.9% for children for the 2017-2018 flu season (4). There is an increased rate of vaccination amongst healthcare workers (78.6%), but as these are the people most likely to come in contact with and spread the virus, even that number could be improved upon (6).
Further complicating the situation, influenza virus has several strains and possesses the ability to change its DNA (referred to as “drift and shift”) as it replicates, making it difficult to produce a highly accurate vaccine (2). Because of this, vaccines cannot be created very far in advance if the most current strain is to be targeted. Vaccine shortages can result if new vaccines are not created at a fast enough rate throughout flu season (6).
There are antiviral medications available for prevention and treatment of flu, however this requires proper identification of those infected or most at risk for infection, and the
administration of these medications is typically time-sensitive (5). Health care professionals should be familiar with common symptoms of flu and be comfortable assessing patients, testing for and diagnosing flu.
All of these considerations for flu illustrate the intense need for educated, proactive health care workers to promote vaccines, quickly identify those most at risk or with active infections, and treat effectively in order to keep the impact of flu minimalized.
The National Institute of Health has ongoing projects to keep available resources robust (14), but this research is only as strong as the health care professionals who implement it and are on the front lines of patient care. Staying up to date on current practice is paramount for national and global management of this resilient pathogen.
Do you think that the current rate of vaccinations among healthcare providers (78.6%) could be improved?
With up to 20% of the US population being affected annually, do you think enough resources are utilized in the prevention, recognition, and treatment of influenza?
What could be done from a national, state, and local level to promote increased prevention, recognition, and treatment of influenza?
What is Influenza?
Viruses are small pathogens containing genetic material that infect host cells and replicate within that host. They can exist for short periods of time outside of a host as an infectious virion and are spread between hosts through a variety of ways. Influenza is a specific group of RNA viruses that replicate within the epithelial cells of the respiratory tract (15).
There are three main types of flu viruses (A, B, and C). Viruses B and C typically only exist in humans, but A has been found in other mammals such as pigs and horses (15). There are also subtypes of each virus, depending on specific structure of the virus; these are labeled as H1-16 and N1-9 for hemagglutinin and neuraminidase, however, further discussion of these is beyond the scope of this course (15).
As the virus replicates within host cells, there can be subtle changes to the RNA over time, eventually adding up to more noticeable changes and resulting in these different subtypes. These slow changes are referred to as antigenic “drift” and are part of why creating a highly accurate flu vaccine is so difficult (2).
Typically viruses that have drifted some are still susceptible to the current vaccine or there is some acquired immunity within the population. However, there is sometimes a more dramatic structural change referred to as antigenic “shift” that results in a completely new viral subtype and a population with virtually no immunity to this new agent (15). This can result in serious infection of pandemic proportions, such as the 2009 H1N1 outbreak (15).
Influenza viruses are typically spread through droplet transmission, when an infected person spreads microscopic drops of bodily fluids, typically through sneezing or coughing, which then come in contact with another susceptible person (8). These droplets usually only travel across air distances of 6 feet or less, however they can be transferred further via indirect contact such as handshaking or by vectors (surfaces or objects where virions survive temporarily while waiting on contact with the next host) (8).
Once a host touches a contaminated vector and then touches their own mucous membranes (nose, mouth, eyes, etc), they can become infected. Other bodily fluids such as loose stools, vomit, and sputum can contain viral RNA and contribute to disease spread (8).
The typical point of replication for influenza is upper respiratory tract, more specifically the nares.
How does this correlate with influenza symptoms?
As you can see, infleunza is spread via many modes. How will you use this information to better protect yourself and patients from influenza infection?
Prevention: Flu Vaccines
Once pathogenicity is understood, providers are better able to prevent spread of infection. The primary and most effective way to help prevent the spread of flu is through a high rate of vaccination in the general population. Current recommendations are for all individuals 6 months of age and older to receive a vaccine unless otherwise contraindicated (8).
It is especially important that those most at risk (children under age 2, adults older than 65, and those with comorbid conditions) and those working with high risk individuals (healthcare and childcare workers) receive vaccines.
For the optimum protection, the goal for vaccine timing should be by the end of October, keeping in mind that full antibody production takes about two weeks after the vaccine is received. Though early vaccination is ideal, a flu vaccine can be administered at any point during flu season and patients requesting immunization later in the season should still be vaccinated (8).
The first time children between 6 months and 8 years of age receive a flu vaccine, they will need 2 doses, 4 weeks apart (8). After receiving 2 doses, children only need 1 dose for all subsequent flu seasons (8).
There are some individuals who should not receive a flu vaccine, but this group is typically very small. Among those who are absolutely contraindicated are infants under 6 months of age and anyone with a previous life threatening reaction to a flu vaccine(6).
It was previously thought that anyone with an egg allergy should not receive the vaccine, since the viral components are grown in an egg medium, however most recent recommendations suggest that this does not cause a reaction for most people and should be reviewed on an individual basis with one’s own primary care provider (6).
Anyone with a history of Guillain-Barré Syndrome should also consult their provider and may be advised to omit the vaccine. Patients with a current cough or cold accompanied by fever may be advised to postpone the vaccine until their symptoms have resolved (6).
Each year, the CDC studies two factors of the current flu vaccine, efficacy and effectiveness. Randomized controlled trials are used to study efficacy, or the intended result, of the vaccine in optimal conditions with healthy participants (6). Less formal observational studies are used to study effectiveness, or how well the vaccine is working in the “real world.”
As previously discussed, antigenic drift and shift mean that the annual vaccine is imperfect and does not always prevent illness as well as intended. For a general idea of the typical effectiveness, we can look at data from recent years: the vaccine was shown to be 48%, 40%, and 38% effective in 2015-2016, 2016-2017, and 2017-2018 flu seasons respectively (6).
Regardless of the lower levels of effectiveness compared to other vaccines, such as MMR, vaccination against flu can still prevent substantial numbers of illness and death when considering the population of the United States.
There are a few side effects to be aware of and to include in patient education with administration of flu vaccines. The most commonly reported side effect is local soreness around the injection site. This occurs in about 65% of patients vaccinated, does not typically interfere with activity, and resolves within a week (6).
More systemic symptoms such as fever, headache, and malaise are sometimes reported, but interestingly these symptoms are reported at similar rates in patients who received a placebo vaccine (6). Rarely, an allergic reaction can occur, ranging from urticaria to anaphylaxis.
Children under age 2 are at a slightly increased risk of febrile seizures, particularly if a flu vaccine is given in combination with Prevnar and DTaP vaccines, therefore timing of routine vaccines in conjunction with a seasonal flu vaccine should be discussed with parents of young children (6).
Though the actual correlation is unclear, there is also a suggested link between flu vaccines and the extremely rare condition of Guillain-Barre Syndrome (GBS). This often life-threatening paralytic condition occurs in about 1-2 people per 100,000 each year, regardless of flu vaccine status.
Ongoing research indicates it is unlikely flu vaccines directly cause GBS and that other triggers such as recent viral illness are more likely to be the culprit, but the CDC estimates there may be a 2 per 1 million chance of experiencing this complication after receiving a flu vaccine (6).
How would you react if a patient refused the influenza vaccine due to potential side effects?
What education would you provide?
In addition to vaccines as the front line of disease prevention, there are multiple ways to help slow or prevent the spread of disease once flu season starts.
Hand hygiene and cough etiquette are amongst the most effective measures to prevent spread of illness (1). These steps are easy and can be followed by anyone, regardless of if they are ill or not.
Avoid touching your mouth and nose. When coughing or sneezing, use a tissue to cover your nose and mouth and then dispose of the tissue and wash your hands. Handwashing should be done with soap and water or alcohol based hand sanitizer (9). In addition to standard precautions, anyone with respiratory symptoms and/or fever is encouraged to wear a surgical mask.
Hospitals and clinics can help stop the spread of infection by separating well patients from those with respiratory symptoms (1). People who are ill should not attend work or school and should limit their contact with well people as much as possible while symptoms are present (9).
Infected individuals are considered contagious 1-2 days before showing symptoms and up to a week after illness begins; they should be fever free for 24 hours before returning to work/school (9).
Recognition and Treatment of Flu: Symptoms
Despite prevention efforts, hundreds of thousands of people nationwide will contract the influenza virus each season.
When prevention efforts fail, the next important step is early identification. It is important for all healthcare workers to be familiar with the symptoms of flu and be able to quickly and accurately identify those with a probable diagnosis of flu.
Typical influenza infections start suddenly with a combination of fever, headache, sore throat, fatigue, nasal congestion or runny nose, body aches, and chills.
Fever and acute symptoms can last more than 7 days, with fatigue and weakness lingering for weeks. While fever is typical of influenza infection, not all who are infected present with a fever (15).
Testing for Influenza
It should be noted that patients with suspected flu can be treated purely based on clinical presentation and regional flu trends at that time; rapid flu tests do not have the highest sensitivity and therefore should not be the determining factor in regards to the necessity of treatment. However, there are several methods of testing for flu that can help confirm a suspected diagnosis of flu.
There are two main types of testing for flu, molecular assaysand antigen detection tests. Molecular assays work by identifying viral nucleic acids or RNA in a respiratory specimen (7). They are highly sensitive and specific, meaning they can detect the virus at even very low levels and the risk of false positive is very low.
There are rapid molecular assays that can result in as little as 15 minutes, identifying flu A or B, and there are also Reverse Transcription-Polymerase Chain Reaction (RT-PCR) and nucleic acid amplification tests available which take closer to 45 minutes to an hour for results and can identify specific subtypes of flu for a more in depth diagnosis (7). Antigen detection tests are typically used in outpatient settings due to their cost effectiveness and rapid results (10-15 minutes) These rapid tests are up to anywhere from 50-70% sensitive and have specificity >90% (7).
While more accessible to the clinic setting, antigen detection tests are less accurate and a negative result does not exclude a diagnosis of flu. In cases where flu is highly suspected and a rapid test result is negative, the result can be confirmed with a molecular assay or treatment can be started based on clinical presentation and a presumed false negative test result (7).
In fact, where high risk populations are concerned, such as asthma, heart disease, immune disorders, and other comorbid conditions, prompt treatment when flu is suspected is recommended regardless of testing results (7).
Viral cultures are also available for the most in-depth results. While not practical for the clinical setting due to long result windows (3-10 days), viral cultures offer extremely detailed and useful information about the genetic details of current flu strains which is helpful when developing the next year’s vaccine (7).
Influenza testing is nuanced and rapid testing cannot be relied upon for diagnosis.
Does this mirror what you see or do in clinical practice?
How could improved education of healthcare providers lead to more accurate diagnosing and treatment of influenza?
Once flu has been identified clinically and laboratory confirmation is obtained (if desired), treatment of flu should be started as quickly as possible in order to maximize benefits of treatment and minimize potential complications of untreated illness.
Three antiviral medications known as neuraminidase inhibitors are available by prescription in the US (oseltamivir, zanimivir, and peramivir). These medications work by blocking neuraminidase, an enzyme that allows newly replicated influenza viruses to be released from host cells (5). Another antiviral, baloxavir, works by stopping replication of the virus within the host cells (5).
Treatment should ideally be started within 48 hours of symptom onset, however there may still be benefits for severely ill patients or those who are very young, elderly, suffering from comorbid conditions, or already hospitalized, and treatment initiation after 48 hours may be considered (5). Treatment should also never be delayed while awaiting laboratory results (5).
Treatment may be initiated based on clinical symptoms alone, if symptoms are highly suggestive of influenza during an endemic period. The decision to treat is based on many factors, including risk of complications and time since symptom onset.
The most common side effects of these medications include nausea, vomiting, headache, dizziness, and sometimes a skin reaction. Typically, these medications are well tolerated and prompt initiation of treatment should be encouraged (5).
In addition to antivirals, supportive care is a mainstay of treatment. Rest, hydration, cool mist humidifiers, antipyretics, and throat lozenges have all been shown to provide comfort and help with symptoms. Multiple studies have shown honey to be an effective cough suppressant and 1 tbsp in warm tea or water can work well to provide some relief.
Patients should be monitored for signs of dehydration, including dry mucous membranes and reduced urine output. Ill patients should also isolate themselves as best as possible to prevent further spreading the illness (12).
Which patients are at highest risk of influenzas complications, including death?
Is it justified to treat these individuals based on positive clinical symptoms even with a negative rapid test? Is it justified to treat them after 48 hours?
“Red Flags” – Potential Complications and What Not to Miss
The majority of flu cases make a full recovery after 1-2 weeks of illness, however there are some more serious complications that can develop, including life-threatening symptoms and even death (11). Flu can sometimes trigger systemic inflammation, leading to myocarditis, encephalitis, rhabdomyolysis, or multi-organ failure.
These conditions can be difficult to diagnose if suspicion is not high. Flu infections attack the usual defenses of the respiratory tract and predispose the body to secondary bacterial infections like pneumonia.
The body’s initial inflammatory response is beneficial to help the body fight off a flu infection, but increasing inflammation or prolonged inflammation puts too much stress on the body and this extreme response can result in autoimmune disorders or sepsis (13). Those with asthma, heart disease, or other chronic conditions are at an increased risk of complications, as are young children and the elderly (11).
Post-influenza pneumonia is a well-described phenomenon and the most common causative pathogen is Methicillin-resistant Staphylococcus Aureus (MRSA). This secondary infection should be considered in patients with respiratory symptoms and/or sepsis after a recent resolution of flu followed by returning or new/acute symptoms. It is important to consider MRSA as a causative agent when prescribing antibiotics to patients with post-influenza pneumonia (15).
“Red Flags” or warning signs that the body is working too hard to deal with the flu virus or is not compensating well include: fast respiratory rate or difficulty breathing, cyanosis, tachycardia, hypotension, chest pain, dizziness, confusion, decreased urine output (>8 hours), severe muscle pain, or seizures. In children, fever >104 (or any fever in children <12 weeks of age) and retracting are concerning signs.
Any other signs/symptoms that are concerning or seem to be worsening warrant further workup and possible hospitalization to prevent further decline (11).
Have you ever seen a patient who displayed “red flags”?
How would this change the patient’s management and what type of treatment / monitoring would they need?
Case Study 1
This case study involves a real patient’s experience with seasonal flu. Names, genders, ages, and some details have been changed to protect patient information.
Jennifer is a 35 year old female who presents to an urgent care clinic in mid February with 2 days of rhinorrhea, cough, sore throat, body aches, and tactile fever. She has not received a flu vaccine this season. Following triage, her vitals are recorded as: HR: 110, RR: 22, Temporal temp: 101.3, SPO2: 97%, BP: 110/76.
She is visibly uncomfortable but sitting up on the exam table and able to cooperate and carry on a conversation. She is breathing a little shallowly and has a frequent, coarse sounding cough, but is overall not in any respiratory distress. She is congested and has clear rhinorrhea, eyes are watery, she has some posterior pharynx erythema, no cervical lymphadenopathy, and some faint rhonchi to her lungs that she is able to clear when coughing.
Rapid strep and rapid flu swabs are collected and the results are negative. She is given a prescription for 5 days of 75mg BID TamifluⓇ (oseltamivir) which she fills and begins taking that afternoon. A viral culture is collected from her via nasopharyngeal swab for confirmation of suspected influenza.
Within 3-4 more days, Jennifer is fever free and beginning to feel better despite some persistent fatigue. She works from home until her fever has resolved and cough is improving. She makes a full recovery without sequelae. Three days later her viral culture indicates she has type B influenza, despite her negative rapid influenza test. This is a typical case of influenza and the
Tamiflu may have hastened her recovery and possibly prevented severe illness. It also illustrates that rapid influenza testing has a low sensitivity and per CDC guidelines treatment may be based on clinical signs and symptoms.
Case Study 2
This case study involves a real patient’s experience with seasonal flu. Names, genders, ages, and some details have been changed to protect patient information.
Braxton is a 9 year old male who presents to his PCP’s office with sudden onset of high fever (tmax 103), headache, and cough that started that morning. It is December and he has not received a flu vaccine. His vitals are stable.
Exam reveals clear rhinorrhea, erythematous and enlarged tonsils, and frequent barky cough. Rapid strep is negative and rapid flu is positive for Influenza A. He is given a prescription for tamiflu (oseltamivir), however his parents have some reservations about the medication due to an article they read on social media and decide not to give him the medicine.
They manage his symptoms with analgesics, gatorade, and rest. About 11 days later he follows up in the office with complaints of persistent fatigue and new complaints of dizziness and abdominal pain. Parents report a syncopal episode at home that morning, prompting today’s visit.
His cough is still present, but better than it was, and he has been afebrile for about 5 days now. He looks very pale and complains of some dizziness as he gets up onto the exam table, his behavior is sluggish. He has some abdominal bloating and tenderness with mild spleen enlargement. He has lost 4 lbs since his previous visit. Vitals are somewhat concerning: HR: 145, RR: 27, Temporal temp: 98.8, SPO2: 98%, BP: 90/54.
He seems poorly hydrated and his overall appearance is concerning so you order some stat labs. Multiple abnormal lab values return, the most critical of which is a hemoglobin of 3.4. He is admitted to the local children’s hospital PICU and treated for hemolytic anemia secondary to viral infection as well as multisystem organ failure.
After multiple blood transfusions and aggressive steroid therapy, he is discharged home after over two weeks of hospitalization with no permanent organ damage.
This case illustrates one of the rae (but potential) complications of the viral influenza infection. It is possible that early antiviral treatment may have avoided this complication and/or minimized it.
While influenza is an annual problem and can often seem routine, it is of utmost importance that healthcare professionals stay vigilant in their knowledge of flu and treat each case on an individual basis.
As the front lines for promotion of flu prevention, early identification and treatment of flu, and maintaining alertness for potential complications, health care workers can have the biggest impact on the severity of the current flu season.
Staying up to date on current practice can help reduce overall numbers of infection, rate of complications, and mortality.
(1) Centers for Disease Control and Prevention. (2012). Respiratory hygiene/cough etiquette in healthcare settings. Retrieved from:
(2) Centers for Disease Control and Prevention. (2017). How the flu virus can change: “drift and shift”. Retrieved from: https://www.cdc.gov/flu/about/viruses/change.htm
(3) Centers for Disease Control and Prevention (2018). Estimates of flu vaccination coverage among adults- US 2017-2018 flu season. Retrieved from: https://www.cdc.gov/flu/fluvaxview/coverage-1718estimates.htm#ref3
(4) Centers for Disease Control and Prevention (2018). Estimates of flu vaccination coverage among children- US 2017-2018 flu season. Retrieved from: https://www.cdc.gov/flu/fluvaxview/coverage-1718estimates-children.htm
(5) Centers for Disease Control and Prevention. (2018a). Influenza antiviral medications: summary for clinicians. Retrieved from: https://www.cdc.gov/flu/professionals/antivirals/summary-clinicians.htm#
(6) Centers for Disease Control and Prevention. (2018b). Influenza vaccination: a summary for clinicians. Retrieved from: https://www.cdc.gov/flu/professionals/vaccination/vax-summary.htm
(7) Centers for Disease Control and Prevention. (2018c). Overview of influenza testing methods. Retrieved from: https://www.cdc.gov/flu/professionals/diagnosis/overview-testing-methods.htm
(8) Centers for Disease Control and Prevention. (2018d). Prevention strategies for seasonal influenza in healthcare settings. Retrieved from: https://www.cdc.gov/flu/professionals/infectioncontrol/healthcaresettings.htm
(9) Centers for Disease Control and Prevention. (2018e). Preventing the flu: good health habits can help stop germs. Retrieved from: https://www.cdc.gov/flu/protect/habits/index.htm
(10) Centers for Disease Control and Prevention. (2018f). Prevention and control of seasonal influenza with vaccines: recommendations of the advisory committee on immunization
4.Measles: The Forgotten Virus is Making a Comeback
To inform nurses about the signs and symptoms, diagnosis, treatment, and public health implications of measles despite its intersection with the anti-vaccination movement.
The History of Measles
Medicine has come a very long way in curing diseases that once wiped out entire populations. Before the vaccine, measles was a serious health concern. Each year, millions of people became infected with measles, and in the United States alone, an average of 495 people died of related complications.
Even beyond the mortality rate, 48,000 people experienced hospitalizations and 1,000 of those developed a significant and lifelong disability every year. One of the most dreaded complications of measles involves the spread to the central nervous system causing subsequent inflammation and risk for brain injury from acute encephalitis (4).
Measles is an acute, viral respiratory illness that is one of the most contagious of all infectious diseases. In fact, 9 out of 10 (90%) susceptible persons with close contact will develop measles. The virus is transmitted by direct contact with infectious droplets or by airborne spread. The measles virus lives for up to two hours on surfaces. The disease is active and contagious in the airspace for two whole hours.
Enter the Measles Vaccine
During a measles outbreak in 1954, physicians collected blood samples from affected students in Boston. They isolated the measles virus from a 13-year-old students blood and created a measles vaccine. In 1963, the live measles vaccine debuted in the United States. Five years later, the modern-day vaccine was introduced.
Measles is usually combined with mumps and rubella as part of the MMR vaccine. It is a very effective vaccine that protects over 97% of recipients (5). By 2000, the Centers for Disease Control and Prevention (CDC) declared measles eliminated. Historically, the development of the measles vaccine changed the scope of public health.
For the first time, prevention proactively saved lives. But now, with the advent of the anti-vaccination campaign, we are at risk for a revival of the diseases that healthcare nearly eliminated.
How did the invention of the measles vaccine affect the global burden of measles?
The CDC declared Measles “eliminated” in 2000, do you think this was a premature assumption that opened the door for resurgence?
Signs and Symptoms of Measles
Measles includes the onset of an elevated fever that may be as high as 105 degrees Fahrenheit (4). Other symptoms include:
- Noninfectious nonallergic rhinitis (also known as coryza)
- Koplik’s spots
- Maculopapular rash
Koplik’s spots are unique to measles and highly suggestive of the disease. They occur two to three days before the rash. They are white, clustered lesions on the gums that resemble grains of salt.
The maculopapular rash appears approximately 14 days after exposure and spreads from head to trunk to the extremities. Those with the measles are contagious from four days before they showed symptoms until four days after the rash appears. In some cases, immunocompromised patients may not develop a rash. The rash usually disappears within one week (4).
A diagnosis is made after evaluation of the signs and symptoms, in particular, a widespread skin rash that appears three to five days after exposure and lasts up to one week. The rash consists of red, itchy bumps. Measles is more likely to occur in unvaccinated children, primarily under five years old.
Once a diagnosis is suspected, measles is verified with laboratory confirmation. The lab tests that are performed are the measles antibodies (IgM) and measles RNA by real-time polymerase chain reaction (RT-PCR). To complete the laboratory tests, the nurse should collect a nasopharyngeal swab and serum sample. The serum sample is for public health implications, and diagnostic testing usually occurs in a specialty lab (4).
If measles is not identified and treated, the associated complications can be quite deadly. Possible complications include (4):
- Ear infection (Otitis media)
- Miscarriage or preterm labor in pregnant women
- Severe diarrhea and dehydration
One of the most dreaded complications of Measles is encephalitis.
What signs and symptoms may alert you that a patient is developing Measles encephalitis?
Personal Protective Equipment (PPE)
Because measles is incredibly contagious, it is critical to adhere to all recommendations for isolation and the appropriate personal protective equipment. Patients with measles should be placed on airborne precautions. Airborne precautions are used to prevent the spread of germs through the air (8). Other illnesses with airborne precautions include tuberculosis and chickenpox.
It is vital to place the patient on isolation precautions as soon as you suspect measles to minimize potential exposure to other staff and patients. Place patients in a negative pressure room and wear a fitted N-95 respirator to enter a room. A surgical mask is not appropriate, so a respirator must be worn.
The treatment of measles is broken into different categories, depending on exposure and symptoms: (4)
- Post-exposure prophylaxis for asymptomatic patients who have been exposed to measles. If they are not properly vaccinated or unsure of their immunization status, they should be treated with an MMR vaccine within 72 hours or immunoglobulin within six days of exposure.
- Patients should receive the immunoglobulin if they are not vaccinated against measles and are unable to be vaccinated with the MMR vaccine in the cases of pregnancy, severe immunosuppression, or age less than one-year-old. They should not receive the MMR vaccine for six to eight months following the immunoglobulin administration.
- Patients should avoid public areas for 72 hours due to the contagious nature of the disease (e.g., hospitals, schools, and daycare).
- Immunoglobulin and the vaccine should never be given together as this process invalidates the vaccine.
- There is no antiviral to treat the disease. Treatment after the confirmation of measles is supportive care and has not changed in over 60 years.
- Acetaminophen PRN for fever and myalgia (muscle aches or pains)
- Humidifier for cough and sore throat
- Rest and hydration
- Isolation for four days after the rash appears
- Educate patients that symptoms will last two to three weeks
There is no antiviral available that targets measles.
Do you think the lack of perceived threat from Measles has affected research?
How will this affect morbidity and mortality in cases of Measles outbreaks?
A movement against vaccinations is taking over social media and parenting groups called “anti-vax” or “anti-vaccination.” These groups want to eliminate vaccinations and believe that the benefits do not outweigh the risks. However, the evidence does not show that the risks are significant, especially when compared to the risks of the diseases.
Encouraging vaccination through education
The best strategy to reduce the spread of measles is to encourage all patients and family members to receive all recommended vaccinations. One of the most important nursing interventions is education, and this is the perfect opportunity to educate your patients.
In 2014, families visiting Disneyland left with measles. The state of California later reported 159 cases of measles throughout the next several months. When looking at school data in that same year, only 70 percent of counties had the ideal herd immunity status of 95% vaccinated.
In response to this outbreak, California passed Senate Bill 277 that eliminated all personal belief and conditional vaccination exemptions before entering school. The law went into effect in 2016 and only allowed medical exemptions and required that all schools report the vaccination status of enrolled children. Officials in California found that by tightening the vaccine regulations, more children received vaccinations before entering kindergarten (6). In 2016, 97% of school districts met herd immunity guidelines.
When patients are discussing travel plans it is an excellent opportunity to provide Measles education(6). Many patients are unaware that leaving the country puts them at risk for specific vaccine-preventable diseases, particularly when traveling to endemic countries.
It is also important that patients and families understand the concept of herd immunity. This is the indirect defense from infectious disease that happens when the majority of the population is immune to a specific infection. Herd immunity ensure that even when a person is not vaccinated, they receive protection because the people surrounding them are resistant to the disease and are unlikely to transmit it to them or harbor an outbreak. However, for herd immunity to be effective, 19 out of 20 people (95%) of the population must be vaccinated (7). When many people are immune, the chances of infection to the rest of the population are rare because it is unlikely an unvaccinated person will come in contact with an infected person.
There are medical conditions which make the vaccine unsafe to receive. New babies are at risk for many diseases until they are old enough to receive all vaccinations (5). Many people are at risk for infectious diseases because they are unable to receive the MMR vaccine. Other populations who should not be vaccinated include patients who are:
- An anaphylactic allergic response to a component in the MMR vaccine,
- Immunosuppressed or compromised,
- Recently received blood products,
- Suffering from active tuberculosis or other severe illness.
Lastly, many people are unaware of the risks of measles because they have never seen it. However, measles could become endemic in the U.S. again if vaccine coverage decreases significantly and herd immunity is lost (4). It is critical to discuss this possibility with your patients so that they are aware of the significant risk of the anti-vaccination movement. Most patients and caregivers are unaware that Measles can result in life-threatening complications, such as pneumonia and encephalitis.
Parent Education and Shared Decision Making
While many healthcare professionals have strong opinions regarding vaccination, using shared decision making to further parental understanding of vaccinations is critical. It can be upsetting for parents to see their infant or child receive multiple injections. By opening the discussion of the risks and benefits, the nurse provides parents with essential information regarding vaccination. It is crucial that nurses have an open discussion and to acknowledge the concerns of patients and families.
Despite multiple immunizations in each visit until their second birthday, the CDC states that a healthy child’s immune system will not become overwhelmed by the vaccinations. There is a slight risk for side effects with immunizations up to severe allergy, disease, and death, but most are mild, like redness and swelling at injection site (3). However, vaccine-preventable diseases can be fatal, and the benefits of the vaccine far outweigh the risks. The risks from becoming ill with the measles are far worse than the risks associated with the vaccination (3). These are important point to make families aware of.
The U.S. FDA ensures the safety, effectiveness, and availability of vaccines. Current vaccinations have each been evaluated by scientists and continually monitor for other side effects after FDA licensure. Any complications or adverse effects are tracked by the Vaccine Adverse Event Reporting System (VAERS). If the CDC and FDA find a link between a particular immunization and a specific side effect, they will weigh the benefits against the risks and update the safety information on the Vaccine Information Sheets (VIS) (3).
How will you approach education and support decision making for patients and families?
What information specifically would you provide in these situations?
The Anti-Vaccination Movement and Public Health Implications
In 2018, there was a measles outbreak in Washington that was considered a public health crisis. In the first few months of 2019, more than 100 vaccine-related bills were introduced in 30 states across the country.
Some states have proposed to eliminate vaccine exemptions or tighten the laws surrounding mandatory vaccination to attend school, while other state regulations recommend exemption expansions.
The Food and Drug Administration (FDA) commissioner Scott Gottlieb controversially made a public statement warning state legislators that they must replace lax laws. Mr. Gottlieb notified states that if they do not tighten vaccine exemptions than the federal government would take action (2).
The MMR vaccine is very effective against measles. Receiving two doses of MMR is 97% effective, while just one dose is still 93% effective (5). However, measles is an extremely contagious disease that can spread quickly in an unvaccinated population . In 2013, an unvaccinated teenager returned to New York from the U.K. Over the next three months, measles spread throughout Brooklyn. At the conclusion, 58 people across the city became infected with measles. Not a single person who became ill with measles had documentation of being vaccinated (6).
The “anti-vax” movement goes beyond lay people. In the fall of 2018, a Texas nurse posting on social media about a toddler with measles in the PICU. The nurse shared to an anti-vaccination group that measles was much worse than she expected. “I think it’s easy for us nonvaxxers to make assumptions, but some of us have never and will never see one of these diseases. (1)”
She stated that despite the severity of the disease in the toddler, she wanted to purposely transmit measles from the child to her unvaccinated child at home. While she possessed nursing knowledge, she did not understand epidemiology. She felt that natural immunity would be safer than vaccination. Despite seeing measles for the first time and knowing how ill the child was, she did not change her vaccination stance and acknowledged she never would.
Her beliefs did not affect her employment, but her behavior did. She was fired from the children’s hospital for sharing private health information after families made hospital administrators aware (1). Thus, it is essential to obtain your data from evidence-based resources like the CDC instead of peers.
The moral of this story is that no amount of evidence can convince hardline anti-vaccinations proponents. It is our job to provide information, education, and promote shared decision making. Ultimately it is the parent or patient’s right (in most states) to refuse vaccines.
Nurses are busy working to assess, evaluate, educate, and empower their patients. Administering vaccines piles another task on a nurse’s overburdened list, but it is our job to ensure each patient receives appropriate education on vaccinations. Assessing vaccination status should be a priority for each and every admission and intake. It is critical to evaluate each patient’s vaccination status to ensure that all vaccines have been administered per the wishes of the parents and/or patients.
For further information about immunizations specific to healthcare providers, please visit: www.cdc.gov/vaccines/hcp
If you need more information about measles, see: www.cdc.gov/measles
To report an adverse reaction to a specific vaccination, visit: vaers.hhs.gov
(1) ABC News. (2018, August 29). Texas nurse fired after posting about patient’s
measles on anti-vaccination page. Retrieved from https://abcnews.go.com/beta-story-container/US/texas-nurse-investigation-posting-patients-measles-anti-vaccination/story?id=57443736&fbclid=IwAR3Y7iXlC3-z2IP29aQ8fGQp8EJIxgUE4Tkf4OWgGelZTKGsRNEPP8mhMls
(2) AP News. (2019, February 25). National Vaccination Information Center: Public
hearings on measles outbreaks and vaccine laws provide opportunities for Americans to voice concerns. Retrieved from https://apnews.com/Business%20Wire/1375c31e40d94327a2c873570c1f65ef
(3) Centers for Disease Control and Prevention. (2019a). Making the vaccinedecision. Retrieved from https://www.cdc.gov/vaccines/parents/vaccine-decision/index.html
(4) Centers for Disease Control and Prevention. (2019b). Measles (Rubeola).
Retrieved from https://www.cdc.gov/measles/hcp/index.html
(5) Centers for Disease Control and Prevention. (2018). Measles, mumps, and
rubella VIS. Retrived from https://www.cdc.gov/vaccines/hcp/vis/vis- statements/mmr.html
(6) Fischer, P. B. (2018). Measles from coast to coast: Risks, costs, and potential
interventions. Infectious Disease Alert, 37(12).
(7) Funk, S. (2013). Critical immunity thresholds for measles elimination. Retrieved
(8) Vanderbilt University Medical Center. (n.d.). Type of Isolation Needed.
Retrieved from https://ww2.mc.vanderbilt.edu/infectioncontrol/12177
5.Childhood Asthma: Prevention and Treatment
Introduction to Asthma
One in 13 people are directly affected by asthma (5). Asthma is a chronic disease of the lungs that causes wheezing, coughing, difficulty breathing, and chest tightness (9). For patients with asthma a common cold or allergic rhinitis can quickly escalate into a life-threatening event. Triggers in the environment can quickly initiate trouble among delicate, inflammation prone, airways.
Although asthma is one of the most prevalent chronic diseases among adults and children, it is often not well controlled. While many patients know that they have asthma, many do not know how to manage it to prevent exacerbations. This can be especially devastating in children as their daily schedules, sleep, education, and activities can be significantly altered by uncontrolled asthma.
Educating and empowering patients and their families to prevent disease exacerbation is a key component of successful asthma treatment. We will discuss asthma prevalence, common triggers, signs of asthma exacerbations, and prevention strategies in this course.
What is Asthma?
Asthma is a chronic disorder of the respiratory system that is characterized by four primary components: recurrent respiratory symptoms, bronchial hyper-responsiveness, airway obstruction, and inflammation (9).
Certain factors such as genetics, environment, socioeconomic status, smoking status, and race/ethnicity can increase the chances of developing asthma. Common triggers of asthma include allergens, pollution, cold air, stress, and exercise, among other irritants.
Environmental factors trigger dendritic cells, which produce B and T cell lymphocytes, initiate IgE production of mast cells, eosinophil, and neutrophils. The end result of this cascade is bronchial inflammation.
These cells also activate Th2/Th1 cytokines which amplify the response of the smooth muscle walls leading to persistent inflammation and remodeling of the tissues (long-term) (9).
Airway Remodeling in Asthma
When bronchoconstriction and airway inflammation are persistent airway edema occurs, worsening asthma symptoms. Airway edema can continue to exacerbate symptoms by promoting increased mucus production, mucous plugging, and hypertrophy and hyperplasia of the smooth muscles.
The combination of bronchoconstriction and airway inflammation gives rise to the chronic symptoms of coughing, wheezing, and difficulty breathing.
This is known as airway remodeling and this process makes asthma treatment more complicated as many commonly prescribed medications have limited response on altered bronchial tissues (9).
Importance of Early Diagnosis and Management
While asthma cannot directly be cured, it can be managed. The earlier asthma is diagnosed, the earlier prevention education can be provided, and the earlier pharmacological management initiated, if indicated.
The primary goal in asthma therapy is to prevent and reduce chronic inflammation (which leads to airway remodeling) and acute exacerbations.
Proper management of asthma symptoms helps to reduce chronic damage by way of airway remodeling while reducing the odds of death related to an asthma attack and increasing quality of life.
Why is early diagnosis of asthma key in management?
What are some of the difficulties in diagnosing asthma in young children?
Prevalence and Impact of Pediatric Asthma
Below are statistics of asthma prevalence in children from the Centers for Disease Control and Prevention’s National Health Interview Survey (NHIS) (3,5,6,9):
• Approximately 6,000,000 children in the United States have been diagnosed with asthma.
• 50-80% of children with asthma develop symptoms before their fifth birthday.
• Approximately 1 in 10 school-age children have asthma.
• Approximately 50% of children with asthma have reported having asthma exacerbations and/or having poor control of their asthma within the past year.
• 10.5 million school days are missed every year due to asthma symptoms.
• ⅓ of hospitalizations in children under the age of 15 are related to asthma.
• In 2016, 209 children died from asthma related illness.
Presentation and Risk Factors
Children can be diagnosed with asthma at a very young age. These children usually present with symptoms of persistent allergy, cough, and intermittent wheeze (6). They often present to the primary care office or emergency department with asthma symptoms during periods of increased allergen exposure and/or a viral respiratory illness.
Respiratory viruses attack airway structures causing inflammation and increased mucus production which exacerbate asthma symptoms. Children with asthma symptoms prior to the age of 3 have been seen to have significant lung growth deficits by age 6 (9). Early diagnosis and treatments are critical in reducing such complications.
Gender is a risk factor for asthma development. In early childhood, boys are more likely to have asthmatic symptoms. Later after puberty, that risk flips and girls more commonly have asthmatic symptoms (12). Children of African American and Puerto Rican descent have higher risk than those of Caucasian or Hispanic backgrounds (8).
Children with obesity are more likely to have develop asthma (9). Finally, asthma is more prevalent in households with income <100% below the poverty line (12).
While all children with persistent respiratory symptoms should be flagged and followed for potential asthma disease work-up, clinicians should be aware of the risk factors and be vigilant in screening and diagnosing those patients.
What are some modifiable risk factors for the development of asthma in pediatrics?
How can you educate parents and caregivers on these?
Diagnosis and Treatment Disparities
In a survey completed by the CDC’s National Center for Health Statistics (NCHS), it was recorded that in 2016 only 71.1% of children with asthma had routine healthcare visits (12).
Access to healthcare, especially in many rural and poverty-stricken areas, is a national concern. Creating outreach programs in schools, primary care offices, and local hospitals may help maximize asthma screening and treatment for at-risk children.
It is critical that healthcare providers recognize these care disparities and work with local and national resources to increase screening and diagnosis.
Asthma diagnosis and exacerbations are ranked based on of severity of symptoms, control, and responsiveness to therapies. Severity is the “intrinsic intensity of the disease process” (9). It can be measured by incidence of symptoms without long-term therapy.
Control is “the degree to which the manifestations of asthma are minimized and goals of therapy are met” (9). Finally, responsiveness is how easily asthma symptoms (especially exacerbations) can be managed (9).
A combination of family and individual medical history, lung function testing, and history of asthma-related medication use help determine asthma diagnoses and treatment plans.
Patients with severe symptoms and a decreased response to therapy are at an increased risk for severe, life-threatening asthma attacks.
There are four classifications of asthma severity:
• Persistent Mild
• Persistent Moderate
• Persistent Severe.
In children, components of severity are further separated by age group: 0-4 years, 5-11 years, and >12 years. Each level is described by the quantity of symptoms being experienced.
These symptoms include nighttime awakenings, need for short-acting beta2-antagonists (SABA) for quick relief of symptoms, work/school days missed, ability to engage in normal activities, and quality of life assessments (9).
Lung function testing with spirometry should be performed in a healthcare office to evaluate the child’s lung compliance. This test should be attempted in all children age 5 years old or greater if asthma diagnosis is being considered (9). Spirometry measures the child’s forced expiratory volume in 1 second and in 6 seconds (FEV1 and FEV6) and forced vital capacity (FVC).
Spiromerty should be performed before and after inhaling a SABA medication to help determine if there is airflow obstruction, its severity, and reversibility with use of a SABA (responsiveness) (9). The resulting numbers are compared to expected values for each age group and written as percentages.
Greater than 85% of expected lung compliance is considered normal for children up to age 19. Asthma severity and lung compliance are inversely related- the further the decrease in compliance the more severe the asthma is.
When combined with the child’s history of symptoms and medication use, healthcare providers can determine the classification of asthma severity and appropriate treatment measures using the stepwise approach. The stepwise approach helps to standardize asthma symptoms and initiate related therapies.
Healthcare providers use this information to determine when to move up or down a treatment level to provide the most effective management with the least number of exacerbations from this disease. Provider assessment of a child’s asthma maintenance therapy should be completed every 4-6 weeks with therapy changes and then every 3-6 months with good symptom control (8).
Can a patient with well-controlled asthma experience a life-threatening attack?
Which patients are most at risk for severe asthma attacks?
Some patients have asthma which is not severe but is also not responsive to therapy. How would you categorically describe this?
Stepwise Approach for Classifying Asthma Severity
The chart below outlines the evaluation of asthma utilizing a standard step-wise approach. First choose the child’s age and then ask questions pertaining to the impairment/risk. Based on this you will be given a “step”. The appropriate treatment for each step is outlined a table you will view shortly.
Stepwise Approach for Classifying Asthma Severity (9)
COMPONENTS OF SEVERITY
>2 days/week but not daily
Throughout the day
>2 days/week but not daily
Several times per day
Interference with normal activity
Exacerbation requiring oral systemic corticosteroids
≥2 exacerbations in 6 months requiring oral systemic steroids or ≥4 wheezing episodes/1 year lasting >1 day and risk factors for persistent asthma
Recommended step therapy
Step 3 plus consider short course of oral systemic corticosteroids
>2 days/week but not daily
Throughout the day
>1x/week but not nightly
>2 days/week but not daily
Several times per day
Interference with normal activity
Normal FEV1 between exacerbations
FEV1 >80% predicted
FEV1 = >80% predicted
FEV1 = >60%-80% predicted
FEV1 = <60% predicted
Exacerbation requiring oral systemic corticosteroids
≥2 per year. Consider time since last exacerbation as frequency and severity may change overtime.
Recommended step therapy
Step 3, medium-dose ICS option and consider short course of oral systemic corticosteroids
Step 3 medium-dose option, or Step 4 and consider short course of oral systemic corticosteroids
>2 days/week but not daily
Throughout the day
>1x/week but not nightly
>2 days/week but not daily, and not more than 1 time on any day
Several times per day
Interference with normal activity
Normal FEV1 between exacerbations
FEV1 >80% predicted
FEV1 >80% predicted
FEV1 = >60% but <80% predicted
FEV1/FVC reduced by 5%
FEV1 = <60% predicted
FEV1/FVC reduced by >5%
Exacerbation requiring oral systemic corticosteroids
≥2 per year. Consider time since last exacerbation as frequency and severity may change overtime.
Recommended step therapy
Step 3 and consider short course of oral systemic corticosteroids
Step 4 or Step 5 and consider short course of oral systemic corticosteroids
Asthma is treated in a stepwise approach based on asthma symptom severity. Using the stepwise approach allows providers to prescribe appropriate medications for each child in order to optimizing symptom control.
A review of common asthma medications and their escalation of prescription based on the stepwise approach are listed below.
Stepwise approach for pharmacologic management of asthma (9)
|0-4 years||SABA PRN||Preferred:|
Cromolyn or montelukast
Medium-dose ICS plus either LABA or montelukast
High-dose ICS plus either LABA or montelukast
High-dose ICS plus either LABA or montelukast plus consider oral systemic corticosteroid
|5-11 years||SABA PRN||Preferred:|
Cromolyn, LTRA, nedocromil, or theophylline
Low-dose ICS plus either LABA, LTRA, or theophylline
Medium-dose ICS plus LABA
Medium-dose ICS plus either LTRA or theophylline
High-dose ICS plus LABA
High-dose ICS plus either LTRA or theophylline
High-dose ICS plus LABA plus oral systemic corticosteroid
High-dose ICS plus either LTRA or theophylline plus oral systemic corticosteroid
|≥12 years||SABA PRN||Preferred:|
Cromolyn, LTRA, nedocromil, or theophylline
Low-dose ICS plus either LABA or Medium-dose ICS
Low-dose ICS plus either LTRA, theophylline or zileuton
Medium-dose ICS plus LABA
Medium-dose ICS plus either LTRA, theophylline or zileuton
High-dose ICS plus LABA AND consider omalizumab for patients with allergies
High-dose ICS plus LABA plus oral corticosteroid AND consider omalizumab for patients with allergies
Inhaled Short-Acting Beta2-Agonists (SABA):
SABA medications are the preferred therapy in the event of acute asthma symptoms, asthma exacerbations, and in preventing exercise-induced asthma symptoms (taken before the activity). Albuterol, Levalbuterol, and Pirbuterol relax airway smooth muscles within minutes to allow relief of inflammation and improvement of airflow.
Children with intermittent asthma may not require a daily, preventative medication. They may only be prescribed a SABA medication for acute symptom exacerbation. Frequency of SABA medication use can be an indicator of asthma activity and control.
Using a SABA medication greater than two days a week for symptom relief generally indicates suboptimal control and indication to move up a treatment step. Of note, all children with asthma are prescribed a SABA medication to use as a rescue, quick-relief medication. (9)
Inhaled Corticosteroids (ICS):
Inhaled Corticosteroids work by suppressing cytokine involvement, decreasing the involvement of the airway’s eosinophil cells and preventing an increase in inflammatory mediators. Use of long-term ICS can prevent the need for oral systemic steroid administration by controlling asthma symptoms. Variable dosing of ICS medication is used depending on severity and persistence of asthma symptoms.
Side effects in long-term use include impaired growth in children, decreased bone mineral density, skin thinning and bruising, and cataracts. Children on this medication should be instructed to use a spacer (if applicable) and rinse their mouths after inhalation to prevent oral thrush. Common ICS medications include Fluticasone (Flovent HFA), Budesonide (Pulmicort Flexhaler), Mometasone (Asmanex Twisthaler), Beclomethasone (Qvar RediHaler), and Ciclesonide (Alvesco) (9)
Cromolyn Sodium and Nedocromil:
Cromolyn sodium and nedocromil are alternative treatment options to low-dose ICS for mild persistent asthma and exercise-induced asthma. These medications are generally not preferred in children. Studies have shown inconclusive results to the impact of effectiveness of this medication in children. (9)
Leukotriene modifiers (LTRA):
Leukotriene modifiers may be used as an alternate treatment option for mild persistent asthma and step 2 of asthma management. They are not recommended over LABA medications in ages >12 years. These medications work by preventing the release of mast cells, eosinophil cells, and basophils that cause airway constriction, vascular permeability, and increased mucous.
Medications in this class include Montelukast, Zafirlukast, and Zileuton. Montelukast can be prescribed in children over the age of 1 and Zafirlukast for children over the age of 7. Zileuton is currently not approved for use in children. (9)
Theophylline is a methylxanthine that can be used as an alternative or adjunctive therapy to ICS for mild persistent asthma in children older than 5. In previous trials, theophylline was shown to have little effect on airway reactivity and produced significantly less control than the use of low-dose ICS alone (9). Because of this and it’s narrow margin of safety, it’s use has largely fallen out of favor.
Inhaled Long-Acting Beta2-Agonists (LABA):
LABA medications stimulate the beta2-receptors to relax the smooth airway muscles. They are the preferred medication to be used in adjunct with ICS medications. They are not recommended alone and not recommended to treat acute asthma symptom exacerbation. LABA therapy should be considered in children ages 5+ who are not well controlled on ICS management alone. The LABA medications on the market today are Salmeterol and Formoterol. (9)
Oral Systemic Corticosteroids:
Oral corticosteroids are usually reserved for severe asthma flares or in the event of difficult-to-control asthma. Side effects such as adrenal suppression, growth suppression, dermal thinning, hypertension, Cushing’s syndrome, cataracts, and muscle weakness may occur and are more likely with chronic usage. If oral corticosteroids are being used more than three times a year for management of asthma exacerbations, reevaluation of long-term asthma control should be evaluated.
Immunotherapy for asthma management is a relatively new concept. Research is currently being performed to address and assess the effectiveness of immunotherapy in preventing asthma symptoms.
Some therapy modules being studied include Omalizumab, Methotrexate, Soluble interleukin-4 receptor, anti-IL-5, recombinant IL-12, cyclosporin A, intravenous immunoglobulin (IVIG), and clarithromycin. (9)
Complementary and Alternative Medicine (CAM):
Many CAM therapies have not been proven to statistically to reduce asthma incidence, severity, or risk. Practicing alternative medicine strategies is not recommended as a replacement to scientifically proven pharmacologic management, but they may be used as an adjunct if appropriate.
These therapies include acupuncture, chiropractic therapy, homeopathic and herbal medicine, breathing techniques, relaxation techniques, and yoga. (9)
There are a myriad of treatment options for pediatric patients with asthma. What are the first-line treatments?
What are some of the side effects of long term systemic corticosteroid administration? Are these risks the same for inhaled steroids?
Some patients wish to incorporate CAM therapies. How will you approach this? What kind of education would you provide on this subject?
Asthma Prevention Strategies
Asthma Action Plan:
The Asthma Action Plan (1) is a great tool for families. It can improve recognition of the early signs of asthma exacerbations and facilitate appropriate treatment of asthma symptoms. It was found in the NCHS’s National Health Interview Survey performed in 2016, that only 50.8% of children reported they had received asthma actions plans and only 76% were taught how to recognize early signs of an asthma attack (12). If updated frequently with the child’s healthcare provider and followed in the event of asthma symptoms it may reduce exacerbation severity and duration, primary care office visits, hospital visits, and asthma-related deaths (1).
Asthma action plans are designed to provide families one place to collect all the child’s critical information regarding their asthma including: name, date of birth, current medications for long-term maintenance, quick-relief medications, medication dosing/instructions, and important phone numbers in case of emergency. This information helps guide caregivers to act quickly when exacerbations occur. It also identifies common asthma symptoms that might be overlooked and plans appropriate treatment steps to complete in the event these symptoms occur.
There are three zones on the Asthma Action Plan: green, yellow, and red. Each zone indicates increasing severity of symptoms and identifies appropriate treatments or interventions. With proper control of their asthma disorder, children and adults alike should spend a majority of their days in the green zone. This zone indicates that there are no asthma symptoms, even in play or activity (1). Prevention of trigger exposure is the key to maintaining this zone.
The next zone, yellow, indicates that the child is not feeling well and is experiencing asthma symptoms such as coughing, wheezing, runny nose/cold symptoms, breathing harder or faster, waking at night coughing, and playing less than usual (1).
The final zone, red, indicates the danger zone in which the child’s symptoms worsen so drastically that in addition to giving the medications listed on the plan, taking the child immediately to the hospital or calling 9-1-1 is the necessary course of action (1).
Some children, even if they spend the majority of their days in the green zone, can quickly escalate to the red zone. Educating families on this plan is critical to helping them make the best decisions for their children in both preventing and managing asthma symptoms.
Controlling Allergies and Environmental Triggers
Children with asthma often lead normal lives until a trigger initiates the inflammatory cascade resulting in an asthma exacerbation. Up to 90% of children with asthma symptoms also have allergies (11). Some of the most common allergens and environmental triggers for asthma, both indoor and outdoor, include dust mites, molds, trees or pollens, cockroaches, pet dander, secondhand smoke, ozone, and particle pollution (7,11).
Exercise and stress can also be triggers for asthma symptoms (10). While limiting exercise is not generally recommended unless prescribed by a healthcare provider, choosing less physically demanding exercises may result in better asthma control. Children with well-controlled asthma are often able to complete activities and exercise as desired (10).
Teaching families how to identify asthma triggers and avoid the child’s exposure when possible can significantly reduce asthmatic complications. Below are a few suggestions that can be offered to families to help improve environments for children with asthma.
Avoiding Common Asthma Triggers (2,7,9):
- Frequently wash hands to avoid spread of infection (common cold, alternate viruses, bacteria).
- Close house windows, doors, and car windows to prevent increased exposure to pollens and other outdoor allergens
- Use zippered mattress and pillow covers to reduce exposure to dust mites.
- After playing outside, immediately change clothes and/or bathe to reduce prolonged exposure to outdoor allergens.
- If possible, remove old carpeting and/or frequently vacuum when child is not around.
- Avoid humidifiers that may harbor mold and bacteria.
- Monitor for food allergies including but not limited to milk, eggs, peanuts, tree nuts, soy, wheat, fish, shellfish, and food additives.
- Address pets in the home. If pets are an asthma trigger and rehoming is not an option, bathe pets weekly, keep them outside as much as possible, and avoid having them in child’s bedroom.
- Avoid secondhand smoke. Ask those who smoke to not smoke around the child, smoke in designated rooms, or cease smoking all together.
These interventions, along with providing thorough asthma prevention and treatment education to families have been proven to significantly reduce complications from asthma (12).
Peak Flow Meters
Peak flow meters are small, hand-held devices used to measure exhaled airflow (2). In the event of an asthma exacerbation, airways become inflamed, trapping air in the lungs and increasing the difficulty of proper exhalation. The use of the peak flow meter can help identify narrowing of the airway prior to the actual presence of asthma symptoms (2).
In the National Health Interview Survey (NHIS) performed in 2016, reports determined that only 50.6% of children were taught how to use a peak flow meter (12). Using the peak flow meter presents an opportunity treat early signs of asthma exacerbations with the hope of ultimately reducing the incidence of moderate to severe symptoms.
Peak flow meter education may seem intimidating to families at first. However, it is quite simple. Just like the Asthma Action Plan, peak flow meters have three zones that indicate severity of airway inflammation. The green zone is considered the safe zone, yellow is the caution zone, and red is the emergency zone (2). Each zone indicates a percentage of the child’s personal best exhaled air flow.
The green zone indicates 80-100% of the child’s personal best flow; the yellow zone measures 50 to less than 80%; and the red zone measured less than 50% of the child’s personal best flow. (9) Using the results of the peak flow meter test with the asthma action plan can help families decide the appropriate course of action in asthma management.
To use the peak flow meter, the child should move the marker on the meter to zero, sit or stand-up straight, take a deep breath, put the meter into the mouth closing the lips around the mouthpiece, and blow as hard and fast as possible (9). The number noted on the meter should then be marked in a log and the steps repeated 5-6 more times (9).
The best three numbers should then be recorded in a final log to determine how well the child’s asthma is controlled. Families should be instructed to record a log over the course of a couple weeks to determine the child’s best peak flow rate as well as determine the colored zones for future asthma management.
After the zones are created with the data collected, the child should then use the peak flow meter daily, to determine if the child is experiencing airway inflammation. The child and family should use the results to compare to the treatment plan as written on the child’s asthma action plan (2,9).
What age-appropriate interventions can you use to ensure that patients properly utilize their inhalers and peak flow meters?
For example how would you approach a toddler in comparison to an adolescent?
Proper Medication Administration
Proper medication administration is crucial to asthma control. It is no longer recommended to use inhaled medications without the use of a spacer (4). A spacer device helps deliver doses of inhaled medication in a more streamlined and coordinated movement (4).
However, despite being taught how to properly use a spacer upon prescription of an inhaled medication, many children and families forget to use or improperly use the device. Spacer use and proper medication administration should be reviewed with every child and their family at all asthma related healthcare appointments and/or emergency department visits.
Ensuring that children and families are using medications correctly may reduce and even prevent serious asthma exacerbations in the future.
Asthma is a prevalent, chronic illness in society. Understanding the disease process, therapy options, and promoting prevention strategies can help manage this chronic disease- reducing complications and improving quality of life.
Online resources offered through national organizations, such as the Centers for Disease Control and Prevention, American Academy of Pediatrics, Healthy People 2020, the Asthma and Allergy Foundation of America provide excellent information for both patients and healthcare members.
It has been said that an ounce of prevention is worth a pound of cure. This holds true for asthma even more so than many other diseases. Focusing on prevention strategies, proper and prompt treatment, and appropriate use of resources are the cornerstone of asthma treatment.
A father and his 5-year-old son present to the primary care office: The father states that the child has been coughing at night 2-4 nights a week; coughing every morning; and has difficulty breathing with exercise or exertion. The child experienced a cold a few weeks ago and since then, the coughing has not improved.
The father denies any fever. He describes the coughing as hoarse, hollow, dry, and sometimes barky. The child also frequently experiences rhinorrhea and increased sputum, but father denies those symptoms at present. The father mentions that they have been to the emergency department twice in the past 6 months for similar symptoms and the child has received two treatments of nebulized Albuterol (2.5mg) at each visit.
They were not sent home with any medications. Father states that while the Albuterol treatments in the emergency department helped for a couple days, the coughing would return. The family has one dog in the home and the child frequently spends time at his grandparents’ house where he is exposed to secondhand smoke.
The child appears healthy in clinic today. His vital signs read: O2: 100%, Respiratory Rate: 13, Heart Rate: 119, Blood Pressure: 97/62, and Temperature: 98.2F. He is sitting comfortably in the office but will frequently clear this throat and have a harsh cough. Upon listening to the child’s lungs, wheezes are noted bilaterally in the bases. There are no retractions, rhonchi or rales.
The healthcare provider performs spirometry testing to evaluate the child’s lung compliance and level of obstruction prior to administering a SABA medication. After completing the spirometry, the child is noted to have a FEV1 75% of predicated value. A nebulized Albuterol treatment is completed and the child performs the spirometry again. After the treatment, the child’s FEV1 returns to a normal range >85% of predicted value.
Physical exam reveals improvement in wheezing and the child states he can breathe better. Based on the child’s history of persistent coughing >2 nights a week, coughing every morning, limitations on activity due to respiratory symptoms, and an initial abnormal FEV1 (though resolved after SABA administration), the healthcare provider determines that the child has Mild-Persistent Asthma.
Based on the step-wise approach of managing asthma, the child is treated as a Step 2 for symptoms aligning with mild-persistent asthma disease. The healthcare provider prescribes the child a rescue Albuterol inhaler (SABA) and long-term, low-dose Fluticasone (Flovent HFA) inhaler (ICS). The healthcare provider recommends to the father that the child be tested for allergies to help identify possible triggers to asthma symptoms. If the child is found to have significant allergies, an additional allergy medication may be prescribed at that time.
The father and child are educated on proper administration of the medications with use of a spacer and given a peak flow meter to measure the child’s exhaled airflow. The father is instructed on how to find the child’s best peak flow rate over the next two weeks and use that to determine critical values of expected airflow. The child should continue to record the peak flow measurements daily to assess early changes in airway obstruction.
The healthcare provider then develops an Asthma Action Plan with the father and child to provide a guideline of therapy, write important medication and emergency information, and help to identify early asthma symptoms and emergency treatments.
They discuss common asthma triggers to avoid. The father and child are encouraged to keep their pets out of the child’s room as much as possible and outside whenever feasible. The child should use a zippered mattress and pillow protector to prevent exposure to dust mites and flooring should be mopped or vacuumed frequently while the child is outside of the home.
It is also recommended that secondhand smoke exposure is limited by way of having grandparents smoke outside of the home, see the child at his home where there is less smoke, and change their clothes or use a smoking jacket that can be removed after smoking before being with the child.
With new information in hand, the father and child, while overwhelmed, feel they can start to prevent and treat the child’s asthma symptoms. The family should be encouraged to follow-up closely with their primary healthcare provider to ensure appropriate control and reduce chronic airway inflammation.
(1) American Academy of Pediatrics. (2016). Asthma action plan and school medication authorization. Retrieved from https://portal.ct.gov/-/media/Departments-and-Agencies/DPH/dph/hems/asthma/pdf/sampleasthmaactionplanaapmarch2017pdf.pdf?la=en
(2) Asthma and Allergy Foundation of America. (2015). Preventing asthma episodes and controlling your asthma. Retrieved from https://www.aafa.org/asthma-prevention/
(3) CDC. (2015). Asthma: Asthma-related missed school days among children aged 5-17 years. Retrieved from https://www.cdc.gov/asthma/asthma_stats/missing_days.htm
(4) CDC. (2018). Asthma: Know how to use your asthma inhaler. Retrieved from https://www.cdc.gov/asthma/inhaler_video/default.htm
(5) CDC. (2018). Asthma: Most recent asthma data. Retrieved from https://www.cdc.gov/asthma/most_recent_data.htm
(6) CDC. (2015). Asthma severity among children with current asthma. Retrieved from https://www.cdc.gov/asthma/asthma_stats/severity_child.htm
(7) CDC. (2018). Home characteristics and asthma triggers: Checklist for home visitors. Retrieved from https://www.cdc.gov/asthma/pdfs/home_assess_checklist_P.pdf
(8) Hsu J, Sircar K, Herman E, Garbe P. (2018). EXHALE: A technical package to control asthma. Atlanta, GA: National Center for Environmental Health Centers for Disease Control and Prevention.
(9) National Asthma Education and Prevention Program. Expert Panel Report 3: Guidelines for the Diagnosis and Management of Asthma. (2007). NIH Publication 07-4051. Bethesda, MD: National Heart, Lung, and Blood Institute. Retrieved from http://www.nhlbi.nih.gov/guidelines/asthma/
(10) Schuers, M., Chapron, A., Guihard, H., Bouchez, T., & Darmon, D. (2019). Impact of non-drug therapies on asthma control: A systematic review of the literature. European Journal of General Practice. doi: 10.1080/13814788.2019.1574742
(11) United States Environmental Protection Agency. (2016). Asthma facts. Retrieved from https://www.epa.gov/sites/production/files/2016-05/documents/asthma_fact_sheet_english_05_2016.pdf
(12) Zahran, H., Bailey, C., Damon, S., Garbe, P. & Breysse, P. (2018). Vital signs: Asthma in children — United States, 2001–2016. DOI: http://dx.doi.org/10.15585/mmwr.mm6705e1
6.Fluid Resuscitation in Sepsis: How Much and What Kind?
The Importance of Fluid Resuscitation in Sepsis
- In patients with septic shock, fluid resuscitation is a critical intervention that restores tissue perfusion. However, there is a great deal of variation in the type of fluid, rate of administration, and the total volume of fluid administered.
- IV fluids should be prescribed like any other drug we give our patients: with a critical look at the indication and contraindication for different types, while balancing the risk of administering too little vs the increasingly apparent sequelae of over administering (1)
- Circulatory insufficiency and shock result from inadequate perfusion relative to the tissue demands (2). Often times, the demand side of perfusion imbalance is an overlooked means of reversing the pathophysiology of shock. Early goal-oriented fluid resuscitation may be crucial in deciding the outcome, but it is important to be aware that the pathogenic inability of the mitochondria to utilize available oxygen may limit the effectiveness of hemodynamic interventions.
- What can cause circulatory insufficiency? The three basic contributors are pump failure, insufficient vascular tone (the vasodilation we see in sepsis), and hypovolemia (2).
- Patients with distributive shock (the primary shock seen in sepsis) may experience circulatory insufficiency due to the profound vasodilatation that is associated with the inflammatory reaction to an infection. (3). As shock progresses and the mean arterial pressure (MAP) trends downward, the cerebrocortical functions are the first to be impaired, which often manifests as a change in the level of consciousness or altered mental status (2).
- As perfusion decreases from vasodilation or from decreased cardiac function, tissue beds become globally hypoxic. The GI tract and the kidneys are known to be intolerant of hypotension and precipitous decrease in MAP, which can lead to impaired mucosal function, bowel integrity, or in extreme cases frank ischemic necrosis (2).
- Secondary to developing tissue hypoxia, and as a result of anaerobic metabolism in the absence of adequate tissue oxygenation, patients may develop a high lactic acid level as a response to the progressive tissue hypoxia. A serum lactate of 4 or greater is associated with increased severity of illness and poorer outcomes even if hypotension is not present (3).
- Knowing this, providers should be prepared to fluid resuscitate patients who are hypotensive or have a lactate >/= 4 mmol/L in order to expand their circulating blood volume and restore tissue perfusion pressure (3).
The Great Debate: Crystalloid vs. Colloid
- Crystalloids are the low-cost salt solutions that are known to be the go-to, easy to grab, and often time’s first choice fluids (4). Isotonic crystalloids are the most commonly administered IV fluid internationally- fun fact: crystalloid solutions were first prepared in response to the cholera pandemic in 1832. So they’ve been around since forever.
- Crystalloids evolved over the next century into two broad groups: sodium chloride (ex. Normal saline) and physiologically-balanced solutions (ex. Lactated Ringers or Plasmalyte). Only about 20-30% of administered crystalloid fluid will stay in the intravascular space. (5).
- Colloids are suspensions of molecules in a carrier fluid with high enough molecular weight to prevent crossing healthy capillary membranes, thus a larger percentage of the administered fluid will remain intravascular. (5)
- Colloids are more expensive fluids and are either man-made (starches, dextrans or gelatins) or naturally occurring (albumin or fresh frozen plasma) (4).
- The physiologic rationale behind favoring colloid over crystalloid is the thought that colloids may expand intravascular volume more effectively by remaining in the intravascular space and maintaining colloid oncotic pressure (5).
- The use of human albumin was first introduced during WWII for victims of traumatic or thermal injuries. Interesting- but a bit cringe-worthy to think of the sterility of this WWII human albumin…
- In the Saline versus Albumin Fluid Evaluation (SAFE) study, a prospective, controlled, randomized, double-blind study comparing 4% human albumin with 0.9% normal saline solution in critically ill patients requiring fluid resuscitation, there was near identical mortality rates in both patient groups. However, there was a small, statistically nonsignificant benefit to using human albumin in the sepsis subgroup. The current SSC guidelines have a weak recommendation (2C) for the administration of albumin in patients with severe sepsis or septic shock who are receiving large amounts of crystalloid fluid. (3).
- In 2013, the Colloids versus Crystalloids for the Resuscitation of the Critically Ill (CRISTAL) study, researchers investigated mortality of ICU patients resuscitated with crystalloids versus colloids (6). After 28 days, there was no statistically significant difference in mortality between the two groups. However, the study continued to track patients through day 90 and found fewer deaths in the colloid group as compared to the crystalloid group (30.7% vs 34.2%, p= 0.03) (6). The colloid group also experienced fewer days of mechanical ventilation and fewer days needing vasopressor therapy (6). While these results seem to be impressive, the study used isotonic crystalloid fluid in both patient groups as maintenance IV fluid, and many patients were treated with different fluids that randomized to prior to study enrollment. Thus, these results should be used with caution given the major study design flaws.
- (The Albumin Italian Outcome Sepsis (ALBIOS) trial in 2014 was a large RCT that compared the administration of crystalloid to the administration of 20% albumin with crystalloid (6). At 28 days and at 90 days there was no significant change in mortality between the two groups (6). At 28 days, 31.8% of patients in the albumin group vs 32% of patients in the crystalloid group had died (p=0.94) (6). Similarly, at 90 days 41.1% of the albumin group and 43.6% of the crystalloid group had died (p=0.29) (6).
- The results of the SAFE, CRISTAL, and ALBIOS trials did not show a clear benefit associated with the use of albumin and combined with the increased cost, crystalloids are the fluid of choice for patients with a diagnosis of sepsis. As research continues, we may begin to see a trend towards better outcomes with albumin administration, but it is currently not recommended as first-line treatment.
How will you incorporate the evidence presented in the above information in your practice?
In what types of situations would you use crystalloids VS colloids?
How does the cost of colloid factor into the decision making process, especially when weighed against the negligible potential difference in outcomes?
Choice of Crystalloid Fluid for Resuscitation: Is Normal Saline Really “Normal”?
- The use of saline versus a balanced crystalloid solution has been a topic of ongoing debate.
- Due to the high mortality, the burden to society, and increasing awareness surrounding sepsis, there has been extensive research done to identify the optimal fluid treatment protocols. Ultimately, much of the choice is dictated by provider preference, hospital protocol, and regional availability due to a lack of evidence-based guidelines on specific fluid choice.
- Fluid composition can have unintended physiological effects, such as altering the pH balance through the metabolism of lactate and acetate leading to a decrease in bicarbonate, and eventually metabolic acidosis, and the potential for acute kidney injury (6).
- The Saline Against Lactated Ringers or Plasma-Lyte in the Emergency Department (SALT-ED) study is a pragmatic, cluster, multiple-crossover trial at a single center evaluating the clinical outcomes of patients treated with 0.9% NS versus balanced crystalloids in the setting of resuscitation in the emergency department (7). The trial included 13,347 patients who received a median of 1 liter of fluid (7). Saline increased the risk of death or renal failure when compared to LR/Plasmalyte (5.6% vs 4.7%, p= 0.02). The subgroup of patients with renal injury at the time of admission was more susceptible to adverse kidney events from saline administration (37.6% vs 28%, p= <0.001) (7). This trial confirmed that saline increases the risk of renal failure when compared to balanced solutions.
- These results were then duplicated at Vanderbilt and included critically ill patients. The SMART trial, a pragmatic, cluster-randomized, multiple – crossover trial, was conducted in five intensive care units at an academic center and included 15,802 adult patients (5). Patients were randomized to receive either 0.9% NS or LR/Plasmalyte. Among the 7,942 patients in the balance crystalloid group, 1,139 (14.3%) had an adverse kidney event, compared to 1,211 of the 7,860 (15.4%) patients in the NS group (p = 0.04) (5). In-hospital mortality at 30 days was higher in the NS group when compared to the balanced crystalloid group, as well (11.1% vs 10.3%, respectively, p = 0.06) (5). The mortality difference in the two groups suggests that NS may not only be causing renal failure but may also be causing harm to patients via additional mechanisms, including increased inflammation. (8).
- Normal saline as a resuscitation fluid should not be administered in high amounts as it carries the risk of inducing a hypernatremic hyperchloremic metabolic acidosis (8). Some patients are already extremely acidotic, and by giving them fluid that will exacerbate their academia is poor practice. The truth is that “normal” saline is not physiologically normal. It is a hypertonic, acidotic fluid that can cause more harm than good, especially in patients who need large volume resuscitation. That being said, the development of electrolyte disturbances secondary to fluid administration also depends on the electrolyte status of the patient before resuscitation is initiated.
- In an RCT of patients with pancreatitis that included a comparison between LR and NSS, patients who were treated with NS had higher levels of C-reactive protein one day after the initiation of resuscitation (p = <0.05), meaning that increased saline administration may have a direct correlation to the degree of inflammation (8).
- All of this is not to say that saline is all bad and should never be used, but to point out that just because “it’s what we’ve always used”, “it’s easy to grab”, or “the patient is hyperkalemic!” are not justifiable reasons to use high volumes of NS in the resuscitation of your patients. There are better options, and believe it or not, hyperkalemia is not a contraindication to LR! One liter of LR only contains 4 mEq of potassium!
- While not all balanced crystalloids are created equal, the SALT-ED trial provides good evidence that LR is superior over NS with a number needed to treat (NNT) of 111, which is currently the highest evidentiary support for any balance crystalloid (7).
Balanced crystalloids may have an advantage over saline-based solution for IV fluid resuscitation. How will you incorporate this into your practice?
What types of patients are likely to benefit from a saline-based resuscitation VS balanced crystalloids?
Some of the unintended effects of saline administration can be high-priority, such as renal failure and a higher risk of death according to some studies. Should we always use balanced solutions when electrolytes permit?
How much fluid do septic patients need?
- The concept of prompt IV fluid administration was first accepted after the 2001 study of early goal-directed therapy (EGDT). In the study, patients either received standard therapy, which involved arterial and central venous catheterization and a protocol targeting a CVP 8-12 mmHg, mean arterial pressure (MAP) at least 65 mmHg, and urine output of at least 0.5 ml/kg/hr, or the EDGT group (5). The EDGT group included the aforementioned components but also included a catheter to measure central venous oxygen saturation (SvO2), six hours of treatment in the emergency department before admission, and administration of 500 mLs of crystalloid fluid every 30 minutes to achieve CVP goals, vasopressors, and vasodilators to maintain MAP goals, and blood transfusions or dobutamine to achieve ScvO2 >/= 70% (5). Overall, in-hospital mortality was found to be 16% less with EDGT when compared to standard therapy (46.5% vs 30.5%; p= 0.009) (5).
- The results of this landmark study propelled early and protocolized fluid management to the forefront of sepsis management. Because of this study and future studies that replicated the above results, the Surviving Sepsis Campaign (SSC) began promoting EGDT fluid resuscitation as a cornerstone of sepsis and septic shock management (5).
- The SSC 3-hour and 1- hour bundle both recommend the initial administration of 30 mL/kg of crystalloid fluid for hypotension or lactate >/= 4 mmol/L as a fluid challenge with a target CVP goal >/= 8 mmHg, ScvO2 of >/= 70%, and normalization of lactate (9). A patient may need repeat fluid challenges in the initial phases of sepsis/septic shock, and this bolus dose is meant to rapidly expand the patient’s blood volume to allow for providers to assess the patient’s response to fluid resuscitation.
- A key concept for dosing fluid therapy in the critically ill population is to actively address ongoing losses (drains, stomas, fistulas, or hyperthermia, open wounds, or various causes of polyuria) paired with the frequent reassessment of the need for further hemodynamic support (10). While fluid administration is a critical aspect of resuscitation, excessive fluid accumulation has been associated with worse clinical outcomes- particularly the development of acute kidney injury (AKI), pulmonary edema, pleural effusions, and in some cases an increase in ventilator days (10).
- The idea of interrelated phases of fluid management, coined “ebb and flow”, differentiated according to the patient’s clinical status with evolving goals for fluid need is highly individualized, but an important concept in the management of the septic patient in order to avoid adverse events related to poor fluid management (10).
- In the initial phase of fluid resuscitation, the objective is the restoration of effective circulating blood volume, organ perfusion, and tissue oxygenation. Fluid accumulation and a positive fluid balance are to be expected here (10). This is basically the only phase we’ve discussed thus far.
- In the second phase, the goal is a maintenance of intravascular volume homeostasis (10). The goal is to prevent excessive fluid accumulation and to avoid unnecessary fluid loading. By the second phase, the patient should show evidence of adequate tissue perfusion.
- In the third and final stage, the objective centers around fluid removal and the concept of “de-resuscitation” as dictated by the state of physiologic stabilization, organ injury recovery, and convalescence (10). During this phase, unnecessary fluid accumulation may add to secondary organ injury and adverse events.
- As mentioned previously, resuscitation goals for the septic patient are to return the patient to a physiologic state that promotes adequate organ perfusion along with matching metabolic supply and demand.
- Ideally, resuscitation end points should assess the adequacy of tissue oxygen delivery (DO2), oxygen consumption (VO2), and should be quantifiable and reproducible. Since there fails to be a single resuscitation endpoint despite years of research, providers must be able to rely on multiple endpoints in order to determine the patient’s overall response to therapy (11). The SSC focuses their resuscitation guidelines on the original EGDT protocol with an emphasis on macro and microcirculatory endpoints (CVP 8-12mmHg in spontaneously breathing patients/12-15mmHg in ventilated patients, MAP >/= 65mmHg, urine output >/= 0.5mL/kg/hr, central venous oxygen saturation >/= 70% or mixed venous oxygen saturation >/= 65%) (11).
- The ProCESS, ARISE, and ProMISe trials have all compared the original EGDT protocol with contemporary care and have found no difference in clinical outcomes, thus prompting the thought that the one size fits all approach to sepsis may be an outdated approach to treatment.
30mL/kg can be a very large amount of fluid in patients with high body weights. Would you still follow the recommendation of 30mL/kg in these cases?
There is much debate about the optimal amount of fluid resuscitation. What are some of the concerns with over and under resuscitation. Which is likely more detrimental in terms of mortality?
Macrocirculation End Points of Sepsis Resuscitation: Central Venous Pressure
- A previously well-established starting point in determining a patient’s need and subsequent responsiveness to fluids is to utilize a static measurement, such as the central venous pressure (CVP) or pulmonary artery occlusion pressure (PAOP) (11). As most providers know- using the CVP as an initial resuscitation target and estimate of preload adequacy is fundamentally flawed. Factors such as total blood volume, cardiac output/venous return, pulmonary hypertension, cardiac tamponade, arrhythmias, and human error involving leveling of the transducer are all factors that have the potential to impact the central venous pressure (11). The correct interpretation of a CVP value is as follows: a low CVP value of </= 6 almost always indicates hypovolemia. However, a high value does not exclude hypovolemia nor does it guarantee hypervolemia.
Microcirculation End Points of Sepsis Resuscitation: Lactate
- Moving from a “macro” point of view to a “micro” point of view, there are several clinical and laboratory values that providers use to assess the microcirculation. Most commonly, lactate, central venous oxygenation, and capillary refill time.
- Lactic acid is one of the most widely accepted biomarkers used to diagnose sepsis-related organ dysfunction. Typically, a lactate >/= 4mmol/L was used as the threshold for organ dysfunction, but recently a threshold of >/= 2mmol/L has been used (11). The working theory behind increased lactate in septic shock is that as global tissue hypoxia occurs, oxygenation fails to meet tissue oxygen demand, therefore increasing anaerobic metabolism…and lactic acid level (11). Just like when you show up for that 1st day of spring 5K after spending the last 4 months on your couch watching Netflix documentaries….need.more.oxygen!!!
- Unfortunately, this very basic explanation fails to consider other contributions to elevated lactate. It continues to be widely accepted and used as a marker of microperfusion, but providers should be aware that there are still limitations.
- Elevated lactate can be attributed to 4 broad categories: decreased tissue oxygen delivery, underlying disease, drugs/toxins, and inborn errors of metabolism (11).
- In decreased oxygen delivery, you could see elevated lactate in individuals who have had a tonic-clonic seizure, severe asthma attack, severe anemia, carbon monoxide poisoning, or chose to do one of those Spartan Races in July. In the underlying disease subset, you could have increased lactate in patients who have fulminant liver failure, lymphoma/leukemia, small cell lung cancer, pheochromocytoma, or thiamine deficiency (sepsis would also fall under this category) (11).
- Drugs and toxins that can often be responsible for an increased lactate include Biguanides, Linezolid, Cyanide poisoning, NRTIs, and beta 2 agonists (11). The rarer inborn metabolism errors are the patients who have enzyme deficiencies such as pyruvate dehydrogenase, pyruvate carboxylase, Fructose-1-6,-diphosphatase, and Phosphoenolpyruvtate carboxykinase (11).
Microcirculation End Points of Sepsis Resuscitation: SvO2/ScvO2
- Moving past lactate measurement to more technical measurements tissue oxygenation, both mixed venous oxygen saturation (SvO2) and ScvO2 have been considered as important targets because they can be used to estimate a global balance of cellular oxygen demand vs delivery (11). A ScvO2 <70% is indicative of inadequate oxygen delivery to tissues, increased oxygen extraction, or a combination of the two. It’s important to note that a true ScvO2 has to be obtained via a central venous catheter with the tip appropriately placed at the junction of the superior vena cava and the right atrium (11).
- Assuming it is measured at the correct location, a ScvO2 of 70%-89% is suggestive of a well-balanced VO2/DO2. A ScvO2 >/= 90% suggests poor oxygenation utilization at the cellular level, tissue dysoxia, or microcellular shunting (11). Currently, the routine use of SvO2 and ScvO2 is not supported in the literature, but the role may become more apparent as sepsis end-goal resuscitation research continues to increase in prevalence.
Microcirculation End Points of Sepsis Resuscitation: Capillary Refill Time
- While technology and invasive tests offer pertinent information, these interventions should be performed in conjunction with frequent clinical examinations to assess the response.
- Capillary refill time is a basic examination skill that new literature is examining as a valuable tool to assess regional and global tissue perfusion during septic shock resuscitation.
- Capillary refill time is defined as the duration of the time needed for the patient’s fingertip to regain color after direct pressure is applied to cause blanching. In a healthy patient, the refill time should be <3.5 seconds (11). It’s important to note that skin temperature, room temperature, age, and use of vasoactive medications can impact capillary refill time and should be taken into consideration. Assuming the patient’s extremities are normothermic, a refill time of >5 seconds suggests the presence of abnormal microcirculatory flow (11).
- Serial assessment with normalization within 6 hours is associated with successful resuscitation when compared against traditional resuscitation targets.
Estimating Fluid Responsiveness with SVV and bedside echocardiography
- Dynamic indices such as stroke volume variation (SVV), pulse pressure variation, and inferior vena cava variability all have been found to have a better predictive value, sensitivity, and specificity than the static indices (11). In patients who are spontaneously breathing or have arrhythmias, direct measurement tests such as the expiratory occlusion test and passive leg raise may be preferred (11).
- As SVV of >12 has an 88% sensitivity and 89% specificity for predicting fluid responsiveness in patient without cardiac arrhythmias and requiring mechanical ventilation. Some monitoring equipment may calculate SVV with a standard arterial line only, other times a special arterial line may need to be inserted in order to measure SVV (15).
- Sepsis-induced cardiac dysfunction is well described and often presents as a reduction in left ventricular stroke volume and impaired myocardial performance. Non-invasive ways to measure the cardiac output and cardiac indexes, such as the FloTrac or Vigileo systems or basic bedside echocardiography, have become more common. The use of invasive pulmonary artery catheters are associated with more risk than patient benefit and their use has significantly decreased. Information gained from bedside echocardiography includes: rough estimate of cardiac output, LV and RV function, chamber fluid status, IVC size and variability, and global cardiac function. This information can be invaluable when utilized in real-time, especially to measure the responsiveness of treatments.
There are multiple types endpoints we can use to measure fluid resuscitation and volume status. Which end points are favored in your clinical practice?
As an extension to the previous question- will you incorporate any of the information gained in this module into your practice?
Fluid challenge without the fluid: Passive leg raise and end-expiration occlusion test
- What could be better than determining the effect of a fluid bolus without actually infusing any fluid? Though these techniques are imperfect, they can provide insight into the “fluid responsiveness” of a patient.
- The passive leg raise test is another noninvasive means to assess fluid need by mimicking a fluid bolus. It involves moving a patient from the semi-recumbent position to a position where the legs are lifted at 45 degrees and the trunk remains horizontal (2). This induces a transfer of 250-350 mL of venous blood from the inferior limbs and the splanchnic compartment towards the thoracic and cardiac cavities mimics the increase in cardiac preload induced by fluid infusion. The threshold to define fluid responsiveness with a passive leg raise test is a 10% increase in stroke volume or cardiac output (1). Cardiac output changes can be detected 1-2 minutes after the maneuver is performed using either SVV via a non-invasive technology (Flo-Trac) or by utilizing bedside echocardiography to visualize the changes in cardiac function (12). A positive response may also be noted if blood pressure increases with a decrease in heart rate, though this is less sensitive and specific. Similar to capillary refill, the passive leg raise can be done regardless of arrhythmia or mode of mechanical ventilation (12).
- The end-expiration occlusion test is another fluid responsive test, but specifically for the subset of patients who require mechanical ventilation. The test consists of stopping mechanical ventilation at end expiration for 15 seconds and measuring the changes in cardiac output. By pausing mechanical ventilation there is an increase in cardiac output by stopping the cyclic impediment of venous return that occurs at each ventilator triggered breath. An increase in cardiac output above the threshold of 5% indicates fluid responsiveness.
Putting it together
- The best approach is to use multiple techniques to measure the efficacy of fluid resuscitation. Relying on any single parameters is not ideal practice and may lead to under or over-resuscitation. The best way to use this data is to perform interventions which increase perfusion (usually a fluid bolus in sepsis) and re-measure the end-point. A trend toward better perfusion (lower lactic acid level, faster capillary refill, etc.) indicates a positive response. A negative response can be due to either: 1.) inadequate volume of fluid resuscitation OR 2.) a patient that is no longer fluid responsive. It can be difficult to discern the difference and the passive leg raise or occlusion test may be helpful here. There is no hard and fast rule, but generally it is thought to be better to over-resuscitate than under resuscitate.
- By systematically using this approach, there aim is to properly resuscitate the patient while avoiding the pitfalls of both over and under-resuscitation. End-points should be measured after each intervention.
- For example if you measure a lactic acid level of 8 and note delayed capillary refill on exam, you may determine that fluids will augment cardiac output and increase tissue perfusion. Thus you choose to administer 1L bolus. Once the bolus is complete, you should re-check the lactic acid level and capillary refill. It may not normalize, but there should be improvement.
In summary, fluid resuscitation in sepsis is a controversial topic. Nurses should utilize a variety of end-points to measure fluid status and perfusion status. Newest evidence is suggesting that LR may have a physiologic benefit over NS and albumin may have role in the resuscitation of septic patients.
1) Malbrain, M. L., Regenmortel, N. V., Saugel, B., Tavernier, B. D., Gaal, P. V., Joannes-Boyau, O., . . . Monnet, X. (2018). Principles of fluid management and stewardship in septic shock: It is time to consider the four D’s and the four phases of fluid therapy. Annals of Intensive Care,8(1), 1-16. doi:10.1186/s13613-018-0402-x
2) Marini, J. J., & Dries, D. J. (2019). Shock and support of the failing circulation. In Critical Care Medicine: The essentials and more(5th ed., pp. 47-67). Philadelphia, PA: Lippincott Williams & Wilkins.
3) 3- Hour Bundle. (n.d.). Retrieved March 21, 2019, from http://www.survivingsepsis.org/SiteCollectionDocuments/Bundle-3-Hour-Step4-Fluids.pdf
4) Lewis, S. R., Pritchard, M. W., Evans, D. W., Butler, A. R., Alderson, P., Smith, A. F., & Roberts, I. (2018, August 3). Colloids or crystalloids for fluid replacement in critically people. Retrieved March 21, 2019, from https://www.cochrane.org/CD000567/INJ_colloids-or-crystalloids-fluid-replacement-critically-people
5) Semler, M. W., & Rice, T. W. (2016). Sepsis Resuscitation: Fluid Choice and Dose. Clinics in chest medicine, 37(2), 241-50.
6) Avila, A. A., Kinberg, E. C., Sherwin, N. K., & Taylor, R. D. (2016). The Use of Fluids in Sepsis. Cureus. doi:10.7759/cureus.528
7) Self, W. H., Semler, M. W., Wanderer, J. P., Ehrenfeld, J. M., Byrne, D. W., Wang, L., Atchison, L., Felbinger, M., Jones, I. D., Russ, S., Shaw, A. D., Bernard, G. R., … Rice, T. W. (2017). Saline versus balanced crystalloids for intravenous fluid therapy in the emergency department: study protocol for a cluster-randomized, multiple-crossover trial. Trials, 18(1), 178. doi:10.1186/s13063-017-1923-6
8) Farkas, J. (2018, February 27). PulmCrit- Get SMART: Nine reasons to quit using normal saline for resuscitation. Retrieved March 21, 2019, from https://emcrit.org/pulmcrit/smart/
9) Levy, M. M., Evans, L. E., & Rhodes, A. (2018). The Surviving Sepsis Campaign Bundle. Critical Care Medicine,46(6), 997-1000. doi:10.1097/ccm.0000000000003119
10) Mcdermid, R. C. (2014). Controversies in fluid therapy: Type, dose and toxicity. World Journal of Critical Care Medicine,3(1), 24-33. doi:10.5492/wjccm.v3.i1.24
11) Greenwood, J. C., & Orloski, C. J. (2017). End Points of Sepsis Resuscitation. Emergency Medicine Clinics of North America,35(1), 93-107. doi:10.1016/j.emc.2016.09.001
12) Boyd, J. H., Sirounis, D., Maizel, J., & Slama, M. (2016). Echocardiography as a guide for fluid management. Critical Care,20(1), 1-7. doi:10.1186/s13054-016-1407-1
13) Byrne, L., & Van Haren, F. (2017). Fluid resuscitation in human sepsis: Time to rewrite history?. Annals of intensive care, 7(1), 4.
14) De Backer, D., & Vincent, J. L. (2018). Should we measure the central venous pressure to guide fluid management? Ten answers to 10 questions. Critical care (London, England), 22(1), 43. doi:10.1186/s13054-018-1959-3
15.) Xavier M., Marik, P., Jean-Louis T. (2016) Prediction of fluid responsiveness: an update. Annals of intensive care. doi: 10.1186/s13613-016-0216-7
7.The One Hour Sepsis Bundle: How to Act in 60 Minutes
- It’s nothing new to healthcare workers that sepsis is a big deal, and often at the top of provider’s differential diagnosis when patients begin to decompensate and the cause is not yet clear. There is good reason, too. The incidence of sepsis from 1979 – 2000 increased by 8.7% from 82.7 to 240.4 per 100,000 population (1). The incidence of sepsis is increasing as a result of the aging population, progressive increase in antibiotic resistance, reliance on implanted devices, organ transplantation, and an increasing prevalence of patients with long-term immunosuppressive diseases who are at risk for severe infection and sepsis (1).
- In order to understand the importance of the sepsis bundle and why there is an emphasis on treating sepsis as a medical emergency, similar to a STEMI or a CVA.
- Sepsis is a life-threatening syndrome consisting of numerous signs, symptoms, hemodynamic, and laboratory findings caused by an excessive and dysfunctional host immune response to severe infection that leads to dysregulated organ dysfunction (2). Septic shock is a more severe subset of sepsis that commonly presents with circulatory and/or metabolic dysfunction. Septic shock carries a 30-40% mortality risk (2).
- The current sepsis definitions were published by the Third International Sepsis Task Force in 2016 are based on the fact that it is the dysregulated immune response, and not the infectious agent itself, that is the cause of the pathophysiological process (2).
Diagnostic Approach to Sepsis
- Early phases of sepsis can be subtle even in the carefully monitored patient, but if the subtle signs are missed and the clinical signs of septic shock become glaringly apparent, you and your clinical team are acting much too late.
- Fever is a characteristic sign, but hypothermia can also be present (and has the connotation of a worse prognosis).
- Below is a table depicting the most common hemodynamic changes seen in sepsis (1).
Finding in Sepsis
|Major compensatory mechanism for low systemic vascular resistance|
Mean arterial blood pressure
|Hallmark of septic shock if it remains low after adequate fluid resuscitation|
|Cardiac index usually elevated in early septic shock; may be depressed in late septic shock|
Pulmonary arterial occlusion pressure (PAOP)
|Assure that hypovolemia is not the cause of hypotension; perform fluid resuscitation until PAOP returns to normal|
Central venous pressure (CVP)
|Indicator of volume status. If it is <6 the patient is likely volume depleted. A normal or high value can have many different causes|
Systemic vascular resistance (SVR)
|SVR often low in early septic shock; may become elevated in later phases of septic shock|
|Mixed venous O2 saturation (SvO2) or|
central venous O2 saturation (ScvO2)
|Low mixed venous O2 saturation or central venous O2saturation (from superior vena cava) indicates poor oxygen delivery to tissues|
|Oxygen consumption (Vo2)|
|Typically increased in early septic shock|
- The updated guidelines use the Sequential (Sepsis Related) Organ Failure Assessment Score (SOFA) to define sepsis. The SOFA score assesses the degree of organ dysfunction across numerous domains. A score of 2+ reflects an overall mortality of about 10% in the setting of a suspected infection (1). The laboratory data included in the SOFA score focuses on coagulopathy, hepatic dysfunction, and/or renal dysfunction (1). Other laboratory data (such as WBC) can aid in the diagnosis of infection but are not used to define sepsis or septic shock.
- A bedside tool called qSOFA (Quick SOFA) was developed to quickly identify adult patients with suspected infection who are likely to have poor outcomes (1). The presence of any 2 of the following is equal to a positive qSOFA: 1) respiratory rate >/= 22/min; 2) Glasgow Coma Score <15; and/or 3) SBP </= 100 mmHg (1). The qSOFA is best used to identify early organ dysfunction in adults on general medical/surgical floors, whereas the SOFA score is used more in the critical care setting (1).
- The qSOFA tool can be used to quickly screen and identify patients who are at risk for deterioration. It is being used both on admission and as ongoing tool to track changes in patient condition.
- The chart below illustrates common laboratory findings seen in sepsis (1).
White Blood Cell count
Leukocytosis or leukopenia
|Stress response, increased margination of neutrophils in sepsis can cause transient neutropenia; toxic granulation|
|Look for evidence of fragmentation hemolysis; thrombocytopenia may be accompanied by DIC|
Elevated prothrombin time (INR), aPTT, low fibrinogen levels, elevated D-dimer; evidence of fibrinolysis
|Coagulopathy very common, but overt DIC is not common (< 15% of patients)|
Elevated alkaline phosphatase, bilirubin, and transaminases; low albumin
|Generally a late finding in sepsis, indicates hepatic ischemia and transaminases typically >10 times upper limit.|
>2.2 mmol/L caused by hypermetabolism, anaerobic metabolism, inhibition of pyruvate dehydrogenase
|Poor prognostic feature if not improved rapidly by fluid resuscitation; diagnostic criterion for septic shock (with suspected infection).|
Can have other causes of elevation- high sensitivity with low specificity.
Elevated as an acute phase reactant from hepatic synthesis
|Acute-phase reactant, sensitive, but not specific for sepsis|
Hyperglycemia or hypoglycemia
|Acute stress response can lead to hyperglycemia, inhibition of gluconeogenesis can lead to hypoglycemia|
Arterial blood gas (ABG)
Respiratory alkalosis (early); metabolic acidosis (late)
|Reduced arterial O2 content and mixed venous O2 saturation|
Think about your clinical experiences. Have you seen patients with sepsis who presented with atypical signs (hypothermia, respiratory alkalosis, etc.).
Do you think this delayed their diagnosis and care? How will you use this information to better detect patients who may have sepsis?
Over the years many tools have been identified in hopes of detecting sepsis early. How does the sensitivity and specificity of each of these tools affect their usability?
A Word on Sepsis Shock
- Septic shock occurs in up to 15% of patients with sepsis (1).
- It is defined as hypotension requiring intravenous vasopressors to maintain a MAP >/= 65mmHg and a serum lactate of >2mmol/L (1).
- In a patient with early septic shock, the hemodynamics will reflect a high cardiac output and a low systemic vascular resistance indicative of profound vasodilation and a compensatory increase in cardiac output in an attempt to preserve peripheral vascular perfusion. As shock progresses, myocardial performance diminishes and circulating blood volume is continually lost to the interstitial space, which perpetuates the profound hypotensive state. Sepsis-induced myocardial dysfunction may ensue. This results in a potentially reversible heart failure state due to myocardial depression.
- The management of the patient in septic shock hinges on prompt recognition of the patients deteriorating condition and expeditious administration of antibiotic therapy coupled with infectious source control. Simultaneously, the failing organ systems must be supported through measures such as, fluid resuscitation, vasopressors, blood transfusions, respiratory support, and inotropic agents. You can find more details regarding the initial management of sepsis in the Surviving Sepsis Campaign guidelines.
What Is a “Bundle,” and Why Are They Used?
- The Surviving Sepsis Campaign developed the internationally endorsed “sepsis bundle” separately from their guidelines as a way to guide sepsis quality improvement (3). The bundles consist of various components of sepsis care including, fluid resuscitation, timely and appropriate antibiotic administration, blood cultures, and the use of serum lactate levels (4).
- The bundle elements were designed in such a way so as to be updated as new evidence emerged (3).
- In response to the most recent guidelines published in 2016, there has been a revised “hour-1 bundle” as opposed to the previous 3 hour and 6 hour bundles (3) (5).
- There has been evidence that shows an association between compliance with bundles and improved survival in patients with sepsis and septic shock. In a multi-center, retrospective, observational study of adult patients with a hospital discharge diagnosis of severe sepsis or septic shock, overall mortality was lower in those who received bundle-adherent care (17.9%) when compared to those who did not (20.4%) (4). Interestingly, when the patients in the study were divided into subgroups by suspected source of infection, there was only a statistically significant mortality benefit to bundle-adherent sepsis care in patients diagnosed with pneumonia (4).
How do you think the shift from a 3/6 hour bundle to a 1 hour bundle with affect patient care?
How can hospitals adapt to this measure?
Is the allocation of additional resources justified?
1-Hour Bundle Components and Strategies to Expedite Care
- The most critical change in the Surviving Sepsis Campaign bundles is that the previous 3-hour and 6-hour bundles are now combined into a single “hour-1 bundle” with the intention of beginning resuscitation and management immediately upon presentation (3) (5). While more than one hour may be needed for patient resuscitation to be completed, the initiation should begin immediately upon suspicion that the patient may be presenting with sepsis.
- Measure lactate level: Serum lactate level serves as a surrogate for direct tissue perfusion measurement (3). In the absence of oxygen anaerobic metabolism ensues and lactate levels rise. It often represents the degree of tissue hypoxia present, and increased levels are associated with worse outcomes. If the initial lactate is >2mmol/L, it should be re-measured within 2-4 hours and used to guide resuscitation with the goal of achieving a lactic acid <2mmol/L (3).
Tips for expedited care:
Hospitals should have a threshold of >/= 2mmol/L for a critical lactic acid value, which will prompt any abnormal value to be communicated to the provider. Consider having non-nursing personnel collect the lactate level so that the nursing staff is free to focus on other tasks. The re-collection of lactates >2 can be automated by many electronic order entry systems and will help reduce fallouts due to re-collection. Point of care lactate is now readily available which can be very valuable.
All critical lactate values should be communicated to both the nurse and the provider. Traditionally this has been done by a call to the nurse who then notifies the provider. We suggest that lab calls both the provider and the nurse directly, to reduce the potential for error.
- Obtain blood cultures prior to antibiotics. Blood cultures can become sterile within minutes of the first dose of appropriate antibiotic (3). By obtaining cultures before administering antibiotics, there is a better opportunity to identify pathogens, and therefore improve patient outcomes. Appropriate cultures include at least two sets of both aerobic and anaerobic cultures from two separate venipuncture sites. However, administration of antibiotic therapy should not be delayed past 1 hour in an effort to obtain cultures (3).
Tips for expedited care:
This is another task that can be delegated to non-nursing personnel, and the focus should be on sterile technique as contamination can completely change the treatment course for the patient. It may be helpful to have dedicated personnel and checklists for collecting blood cultures to ensure standardized care. Some evidence suggests that newer cleaning agents may reduce contamination.
- Administration of broad-spectrum antibiotics. Empiric broad-spectrum antibiotic therapy with one or more intravenous antimicrobials to cover all likely pathogens should be started immediately (3). Once a pathogen is identified and sensitivities are established, the empiric antibiotics should be narrowed or discontinued if the patient is found to not to have an active infection (3).
Tips for expedited care:
Since time is of the essence when treating a patient presenting with sepsis, the empiric antibiotics should be kept in the on-unit medication storage for ease of access. Nurses should have immediate access to these medications.
All orders for sepsis antibiotics should be ordered as STAT (for the first dose). The providers should be trained to enter antibiotics orders directly after examining patients, if possible. Delays in ordering obviously lead to a delay in medication delivery. The goal should be to have a culture that recognizes and treats sepsis as a medical emergency, just as a code stroke or myocardial infarction.
- Administer IV Fluid. Early effective fluid resuscitation is critical for the stabilization of sepsis-induced tissue hypoperfusion and septic shock (3). Initial fluid resuscitation should be begin immediately upon recognizing that a patient is presenting with sepsis and/or hypotension and elevated lactate (3). Fluid resuscitation should be completed within 3 hours of recognition. Current guidelines recommend that intravenous fluid resuscitation consist of 30 mL/kg bodyweight of crystalloid fluid (3).
Tips for expedited care:
Providers should communicate the need for intravenous fluids verbally to the nursing staff and place orders into the order entry system directly after examining patients. The patient should have 2-3 large bore IVs placed to facilitate the administration of IV fluids and IV antibiotics without sacrificing the timing of one or the other. Often times, placing a central line takes anywhere from 15-30 minutes, and will delay overall patient care during the first minutes. If additional venous access is needed, it is advisable to wait until the patient is stabilized so long as adequate reliable IV access is obtained.
- Apply vasopressors. A critical part of sepsis resuscitation is restoring perfusion to the vital organs. If a patients blood pressure does not return to normal after the initial fluid resuscitation, then vasopressors should be initiated to maintain a mean arterial pressure (MAP) of >/= 65 mmHg (3). If a patient has profound hypotension and the decision is made by the medical team to initiate vasopressor therapy, there is no need to wait to initiate until central access is obtained (3). Vasopressors can be infused through a large bore peripheral IV safely for a short amount of time (3).
Tips for expedited care:
Within the ER and ICUs, there should be easy access to vasopressors, specifically norepinephrine, vasopressin, and epinephrine, in the event that a patient needs a vasopressor started. Additionally, institutions should have standing protocols for nurses to initiate a vasopressor in the event that a patient is consistently hypotensive despite adequate fluid resuscitation. This will save vital time by allowing the nurse to use their clinical judgment and restore vital organ perfusion quickly and efficiently while awaiting provider guidance.
How can you incorporate these tips and techniques for expedited care into your practice?
What are some barriers you anticipate facing if you attempted to adopt these strategies?
Do you think it is feasible for hospitals to adapt a 1 hour bundle?
- Despite bundle care and the diligent work of healthcare providers and beside nurses alike, many hospitals have identified an opportunity to save lives and reduce suffering through early sepsis detection, compliance with current standards of care and determining the appropriate level of care.
- The Emergency Department Code Sepsis Project focuses on timely implementation of the SSC care bundle to reduce mortality and costs and to ensure appropriate level of care placement. By activating a ‘code sepsis’ it allows not only doctors and nurses to be aware of the urgency at hand, but also pharmacists, respiratory therapists, lab technicians, nursing support staff, and unit secretaries.
- In some facilities, a ‘code sepsis’ is worked into the framework of the rapid response team. For example, if a nurse screens a patient for SIRS criteria and the patient meets the criteria, a page can be sent out from the patients current floor and this will mobilize the appropriate resources in order to facilitate swift and effective resuscitation.
- In a retrospective observational quasi-experimental study conducted at the Hospital Clinico Universitario de Valladolid, researchers found that the in-hospital, intra-ICU, and 28-day mortality rates were all higher in the “pre code-sepsis” group (6). In –hospital mortality was 56% in the pre-code sepsis group, compared to 31% in the code sepsis group, p=0.035 (6). 28-day mortality also exhibited a statistical significant change (p= 0.035) with 44% and 23%, respectively (6). Intra-ICU stay was also longer in the pre-code sepsis group with an average stay of 10.5 days compared to 5 days in the code sepsis group, p = 0.05 (6).
- The multidisciplinary nature of the code sepsis project creates a strong sense of teamwork centered around applying best evidence-based practice, mobilizing resources, avoiding procedure variability, and improving patient care and safety (6).
- Hospitals that are struggling to meet sepsis measures should consider the addition of a “code sepsis” or “sepsis response team”.
Sepsis as a Medical Emergency
- Each organization should strive for a culture that treats sepsis with the same urgency as any other medical emergency. Much of the delay in treatment with sepsis is due to a lack of standardized processes. Hospitals should work to develop sepsis protocols and sepsis response teams in order to increase compliance with bundles and decrease mortality.
How could a code sepsis benefit your sepsis patients?
Do you think that a code sepsis would expedite care in your facility?
- Ultimately the one hour bundle is a call by the Surviving Sepsis Campaign and does not affect hospital reporting to Medicare/Medicaid. These measures (at the time of this writing) are still collecting data and reporting based on the 3/6 hour bundles previously set forth by the Surviving Sepsis Campaign. Expediting care may reduce mortality and morbidity associated with sepsis.
1) McCulloh, R. J., & Opal, S. M. (2017). Sepsis, Septic Shock, and Multiple Organ Failure. In Lange Critical Care. Retrieved March 8, 2019, from https://accessmedicine.mhmedical.com/book.aspx?bookid=1944
2) Marini, J. J., & Dries, D. J. (2019). Sepsis and Septic Shock. In Critical Care Medicine: The essentials and more(pp. 576-594). Philadelphia, PA: Lippincott Williams & Wilkins. Retrieved March 8, 2019, from http://ovidsp.dc1.ovid.com/
3) Levy, M. M., Evans, L. E., & Rhodes, A. (2018). The Surviving Sepsis Campaign Bundle: 2018 update. Intensive Care Medicine,44(6), 925-928. doi:10.1007/s00134-018-5085-0
4) Milano, P., Desai, S., Eiting, E., Hofmann, E., Lam, C., & Menchine, M. (2018). Sepsis Bundle Adherence Is Associated with Improved Survival in Severe Sepsis or Septic Shock. Western Journal of Emergency Medicine,19(5), 774-781. doi:10.5811/westjem.2018.7.37651
5) Hour-1 Bundle. (n.d.). Retrieved March 11, 2019, from http://www.survivingsepsis.org/Bundles/Pages/default.aspx
6) García-López, L., Grau-Cerrato, S., Frutos-Soto, A. D., Lamo, F. B., Cítores-Gónzalez, R., Diez-Gutierrez, F., . . . Andaluz-Ojeda, D. (2017). Impact of the implementation of a Sepsis Code hospital protocol in antibiotic prescription and clinical outcomes in an intensive care unit. Medicina Intensiva (English Edition),41(1), 12-20. doi:10.1016/j.medine.2017.02.001
8.Chest Tubes 101
The ancient Greeks were the first to record techniques used to drain the pleural space (1). Though the process and equipment have evolved over the centuries, the basic principles have not changed (1). Today, thoracostomy tube (more commonly known as a chest tube) placement continues to be a very common procedure.
Chest tubes are utilized for a variety of reasons, ranging from emergent placement to routine use after an elective surgery (1). They can be placed just about anywhere– the bedside, the operating room (OR), and interventional radiology.
Most nurses will encounter chest tubes at some point during their career– perhaps frequently, depending on where you work. Thus, it is essential for nursing staff to feel comfortable with chest tube management. Unfortunately, like anything else in healthcare, chest tubes are at risk for complication. Quick identification of potential complications could be the difference between life and death. This course aims to expand your knowledge and increase confidence in chest tube management.
What Is a Chest Tube?
Licensed and retrieved from Adobe Stock
Let’s start with a quick refresher on the structure of our lungs. First comes skin (obviously). Beneath that is a layer of subcutaneous tissue, followed by muscle. Then we come to the ribs, which form the basic protective cage that holds our lungs, heart, and some very important blood vessels. Between each rib from top to bottom is a vein, artery, nerve, and more muscle (2). Behind the ribs lies the first layer of the pleural space, called the parietal pleura (2).
This membrane lines the entire chest cavity. Then comes the pleural space, which measures about 15-20 microns wide in its normal state (2). On the other side of the pleural space lies the visceral pleura, which is a membrane that covers the lungs, and then finally the lungs themselves (2).
What this means is that in a normal person, a small potential space exists between the lungs and the chest cavity, called the pleural space. When the pleural space becomes compromised and fills with extra fluid or air, the precarious negative pressure balance that keeps the lungs inflated is disrupted, forcing lung tissue to collapse.
A chest tube comes to the rescue. Known officially as a thoracostomy tube, the chest tube is a hollow plastic tube that is carefully placed by a licensed provider. The tube is driven through the outer skin and muscle, between two ribs and past the parietal pleura to rest inside the pleural space.
Its purpose is to drain the excess fluid or air out of the pleural space so the affected lung can reinflate. The tube is attached to a drainage system to facilitate the movement of the abnormal fluid/air out of the chest. The tube remains in place until it is no longer needed or becomes nonfunctional (3).
Chest tubes are generally divided into three categories based on size and method of insertion: large bore, small bore, and tunneled.
Large Bore (Blunt Dissection Technique)
Generally greater than 20Fr in size, large bore chest tubes are placed using the blunt dissection technique (3). A quick aside here: the size “Fr” refers to “French” or the actual french word “Charrière”, which is the name of the frenchman who invented the sizing (3). The sizing is based on the diameter of a tube, with 1Fr = ⅓ mm (for example, a 12Fr tube is 4mm, 12÷3=4).
The blunt dissection technique requires a skin incision large enough to fit a finger (3). A clamp or forceps is used to bluntly dissect intercostal tissues. The tube is inserted and held in place with heavy suturing (3). This technique is more invasive. It also comes with some risks, including damage to surrounding structures, tube misplacement, bleeding, and increased pain.
Small Bore (Seldinger Technique)
Small bore chest tubes are generally less than 14Fr in size. They are placed using the Seldinger technique, which involves using an introducer needle to get access into the pleural space (3). A guidewire is threaded through the needle and the needle is removed. Then the chest tube is threaded over the wire and the wire is pulled out, leaving only the chest tube. The tube is held in place with a suture and/or adhesive dressing. Advantages include a smaller incision, less pain, and it’s less invasive (3). Conversely, they are more prone to blockage because they are smaller (3).
The decision to use a small or large bore chest tube is made by the provider. For the treatment of most pneumothoraces, research shows that small bore chest tubes are as effective as larger tubes and may be less painful (4). Large bore tubes are recommended to treat traumatic pneumothorax due to the need for removal of blood and air (4). In the past, providers used large bore chest tubes to drain thick fluid like blood and pus, but more recent research suggests that small bore chest tubes are also effective if they remain patent and are properly maintained (4).
Indwelling chest tubes are indicated for long term chest drainage, primarily as a treatment for malignant pleural effusion (3). These tubes consist of a special catheter equipped with a cuff that remains under the skin and acts as an infection barrier (3). The Seldinger technique is used to get access into the pleural space, along with a “peel-away” dilator that allows the tube to be tunneled under the skin. Two small incisions are required for placement. A special vacuum bottle is attached periodically to collect the drainage (3).
Think about the anatomy of the lung, including the pleural space.
Where exactly in this space are chest tubes placed?
Is the potential space between the visceral and parietal pleura large enough for chest tube placement in the absence of pathologic conditions (pleural effusions, pneumothorax, etc.)?
Bedside chest tube placement has become increasingly routine. Thus, bedside nursing staff may be directly involved with the initial chest tube placement (5).
The nurse may be asked to gather the necessary supplies for placement, obtain patient consent, and assist with patient education (5). The nurse may then be expected to assist the provider during the procedure. Afterward, the provider will order a chest x-ray to verify placement. As always, nursing staff is responsible for ensuring any post-procedure orders are carried out.
Once the chest tube is in place, verified by x-ray, and attached to a drainage device, nurses are tasked with monitoring. This would include monitoring vital signs as directed, observing for pain and signs of infection, and assessing the tube and drain system (5). An important part of monitoring includes recording the amount and color of chest drainage. How often this is done depends on facility policy and the provider’s written orders.
Perhaps the most intimidating aspect of chest tube management is ensuring proper function. It is the nurse’s job to look for signs that there may be a problem. Rest assured, these signs and symptoms will be discussed in detail later in the course.
There will also be orders for the nurse to change any dressings and provide necessary wound care. This includes routine observation of the chest tube insertion site. Depending on how long the chest tube is in place, nurses may also have to change out the drainage system if it becomes full of fluid.
Patients with chest tubes may also have to travel. This could be a short distance, like to the bathroom, or across the hospital to surgery or imaging. Nursing staff is responsible for ensuring the chest tube is properly packed up and stowed away for every adventure.
Why is it pivotal that imaging be obtained after every chest tube placement?
Indications for Chest Tube Placement
A chest tube may be indicated for the following reasons: pneumothorax/hemothorax, pleural effusion, empyema, chylothorax, and post-operatively after cardiac/thoracic surgery (1).
A pneumothorax, also known as a “lung collapse”, occurs when the normal negative pressure gradient within the lungs is compromised (6). Air is introduced into the pleural space where it is not welcome. A pathway to the pleural space may form on the inside of the body when lung tissue is damaged. The connection typically forms at the airway or alveoli (the little air sacs in the lungs that encourage gas exchange) (6).
For example, a patient with COPD or chronic bronchitis may develop enlarged, weakend alveoli called blebs that are prone to rupture. When this happens, air flows into the pleural space because of the difference in pressure, forcing the lung tissue to shrink or collapse in response to the expanding pleural space (6).
A pneumothorax may also occur from an outside source if an abnormal connection forms between the pleural space and the chest wall (6). For example, during a lung biopsy, a needle is introduced into the lungs from the outside. Sometimes a pathway forms, allowing air from the environment to flow into the chest. In an attempt to equalize the pressure, air rushes into the pleural space.
A pneumothorax may also be spontaneous in a condition known as primary spontaneous pneumothorax (PSP) (6). PSP usually occurs in tall, thin young men between the ages of 10-30 (6). The risk is significantly increased with current or past smoking (6).
Finally, a hemothorax is diagnosed when blood becomes trapped within the pleural space. It often occurs with pneumothorax. Hemothorax may result from trauma, abnormal coagulation, spontaneously, or after certain medical treatments (such as a biopsy) (7).
Symptoms of pneumothorax and hemothorax include acute chest pain and shortness of breath (dyspnea). The pain may be worse during inhalation and localized to the affected side (6). The degree of dyspnea is often proportional to the size of pneumothorax (bigger pneumo = more pain), but not always- a small percentage of people are asymptomatic (6).
Licensed and retrieved from Adobe Stock
In a healthy person, the pleural space contains a small amount of serous fluid (about 5-10 ml) that is secreted by the parietal pleura and reabsorbed by the lymphatic system (8). When this carefully balanced system is disrupted, extra fluid can accumulate, known as a pleural effusion.
Pleural effusion is the result of leaky capillaries. Capillaries leak for two reasons: changes in pressure or damage to the vessels themselves (8). Congestive heart failure and cirrhosis are the two most common causes of pressure changes. Capillary damage is most commonly caused by pneumonia, pulmonary embolism, cancer, and GI disease (8).
Pleural effusion in the pediatric population usually stems from congenital heart disease, pneumonia, and cancer (8).
Large right-sided pleural effusion
Licensed and retrieved from Adobe Stock
Empyema is the development of infected, purulent fluid inside the pleural space (8). Pneumonia is the usual suspect, but empyema can also form from a lung abscess, bronchopleural fistula (an abnormal tract/pathway between the bronchus and the pleural space), esophageal perforation, or complications of trauma and surgery (8).
The development of empyema may begin with just a small amount of extra, sterile fluid that accumulates in the pleural space (8). When an infectious agent is introduced, inflammation brings white blood cells and even more fluid. Eventually, the infected material can grow into the pleural walls and cause tissue thickening, prohibiting lung expansion (8).
Purulent drainage associated with empyema can be thick and therefore difficult to drain. Fibrinolytics (medicines that dissolve blood clots) can be directly administered through the chest tube into the pocket of infection to help break it down and improve drainage (2). tPA is the medication of choice. A small amount of tPA is diluted in saline and infused through the chest tube, which is clamped for a while (1-2 hours) before drainage is resumed (2). The dose may be repeated if necessary.
Symptoms for pleural effusion and empyema include dyspnea, pleuritic chest pain, cough, fever & chills if infection is present, and weight loss. If a large volume of fluid collects, cardiac function may be impaired: the heart cannot pump effectively if there is no room (8).
Think about the different conditions that can necessitate chest tube placement.
What is the difference between a pneumothorax, hemothorax, pleural effusion and empyema? What are the causes for each?
Chest tubes are often placed after heart or lung surgery because of the risk for developing pleural effusion or pneumothorax during recovery. They are inserted while the patient is still sedated prior to leaving the operating room.
Chest tubes are routinely placed following open heart surgery, including cardiac bypass and valve replacements. They are also indicated in major thoracic surgeries, such as pneumonectomy, lobectomy, lung transplants, segmentectomy, and wedge resection.
Patients with chest trauma may require a chest tube in the presence of pneumothorax or hemothorax.
When considering chest tube placement, it is important to evaluate the patient. Because the indications for chest tubes range from routine post-op care to life threatening emergency, the presentation of these patients varies significantly. In all cases, patient or family consent is paramount and should be obtained prior to the procedure.
The only exception to this is a true emergency, the process for which is outlined in your facility’s policies (all the more reason to be familiar with policy!).
Contraindications in chest tube placement should be considered as part of a risk/benefit analysis. For example, there are no contraindications for using chest tubes in the treatment of tension pneumothorax (1).
Tension pneumothorax is a medical emergency. It occurs when a pneumothorax or hemothorax becomes so severe that air can no longer escape from the pleural space. The pressure increases within the chest and forces the mediastinum (heart, great vessels, etc.) to shift out of the way, compressing the remaining unaffected lung.
These patients are at high risk of going into shock or cardiac arrest. Signs and symptoms of tension pneumothorax include decreased breath sounds, hypotension, tachycardia, and hypoxia.
Relative contraindications to chest tube placement include abnormal coagulation or infection at the insertion site (2). Abnormal coagulation puts the patient at higher risk of bleeding. The parameters for placement will vary between facilities, but generally speaking, prospective patients should have an INR < 1.5 and platelets > 50,000 (2).
Infection at or near the insertion site increases the risk of infection in the chest cavity (3). In many cases, an alternate insertion site is available and should be utilized. For patients seeking elective or semi-elective chest tube placement, these relative contraindications should be resolved prior to placement, if possible.
A chest tube is considered elective if the patient is stable. The American College of Chest Physicians (ACCP) guidelines state that a patient is clinically stable with a respiratory rate less than 24 breaths/min, pulse rate 60-120 beats/min, normal blood pressure, and oxygen saturation greater than 90% on room air (6).
The ACCP recommends that all patients with a large pneumothorax (great than 3 cm apical length) get a chest tube (6). Ultimately, the ordering provider will decide if a patient requires a chest tube as an elective procedure or an emergency.
When preparing a patient for chest tube placement, it is important to be aware of potential complications. Chest tubes can be lifesavers but they are not without risk: when placed at the bedside or during an emergency, it is essentially a blind procedure.
Injury to Surrounding Structures
Gastrointestinal Tract. Although rare, it is possible to for chest tubes to be placed beneath the diaphragm into the abdominal cavity. Insertion into the abdominal cavity poses risk for injury of the stomach, bowel, liver, spleen and other abdominal structures (1).
Though the overall risk is <1%, a third of all chest tubes that find their way into the abdomen result in injury to the patient (1). Signs of abdominal placement include the presence of stomach contents within the tube or peritonitis (1). An x-ray would confirm that the chest tube is located below the diaphragm. Inserting the chest tube no lower than the 5th intercostal space helps prevent this problem (1).
Diaphragm. Many chest tubes are placed at the bedside without imaging guidance. Improper placement poses a risk for injury to the diaphragm (1). Laceration, perforation, and muscle injury are the most common injuries (1). Certain conditions increase the risk of diaphragmatic injury, including diaphragm paralysis, late pregnancy, obesity, ascites, and abdominal tumors (1).
Lungs. The lungs are at highest risk of injury during chest tube placement, especially if a patient suffers from decreased lung compliance or pleural adhesions (1). Lung injury is commonly missed because it cannot be visualized on imaging and patients may be asymptomatic (1).
A rare complication of chest tube placement is infarction of the lung. Excessive suction causes aspiration of lung tissue into the chest tube, leading to infarction and tissue death (1). Providers must also beware of lung perforation and accidentally puncturing the pulmonary artery (as evidenced by rapid blood loss, massive hemoptysis, shortness of breath, tachycardia and hypotension) (1).
Cardiac Structures. If the chest tube is advanced too far, the tip may rest too close to the mediastinum, resulting in compression of nearby structures (1). Although rare, it can lead to hemodynamic instability (1). There have also been cases of penetration of cardiac structures.
Like all procedures, chest tubes are not without risk.
Think about the complications above.
What signs and symptoms might you see if these are encountered?
Other Potential Complications
Pain- Some pain is associated with chest tube placement. At the very least, providers will provide local anesthetic to numb the area while the tube is inserted. Sometimes, patients are also given IV pain medicine or sedation during placement. Patients may also experience pain while the chest tube is in place, so providers will often prescribe PRN analgesia to improve comfort. Some studies have suggested that large bore chest tubes are generally more painful than smaller ones (4).
Fistula- Bronchopleural fistula is both an indication for and potential complication of chest tube placement (1). A fistula is an abnormal pathway or tract that forms between two structures, in this case between the pleural space and the bronchial tree. A chest tube may benefit a patient if a bronchopleural fistula already exists (1). However, if a fistula forms as a result of the chest tube itself, it is associated with high morbidity and mortality (1). Patient symptoms of fistula include dyspnea, hypotension, cough, and persistent air leak (1). Timely chest tube removal can help prevent the formation of a fistula because it limits tube erosion (1).
Bleeding- Providers must be careful when placing chest tubes because the space between each rib contains a vein, artery, and nerve (1). Although rare, cases of hemorrhage and death have been reported as a result of chest tube placement. Luckily, abnormal bleeding is usually apparent right away. However, early diagnosis can be missed if the tube compresses the artery in such a way that it prevents any bleeding while in place (3).
Recurrent Pneumothorax- One of the worst complications is recurrent pneumothorax, simply because it means the chest tube has failed. A new pneumothorax is more likely to occur when the tube is pulled too early and the lung has not properly re-expanded (1). It can also be caused by an air leak or if air enters the pleural space during tube removal (1). If the recurrent pneumothorax is small and the patient is asymptomatic, it can typically be managed with follow up imaging and close observation. Otherwise, the chest tube will have to be reinserted.
Where Are Chest Tubes Placed?
As previously mentioned, there are several different techniques used to place chest tubes: the blunt dissection technique for large bore tubes, Seldinger technique for small bore tubes, and the Seldinger technique with a peel-away dilator for tunneled chest tubes. Interestingly, these chest tube techniques can be performed just about anywhere: the OR, IR, and the patient’s bedside.
Chest tubes are usually placed in the OR after cardiothoracic surgery. The tube should be positioned no lower than the 5th intercostal space along the midaxillary line to avoid injury to the diaphragm (1). The second intercostal space at the midclavicular line is an alternate site. However, it is never the first choice because the tube must be driven through the pectoralis muscle (ouch) and it is more likely to produce an ugly scar (3).
Mediastinal chest tubes are commonly placed after cardiac surgery to facilitate drainage of blood and other fluid from the pericardial and pleural spaces (1). The goal is to prevent cardiac tamponade and pleural effusion. These tubes are easy to identify because they emerge from the mediastinum.
Interventional Radiology (IR)
Interventionalists have the advantage of using imaging to assist with chest tube placement. Ultrasound, CT and fluoroscopy (live x-ray) may be used. Imaging allows the provider to observe the chest tube as it enters the body, which helps ensure proper placement.
When placing a chest tube for the treatment of pneumothorax, the provider often uses fluoroscopy for guidance. The pneumothorax is visualized on the monitor while the tube is positioned. Using the Seldinger technique, the final catheter is threaded over the wire to rest in the pleural space.
Interventional radiologists are commonly enlisted to place drainage tubes for the management of empyema or lung infection (8). CT is the modality of choice because it allows better visualization of surrounding structures than fluoroscopy. The provider will take frequent CT scans while a wire is guided into place, then thread the catheter over the wire into the infection (8). Small bore tubes have been shown to be effective in the drainage of thicker fluids, like pus (4).
Finally, approximately 50% of cancer patients develop malignant pleural effusion (8). Malignant pleural effusion is recurrent, usually due to diseased pleura, obstructed lymph channels, or atelectasis (8). Breast, lung, lymphoma, ovarian, and gastric cancers have been known to cause malignant effusion (8). At first, these recurrent effusions may be treated with thoracentesis, a procedure in which the interventional radiologist positions a small catheter into the pleural space, where it remains temporarily to allow pleural fluid to drain. After drainage has ceased, the catheter is removed and a dressing is applied.
Over time, malignant effusions require drainage more frequently, which can be hard on the patient (8). Thoracentesis provides only short term relief of symptoms. Tunneled chest tubes are a more long term alternative for malignant pleural effusion. The catheter contains a special cuff and is tunneled under the skin to minimize the risk of infection. Prior to placement, the interventional radiologist will use ultrasound to locate the effusion.
Providers often insert chest tubes at the bedside. After discussing the risks and benefits of the procedure with the patient, providers should obtain informed consent. Nursing staff would be required to assemble the appropriate supplies and be available to assist as needed. Full aseptic technique is required, so medical staff should wear gowns, gloves, masks and use sterile drapes (3).
Chest tube insertion is made much simpler if the patient is positioned appropriately. The head of the bed should be raised to 45-60 degrees with the patient resting in the supine position and slightly rotated. The ipsilateral arm is placed behind the neck or head so it is out of the way, providing easy access to the chest (ipsilateral meaning “same side”).
For posterior fluid collections, the patient should sit on the side of the bed with the provider standing behind (3). The position can be made more comfortable by allowing the patient to rest his or her arms upon a side table. Bedside ultrasound will allow the provider to visualize any fluid collections.
Note: In all cases, post-procedure x-ray is required as soon as possible to confirm chest tube placement.
Large right-sided pneumothorax
Notice the lack of parenchymal (lung) markings on your left side. Remember that chest radiographs are flipped, thus this is the patient’s right side. This lack of lung marking is due to a pneumothorax- thus the lung is compressed by air in the pleural space.
Licensed and retrieved from Adobe Stock
Chest Tube Drainage Systems
After a chest tube is in place, it must be attached to a drainage system to facilitate the removal of excess fluid and promote lung reinflation. There are four basic types of drainage systems: Heimlich valves, three-compartment systems, digital systems, and vacuum bottles.
A Heimlich valve is a one-way valve shaped a bit like a thin cylinder that attaches to the distal end of the chest tube. It is called a one-way valve because air is permitted to flow only one direction: out.
The valve itself is composed of a rubber flutter that occludes with inspiration to prevent air from entering the chest. The flutter opens during exhalation to allow the trapped air to escape the pleural space. The pneumothorax shrinks slowly over time with each breath. Heimlich valves are more commonly used for ambulatory patients when suction is not required (3). Its small size allows patients to move freely. Figure 1 is an example of a Heimlich valve (11).
The most commonly used drainage systems are three-compartment systems, such as Atrium® and Pleur-evac®.
Like the name suggests, they contain three interconnected chambers: the collection chamber, water seal chamber, and a suction chamber. The collection chamber fills with air or fluid that drains from the chest tube. The water seal uses a column of water to prevent air from flowing into the pleural space with inhalation (3). Finally, the suction chamber allows the provider to adjust the level of suction against the chest tube.
If needed, the drainage system is attached to a wall regulator to apply active suction (3). Alternatively, these drainage systems can also be set to drain by gravity if the device is positioned below the chest (3). These drain systems require careful observation for air leaks. Figure two is a drawing of a three-compartment system (11).
Figure 2: Drainage system
Digital Drain System
A more modern approach to chest tube management, digital systems use a computer to monitor drainage, air leaks, and pleural pressure (3). All measurements are calculated internally and displayed on a screen. They do not require wall suction, so patients may ambulate with ease (3). Because they are more compact and basically manage themselves, some patients are discharged with their chest tube in place, resulting in shorter hospital stays overall (3). Digital systems are typically used for patients who develop a pneumothorax after thoracic surgery.
Remember, tunneled catheters are commonly used to drain recurrent pleural effusions associated with malignancy. Instead of constant suction and drainage, pleural fluid is allowed to accumulate and then drained periodically as needed. Frequency of drainage ranges from occasionally to multiple times a week. The tunneled catheters are equipped with a special one-way valve that opens and drains when a vacuum bottle is attached (3).
Think about the different types of drainage systems.
What are the pros and cons of each system?
How does the troubleshooting differ for each system?
Nurse Roles and Responsibilities: How to Manage Chest Tubes
It is the responsibility of the nursing staff to monitor chest tubes and report any potential malfunction. Because chest tube patients may reside in virtually any hospital department (or even as an outpatient), it is essential that nurses feel comfortable around them. Chest tube management includes observing and maintaining the insertion site, recording output, and managing the drainage system.
Observe the Patient
Perhaps most importantly, the nurse should observe the patient. Check vital signs as ordered by the provider or facility policy. Assess for pain. Some discomfort is expected after chest tube placement. Provide pain medicine as needed. Auscultate breath sounds frequently and encourage deep breathing, especially during the post-procedure period. Diminished breath sounds, changes in vital signs and increased work of breathing could indicate the re-accumulation of air or fluid in the pleural space.
Maintain the Insertion Site. Chest tubes are commonly sutured to the skin to hold the tube in place. The insertion site is covered with a dressing to protect the area. Dressing changes occur as ordered by the provider or are dictated by facility policy. Most chest tubes require an occlusive dressing, meaning the dressing should adequately cover the site and be well-secured, which reduces the risk of developing an air leak (1). Expect to change the dressing if it becomes soiled. Nurses should observe the insertion site frequently for signs of infection, including fever, redness at or around the site, swelling, warmth, and purulent drainage.
Although they are sutured in place, there is a risk for dislodging the chest tube if it is pulled too hard. Securing the tube to the patient’s side with a piece of tape is one way to reduce the risk of dislodgement (9). Advise the patient to ask for help when getting out of bed.
Record Output. Nursing staff is also in charge of observing and recording chest tube output. The frequency of recording the output is dictated by written orders from the provider or facility policy. Drainage fluid is often pink or bloody in color. The most common type of drainage system is the three-compartment system, such as the Pleur-evac® or Atrium®. All drainage is contained within these system, meaning the container cannot be emptied. Instructions vary between facilities, but it is common practice to document the amount of drainage directly onto the container by marking the level of output with a pen or marker. When full, the drain system is removed and a new, clean one attached.
Manage Drain Systems
Heimlich Valve. Nurses should assess that the Heimlich valve is securely attached to the distal end of the chest tube. The one-way flutter valve allows air to leave the chest but prevents air from seeping back inside. It does not require suction, so the patient may move around freely. Heimlich valves do not possess a collection chamber, rather, any drainage will freely leak from the distal end of the valve. Thus, the Heimlich valve is not the system of choice for patients with significant drainage.
Three-Compartment System. Again, these are the most commonly used systems. They should be positioned below the patient’s chest at all times. The nurse is responsible for monitoring the three compartments: collection chamber, water seal, and suction. As discussed above, the nurse will simply document the drainage any drainage that collects in the collection chamber.
The water seal serves two functions: to prevent outside air from flowing into the chest and the detection of air leaks. An air leak within a chest tube may indicate a serious problem. The water seal should be easy to find. When the water seal is functioning correctly, the water level will fluctuate (rise and fall) with breathing. If the nurse observes intermittent or constant bubbling within the water seal, an air leak is present (1). The more bubbling, the bigger the leak.
Chest tubes often require suction to help gently pull excess fluid and air from the body. Three-compartment systems are equipped with a dial that allows staff to set the level of suction, usually between 0 and -40 cm H2O. The provider’s orders or facility policy will dictate the level at which suction should be set. Part of the nurse’s assessment is verifying that the suction dial is set correctly. Additionally, nursing staff should check that the suction tubing is connected securely to the wall suction regulator.
Digital Drain System. Thanks to technology, digital drain systems are pretty easy to manage. The device collects and displays all of its data to the nurse, including the amount of drainage, intrapleural pressure, and the presence of any air leak. It simply needs to be recorded.
Tunneled Catheters. Tunneled catheters should be clamped unless they are being drained. These catheters contain a one-way valve that will not open unless a vacuum bottle is attached. Tunneled catheters are usually managed at home by a willing family member or trained home health provider, thus the patient and family may require extensive education prior to discharge.
Clamping the Tube. With the exception of tunneled catheters, as a general rule, chest tubes should not be clamped unless it is necessary to replace the drain system or it is ordered by the provider (9). If an air leak is present, a clamped tube can lead to tension pneumothorax (9). There is no need to clamp a chest tube during patient transportation or ambulation. If the drainage system is positioned below the chest as indicated, it will continue to drain with gravity after suction is turned off (9).
Chest Tube Troubleshooting: When to Call the Doctor
Like anything else, chest tubes are prone to complications. It is essential for nurses to be able to identify a malfunctioning tube quickly and know when to alert the provider. A worsening pneumothorax can lead to a longer hospital stay for the patient, or at worst tension pneumothorax and death.
Chest tubes should be assessed regularly by nursing staff. The chest tube must be well-connected to the drainage system and wall suction (if necessary). If the chest tube becomes disconnected from the drainage system, the two ends should be cleaned well with an antiseptic, like alcohol pads, prior to being reconnected (1). Do not clamp the tube in case there is an air leak, as the patient could develop a tension pneumothorax (1).
Infection. Infection is always a risk when a foreign body is present. Because chest tubes allow direct access into the chest cavity, it is essential to watch closely for any signs of infection. Infection may develop at the insertion site or inside the chest cavity (empyema/abscess).
Signs of infection at the insertion site include fever, redness, swelling, warmth, or purulent drainage. The site needs to be kept clean and soiled dressings should be replaced quickly and efficiently.
Chest tube patients that also have pleural effusions are at higher risk of developing empyema (1). Chest tubes are considered a “clean contaminated” procedure, meaning the chest cavity is accessed cleanly, but a risk for contamination remains as long as the tube is in place (1). The risk of empyema after chest tube insertion is as high as 25% in some populations. A nurse might suspect the development of empyema/abscess if the patient exhibits symptoms of infection: fever, tachycardia, respiratory distress and purulent drainage from the chest tube. A prompt call to the provider is warranted.
Kinks & Clots. The smaller the chest tube, the more likely it is to become clogged or kinked. Sometimes it is easy to spot a problem with a simple inspection of the entire apparatus. Pay particular attention to areas of the tubing covered with tape, such as the insertion site or taped connections. Straighten out the the tubing when patients are lying in bed or sitting in the chair.
Pay close attention to the drainage system. A digital system or three-compartment syndrome will alert you if there is a problem. A digital system will literally sound the alarm in the event of a kink or clot because it monitors pressures. Three-compartment systems are not fitted with alarms, so they require closer observation to detect an issue. Earlier, it was mentioned that it is normal for the water seal in three-compartment systems to fluctuate with breathing or coughing. If the water seal is not fluctuating with breath, you may have a kink or clot. The water seal is not fluctuating because the tube cannot drain past the blockage.
Kinks are easy to fix: simply straighten out the tube or resolve kinked connections. Clots can be a little more difficult to handle. Luckily, ⅔ of clots resolve themselves (1). Historically, providers have used techniques such as milking or stripping the tube to help remove clots. The use of these procedures is questionable. Prophylactic milking/stripping has not shown any tendency to prevent clots from forming (1). Also, these techniques have actually been shown to cause harm by increasing pressure within the pleural cavity, resulting in increased bleeding, tissue entrapment, and dysfunction of the left ventricle (1). Thus, tube milking and stripping should probably be avoided altogether.
What do you do if you see a clot then? If the clot is located in the drain system tubing, simply replace the system. Attach a new Pleur-evac® or Atrium® system and remove the affected tubing. If that doesn’t resolve the problem, notify the provider. Chest tubes can also become kinked inside of the patient, so the provider may order a chest x-ray to confirm proper tube placement (2).
Loss of Suction. Ensure that the drain tubing is securely attached to the wall suction regulator and that the tubing is unclamped. The regulator should be turned on. Check that the suction dial on the drain system is set to the appropriate suction setting. If all connections are appropriate, the wall regulator or drain system is malfunctioning and should be replaced. Maintaining appropriate suction is critical, as too little suction will prevent lung re-expansion, while too much suction can damage lung tissue (9).
Drain System Malfunction. The best course of action is to replace the drain system and re-assess the problem. If it was truly an issue with the drain system it should resolve by replacing it.
The easiest way to assess for an air leak is to observe the drainage system. Again, a digital system will alarm if it detects a problem. With a three-compartment system, an air leak will cause intermittent or constant bubbling within air-leak detection compartment of the water seal. Air leaks are a concern because they allow air to flow back into the pleural space (1). The whole point of the chest tube is to get the air out of the chest. Air leaks can occur in a couple places: at the insertion site or within the tubing/drain system (1).
If an air leak is observed in the water seal chamber, the next step is to find out where it is coming from. This is one case where clamping the tube (temporarily, of course) can help diagnose a problem. First, clamp the tube close to the patient (10). If bubbling within the water seal continues, this means there is a leak in the tubing or drain system. Although made of strong material, these drain systems are not infallible. Tubing can be cut or damaged accidentally, and it may not be easy to spot. Assess the tubing for cuts or holes. Ensure all connections are secure, as loose connections are an easy way for air to sneak inside. Replace the drain system if the tubing or container is damaged.
On the other hand, if you clamp the tube and the air leak disappears from the water seal, this means air is leaking near the patient (10). In this case, the leak stems from the insertion site or somewhere inside the chest (10). An air leak at the insertion site occurs because the dressing is insufficient or the hole is too big. This is why an occlusive dressing is a must. Apply new petroleum gauze and cover with a sterile, occlusive dressing at the site where the tube enters the skin (10). This prevents air from leaking into the chest at the skin.
Unfortunately, sometimes the skin site is too large relative to the tube itself, meaning the tube is too small for the skin incision that was created (1). The tube should fit snugly into the skin incision, without gaps. If you suspect the skin incision is too large, notify the physician. Often, a simple stitch can tighten any loose skin at the insertion site (1).
Finally, if you have accounted for all of the potential problems listed above and an air leak remains, the problem is likely inside the chest (10). Potential causes of persistent air leak include residual pneumothorax, pleural injury, a malpositioned chest tube, or fistula (10). Notify the provider right away if all attempts to resolve an air leak have failed.
Sometimes, the tube comes out despite every precaution. It may be pulled out partially or completely. After a partial removal of the tube, quickly and calmly secure the tube to the patient with a new dressing and tape. Obtain a set of vital signs and assess for pain and any new symptoms, such as shortness of breath or dyspnea. Notify the provider immediately. Follow up imaging (usually an x-ray) may be ordered to determine chest tube location and assess for any residual pneumothorax.
If the tube is pulled completely out, put on gloves and quickly cover the insertion site with your hand to prevent air from flowing into the chest (10). Stay with the patient and call for help. When help arrives, ask a coworker to get the necessary supplies for a new occlusive dressing: petroleum gauze, dry sterile gauze, and tape. Apply the dressing and notify the provider immediately. If the patient is in distress, call for help. Remember, chest tubes can be placed at the bedside pretty quickly in an emergency. And try to stay calm!
Under normal circumstances, chest tubes are removed once drainage has ceased, breath sounds return to normal, and/or imaging shows a resolution of the pneumothorax (9).
Think about the different types of complications that can occur.
How would you react and manage each complication?
When would you call the provider/doctor for further assistance?
What are some life-threatening complications that can occur as a result of chest tube malfunction?
Chest tubes are a life-saving intervention for the patient with pneumothorax, hemothorax, chylothorax, pleural effusion, empyema/infection, and also those recovering from major cardiothoracic surgery. The technique for chest tube placement depends on the size: large tubes are placed using the blunt dissection technique and small tubes are inserted with the Seldinger technique. Radiologists use the Seldinger technique and a peel-away dilator to insert tunneled chest tubes.
Both small bore and large bore chest tubes are effective in treating pneumothorax, hemothorax, empyema/infection, and preventing complications after surgery. The size of the tube really depends on provider preference. There are advantages and disadvantages to either size. Large bore tubes are less likely to form kinks or clots, but may be more painful. Small bore chest tubes are less invasive, but form clots much more easily. Tunneled chest tubes are a great way to provide a palliative care to patients suffering recurrent malignant pleural effusions.
While there are no true contraindications for chest tube placement, a few relative complications exist. Sometimes, chest tube placement is a true emergency, such as the need to treat a tension pneumothorax. In these cases, the benefits outweigh the risks. For more stable patients, providers should ensure that consent is obtained and the patient’s blood is coagulating appropriately prior to chest tube insertion.
When possible, patients and their families should be aware of potential risks with chest tube placement. Bleeding, damage to surrounding structures, bronchopleural fistula, recurrent pneumothorax, and pain are some potential complications of initial chest tube placement.
Chest tubes may be placed in the OR, IR, or even at the bedside. Once inserted, the tube should be connected to a drainage system to pull air out of the chest and prevent air from returning to the pleural space. Types of drainage systems include Heimlich valves, three-compartment systems, digital systems, and vacuum bottles for tunneled catheters.
Nurses are responsible for chest tube management after insertion. Roles and responsibilities include monitoring and recording drain output while continually assessing for signs of infection, air leaks, suction loss, or drainage system dysfunction. The ability to quickly identify a malfunctioning tube is essential for protecting our patients. Often, a problem is solved with a quick fix, like replacing the drainage system if the tubing becomes damaged. However, persistent questions and concerns require a prompt call to the provider.
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9.Drains: Everything You Need to Know
Picture this: you walk into your hospital unit, fresh off a good night’s sleep. You find your patient assignment and head over to get report. Then the outgoing nurse says something that makes your heart skip a beat. “This patient has an abscess drain. You need to flush it every X hours, record the output every X hours, call the doctor if __ happens…” Before long, your head is spinning, and then you realize you’ve been spelling ‘abscess’ incorrectly for who knows how long!
Drains can be intimidating, especially with little to no prior experience in drain management. They often come with a specific set of instructions that can be somewhat confusing. What’s worse, a patient may suffer a serious delay in recovery if something goes wrong. Nobody wants to be the one to make that call to the doctor about a malfunctioning drain. Fortunately, like anything else, managing drains becomes much easier with experience and a little education.
Types of Drains
A patient may require drain placement for various reasons. Often, they are placed at the end of a surgery to help eliminate any fluid that may accumulate within the wound. A common type of surgical drain is the Jackson-Pratt ® . Certain organs may require a drain to assist with the removal of their contents, such as foley catheters or nasogastric tubes. Drains may also be placed to help remove fluid or air from body cavities. A chest tube is a good example of this type of drain. Finally, if a patient develops an abscess, a drain is often required to help remove the infected fluid more quickly.
Drains serve a very important purpose (other than driving the patient and his/her nurses crazy). The accumulation of fluid in the wrong place can have a detrimental effect on the patient’s health and healing (1). Excess fluid in the surgical site can cause significant pain as well as injury to surrounding tissues and organs (1). It can also increase the chance of infection (1).
Medical drains can be divided into multiple categories.
Drains are often described as being active or passive. Passive drainage allows for gravity to help remove excess fluid, without the use of pressure (2). An example of passive drainage would be placing a foley catheter to gravity or using a penrose drain. A penrose drain is a relatively flat, ribbon-like tube that creates a passage from a wound to the open air, which allows any excess fluid to simply flow outward (2). The area surrounding the opening is often lightly covered with gauze to collect fluid as it drains and must be changed when saturated (2).
The following image is an example of a penrose drain (3).
Active drains use actual pressure, typically negative pressure, to help remove excess fluid from the body. An example of an active drainage system would be a Jackson-Pratt (JP) ® drain or hemovac ®. With both types of drains, the pressure is created by compressing the collection container, which creates a low pressure vacuum that pulls the fluid out of the body (2). The following image is an example of a JP ® drain (3).
Open vs. Closed
Drains can also be described as open or closed. An open system simply means that it is open to air. An example of an open system would be a penrose drain, as described above. A closed drain, on the other hand, is not open to the environment. Rather, the draining fluid is contained within the system, and the collection bulb or bag is simply emptied from time to time, as needed. A JP ® drain is an example of a closed drain.
Surgical vs. Percutaneous
While not a technical classification, it is interesting to note how the drain is placed. Surgical drains are usually positioned in the operating room or, more rarely, at the bedside by the physician. The JP ® is an example of a surgical drain.
Drains may also be placed percutaneously:
Percutaneous: (adjective) effected or performed through the skin (4)
Percutaneous drains are placed without surgical intervention. Rather, Interventional Radiologists use imaging, such as CT, ultrasound, or fluoroscopy to guide a needle into a fluid collection (5). This technique is generally less invasive (6).
What are the advantages and of open vs closed drainage systems?
Infections 101: A Brief History of Drains
Before the advent of antibiotics, the development of an abscess or postoperative infection was often a death sentence (7). Thanks to advances in modern medicine, suffering patients now stand a chance. In certain situations, infections can be treated simply with a course of antibiotics. However, if there is any concern for the development of sepsis, further intervention is needed (6).
Until the 1970s, the most effective (and only) way to treat infection and abscess was surgical intervention (7). Surgeons would attempt to remove the infected material while striving for “directness, simplicity, and above all, avoidance of unnecessary contamination of uninvolved areas” (7). Unfortunately for these patients, this meant that a second surgery was required to heal them from complications of their first surgery. Even with the addition of antibiotics, these situations were associated with significant morbidity and mortality (6).
Luckily, rapid advances in technology allowed for the development of a less invasive solution. The advent of fluoroscopy, ultrasound, and especially CT provided physicians with a tool to see inside the body without having to cut someone open. The first studies involving the use of medical imaging for percutaneous drain placement were published in the late 1970s (7). Over the next several years, multiple studies reported success rates ranging from 60-80% using these new techniques (8).
Doctors are now able to drain up to 3 separate abscess/infection sites percutaneously (8). Recent studies report technical success of up to 90% with percutaneous drain placement, and it can offer immediate improvement in sepsis, with return to hemodynamic stability within 1-2 days (9). CT is considered the imaging modality of choice because of its ability to fully visualize the infection and surrounding structures as well as provide a pathway from the skin to the destination (9).
How has the increased use of medical drains altered the medical care and approach to managing abscesses?
Patient Considerations for Percutaneous Drain Placement
Not every infection or fluid collection requires percutaneous drain placement or even surgery. Thus, it is important for physicians to work together to determine the appropriate treatment for each patient individually. When a patient is found to have an abscess, multiple doctors may get involved, usually either a surgeon or interventional radiologist- sometimes both!
It is essential that providers choose patients carefully, as ineffective or incomplete drainage of the infection can lead to significant morbidity and mortality (8). For example, percutaneous drainage is sometimes avoided in patients with chest infections, such as empyema, abscess, and pleural effusion because of the risk of pneumothorax (9). Additionally, pyogenic and fungal abscesses in the lung parenchyma often resolve with more conservative management, namely through supportive care and antibiotics (9). Pancreatic abscesses remain at high risk of treatment failure with percutaneous drain placement, thus surgery is usually still the intervention of choice (9).
Conversely, there are many types of abscesses that respond well to percutaneous drainage. Liver abscesses have a very low risk of complications with this type of drain placement, around 1-4% (9). It is also very effective in managing infections related to visceral perforation, which may result from Crohn’s disease, prior operations, diverticulitis, and appendicitis (9). Deep pelvic abscesses respond well to percutaneous drainage, although these can be more challenging and require careful planning because of the presence of nearby organs (9).
Percutaneous drainage is often considered for patients who are too ill for surgery, in the hopes that it may improve sepsis and promote increased strength/rest (8). It is also recommended for patients who have a good response to antibiotics and low risk of mortality.
Deciding who may benefit from a drain and who needs conservative therapy is difficult and nuanced.
How would you consult with on this subject?
Should medical therapy be initiated while awaiting intervention?
Image-Guided Drainage: How Does it Work?
When first contemplating percutaneous drainage, doctors must first decide which modality to use: fluoroscopy, ultrasound, or CT. As mentioned previously, CT is most often used to guide drain placement because of its superior visualization.
The interventional radiologist will typically review any available imaging beforehand to plan the most appropriate route for drain placement. Care must be made to avoid major vessels and other important structures (6). To minimize the risk of complications, physicians are advised to use the safest, most direct route and attempt placement in the most dependent part of the fluid collection to encourage effective drainage (6).
Once the patient is properly positioned on the table, the physician will use the CT, ultrasound, or X-ray to guide the placement of a special needle, taking frequent pictures to monitor its progression from the skin through soft tissue and into the infection (6). Once the needle is in place, a wire is passed through the needle into the fluid collection and then the needle is removed, leaving only the wire in place.
Next, a drainage catheter is threaded across the wire to its final resting place. The tip of the catheter rests within the fluid collection. The drainage catheter contains holes to help fluid pass out of the body. Once the tube is in place, the wire is removed. A drainage bag is attached. Throughout the procedure, pictures are taken to ensure correct placement. Patients are often given moderate sedation to make them more comfortable, but not in every case.
Care for the patient with a drain can seem intimidating, but it doesn’t have to be. Often, the physician will write orders to guide nursing staff while caring for these patients. Drain management may also differ depending on what type of drain the patient has. If there are no orders it is reasonable to contact the physician who placed the drain for clarification.
Two of the more common types of surgical drains are the hemovac ® or JP ® drain. As mentioned previously, both of these drains are active, closed systems, meaning they use negative pressure to help remove excess fluid from a surgical wound, all of which is stored within the collection device.
When managing JP ® or hemovac ® drains, it is important to note the color of the drainage fluid. The fluid is typically bloody at first, but should gradually lighten to a light pink, clear, or yellow color (10). Indications for removal may vary, but in general, these drains remain in place until the daily output decreases to less than 30 ml (10).
Follow any written instructions provided by the ordering physician. Nurses will also be responsible for emptying the drain, observing the site and documenting findings. The drain should be emptied no later than when it becomes half full, as it will lose suction and become ineffective (2). Observe the insertion site for drainage and signs of infection. Be sure to keep the skin clean. These drains may also be sutured in place.
Percutaneous drains usually look a little bit different. The interventional radiologist uses a special type of drainage tube that is also sometimes called a ‘pigtail’. These tubes do not always have to be sutured in place, for they may contain a string that, when pulled, curls the distal end of the tube, making it a bit harder to pull out. They are then usually adhered to the skin with a dressing.
Again, it is important to note the color of the drain output. Keep in mind that percutaneous drains are often used for abscess or infection, meaning fluid will be purulent and/or bloody. Check for any specific written instructions for drain management. Monitor the drain site regularly for signs of infection or drainage. Empty the drainage bag as directed or as needed and document findings. These drains may also use a collection bag that applies suction through negative pressure.
Percutaneous abscess drains are more likely to require flushing because the purulent drainage can be thick and pose a risk for occluding the drain. They may be equipped with a three-way stopcock to allow for easy flushing.
Image guidance has revolutionized drain placement.
What are the advantages of surgical drains and what is their role currently?
How to Flush a Drain Using a Three-way Stopcock
The first step is to review any written orders and become familiar with policies regarding drain flushing. You may be required to have a provider order in order to flush a drain. Then gather some supplies: gloves, an alcohol pad, “dead end” cap or clave, clean pad/towel, and saline flush syringes. Prepare by applying gloves and laying out a clean towel or pad underneath to create a workspace and catch any drainage. Flushing a drain is usually painless, but advise patients that they may feel a little discomfort.
Take a look at the figure below (11). It is an example of a three-way stopcock. It has three different ports and an “off switch” that swivels. Whichever direction the off switch is pointing closes that port so fluid cannot flow. In the example provided, the switch is closed to the patient, meaning that fluid cannot pass into the bag.
Step 1. Find the Flush Port
To flush the drain, find the flush port located on the stopcock. It should be pretty easy to spot, as it is usually the only port that is free (since one end of the stopcock is connected to the actual drain tube, the other to the drain bag). The flush port should be capped with either a “dead end” cap or a clave. If there is a dead end cap, it will have to be removed, since saline cannot be flushed through. If a clave is present, the saline syringe can be screwed in directly.
Step 2. Prepare the Flush Port
Next, turn the off switch so it is pointing toward the flush port, if it isn’t already. This will close the flush port or “turn it off” so that drainage cannot leak out. If a dead end cap is present, remove it. Wipe the flush port with an alcohol pad and attach a new, sterile clave, if available. Claves make future flushing much easier because the flush syringe can be attached directly. If a clave is already present, wipe it thoroughly with an alcohol pad.
Step 3. Prepare the Saline
Attach a saline syringe to the flush port. 5-8 ml is usually plenty. If the ordering physician wrote specific instructions on how much saline to infuse, follow the directions closely. The off switch will have to be turned before flushing is possible. At this point, the switch is facing the flush port, which prevents fluid from exiting or entering. The attached saline simply will not flush, no matter how hard the plunger is pushed.
Step 4. Flush the Drain
Saline can be flushed either into the drain or into the bag, depending on which way the off switch is turned. To flush the drain itself, a nurse would have to direct the saline toward the patient. This means the off switch needs to be turned toward the bag. The bag is now “off” and won’t get any flow, allowing saline to travel through the flush port and up the drain into the patient. Once the saline is flushed, turn the off switch back to the flush port. This will reopen flow into the bag. The saline that was just infused should now travel freely through the drainage tube and into the bag. Observing this allows the nurse to know that the tube is draining correctly.
Sometimes the contents of the abscess can be thick or contain particles that can clog the tube leading to the bag. Thus, the drain bag may also need to be flushed. Simply follow the same steps listed above, only, instead of turning the off switch to the bag, it should be turned to the patient. This will prevent flow from entering the drainage tube, leaving a pathway from the flush port into the drain bag. The nurse should be able to see the saline traveling into the bag. Once the bag is flushed, return the off switch to face the flush port. This allows for an open pathway from the drain into the bag.
Step 5. Assess the Drain
After flushing, it is important to note any patient discomfort, as well as document how much saline was flushed. Before leaving the bedside, and always when assessing a patient’s drain, ensure that the off switch on the stopcock is turned toward the flush port. This will allow drainage to flow seamlessly from the patient into the bag.
*Note, not all drains are meant to be flushed, especially those that do not contain a flush port and/or three-way stopcock. Never flush a drain without a provider’s order. Do not attempt to flush a drain if you suspect it has been pulled away from its original position.
Properties of a Well-Functioning Drain
Since humans lack x-ray vision, the inner workings of a drain can seem a little mysterious. What is going on in there? How can a nurse know if it is doing what it is supposed to do? Repeat imaging (CT, ultrasound, etc.) is the best way to visualize how infections and abscesses change over time. However, it is costly and unnecessary to expose patients to extra radiation as a matter of curiosity.
To get some idea of how a drain is functioning, one has to look at the drain itself. Even though drains may look different, they function in similar ways, thus these considerations can be applied to both surgical and percutaneous drains.
The hallmark of a well-functioning drain is output. The purpose of a drain is to get fluid out of the body. Therefore, if the collection bag/bulb is capturing drainage fluid, this is a good indication that it is working correctly. Remember that the fluid is often bloody at first, but should lighten over time. The drainage from an abscess may also be bloody at first before appearing purulent.
Skin Site Clean/Dry
The skin at the site of a drain should be kept clean and dry (2). Minimal amounts of fluid may leak around the tube, causing crusting on the skin or a small amount of visible drainage. This can be gently wiped away with clean gauze soaked with normal saline or warm, soapy water (10). Apply a fresh clean gauze at the site to protect the skin from breakdown (10). If a large amount of drainage is leaking from the skin and around the tube, this is not normal and should be addressed.
Stopcock in the Proper Position
Ensuring that the three-way stopcock (if present) is in the proper position is essential for proper function. The off switch should be pointing to the flush port at all times, unless the nurse is preparing to flush the drain. Turning the off switch to the flush port prevents fluid from draining outside of the system and creates an open pathway from the drain into the drain bag.
All active drains should be monitored closely to ensure that the bulb or accordion is adequately compressed (2). Constant negative pressure must be maintained in order for the drain to work. These drains may require frequent assessment and emptying, especially at first. Examples of active drains include JP®, hemovac®, and most percutaneous drains.
Is this Normal? Drain Troubleshooting
Unfortunately, drains can develop complications. It is essential to know what to look for so that potential problems can be identified early. As mentioned previously, a delay in reporting or discovering a drain malfunction may cause delays in patient healing. Luckily, the problems are fairly easy to spot if you know what to look for.
Some bleeding is normal. The act of placing a drain may cause bleeding from nearby small vessels (9). This is usually self-limiting, which is why the nurse may note bleeding in the early hours after placement. The drainage should gradually lighten. Prolonged bleeding or the development of new bleeding warrants a prompt call to the physician.
A leaky drain can be a messy business. If the source of the leak is not immediately known, the nurse should evaluate the drain. Assess the tubing for cracks or holes. Ensure all connections are tight. Sometimes the drainage bag/bulb may be punctured. If so, it is often easily replaced.
Leaking may also occur because the drain is occluded or kinked (2). Assess the tubing carefully for signs of obstruction. Flushing the drain can help dislodge occlusions. Again, never flush a drain without orders from the physician.
A drain may also leak at the skin. Minimal amounts of leakage can be expected because the drain creates a track for small amounts of fluid to escape. Moderate to severe leakage can cause skin breakdown and is not normal. It suggests that the drain is malfunctioning in some way, often due to an occlusion or displacement of the drain. Fluid travels the path of least resistance. If it can’t pass easily through the tube, it will find another way out. Notify the physician, who may order follow up imaging, like a CT scan. If a percutaneous drain is leaking, the patient may have to be sent down to interventional radiology for assessment and possible replacement.
Drain output may cease for two reasons: there is no more fluid or the fluid can’t get out. It is easy to assume the former. Yet, when faced with a drain without drainage, It is important to use critical thinking and common sense. Drainage usually tapers off, meaning it will drain a little less over time. An abrupt cessation of fluid could indicate a problem. Assess the drain for kinks or obstructions. If the drain is occluded, fluid may begin to leak around the tube at the skin. Carefully document drain output as dictated by the physician or facility protocol. Any time there is a concern, the physician should be notified.
Infection may occur with both surgical and percutaneous drains. It usually forms one of two ways: during initial drain placement or as a result of continued catheter presence (9). Infection may form during initial placement if the needle punctures a non-target area (such as the colon) or from prolonged dilation, which is why the procedure should be completed in a timely manner (9). Infections may also form at the skin if a drain is present for a long time (9).
The nurse should assess the drain site frequently. Signs of skin infection include redness, increased pain, swelling, fever, and purulent drainage (10). Additionally, sepsis is always a concern for the patient with an abscess (9). A patient with sepsis will sicken very quickly, with rapid increase in fever, chills, and rigors (9). Vital sign monitoring is essential. If the nurse suspects a new infection of any kind or deterioration, notify the physician immediately.
Living with a drain takes some getting used to. It can be easy for patients to forget it’s there. Sometimes the tubing can become tangled up in the bed sheets or left behind when a patient stands up. Although drains come equipped with reinforcements, such as a suture or dressing to help keep the tubing in place, it is possible to pull the drain at least partially or sometimes completely out of the body.
If a drain is pulled out entirely, the nurse should cover the site with some gauze to catch any drainage. When drains are placed, they form a pathway from the abscess or infection to the skin. The tube’s job is to provide a conduit for the fluid to escape. If the tube is removed abruptly, that pathway still exists temporarily, so fluid will continue to leak out of the body in the absence of the tube. Do not attempt to put the tube back in, as it is no longer sterile. Notify the physician.
If the drain is only partially removed, reinforce the dressing as best as possible to maintain its current position and call the physician. Again, do not attempt to push the tubing back inside the patient. The physician may order imaging to assess the drain’s location (2). Removal and/or replacement may be necessary.
Managing drains can be intimidating at first.
How would you troubleshoot the common issues listed here?
This course is designed to help readers become more familiar with drains. They come with all sorts of indications: to facilitate healing after surgery or infection, to assist with draining contents from affected organs, or remove fluids that have accumulated in body cavities.
Drains are classified based on their function: open or closed, passive or active. Familiarity with the different types of drains gives the nurse a basic understanding of how they work- which is important because they can look very different, depending on the manufacturer.
In the old days, surgery and antibiotics were the only way to treat intra-abdominal infections. Significant advances in technology have allowed interventional radiologists to specialize in using medical imaging (CT, ultrasound, X-ray, and MRI) to place drains without making an incision. However, patient selection is still very important, and physicians must know which patients are good candidates for percutaneous drain placement and which are better off heading to the OR.
This course is also designed to provide a basic understanding of drain management and troubleshooting. It is important for nursing staff to understand how a drain is supposed to behave when it is functioning normally so that potential problems are easier to spot. When in doubt, consult the physician. Always be aware of any written orders or policies that dictate drain management, as practices may vary from place to place.
As with anything else, the best way to become more comfortable with drains is to be around them!
(1) Makama, J. G., & Ameh, E. A. (2008). Surgical drains: What the residents need to know.
Nigerian Journal of Medicine: Journal of the National Association of Resident Doctors of Nigeria, 17(3), 244-50. doi: 10.4314/njm.v17i3.37389
(2) Knowlton, M. C. (2015). Nurse’s guide to surgical drain removal. Nursing 2015, 45(9),
59-61. doi: 10.1097/01.NURSE.0000470418.02063.ca
(3) Lemone, P., & Burke, K. (2008). Medical-surgical nursing(4th ed.). Upper Saddle, New
(4) Percutaneous. (2019). In Merriam-Webster Dictionary Online. Retrieved from
(5) Wallace, M. J., Chin, K. W., Fletcher, T. B., Bakal, C. W., Cardella, J. F., Grassi, C. J., …
Kundu, S. (2010). Quality improvement guidelines for percutaneous
drainage/aspiration of abscess and fluid collections. Journal of Vascular and Interventional Radiology, 21(4), 431-435. doi: https://doi.org/10.1016/j.jvir.2009.12.398
(6) Hearns, W. C. (2012). Abscess drainage. Seminars in Interventional Radiology, 29(4),
325-336. doi 10.1055/s-0032-1330068
(7) Rivera-Sanfeliz, G. (2008). Percutaneous abdominal abscess drainage: A historical
perspective. American Journal of Roentgenology, 191(3), 642-643. doi:
(8) Cinat, M. E., & Wilson, S. E. (2002). Determinants for successful percutaneous
image-guided drainage of intra-abdominal abscess. Arch Surg., 137(7), 845-849. doi:10.1001/archsurg.137.7.845
(9) Lorenz, J. & Thomas, J. L. (2006). Complications of percutaneous fluid collection.
Seminars in Interventional Radiology, 23(2), 194-204. doi: 10.1055/s-2006-941450
(10) National Institutes of Health. (n.d.) Patient education: How to care for the Jackson-Pratt
drain. Retrieved from https://www.cc.nih.gov/ccc/patient_education/pepubs/jp.pdf
(11) St. Jude Children’s Research Hospital. (2019). Caring for a pigtail drain. Retrieved from
10.Care of the Aortic Stenosis Patient Undergoing Transaortic Valve Replacement (TAVR)
Aortic stenosis is the second most common valvular heart disease in the Western world, and it is usually diagnosed in patients over the age of sixty-five. (1) With a burgeoning elderly population, it is estimated that the number of Americans over the age of sixty-five will double by the year 2060 (2). Consequently, many more patients with aortic stenosis will be encountered in the clinical context.
Intervention to replace the aortic valve in these patients is crucial because once diagnosed with critical stenosis patients have a mortality rate of 75% within three years. (1) Aortic stenosis is the second most common valvular heart disease in the Western world, and it is usually diagnosed in patients over the age of sixty-five. (1) With a burgeoning elderly population, it is estimated that the number of Americans over the age of sixty-five will double by the year 2060 (2).
Consequently, many more patients with aortic stenosis will be encountered in the clinical context. Intervention to replace the aortic valve in these patients is crucial because once diagnosed with critical stenosis patients have a mortality rate of 75% within three years. (1)
In previous generations, definitive treatment meant open heart surgery performed with the patient on circulatory bypass. However, the less invasive option of trans-catheter aortic valve replacement (TAVR) has recently grown in popularity and has shown to be as effective as an open aortic valve replacement in patients classified as intermediate to high risk (3-5).
The number of TAVR procedures is likely to increase as the procedure matures and the elderly population continues to grow.
The rate of aortic stenosis in the elderly population is estimated to be between 3.4-12% depending on severity. A recent metanalysis compiled data from seven studies and observed a total of 9,723 patients aged seventy-five years or older. The study showed the prevalence of aortic stenosis to be approximately 12%. The estimated rate of severe aortic stenosis, in the same study, was estimated at 3.4%.
Figure 1: Valves of the heart
This image depicts the left and right coronary arteries as they branch off the aortic valve. The left coronary artery sits behind the left coronary cusp and the right coronary artery sits behind the right coronary cusp. The remaining cusp is termed the non-coronary cusp as there is no coronary artery associated.
2011 Heart Valves [Digital image]. (2011) Retrieved March 19, 2019, from https://commons.wikimedia.org/wiki/File:2011_Heart_Valves.jpg Additional Anatomy Marking by M. Le, https://creativecommons.org/licenses/by/3.0/legalcode
Given the prevalence of aortic stenosis in the sample population, researchers estimate that approximately 27,000 patients will become eligible for trans-aortic valve replacement each year. (6) Therefore, having a full understanding of aortic stenosis and its effects on the body is essential to provide care for patients undergoing a TAVR procedure.
Normal Anatomy and Function of the Aortic Valve
The aortic valve works in conjunction with the other three valves of the heart to keep blood moving forward. A brief review of a normally functioning aortic valve helps us understand how the pathology of aortic stenosis causes such profound effects on the rest of the body systems.
The aortic valve is situated between the left ventricle and the aorta. This area is also called the left ventricular outflow tract or LVOT, which simply means the track that flows out of the left ventricle. The opening of the aortic valve, known as the valve area, normally measures 2.6-3.5 cm2. (7)
The aortic valve is referred to as a semilunar valve because when closed it looks like three semilunar structures coming together to form a Y-shape (Figure 1). The aortic valve can be divided into four elements (8) and they are as follows:
- One annulus
- Three cusps (leaflets) with four layers
- Three sinuses
- Three commissures
The three semilunar shaped pockets, known as cusps (or leaflets), attach to a fibrous ring known as the annulus. The annulus is a part of the cardiac skeleton, a dense network of connective tissue that lies between the atria and ventricle reinforcing the structure of the heart (9). The annulus also acts as a shock absorber by transferring the force of the high-pressure circulatory system into the framework of the cardiac skeleton causing less wear and tear on the leaflets.
The cusps are named as the right coronary cusp, the left coronary cusp, and the non-coronary cusp. They are named this way because just behind the cusps, on the ventricle side of the outflow tract, lie three nodules, known as the sinus of Valsalva. The sinus is the area where the left and right main coronaries attach to the aorta (Figure 1). During diastole, the sinuses fill with blood that was just pushed out of the ventricles. As the ventricle begins to relax, the coronary sinuses drain blood into the coronary vessel system, preparing for the next contraction by providing oxygen and nutrients to the heart muscle.
The cusps are pearlescent in appearance and have four layers all less than 1mm thick; each layer has a distinct function (Table 1) (10). The names of the layers are as follows:
The layers are connected in the following arrangement starting from the aortic endothelium and working toward the ventricular endothelium:
Aortic Endothelium > Fibrosa > Spongiosa > Ventricularis > Ventricle Endothelium
Figure 2. Aortic Valve Histology – Microscopic view of the aortic valve leaflet layers.
Korossis, Sotirios. (2018). Trilaminar leaflet structure of the semilunar valves [Digital Image] Retrieved March 25, 2019 from https://www.researchgate.net/figure/a-Trilaminar-leaflet-structure-of-semilunar-valves-showing-the-fibrosa-spongiosa-and_fig4_328084726 Rearrangement of images by M. Le, https://creativecommons.org/licenses/by/3.0/legalcode
Table 1. Layers and Function of the Aortic Valve Leaflets
|Fibrosa||fibroblasts and collagen fibers in a circular arrangement||Faces the aorta||Fibers are arranged in a circular pattern. Distributes the pressure load from the surface of the leaflet out to the annulus|
|Spongiosa||Mucopolysaccharides, mesenchymal cells, and fibroblasts||The base where the leaflet attaches to the annulus||Resists the compression of the cusps|
|Ventricularius||mucopolysaccharides, mesenchymal cells, and fibroblasts||Faces the left ventricle||Fibers are arranged in a radial pattern to distribute force and maintain shape of the valve|
|Epithelium||Squamous Cells||Wraps the outside of the leaflet continuous with the aorta and ventricle||Provides protection from shearing forces|
Aortic Valve’s Role in the Cardiac Cycle
We have looked at the composition of the aortic valve now let’s look at its role in the cardiac cycle, starting with the venous circulation. (Figure 32) Deoxygenated blood from the body travels to the heart through the superior and inferior vena cava:
- The superior and inferior vena cava empty into the right atrium of the heart. The atrium contracts, the tricuspid valve opens, and the blood flows into the right ventricle. As the right atrium relaxes, the tricuspid valve closes.
- The right ventricle contracts and opens the pulmonic valve. Blood travels into the pulmonary circulation to eliminate waste and reoxygenate. The oxygen rich blood then travels from the pulmonary circulation into the left atrium of the heart.
- The left atrium contracts, opening the mitral valve and blood flows into the left ventricle. The atrium relaxes and the mitral valve closes. The left ventricle contracts, sending blood out of the aortic valve and to the body through the aorta and carotid arteries. The valve will close when the pressure in the aorta is higher than the pressure in the ventricle.
Closure of the aortic valve is part of the second heart sound, S2, and is heard as the “dub” part of “lub-dub.” Originally, the S1 and S2 heart sounds were thought to be the sounds of the valves snapping shut. However, we now know that the heart sounds occur because of vibrations that happen just after the valve has shut (11).
For example, as the aortic and pulmonic valves initially close some blood flows back and hits against the valves. The blood hitting against the valves causes vibrations that travel along the corresponding chamber producing the “lub” or “dub” sound as it travels.
Figure 3: Blood Flow Through the Heart
ZooFari (2010) Heart Diagram Blood Flow [Digital Image] Retrieved March 19, 2019 from https://wikimedia.org/wiki/File:Heart_diagram_blood_flow_en.svg https://creativecommons.org/licenses/by-sa/3.0/legalcode
Pathophysiology and Assessment
In aortic stenosis, the leaflets of the aortic valve become calcified, scarred, and stiff. The calcifications narrow the valve opening from the normal 2.6-3.5 cm2 to ˂1 cm2. The narrow valve obstructs the left ventricular outflow tract (LVOT), increasing the work the heart must do to overcome the obstruction or the afterload. To compensate for this obstruction and increased afterload, the heart begins to squeeze harder, increasing pressure in the left ventricle.
Left ventricle pressures have been reported as high as 300 mmHg in some cases (11). The constant exposure to high pressure causes the left ventricle to fibrose, thicken, and remodel. The increased muscle mass also demands more oxygen which causes stress on the microvasculature of the heart and contributes to the symptom of angina (12).
Typically, the left ventricle can relax and to allow for passive filling from the left atrium. The passive filling of the ventricle makes up the 80-85% of the end-diastolic volume, and the remaining 15-20% is provided by the “atrial kick” at the end of diastole. However, aortic stenosis patients have stiff, non-compliant ventricles that do not relax enough for proper filling during diastole; these patients depend on the atrial kick for 40% of their blood volume (7).
Therefore, abnormal rhythms such as atrial fibrillation or tachycardia cause patients with aortic stenosis to lose the benefits of the atrial kick, which causes a subsequent decrease in cardiac output to the body which leads to syncope and in some cases sudden cardiac death.
Ultimately, in the course of aortic stenosis, the left ventricle will dilate, fail, lead to pulmonary congestion, shortness of breath, and chest pain, which are the hallmark symptoms of aortic stenosis. Patients presenting with the classical triad of aortic stenosis have a 2-5 year prognosis if untreated (7).
Hallmark symptoms: Syncope Angina Dyspnea
In severe aortic stenosis, blood from the left ventricle is being pushed out of a tiny calcified and critically stenosed opening at tremendous pressures creating what is called a “nozzle effect”. It is termed the “nozzle effect” because blood is spraying out of the aortic valve like water out of a fire hose (11).
As the blood hits the sides of the aorta, it causes vibrations that are heard, sometimes even without a stethoscope, and are felt like the thrill of a fistula. The murmur of aortic stenosis is heard and felt loudest in the 2nd intercostal space on the right side (Figure 5) this is the area directly over the aorta (13). The murmur can be heard best during systole since this is when blood is spraying out of the ventricle and creating turbulence in the aortic arch.
Figure 4: Left Ventricular Remodeling
Left ventricular hypertrophy (LVH) develops in response to elevated pressures in the ventricle. Patients who develop LVH are 4.5 times more likely to experience adverse events. Sustained exposure to increased afterload causes apoptosis, or cellular death, in the ventricles which leads to dilation and heart failure. Heart failure contributes to the hallmark symptoms of syncope, angina, and dyspnea.
Patchett, N. (2015) Ret March 19, 2019 from https://en.wikipedia.org/wiki/Cardiomyopathy#/media/File:Tipet_e_kardiomiopative.png one element removed and rearrangement by M. Le, CC BY-SA 3.0
It is important to be able to identify the murmur of aortic stenosis given that many patients can go decades without any symptoms, and earlier detections can lead to earlier treatment and fewer long-term complications and morbidity. The murmur of aortic stenosis is considered a mid-systolic murmur described as a harsh crescendo-decrescendo murmur. Initially, as blood is pushed out of the ventricle, there is no sound, but as the ventricle squeezes harder the turbulence of the blood flow causes the crescendo and gradually as the ventricle begins to relax the decrescendo ensues.
In the late stages of the disease, S2 may be obscured by the murmur or even lost as the aortic valve becomes less compliant; this is an abnormal finding. The presence of S4 is indicative of left ventricular hypertrophy that develops over time in aortic stenosis (13). The S4 rhythm is called a gallop rhythm because it sounds like the hoof-beats of a horse (13).
When listening to a normal heartbeat, during S2 with inspiration, you may be able to distinguish two heart sounds; this is a normal finding called physiological splitting, and it only indicates that the pulmonic valve is taking a bit longer to close due to the inspiration. However, in aortic stenosis, it takes the aortic valve longer to close due to delayed emptying and the ventricles inability to relax. This abnormal finding is called paradoxical splitting, and it is heard during expiration rather than inspiration. (7)
Pulsus Tardus is a weakening of the carotid pulse that can be felt with light palpitation of the carotid artery. Pulsus parvus et tardus is when the carotid upstroke is delayed (7, 13). The carotid upstroke can be assessed by listening to the heart for systole and noting by palpation how long it takes to travel to the carotid artery.
Have you ever cared for a patient with severe aortic stenosis?
Did they exhibit any of the hallmark symptoms?
How did their AS affect their care plan?
Figure 5. The Murmur of Aortic Stenosis
The murmur of aortic stenosis is best heard over the second intercostal space at the sternal border and may radiate toward the carotids. Also, depending on the turbulence of blood flow the murmur may be palpable as a thrill
Blausen.com staff (2014). Medical gallery of Blausen WikiJournal of Medicine 1 (2). DOI:10.15347/wjm/2014.010. ISSN 2002-4436. https://commons.wikimedia.org/wiki/File:Blausen_0467_HeartLocation.png, „Blausen 0467 HeartLocation“, https://creativecommons.org/licenses/by/3.0/legalcode
Etiology & Risk Factors
There are a few ways in which aortic stenosis can occur. These causes are listed below from most to least common.
- Idiopathic calcification
- Congenital bicuspid valve
- Rheumatic heart disease
- Radiation or Endocarditis
- Genetic elevation of lipoprotein (a) (13)
Idiopathic calcification occurs mostly in patients over the age of sixty-five; this by far is the most common cause of aortic stenosis and is found in 3 to 5% of the general population (14). Risk factors for patients in this class to develop aortic stenosis include smoking, male gender, hypertension, hyperlipidemia, and diabetes. They are mostly the same risk factors associated with atherosclerosis (1).
Bicuspid aortic valve disease, a congenital condition, is a condition where a person is born with only two cusps on the aortic valve. Bicuspid valve disease is the most common congenital heart disease and is found in 1 to 2% of the population (15). Symptoms usually show up in this group around 40-50 years of age as age-related changes begin to affect the bicuspid aortic valve. Nearly 40% of these patients also have aortic dilatation which can lead to rupture, a medical emergency (15).
Rheumatic aortic disease, now a rare cause of aortic stenosis, is caused by an autoimmune response to group A streptococci, which leads to scarring along the commissure of the valve leaflets lessening their pliancy and causing an obstruction to the outflow tract of the left ventricle (14). Rheumatic aortic stenosis can easily be remedied with antibiotics and with the combination of rapid strep testing and access to antibiotics this is very rarely encountered in the clinical area.
Some cases of aortic stenosis are believed to be caused by a genetic variation in the genes that express lipoprotein (a). The elevation of lipoprotein (a) along with low-density-lipids are thought to induce inflammatory changes on the layers of the valve leaflets leading to valve calcification and stenosis (16, 17). Other rare causes of aortic stenosis include; endocarditis, radiation therapy, Paget disease, Fabry disease, ochronosis, and end-stage renal disease (14).
Natural History of Aortic Stenosis
In aortic stenosis the aortic valve causes and obstruction of the left ventricular outflow tract. The heart attempts to overcome this obstruction by pushing harder. This causes a tremendous difference in pressure between the left ventricle and the aorta. This difference is measured and termed the transvalvular gradient. Transvalvular gradients higher than 50 mm Hg with a small valve area such as 0.8 cm2 is considered “severe aortic stenosis”.
In severe aortic stenosis the left ventricle compensates in two ways:
Remodeling happens on a cellular level and is caused by changes to the cellular matrix in response to elevated pressure. Thickening of the heart muscle occurs because of how hard the heart must push against the transvalvular gradient (Fig. 4.). The more the heart muscle is worked the larger it becomes, just like any other muscle of the body. The thickening, however, has consequences.
The first being that the muscle of the left ventricle has thickened, but the excess tissue leaves no room for blood in the ventricle. Less blood in the ventricle leads to less blood being pushed out to the body. This leads to diastolic heart failure. These patients can appear to have a normal Ejection Fraction (EF), but this can be deceiving. Let’s look at normal ejection fraction vs. the ejection fraction of a patient with diastolic dysfunction.
The Normal Ejection Fraction
A. The heart fills will 100 ml
B. The heart ejects 60 ml
B/A=0.60 or 60%
The Ejection Fraction of Diastolic Dysfunction
A. The heart can only fill 50 ml
B. The heart ejects 30 ml
B/A=0.60 or 60%
The ejection fractions are identical, but the patient with diastolic dysfunction is filling up with half the blood and pumping out half the blood of the normal patient. The deficit leads to under perfusion to the body, which leads to exertional chest pain. On the other hand, because the ventricle cannot fill up enough or pump out enough blood begins to backup from the left ventricle to the left atrium and finally all the way back to the vasculature of the lungs.
The vessels of the lungs begin to leak excess fluid causing pulmonary edema and dyspnea. This dyspnea is especially increased during exertion, because on top of the fact that the heart cannot push out enough blood, now there is tachycardia which decreases the amount of time the heart has to fill up. Patients with aortic stenosis often adjust their activity level over time so that they do not over exert themselves which leads to the chest pain and shortness of breath.
Now let’s look at the other scenario. Aortic stenosis patients with systolic dysfunction usually have an ejection fraction that is lower than normal. In this scenario the left ventricle has become worn out and is unable to pump blood to the rest of the body. The ventricle dilates and thins causing it to lose its ability to pump effectively (fig. 4). Let’s compare the ejection fraction to that of a normal patient.
The Normal Ejection Fraction
A. The heart fills with 100 ml
B. The heart ejects 60 ml
B/A=0.6 or 60%
The Ejection Fraction of Systolic Dysfunction
A. The heart fills with 100 ml
B. The heart ejects 30 ml
B/A=0.30 or 30%
In this case the ventricle has enough room for the normal amount of blood, but the muscle of the ventricle is only able to squeeze out 30 ml to the body. If you notice in both scenarios the patient is only pushing 30 ml of blood out of the ventricles; so regardless of whether the patient has systolic or diastolic heart failure they end up with the same consequences of chest pain from under-perfusion and shortness of breath from blood backing up into the pulmonary vasculature.
As patients with aortic stenosis progress slight changes in heart rate, afterload, and vascular resistance mean wide swings in symptoms and if not corrected can lead to sudden death. With excessive fluid volume aortic stenosis patients will develop dyspnea while dehydration will not allow the ventricle to fill adequately.
Tachycardia does not allow the ventricles to fill while bradycardia will decrease the cardiac output further. Patients with aortic stenosis are best kept close to their baseline vital signs while preparing for the TVAR procedure.
Overview of Procedure
The transcatheter aortic valve replacement or TAVR procedure is approved for patients who have severe symptomatic aortic stenosis and who are at high risk for surgical valve replacement.
Sheaths are used to make a conduit for the valve deployment device. The valve is round and made of a metal mesh network to which bovine leaflets attached.
The TAVR procedure does not require that the heart is stopped to perform the valve replacement, though the heart is usually paced at a high rate during deployment.
Diagnostic imaging is crucial if a TAVR is to be planned. Solid imaging of the aortic valve decreases the risk of sub-optimal valve deployment during procedure, which can result in paravalvular regurgitation, aortic injury, heart block, or embolization of the valve prosthesis (18).
The gold standard of evaluation of aortic stenosis is the transthoracic echocardiogram (TTE). In this section we will look at what a diagnostic TTE assesses. Performing a TTE helps to (19):
- Confirm the diagnosis of AS
- Identify the cause of AS
- Assess valve morphology
- Identify the severity of the valve lesion
- Note left ventricular remodeling
- Estimate functional capacity of the left ventricle
- Assess for the presence of mitral valve regurgitation
- Assess for concomitant pulmonary hypertension
Echocardiography can be used to determine the number of leaflets that are present and if the valve is tricuspid or bicuspid. This is of importance since the bicuspid valve is not yet approved for replacement via TAVR.
Another morphological notation on echocardiography is the presence of calcification on the valves. The ultrasound can quantify the amount, location, and severity of the calcium deposits (20).
Rheumatic valve disease is usually differentiated by the pattern of calcification. While rheumatic heart disease usually shows calcification at the commissure line, aortic stenosis usually affects the base of the leaflet and works in an outward pattern (14).
Echocardiographic parameters classify the severity of the valve lesion into mild, moderate, and severe stenosis. The severity of the disease is determined by the valve area, valve gradients, and peak velocity.
Table 2. Measure of Severity in Aortic Stenosisb
|Aortic Valve Area (AVA) cm2||>1.5 cm2||1.1-1.5 cm2||≤1 cm2|
|Mean Gradient mm Hg||˂20 mm Hg||20-39 mm Hg||≥40 mm Hg|
|Peak Velocity (m/sec)||2.0-2.9 m/sec||3.0-3.9 m/sec||≥4 m/sec|
Based on information from Mixon & Dehmer
Aortic Valve Area
The aortic valve area (AVA) is a calculation that measures the obstruction of the left ventricular outflow tract, by the stenosed valve. The normal aortic valve area is 2.5-3.5 cm2. The more stenosed the valve, the smaller the aortic valve area.
Figure 6. Peak Velocity Illustration
The narrowed opening in aortic stenosis causes a “nozzle” effect as the force from the ventricle ejects blood across the valve at a high speed, known as peak velocity. (figure B) The normal peak velocity shown in (figure A) is smooth with laminar flow
Le, K. (2019) Peak Velocity Illustration. BA.
The valve gradient is another calculation that measures the difference in flow across the valve. The gradient can be calculated on echocardiography or performed directly in the cath lab. In the cath lab, the pressure in the left ventricle and the pressure in the aorta are measured simultaneously. The difference between the two numbers is the gradient. High pressures in the ventricle with low pressures in the aorta is indicative of aortic stenosis. The normal mean gradient is ˂20 mmHg.
The peak velocity is a calculation that estimates how fast the blood is traveling across the valve and is measured in meters/second. The standard peak velocity is 2.0-2.9 m/sec. Peak velocity is related to the “nozzle effect,” where the ventricle is trying to push blood out of a narrowed opening. The enormous pressure generated translates into a higher peak velocity.
Left Ventricular Hypertrophy
Left ventricular hypertrophy (LVH) is abnormal thickening and reshaping of the left ventricle in response to the extreme pressures generated in the ventricle as it pushes against the stenotic valve. LVH is present in approximately 67% of patients diagnosed with asymptomatic severe aortic stenosis (12). The onset insidious and can develop long before the onset of symptoms. LVH increases the risk of adverse cardiovascular outcomes up to 4.5-fold (12). Therefore, echocardiographic evaluation of the left ventricle is useful to estimate the functional capacity and determine the severity of LVH before the TAVR procedure.
The echocardiography is also able to detect concomitant Mitral Regurgitation (MR). MR is when the blood flows backward from the left ventricle into the atrium. This process can either be acute or chronic. Acute cases of MR usually occur in the setting of myocardial infarction, infective endocarditis, rupture of a chordae tendineae, or malpositioning of the aortic valve during TAVR (18).
In acute cases, there is an overwhelming back up of blood from the left ventricle to the left atrium and back to the pulmonary circulation. The rapid onset does not allow time for compensation, and it can easily lead to pulmonary congestion, hypoxia, reduced cardiac output, hypotension or even shock (18).
Non-acute cases of MR can occur when the left ventricle becomes hypertrophic, and subsequently the annulus of the mitral valve becomes dilated, which is common in aortic stenosis (18).
Regurgitation can lead to pulmonary congestion and edema. The mitral valve can be repaired along with the aortic valve in patients undergoing SAVR, but it is not yet performed in conjunction with TVAR. Ultimately, the decision to perform TAVR vs. SAVR in these patients is based on the heart valve team and the patient.
Other Imaging Modalities
Other imaging modalities include computed tomography (CT) or cardiac magnetic resonance (CMR). Cardiac catheterization is recommended in all patients since concomitant coronary artery disease is found in 50% of patients with aortic stenosis (7).
Many modalities are used so that a complete picture of the valve can be obtained before the procedure.
To recap the information we have covered thus far, answer the following questions:
What is the most common cause of AS?
What is the natural history of untreated AS?
What type of imaging is considered the “gold standard” for evaluation of AS?
Decision to Intervene
The heart valve team is tasked with deciding the best pathway for the patient based on current evidence and guidelines. The team typically consists of cardiologists, structural interventional cardiologists, imaging specialists, cardiovascular surgeons, a cardiovascular anesthesiologist, and cardiovascular nursing professionals (18).
The patient and family are involved in each step of the process, and they may be assigned a heart valve coordinator that works closely with them ensuring high-quality education and information for the decision-making process.
The decision to proceed to intervention is based on several factors (18):
- The patients goals and beliefs
- The presence or absence of symptoms
- The severity of the lesion
- Remodeling of the ventricles
- Pulmonary or systemic congestion
- A change from baseline heart rhythm
- Risk/benefit based on age
- Co-morbidities and life expectancy
Evaluation of Risk
The Society of Thoracic Surgery Predicted Risk of Mortality (STS-PROM) is a scoring system that is based on years of data collected by the Society of Thoracic Surgery. The heart valve team takes the STS score and classifies the patient into low, intermediate and high risk for surgical intervention.
Before surgery other factors are also measured such as the frailty index which takes into consideration the patients ability to perform activities of daily living, assesses any weight loss in the previous year, and tests the patient’s ability to rise from a chair. The patient may also be asked to perform a six-minute walk test or pass the Mini-Mental State Exam that assesses cognitive function.
Patients are further classified into stages A-D3 (Table 4.). These stages describe the severity of stenosis, characteristics of the stenosis, and presences or absences of symptoms.
The AHA/ACC guidelines are made to go along with the STS-PROM assessment. For example, a patient at high surgical risk, with symptomatic severe aortic stenosis would fall into the TAVR category, while a patient at intermediate risk with severe symptomatic stenosis would be recommended for SAVR. Intervention recommendations for stage A-D3 can be found in Table 4., while absolute contraindications for TAVR are listed below:
Contraindications for TAVRc
Based off information from Nitya & Kumar
- Bicuspid or non-calcified aortic valve
- Peripheral vascular or aortic disease
- Coronary artery disease requiring revascularization within 30 days
- End stage renal disease
- Severe left ventricular hypertrophy
- LVEF<20%, severe mitral regurgitation
- Significant neurological disease
- Life expectancy <1 year
Ultimately, Surgical Aortic Valve Replacement (SAVR) is preferred in patients with low to intermediate surgical risk. However, for patients at high surgical risk measured by STS score>10% TAVR is the preferred intervention (7).
Table 4. Staging and Timing of Intervention
Based on information from Kanwar, A., Thaden J.J., and Nkomo, V.
Criteria for Intervention
At risk of AS
Watch and Wait
ACE, ARB, Beta Blocker if tolerated.
Watch and Wait
ACE, ARB, Beta Blocker if tolerated.
Intervention AVR largely based on decision between surgeon and patient.
TTE every 3-5 years for mild severity (Vmax 2.0-2.9 ms)
TTE every 1-2 for moderate severity (Vmax 3.0-3.9 ms)
TTE with any change in symptoms.
Asymptomatic severe AS
SAVR is recommended once patient becomes symptomatic, symptoms are elicited on stress test, or undergoing another cardiac procedure.
calcified AVA ≤ 1.0 cm2 and an aortic velocity ≥ 4-5 m/s or mean gradient ≥ 40-60 mm hg
None or May have exercise induced symptoms
TTE every 6-12 months for
(Vmax ≥ 4 ms)
Exercise stress testing to:
Confirm otherwise hidden symptoms, assess response to exercise, determine next steps.
Asymptomatic severe AS with LV dysfunction
LVEF <50% with calcified AVA ≤ 1.0 cm2 and an aortic velocity ≥ 4 m/s or mean gradient ≥ 40 mm hg
Symptomatic severe high-gradient AS
In the absence of severe co-morbid disease SAVR is recommended.
In presence of severe co-morbid disease TAVR is recommended.
calcified AVA ≤ 1.0 cm2 and an aortic velocity ≥ 4 m/s or mean gradient ≥ 40 mm hg
Symptoms mainly with exertion: dyspnea,
angina, syncope, heart failure
Symptomatic Severe low gradient AS with low LVEF
In the absence of severe co-morbid disease SAVR is recommended.
In presence of severe co-morbid disease TAVR is recommended.
UNDER STRESS TEST: LVEF <50% with calcified AVA ≤ 1.0 cm2 and an aortic velocity ≥ 4 m/s or mean gradient ≥ 40 mm hg
Symptoms at rest: syncope, dyspnea, heart failure
Low dose dobutamine stress test
Symptomatic Severe low gradient/low flow
In the absence of severe co-morbid disease SAVR is recommended
In presence of severe co-morbid disease TAVR is recommended
UNDER STRESS TEST: LVEF ≥50% with calcified AVA ≤ 1.0 cm2 and an aortic velocity ≤ 4 m/s or mean gradient ≤ 40 mm hg
Symptoms at rest: syncope, dyspnea, heart failure
Low dose dobutamine stress test
Many patients with AS are not surgical candidates due to the above mentioned contraindications.
How will you approach this with patient and families?
How will you explain the rationale behind the risk stratification?
Choice of valve
Multi-detector computed tomography (MDCT), is the preferred imaging method to determine the annular size of the aortic valve, and it facilitates the decision of what valve should be chosen (18). The 3D data set that MDCT provides produces a more tangible image by which to choose valve size; and it is also able to measure the annulus of the aortic valve during systole when the valve is usually wider and fully open.
The MDCT scan measures the aortic root which produces an anatomical image of the sinus of Valsalva, the coronary ostia, and the size of the aorta and sinotubular junction (18). These views can be used to seat the valve properly since any obstruction to the coronary ostia can lead to ischemia and possible cardiovascular arrest.
MDCT imaging can help determine whether a balloon-expandable, self- expanding, or mechanical deploying valve should be chosen. The balloon-expandable valve fits over a balloon and when the balloon expands it pushes the valve onto the annulus of the aortic valve.
Figure 7. Common TAVR Access Sites
A self-expanding valve expands in a spring-like manner without the need for a balloon. The mechanical valves have a seal to reduce paravalvular leak and can be expanded by the cardiologist in a controlled manner. However, the Lotus valve was the only mechanical valve on the market and has been pulled temporarily due to issues with its locking mechanism (21).
Regarding preference, Otto et. Al states that a self-expanding valve is a gentler option and may be preferred in patients with “severe calcification of the valve and outflow tract with a risk of rupture, patients with an extremely oval-shaped annulus, or for small transfemoral access” (18).
If a patient requires the transapical approach, as in the case of severe atherosclerosis of the vasculature, the only valve approved for use is the balloon-expandable version (18). Many versions on the market today can be repositioned if malpositioned (18). Often, however, the choice of valve is merely physician preference.
Choice of Access
The outer diameter (OD) of the sheaths used for valve deployment range anywhere from 6.9 cm to 8.68 cm depending on the intended valve. Access sites are thoroughly imaged to ensure an entry point that is non-tortuous and mostly free of atherosclerosis which can put the patient at risk for cerebral embolization (18). If entry through the femoral artery is not feasible, other options include transaxillary, transapical, direct aortic, carotid, or transvenous approach (Figure 7).
Hybrid Operating Room
Facilities, where TAVR procedures are performed, have a dedicated hybrid operating room that is a mix between a cath lab and a standard operating room. There is a cardiopulmonary bypass machine available if the procedure is converted to open-chest. Coronary occlusion wires are on hand if coronary embolization occurs intra-procedure, and anesthesia is equipped with advanced airway supplies if necessary. A crash cart and defibrillator are nearby, and defibrillator pads are placed on the patient per routine.
Many of these patients have both cardiovascular and non-cardiovascular risk factors. Cardiovascular collapse is a real concern and proper anesthetic management can decrease this risk. Optimal hemodynamics should be maintained through the case, and attention should especially be paid to hypotension. Prompt administration of vasoactive medications aids in the avoidance of hypoperfusion.
While general anesthesia with endotracheal tube is the most common delivery method of anesthesia in TAVR patients, studies have shown that moderate sedation decreases the need for vasoactive medications (18, 22). However, an endotracheal tube should be considered if imaging by TEE is expected due to patient comfort.
If moderate sedation is to be utilized, the practitioner must be certain that airway securement can be done quickly in the event of respiratory or circulatory collapse. Due to the amount of equipment surrounding the patients head, attention should be paid to the environment and maneuverability in the event of emergent intubation (18).
This procedure is performed on a high-risk population; therefore, complications are not uncommon. There are many different types of complications; however, if recognized promptly most can be managed or reversed.
Some complications are caused by improper placement of the new valve; these complications look different based on whether the valve is deployed too high or too low. Valve placement on the aortic side can cause a blockage of the aorta, injury to the aortic intima, or blockage of the coronary arteries. Valve placement too far into the ventricle can interfere with the mitral valve, causing mitral regurgitation, and subsequent pulmonary edema.
Also, pressure on the atrioventricular node can lead to conduction abnormalities and possible heart block (20). In these cases, the valve is retrieved and repositioned if possible. A transvenous pacer is inserted at the start of the procedure, which is used if the patient experiences complete heart block or any other non-perfusing rhythm.
If the surgical valve fails to cover the entire annulus, a paravalvular leak may occur. The leak can usually be corrected by inflating a balloon inside the valve, effectively pushing it outward to create a better seal, if this fails the valve may need to be recaptured and repositioned or replaced with a larger size.
Some complications are systemic such as cardiovascular collapse, shock, stroke, and myocardial infarction. Shock or hemodynamic collapse is always a risk in unrepaired aortic stenosis patients. The best management is to keep the patient within tight hemodynamic parameters, however, if cardiovascular failure ensues, and is irreversible the patient should be placed on coronary bypass.
If the ventricle or annulus is ruptured the procedure should be converted to an open heart. Also, if coronary occlusion and subsequent ischemia ensues the procedure should be converted to an open CABG. In the event of an embolic stroke catheter-based retrieval should be attempted.
In the event of a hemorrhagic stroke anti-coagulation should be reversed and treatment with this type of stroke is conservative. Access site complications such as dissection of the artery may require endovascular or surgical repair. Lastly, bleeding complications can be related to systemic heparinization that may need to be reversed.
Information about the patient’s history can be gleaned from the chart; however, obtaining a thorough report and being aware of the most common complications will aid in swift recognition and correction of adverse events.
When obtaining report some items to note are; size and type of valve placed, concern of mal-placement or leak, the type of sheath that was used, and the number of vascular access sites the patient has.
Was the repair transapical and if so were any drains placed? Were any irregular arrhythmias noted post-deployment? Does the patient have a transvenous pacer still in place? Is the patient pacer dependent, if so what are the settings, and where is the sheath and control box? What type of closure device was used? Were there any bleeding incidences in the surgery suite? When and what was the last ACT? Does the patient have any risk factors for bleeding; such as von Willebrand factor deficiency? Are any hematomas noted?
TAVR Complications Ordered Most to Least Common
Based off information from Nitya & Kumar (7)
- Bleeding (15%)
- Vascular site complications (10-15%)
- Need for permanent pacemaker (5-15%)
- Significant perivalvular leak (10%)
- Stroke (2-5%)
- Death (2-5%)
- Acute kidney injury (1-2%)
- Coronary Occlusion (0.6%)
- Valve embolization (0.3%)
If there are hematomas what size and how firm are they? If the patient has a femoral access as they are at risk for retroperitoneal hematomas- this may manifest as back pain, hemodynamic instability, and bruising along the flank. It is also advisable to mark the borders of the hematoma as a reference since patients can bleed insidiously. Is the patient having any pain?
What type of anesthetic was used local, monitored anesthesia care, or general? If it was general anesthesia, what type of airway was used? Time and dose of last known pain medication and was local anesthetic used at the access site? How much vasoactive medication was necessary during the procedure? How much fluid was administered intraoperatively? Is there a urinary catheter and how much was the urine output during the procedure? How much contrast dye was utilized for the procedure?
These questions take into consideration some of the most common complications such as; bleeding, vascular site complications, need for permanent pacemaker, significant perivalvular leak, stroke, and acute kidney injury. Occurrence rate on each complication can be found above (TAVR Complications Ordered Most to Least Common).
Knowing the most common complications, how will you adjust your assessment and monitoring of post-op TAVR patients?
What signs and symptoms are you likely to see if any of these complications occur?
Bleeding and Vascular Site Complications
Before the procedure, patients undergo a series of imaging scans to identify potential vascular access sites. The scans included are a left and right heart catheterization and aortography, transthoracic and transesophageal echocardiography, computed tomography and angiography of the chest, and computed tomography of the abdomen and pelvis (23).
However, it is still estimated that about 15% of patients experience periprocedural bleeds which outranks all other complications (7). Many of these bleeds are related to the vascular entry site which carries a complication rate of 10-15%.
Proper monitoring of the access site, and the 5 P’s pain, pallor, pulse, paresthesia, and paralysis helps to identify any occlusion of the artery which is considered a surgical emergency. Most bleeding can be resolved by proper monitoring and intervention by manual pressure applied to the site. However, for continuous uncontrolled bleeding manual pressure should be applied, an ACT should be assessed, and if manual pressure is not adequate, the patient will require surgical stenting of the vessel (24).
Acquired Von Willebrand Syndrome
Aortic stenosis patients are also at high risk to acquire von Willebrand syndrome. (25) This happens because the stenosed aortic valve causes shearing forces and as blood crosses the valve clotting factors are destroyed; which in some cases this can lead to an induced VonWillebrand syndrome.
This condition can subsequently cause Heyde’s syndrome which is a gastrointestinal bleed caused in the setting of absent or defective von Willebrand factor. Replacing the valve may decrease the shearing effect, but it takes time for clotting factors to stabilize. The adenosine diphosphate closure time (CT-ADP) is a bedside test that is run much like an activated clotting time which may be useful in helping to identify paravalvular leaks and patients at risk for bleeding complications (25).
Complete heart block is a condition where the electrical signal of the heart is blocked and cannot travel through the atrioventricular (AV) node. This is characterized by a complete dissociation of p-waves and QRS complexes. Patients can also experience different degrees of AV dissociation which may lead to 1° AVB and 2nd° AVB.
While it is known that AV blockage can occur after TVAR, it is not well understood why this happens. Some studies have attempted to predict which patients are at risk for AV blockage post-TAVR. Studies have shown that larger valve sizes and the Edwards Sapien 3 Valve in particular have a higher rate of AV block. (27)
In another interesting study, patients with a QRS >120s were found to have a 38% rate of permanent pacemaker placement after TVAR, while none of the patients with a QRS ≤120s had any semblance of heart block. (28) In yet another study they found that longer P-R intervals, QRS duration, history of Right Bundle Branch Block (RBBB) and pre-existing 1°/2° block were more common in patients that required permanent pacemakers post procedure.
(29) Most incidences of heart block occur immediately after the procedure (30) while the patient is in the critical care unit. A thorough look at the patients pre-operative EKG and cardiac history may reveal patients at risk of needing a pacer post-operatively, allowing the nurse to prepare for placement of a transvenous pacer or utilization of one that is already in place.
The mechanism by which stroke occurs after procedure is debatable, but both embolic and hemorrhagic strokes may occur after TAVR. However, more advanced catheters and valves lessen the risk of stroke. (31) The risk of stroke does appear to be the same as patients undergoing surgical aortic valve placement (SAVR), however, one study found that TVAR patients who experienced a TIA post-procedure had a lower 1-year survival rate (31).
Patients who are immediately post-op and in the ICU are at the most risk of experiencing a stroke or transient ischemic attack (TIA). However, after the immediate preoperative period, the risk of stroke/TIA decreases dramatically (31). Since it is postulated that debris from the valve is the cause of many neurological events studies are examining the use of cerebral protective devices such as a filter to decrease the incidence of embolic stroke. (32) Additionally, the use of antiplatelet therapy does seem to minimize the risk of embolic type strokes. (31) A full neurological exam should be performed upon admission per standard practice.
Patient may still be sleepy from procedure at this time, but it is important to assess for a proper baseline since TVAR patients are at high risk for stroke especially within the first twenty-four hours. Full neuro assessments that include a pupillary check should be performed every four hours at minimum or per hospital policy. Abbreviated neuro assessments may be performed in between full assessments and they should include at minimum an assessment of balance, dizziness, headache, blurred vision, facial drooping, and speech difficulty. Performing regular neurological checks will aid in early identification and treatment for TAVR patients Policies will vary by institute but a sample schedule may be as follows:
- Full neurological exam x1 then q 4hrs
- Abbreviated exam q 15 min x 8
- Abbreviated exam q 30 x4
- Abbreviated exam q hr
Acute Kidney Injury, Pain Management and Early Mobilization
Acute Kidney Injury
The development of acute kidney injury after TVAR is associated with a four-fold increase in mortality. (33, 34) Risk factors for AKI after TVAR are hypertension, COPD, pulmonary disease, and blood transfusions (33-35). Some hospitals employ a preoperative infusion of acetylcysteine and IV bicarbonate as a protective measure against the contrast dye, but there is conflicting evidence as to whether this actually decreases risk.
Measuring intake and output for patients at risk for AKI are nursing measures that may help with early diagnosis and treatment. Proper fluid management and avoidance of hypovolemia may reduce the risk of AKI.
Pain Management and Early Mobilization
Pain management should be titrated to the patient’s needs. Ideally, pain medication should be adjusted so that the patient is comfortable during early ambulation and remains alert and oriented. Early mobilization is linked to shorter hospital stays and a decreased risk of venous thrombus. (36) Patients with femoral access sites will usually need to lie with the head of the bed in ≤15° for a minimum of six hours to ensure hemostasis, then they may resume sitting and walking activities.
Patients with other access sites may be able to ambulate sooner dependent upon hospital policy. Patients should make a goal of walking the unit at least 3-4 times a day if possible.
Respiratory problems, infections, and bleeding events are the main reasons that TVAR patients are readmitted (18). Proper education throughout the hospital stay may help decrease the incidence of these events.
Most patients will be sent home on a regimen of aspirin and clopidogrel for at least six months to prevent thrombus formation of the newly placed valve. Education should be provided for the patient on how to monitor their access site for any signs of bleeding and they should be aware that the clopidogrel will put them at greater risk for bleeding.
The patient should be instructed on how to keep the incision site clean and how to apply any dressings if necessary. Educate the patient making them aware that ambulation along with coughing and deep breathing will decrease the chance of pneumonia and respiratory infections.
Any medication changes should be discussed, and the patient should go home with a medication reconciliation form stating what dose should be taken and at what time.
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- Elhmidi, Y., Bleiziffer, S., Deutsch, M. A., Krane, M., Mazzitelli, D., Lange, R., & Piazza, N. (2014). Acute kidney injury after transcatheter aortic valve implantation: Incidence, predictors and impact on mortality. Archives of Cardiovascular Diseases, 107(2), 133–139. https://doi.org/10.1016/j.acvd.2014.01.002
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- Hall, J.E. Guyton, A. C. (2011). Guyton and Hall Textbook of Medical Physilogy.Philadelphia, PA: Elsevier Inc.
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- Ho, S. Y. (2009). Structure and anatomy of the aortic root. European Journal of Echocardiography, 10(1), 3–10. https://doi.org/10.1093/ejechocard/jen243
- Kanwar, A., Thaden, J. J., & Nkomo, V. T. (2018). Management of Patients With Aortic Valve Stenosis. Mayo Clinic Proceedings, 93(4), 488–508. https://doi.org/10.1016/j.mayocp.2018.01.020
- Kapadia, S., Agarwal, S., Miller, D. C., Webb, J. G., MacK, M., Ellis, S., … Leon, M. B. (2016). Insights into Timing, Risk Factors, and Outcomes of Stroke and Transient Ischemic Attack after Transcatheter Aortic Valve Replacement in the PARTNER Trial (Placement of Aortic Transcatheter Valves). Circulation: Cardiovascular Interventions, 9(9), 1–10. https://doi.org/10.1161/CIRCINTERVENTIONS.115.002981
- Kar, B., Zhao, Y., Smalling, R., Balan, P., Hadidi, O., Ocazionez, D., … Ekeruo, I. A. (2017). Predicting Risk Factors for Permanent Pacemaker Placement Following Transcatheter Aortic Valve Replacement: a Uthealth Experience. Journal of the American College of Cardiology, 69(11), 1246. https://doi.org/10.1016/s0735-1097(17)34635-1
- Kibler, M., Marchandot, B., Messas, N., Labreuche, J., Vincent, F., Grunebaum, L., … Morel, O. (2018). Primary Hemostatic Disorders and Late Major Bleeding After Transcatheter Aortic Valve Replacement. Journal of the American College of Cardiology, 72(18), 2139–2148. https://doi.org/10.1016/j.jacc.2018.08.2143
- Kovacs, R. J., Halperin, J. L., Stevenson, W. G., Otto, C. M., Brindis, R. G., Bozkurt, B., … Ohman, E. M. (2014). 2014 AHA/ACC guideline for the management of patients with valvular heart disease. The Journal of Thoracic and Cardiovascular Surgery, 148(1), e1–e132. https://doi.org/10.1016/j.jtcvs.2014.05.014
- Le Tourneau, T., Jude, B., Vincentelli, A., Bauters, A., Juthier, F., Decoene, C., … Six, I. (2003). Acquired von Willebrand Syndrome in Aortic Stenosis. New England Journal of Medicine, 349(4), 343–349. https://doi.org/10.1056/nejmoa022831
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11.Liver Transplant: Beyond the Basics
In 1967, Dr. Thomas Starzl was the first to successfully perform an orthotopic liver transplant (OLT) in a hepatoblastoma patient. Although the patient ultimately died 18 months later of metastatic disease, this was the beginning of several major transplant surgery breakthroughs including the introduction of brain-death criteria in 1968, and the introduction of immunosuppressive medications in 1979 (1).
52 years later and the process of a liver transplant is far from a perfect science. Patients require lifelong close follow up, have frequent infections, and can occasionally need re-transplantation due to graft dysfunction.
Liver transplant patients require meticulous care both pre and post-transplant, and it is paramount that advanced care clinicians in all medical subspecialties are knowledgeable on the basic medical problems and risks of organ transplant.
The purpose of this module is to provide a comprehensive overview of the liver transplant process and an extensive review of the inpatient management of the post-transplant patient. By educating clinicians on the transplant process and the care of the transplant patient, it is the hope of the medical community that the success of liver transplant will continue to grow.
Stages of Liver Disease
As most of us know, there are litanies of liver diseases that can cause organ dysfunction. Despite the long list of liver diseases, they tend to all progress in a similar fashion. Here, we will break down the stages of liver disease from the healthy liver to cirrhosis.
A healthy liver has numerous important functions including helping to fight infection, cleaning the blood of bacteria, produces coagulation factors, produces bile to digest fat and absorb certain vitamins, metabolizes and removes toxic byproducts of medications, and processes food into storable energy. It has the ability to regenerate when injured, but as damage occurs from infection or disease the liver loses the ability to function at full capacity (2).
The first stage of liver injury is inflammation, where the liver may be tender and enlarged (2). This can be during the course of your immune system trying to fight off an infection, and can cause a patient discomfort or they may be asymptomatic depending on the severity of inflammation (2).
If the liver dysfunction is left untreated, the liver will begin to develop scar tissue and slowly replace healthy tissue. This process is referred to as fibrosis. As scar tissue replaces healthy tissue, blood flowing through the portal system can be impaired therefore making it more difficult for the healthy parts to function appropriately. There numerous scoring systems to grade fibrosis in order to give an objective trajectory of the degree of liver fibrosis and a prediction of how the fibrosis will progress. A popular scoring system is the METAVIR scoring system, which uses a liver biopsy sample to assign a score for “activity” or how the fibrosis is projected to progress and a score for the degree of fibrosis itself (3). The scores range from A0 (no activity) to A3 (severe activity), and F0 (no fibrosis) to F4 (cirrhosis) (3).
As fibrosis progresses, it leads to cirrhosis which is defined as irreversible scarring of the liver. At this stage of liver disease, the liver cannot heal, but progression of scaring can be prevented. There are four stages of cirrhosis: Stage 1 is considered to be compensated cirrhosis as it involves scaring of the liver, but few symptoms (4). Worsening of portal hypertension and the development of varices characterize stage 2 cirrhosis (4). Stage 3 cirrhosis is characterized by the new onset of ascites and is the hallmark stage of decompensated cirrhosis (4). Stage 4 cirrhosis is characterized by the development of end-stage liver disease (ESLD) and is fatal without a liver transplant (4).
How will you explain the stages of liver disease to patients?
Causes of Liver Disease
Liver transplant is indicated in patients with severely decompensated cirrhosis that has surpassed the limits of medical management or once a patient with cirrhosis has experienced complications such as ascites, hepatic encephalopathy, variceal hemorrhage or hepatocellular dysfunction and results in a MELD >/= 15 (6). The most common cause of decompensated cirrhosis remains the hepatitis C infection (HCV). The fortunate caveat to this is that direct-acting antiretroviral agents (DAAs) are becoming more readily available and the incidence of OLT related to HCV infection is expected to decrease (7).
Due to the high prevalence of HCV in the community and in-patient settings, providers should be aware of the DAA classes and the basic mechanisms of action. DAAs work by directly targeting the hepatitis C virus to prevent viral duplication, and therefore offer shorter treatment times, less side effects and higher overall cure rates (8). There are four classes of DAA, and the drug chosen is based on the patient’s specific hepatitis C genotype. Most DAA drugs are combination drugs that combine two separate classes of DAAs to maximize viral replication inhibition. Common combination DAA drugs include Mavyret, which is a combination of two DAA drugs, and has an approximate cure rate of 97-100% (9). Treatment is between 8-12 weeks and costs $26, 400 for 8 weeks of treatment (9).
Common side effects reported in clinical trials include; headache, insomnia, nausea, fatigue and asthenia (9). Another well-known DAA is Harvoni (Ledipasvir and Sofosbuvir), which has a sustained viral response of 93-99%, and has varying treatment lengths depending on the patient’s degree of liver disease (10). Treatment length ranges from 8 weeks in patients who are treatment naïve with no cirrhosis to 24 weeks for patients with previously treated HCV and compensated cirrhosis (10). The cost of a 12 -week regimen is averaged at $94, 500 (10). Most insurance plans offer partial coverage, but even if a patient’s plan does not cover the cost there are numerous patient assistance programs that can be used to assist with the cost of the treatment.
The other main indications for liver transplant in order of decreasing frequency are; alcoholic liver disease (18%), idiopathic/autoimmune hepatitis (12%), primary biliary cirrhosis (10%), acute liver failure (7%), hepatitis B virus (6%), metabolic liver disease (3%), cancer (3%), and fulminant hepatic failure (2%) (11)
Less common reasons a patient may qualify for a transplant in the absence of liver failure include treatment of portopulmonary hypertension, hepatopulmonary syndrome, correction of primary hyperoxaluria (done with a simultaneous kidney transplant), and management of cystic fibrosis induce cirrhosis (10).
What are some modifiable and non-modifiable risk factors for liver disease?
How can patients alter their lifestyles in order to reduce their chances of developing liver disease?
HCV infection treatment represents an opportunity to reduce the burden of liver disease. What type of screening and treatment programs are being offered to patients?
Case Study: Meet The Patient
You are an acute care nurse practitioner working in a busy ICU. You begin your shift with a new admission, Ms. Mino. She was an ICU to ICU transfer overnight, and the overnight resident figured you’d just do the HPI on pre-rounds because the patient “wanted to sleep”!
Ms. Mino is a 65-year-old woman with a PMH of all the good stuff. HTN, T2DM, hypercholesterolemia, and arthritis. She drinks 1-2 glasses of wine on special occasions and does not smoke.
When Demand Exceeds Supply: How Do We Allocate Livers?
While the best results are achieved in patients who are still relatively healthy, the patients who need a transplant most urgently are those who are critically ill and have acutely decompensated. In order to properly allocate organs, a model that prioritizes the sickest first was developed. The Model for End-Stage Liver Disease (MELD) was originally developed to predict the 3-month mortality of patients who underwent a transjugular intrahepatic portosystemic shunt (TIPS) placement (12). It was adopted by the United Network for Organ Sharing (UNOS) in 2002 as the model for liver allocation in the United States.
The MELD score is the product of an equation using the patient’s bilirubin, INR, and creatinine to produce a number that directly correlates to the patient’s need for a transplant in the next 3 months (9). The equation is as follows: MELDScore = 10 * ((0.957 * log(Creatinine)) + (0.378 * log(Bilirubin)) + (1.12 * log(INR))) + 6.43 (12).
In 2016, UNOS modified the MELD score to also take the patient’s sodium level into account. Hyponatremia is directly correlated with the severity of cirrhosis and independently predicts mortality independently of the MELD score. MELDNa score benefits patients who have a low MELD score but suffer from profound hyponatremia. The equation for MELD-Na is: MELDNa= MELD – Na – [0.025 × MELD × (140 − Na)] + 140 (12).
Additionally, there are certain patient populations such as those with HCC or portopulmonary hypertension that receive MELD exception points in order to accurately depict their waitlist mortality. The exception to the MELD system is referred to as Status 1A and is reserved for patients who have a sudden and severe onset of liver failure and are expected to only live a matter of hours without a transplant (13).
What are the strengths and weakness of our current transplant system?
Case Study: History of Present Illness
On exam, she is awake, alert and able to participate in your HPI. Her husband, Jim, is with her and looks concerned. She states that she has been mostly in her normal state of health minus a chest cold that her grandson gave to her last week, but “with some cold medicine, I felt good enough to work on my garden all week!. “All the kneeling on the hard ground really made my back and knees hurt, though.
Don’t ever get old! It’s all-downhill from 40, I swear. I actually fell just once trying to get up from doing some planting in my flowerbeds the other day. Nothing major just kind of toppled over and landed pretty hard on my right knee and side. Can you believe that! I used to be an athlete!”
When asked what brought her into the hospital originally, Jim states that he noticed the whites of her eyes that a strange tint to them. “Almost yellow-ish”, he says. She replies “yes, and my urine has gotten very dark and I don’t have much urge to urinate, but I probably wasn’t drinking enough when I was out in the yard. This pain in my right side hasn’t really gotten any better either”.
You review her home medications, and they are as follows: Glipizide 5mg daily, Amlodipine 10mg daily, Tylenol for arthritis PRN. She states that due to her fall she’s been taking a little more than her doctor told her to take- 3 tablets 3x/day as needed. She’s also been taking NyQuil to help her coughing at night- 2 tablespoons before bed and 2 tablespoons if she wakes up coughing in the middle of the night.
You do some quick math, and yes- that comes out to about 6,500- 7,150 mg of Tylenol a day. Acute Acetaminophen Toxicity with Acute Liver Failure jumps to the top of your differential. Luckily, she is encephalopathic, but she could become critically ill very quickly. Around this time, her labs come back.
Cr 2.5, Bilirubin 4.8, INR 3.2, Sodium 133. Acetaminophen level: 50
AST 7,377 ALT 3,570 Alk Phos 109
Using the MELD calculator, this is a MELD score of 35, which would be enough to list her as a Status 1A transplant candidate.
Evaluation for a liver transplant is an extensive and multidisciplinary process that focuses mainly on the allocation of donor organs to recipient’s with the physical and psychosocial health to withstand a taxing surgery, and adopt the new lifestyle that comes with being a transplant recipient. The evaluation process is a multifaceted process involving; transplant hepatologists, transplant surgeons, social workers, nutritionists, financial counselors, transplant coordinators, and a psychiatrist.
Patients are expected to abstain from alcohol consumption, tobacco and ilicit drug use, which can pose a challenge if the patient had a prior substance abuse problem. Additionally, patients are educated to avoid NSAIDs and use less than 2,000 mg acetaminophen daily for pain control. Patients are also educated on adopting healthy eating habits. Transplant medications can increase the risk of developing obesity, heart disease, diabetes, bone loss, and hyperkalemia, and diet modifications can help manage these side effects.
During the evaluation by the hepatology and transplant surgery team, the patient’s history is reviewed with focus on the duration, severity, complications, and past medical management treatments of the primary liver disease (14). Drug and alcohol dependency issues, current functional level and level of debility as it relates to the liver disease are discussed at length. The physical exam aids in confirming signs of advanced liver disease, as well as, identifying exam findings that may impact the success of OLT (cachexia, muscle wasting, overall debility) (14).
This is also when the patient can be assessed for variceal hemorrhage prophylaxis, hepatitis A/B vaccination if applicable, and HCV treatment pre and post-transplant, if applicable (14). The surgical consultation serves as a first-pass education to the patient and family regarding the surgical procedure, donor and graft types, potential complications, rejection rates, and the necessity of lifelong immunosuppression.
During the psychosocial evaluation, social workers and mental health professionals evaluate the potential organ recipient for evidence of compliance with medical directives, adequate support from caregivers, and no psychiatric disorders that may impact compliance post transplant or include harmful behaviors, such as alcohol, tobacco, or illicit drug use (14). There is no psychiatric disorder that leads to an absolute contraindication to transplant as long as there is adequate preparation, education, and able social support (14).
A large part of the psychosocial evaluation is making sure the patient has active insurance that will help to pay for their new lifelong need of medical care, and ensuring that the patient has a caregiver identified that will assist them in getting to and from clinic appointments especially if they patient is under the influence of narcotic pain medication post-operatively (14).
The patient undergoes a battery of laboratory tests to evaluate hepatic function, electrolytes, renal function, viral serologies (to establish Hepatitis A/B/C, CMV, Epstein-Barr virus, and HIV status), tumor markers, ABO-Rh blood typing, and creatinine clearance (14).
Results of the hepatic panel, chemistry panel, and electrolytes have the potential to change the patients MELD score, therefore increasing their status on the waitlist. Conversely, if the patient responds to medical management and the lab work improves, their MELD score will reflect improvement in their hepatic function and therefore move them to a lower position on the waitlist.
The renal function and creatinine clearance are crucial to establish a baseline, evaluate the patient for the need of a simultaneous liver-kidney transplant, and to renally dose their medications post-transplant.
Results of viral studies will dictate whether the patient needs treatment pre or post transplant for a viral illness. There are also programs in place that match HIV + donors to HIV + recipients, and new programs are beginning to emerge that include HCV + recipients with HCV + OR – recipients. As transplant surgery continues to advance, it is very likely that practitioners will be seeing HCV – recipients receiving HCV + organs and undergoing acute HCV treatment post-operatively.
The patient will also undergo ultrasonography to assess the patency of the portal vasculature and triple-phase computed tomography or gadolinium MRI to exclude a complicating hepatocellular carcinoma (HCC). If there is identification of HCC, attention will be paid to the size and number of lesions in order to direct the next steps in the evaluation process (14). The Milan Criteria uses tumor size, number, presence of extrahepatic and major vessel involvement to aid in differentiating between patients who should undergo OLT and those who would not be suitable (14).
An important aspect of the transplant evaluation process is cardiac evaluation. As with any surgical procedure, there is a great cardiovascular risk and the patient must undergo a noninvasive echocardiogram, as well as, noninvasive stress testing and a basic cardiovascular exam to rule out a severe cardiovascular disease that would hinder a good long-term outcome (14).
Patients who have advanced liver disease may not be able to achieve the target heart rate during an exercise stress test, and may need to undergo a stress test with pharmacological stress test and cardiac catheterization if coronary artery disease cannot be confidently excluded (14).
If >70% coronary artery stenosis is detected, revascularization may be attempted prior to liver transplant, although cardiac surgery in a patient with decompensated cirrhosis carries a risk that does not have documented benefit. In addition to evaluation of the patient’s coronary arteries, attention must be paid to the assessment of valvular heart disease and the presence of ventricular dysfunction.
There is no fast and hard rule of when heart function is too poor to undergo transplant surgery. Traditional medical therapies are utilized to optimize the patient’s cardiac function prior to surgery, and they are closely monitored post-transplant to ensure that medical management is sufficiently treating their underlying cardiac disease.
The evaluation process can be difficult for patients and families.
It provides an opportunity for hope but at the same time may end without a definitive treatment.
How can you explain the process and offer emotional support during the evaluation?
Case Study: The Workup
After completing your HPI, you go back to the office and call a STAT consult to both hepatology and transplant surgery. You explain the patient’s background, your preliminary data, and concern for acute decompensation if she remains untreated. The transplant surgery team comes to evaluate the patient, and on their exam she was lethargic, answered questions but quickly fell back to sleep.
When she extended her hand to shake the physicians hand, he noted a flapping tremor. Her husband provided the details of the HPI for her. They ask for a full hepatic panel, viral serologies including CMV, EBV, hepatitis panel, and HIV status. They also ask for ABO-Rh blood typing to be done in case the patient needs to be cross-matched with an organ donor. Her standard labs are increased in frequency to every 8 hours to assess for metabolic changes, decline in coagulation ability, and trend of liver enzymes.
A MRA abdomen and pelvis is ordered to evaluate her portal vasculature. Cardiology is consulted for pre- surgical cardiac clearance, an EKG is done and records of her last stress test are requested from her private cardiologist that she sees for her hypertension management.
Her viral serologies are all negative, and her abdominal imaging shows no contraindications to liver transplant. She is listed as a Status 1A transplant candidate by the afternoon.
Hepatology recommended initiated an N-acetylcycstine infusion to help medically manage her acetaminophen toxicity, and to give Vitamin K 10mg IV to help with her coagulopathy while organ offers are evaluated. Both teams will continue to follow her case closely, and update the ICU team and family if an organ becomes available.
Living Donor Liver Transplant: The Other Kind of Transplant
Organ transplant has become a victim of its own successes. The number of patients awaiting an organ transplant far exceeds the availability of deceased donor organs. Living donor liver transplantation (LDLT) has expanded the donor pool while also providing patients with a lower MELD score a chance to receive a transplant.
Indications for LDLT vary between the pediatric and adult populations. In adults, the concept of putting a healthy individual at surgical risk poses an ethical dilemma if the organ recipient has an increased risk for mortality post-transplant. Ideal LDLT candidates are separated into two main categories.
First, patients with hepatocellular carcinoma that is confined to the liver and is not associated with liver decompensation (15). This group of patients will not mount a MELD score suitable for deceased donor liver transplant (DDLT), but as their disease progresses and becomes extrahepatic they will quickly become unsuitable for a transplant altogether.
The second group of patients includes those with disease severity that is not reflected in their MELD score, such as patients with severe refractory encephalopathy, complicated cholestatic liver disease, ascites, or cachexia (15).
The projected outcome of the transplant recipient is weighed considerably before putting a healthy live donor at surgical risk. In a report by Berg et al. (16) the mortality rate associated with receiving an LDLT was lower than receiving a deceased donor liver transplant, but this depends largely on the severity of illness in the recipient.
As discussed previously, the sicker the patient prior to transplant the higher their post-operative mortality. Sicker patients with higher MELD scores tend to do poorly with an LDLT because the partial graft is unable to meet the needs of a severely chronically ill patient (15).
Evaluation of the living organ donor is comprehensive and aims to medically and psychologically assess the patient. The medical evaluation begins with a detailed history and physical exam, which should include assessing the patient’s BMI, as obesity is a risk factor for developing hepatic steatosis.
Patients undergoing the preliminary work up to be a live organ donor should be assessed for risk or history of viral hepatitis, non-alcoholic fatty liver disease, cardiovascular disease, malignancy, and bleeding disorders. Further medical workup includes routine blood work, including blood typing, viral serologies (HBV, HCV, HIV, CMV, EBV), autoimmune markers, and coagulation studies (18).
A CT scan or MRI is completed to estimate the volume of the left lateral segment or right lobe to assess whether the mass is appropriate for a particular potential recipient (18). Imaging also allows for the identification of any space-occupying lesions or the presence of steatosis. The role of liver biopsy in the donor is dependent on the transplant site’s protocol and the patient being evaluated.
A biopsy may be indicated in the potential donor who has elevated liver enzymes, an elevated BMI, or steatosis is suspected (18). The psychological evaluation of the patient centers around ensuring that the potential donor is educated on the procedure and is afforded ample time to make an informed decision about the procedure.
Due to the rigorous process, only a small number of potential donors end up being suitable for participating in an LDLT. In the Adult-to-Adult Living Donor Liver Transplantation Cohort (A2ALL) only 40% of donor candidates were accepted for donation (18).
While LDLT has many advantages, it is not without risk to the healthy donor. Farkas et al. (1) reports that the donor has a post-surgical morbidity risk of 30% and a mortality risk of 0.8%. The most common cause of morbidity was mild pleural effusions (16.4%), followed by biliary leaks and strictures (15). A significant risk of LDLT for the adult donor is small for size syndrome (SFSS).
This syndrome can occur when there is inaccurate size matching and the residual hepatic mass is inadequate for the donor’s metabolic needs. SFSS is characterized by prolonged cholestasis with elevated serum bilirubin levels, elevated liver enzymes, coagulopathy, ascites, and in severe cases primary non-function with subsequent shock and death (19).
Despite these potentially life-threatening complications, the overall risk for the donor in LDLT is low, and patients are supported medically, and psychologically by the medical team throughout their entire transplant process.
What are the advantages and disadvantages of living donor transplants?
Contraindications of Transplantation
Contraindications to liver transplant can be grouped into two categories: absolute contraindications and relative contraindications. While absolute contraindications are dependent on the patient’s disease process, relative contraindications rely heavily on the clinical judgment of the medical team. Absolute contraindications include active alcohol abuse, or less than 6 months of sobriety, uncontrolled sepsis, metastatic hepatocellular carcinoma, and uncorrectable cardiopulmonary disease causing a surgical risk (1).
Traditionally, patients infected with HIV were considered to be unsuitable for transplant due to the concern that immunosuppression post-transplant would accelerate their HIV infection (20). However, due to the use of antiretroviral therapy, the prognosis of HIV patient’s has improved substantially and HIV/AIDS without co-infection of hepatitis B or hepatitis C is viewed as a relative contraindication to transplant and are viewed on a case-by-case basis (20).
Relative contraindications include psychosocial conditions, such as poor social support, or repetitive noncompliance with medical care (21). Additional relative contraindications include advanced age, severe obesity, severe malnutrition, and other comorbidities that could potentially outweigh the benefit of transplant.
Patients recovering from a liver transplant typically spend some time in the intensive care unit. As the practice of liver transplantation has evolved, the length of ICU stay has decreased dramatically where most patient’s requiring ICU level of care post-transplant have a 24-hour median length of stay (22). Patients with preexisting conditions, intraoperative events or postoperative complications may require a prolonged ICU stay, and often require the expertise of multiple disciplines to manage their postoperative care.
Infections are the leading cause of postoperative morbidity and mortality in liver transplants. Razonable et al. (22) estimated that more than half of liver transplant patients will develop an infection in the first year post-transplant.
The risk of developing a postoperative infection is directly related to the patient’s level of exposure to infectious agents and the level of immunosuppression. Commonly seen infections include urinary tract infections, wound infections, bacteremia, and fungemia.
Many times, the causative bacteria will be a drug resistant organism and require home IV antibiotic administration. Additionally, transplant patients are at higher risk of contracting viral illnesses and frequently get readmitted with enterovirus, adenovirus or rotavirus.
In the first month postoperatively patients are most likely to develop infections related to the surgical procedure and hospitalization, such as bacterial and fungal wound infections, urinary tract infections, bloodstream infections, pneumonia, and Clostridium difficile colitis (22).
Patients should be treated empirically with antibiotic coverage, ideally with a third-generation cephalosporin, perioperatively to decrease the risk of postoperative infectious complications (22). Treatment of bacterial infections involves characterization of the causative organism, source control, and an appropriate antibiotic regimen.
Immunosuppression should be immediately decreased and may need to be temporarily stopped in order to adequately control a post-operative infection (16).
Patients are also at risk for specific opportunistic infections in the early postoperative period. Herpes simplex virus (HSV) reactivation disease is the most common opportunistic viral infection and can quickly progress to disseminated multi-organ infection and failure (22). Dissemination to visceral organs is primarily observed in immunocompromised patients, and should be on any practitioner’s differential if a patient appears to be ill and has had previous herpes viral outbreaks even if there are no active lesions present.
Although the incidence of viral sepsis is somewhere around 1% in developed countries, there is clear documentation of HSV dissemination leading to fulminant hepatitis, pneumonia, encephalitis, and sepsis (12). Treatment of HSV should focus on prophylaxis with antiviral agents, such as acyclovir or ganciclovir.
Cytomegalovirus (CMV) status of the donor, regardless of positive or negative must be recorded in the recipient’s chart. CMV affects the recipient’s ability to mount an immune defense and may cause a predisposition for developing postoperative infections (23).
To combat this, patients are started on either a prophylactic or treatment dose of valganciclovir immediately after transplant depending on their risk of contracting CMV from their donor.
For example, if a recipient is CMV negative pre-operatively, but the donor is CMV positive then this patient will require treatment levels of valganciclovir and close monitoring of their CMV titers to ensure they don’t contract CMV viremia.
Post-transplant acute kidney injury (AKI) has been reported to occur in 9-78% of cases with 10% progressing to end-stage renal failure (22). Early identification of potential AKI is crucial to improving patient outcome as evidence shows that even small increases in serum creatinine are associated with a decline in overall mortality.
The etiology of post liver transplant can be related to numerous causes, including sepsis or bacteremia, hemodynamic instability, or hypovolemia. Immunosuppressive agents, such as calcineurin inhibitors (tacrolimus, cyclosporine), are known to cause a drug-induced kidney injury. Unfortunately, many OLT patients will end up back on the transplant list for a kidney transplant due to CNI induced renal failure.
Tacrolimus is the immunosuppressive drug of choice in solid organ transplant, and it is never completely held due to renal dysfunction. If a transplant patient is exhibiting progressively increasing creatinine, the tacrolimus dose may be decreased and the goal trough lowered in order to protect renal function. Patients are instructed to increase their oral rehydration and have repeat lab work in 2-3 days to assess changes in their creatinine.
Knowing the potential complications of liver transplants- what physical exam, history, and clinical data will you examine to monitor for these?
What education would you give a family prior to transplant regarding the potential risks?
Case Study: The Post-Operative Period
Ms. Mino receives an orthotopic liver transplant from a local deceased donor less than 24 hours after transfer to your ICU. You are returning for your 3rd shift in a row, just in time for her to be returning to your care from the operating room.
You get sign out from the transplant surgery fellow. “Yeah, the case went great. EBL 8.5L, we gave 5 units PRBC, 3 units platelets, 3 units FFP, 6L crystalloid and 2L albumin. She has 3 JP drains to bulb suction. I wouldn’t start anticoagulation yet. Case was pretty oozy since her INR was >3 at the start of the case. Pressures are a little soft, but we took her off vasopressors before we transferred her back here. Okay, thanks. Oh yeah…she’s still intubated, but can be extubated at your discretion.”
You assess your patient and find that she has a traditional Mercedes incision with 2 JP drains on the right side, and 1 JP drain on the left all with a moderate amount of serosanginuous drainage. Her abdomen is full, but soft. She is still sedated from the procedure, but you ask the nurse to titrate the sedation down in hopes of doing a spontaneous breathing trial and extubating in a few hours. Her blood pressures are 110/65 via arterial line. She is making adequate amounts of clear yellow urine, which will be monitored closely for signs of intravascular depletion or ongoing AKI.
If her SBP drops below 95, you will plan to give a bolus of albumin and watch for response. Due to the high EBL of the case, she could need a blood transfusion at some point. Her routine labs are cycled at every 6 hours for the first 24 hours. Her first set of post-operative labs show an H/H of 8.5/24, WBC 17 and her liver enzymes are now all under 1,000.
You review her post-operative orders and see that the transplant team entered most of them. Mrs. Mino received induction immunosuppression in the operating room, and will begin Tacrolimus, Mycophenolate mofetil, and a Methylprednisolone taper today. Tacrolimus levels will be drawn every morning, and the transplant surgery team will manage the medication dosage. You see that she is on a perioperative antibiotic for five days, as well as prophylactic doses of Bactrim to protect against toxoplasmosis, IV Gangciclovir for CMV prophylaxis and IV Fluconazole for fungal prophylaxis.
Knowing that her WBC will be elevated due to the surgical stress and high doses of steroids, you will have to remain diligent to assess for additional signs of infection.
Ultimately, Mrs. Mino does well and is extubated 8 hours post surgery. She is comfortable on 2L nasal cannula. Her pain is well controlled with IV Dilaudid, which will be transitioned to oral medications once she has return of bowel function. She is stepped down from the ICU on post op day 3, and discharged from the hospital on post op day 7 with close outpatient follow up.
Post Transplant Management: Immunosuppression, Infection Prevention, and Long Term Outcomes
Management of the post liver transplant patient requires diligent and comprehensive care.
Liver enzymes, bilirubin, protein synthesis markers, and coagulation factors are monitored frequently to detect early graft dysfunction and the need for aggressive intervention. Enzyme levels are expected to be markedly elevated in the immediate post-operative phase but begin to decrease over the course of several days (23). Persistent elevation in a patient’s liver enzymes may be indicative of ongoing hepatocellular necrosis (23).
Diligent immunosuppressive therapy is required to prevent rejection, and while immunosuppression pharmacology is always improving, the basic regimens are worth mentioning. In the early postoperative phase, immunosuppressive therapy is complex and must be patient specific. The most common immunosuppression regimens include calcineurin inhibitors, such as Tacrolimus. Tacrolimus is typically started on post-op day one at a dose of 4mg BID, and titrated based on the patient’s goal trough. In the immediate post-transplant phase, a goal trough is typically 10-12 ng/mL.
After approximately 4 weeks of initial treatment, the Tacrolimus trough goal will stabilize to a maintenance lifelong goal of 5-8. ng/mL. Corticosteroids play a major role in solid organ transplant immunosuppression and are critical in treating acute organ rejection (23). Typically, patients will begin with high doses of methylprednisolone intraoperatively, and transitioned to prednisone to complete their taper over the course of 3-6 months.
An additional agent, Mycophenolate mofetil, is used to treat acute rejection but is often used as an adjunct to immunosuppressive therapy (23). Mycophenolate is the first immunosuppressive drug to be held when there is a concern of infection, due to its adjuvant nature. Many of these drugs have harsh side effects making long-term compliance difficult and frustrating.
Most commonly, patients on immunosuppressive medications will suffer from diarrhea, headaches, tremors from the neurotoxicity risk of tacrolimus, and insomnia. In cases of neurotoxicity, the tacrolimus trough goal will be lowered as able, and other side effects are managed with supportive medications (Imodium, Lomotil, Melatonin). Immunosuppression regimen education is a focus of the post-transplant recovery process and should begin as early as possible.
Long term, patients require close follow up, including weekly clinic appointments the first several months post-transplant. As they recover from the surgery, clinic appointments become less frequent, but they still require frequent lab work to assess immunosuppressive drug levels.
Liver transplantation has come a long way since the first successful surgery 50 years ago, but patient’s today are facing new challenges that have yet to become medical triumphs.
The number of transplant organs continues to grow each year. In 2016, a total of 7,841 liver transplants were completed, a 10% increase from 2015 (24). As transplant medicine continues to grow, long -term outcomes improve as well. In 2016, the incidence of graft failure at one year decreased to 9.8% for recipients of deceased donor organs, a 10% reduction from 2015 (24). The three and five-year mortality rates continue to improve, especially in those who received living donor liver transplants (24).
As of June 30, 2016, there were 79,188 liver transplant patients living with a functioning graft (24), making the knowledge and care of a post- transplant patient crucial to both acute care and primary care practicing providers.
Course References and Disclaimer
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2) The Stages of Liver Disease. (n.d.). Retrieved February 12, 2019, from https://liverfoundation.org/for-patients/about-the-liver/the-progression-of-liver-disease/#1503432933768-040e8645-d918
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4) Cunha, J. P. (n.d.). What Is Cirrhosis of the Liver? Symptoms, Treatment & Stages. Retrieved February 12, 2019, from https://www.medicinenet.com/cirrhosis/article.htm
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10) Harvoni (ledipasvir and sofosbuvir) | Hepatitis C TIP | PHCN. (n.d.). Retrieved February 13, 2019, from http://www.hepctip.ca/harvoni-ledipasvir-and-sofosbuvir/
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13) Questions and answers for transplant candidates about liver allocation. (2017). Retrieved from http://www.unos.org/wp-content/uploads/unos/Liver_patient.pdf
14) Martin, P., DeMartini, A., Feng, S., Brown Jr, R., & Fallon, M. (2014). Evaluation for liver transplantation in adults: 2013 practice guideline by the American Association for the Study of Liver Diseases and the American Society of Transplantation [Practice Guideline]. Clinical Journal of the American Association for the Study of Liver Diseases, 59(3). http://dx.doi.org/10.1002/hep.26972
15) Arvelakis, A., & Shapiro, R. (2013). Living donor hepatectomy. Retrieved from http://emedicine.medscape.com/article/1830182-overview#a4
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18) Cotler, S. J. (2017). Living donor liver transplantation. Retrieved from https://www.uptodate.com/contents/living-donor-liver-transplantation
19) Sun, Z., Yu, Z., Yu, S., Chen, J., Wang, J., Yang, C., … Zhang, M. (2015). Post-operative complications in living liver donors: A single-center experience in China. PLoS One, 10(8). http://dx.doi.org/10.1371/journal.pone.0135557
20) Tebas, P. (2015). Solid organ transplantation in HIV-infected individuals. Retrieved from https://www.uptodate.com/contents/solid-organ-transplantation-in-hiv-infected-individuals#H1
21) Dove, L., & Brown, R. S. (2015). Liver transplantation in adults: Patient selection and pretransplantation evaluation. Retrieved from https://www.uptodate.com/contents/liver-transplantation-in-adults-patient-selection-and-pretransplantation-evaluation?source=see_link§ionName=CONTRAINDICATIONS&anchor=H5#H5
22) Razonable, R. R., Findlay, J. Y., O’Riordan, A., Burroughs, S. G., Ghobrial, R. M., Agarwal, B., … Gropper, M. (2011). Critical care issues in patients after liver transplantation [Review]. Liver Transplantation, 17, 511-527. http://dx.doi.org/10.1002/lt
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24) Kim, W. R., Lake, J. R., Smith, J. M., Skeans, M. A., Schladt, D. P., Edwards, E. B., . . . Kasiske, B. L. (2018). OPTN/SRTR 2013 Annual Data Report: Liver. American Journal of Transplantation,15(S2), 1-28. doi:10.1111/ajt.13197