Written communication is an essential skill for a consultation-liaison (C-L) psychiatrist, but unfortunately, how to write a consultation note is not part of formal didactics in medical school or residency training.¹ Documentation of a consultation note is a permanent medical record entry that conveys current physician-to-physician information. While considerable literature describes the consultation process, little has been published about composing a consultation note.^1,2 Residents and clinicians who do not have frequent consultations may be unfamiliar with the consultation environment and their role as an expert consultant. Therefore, more explicit guidance on documentation and optimal formatting of the consultation note is needed.

The Box provides an outline for completing the Recommendations/Treatment Plan section of psychiatric consultation notes. When providing your recommendations, it is best to use bullet points, numbering, or bold text; do not bury the information in a dense paragraph.³ Be sure to address each of the following 6 elements.

1. Primary consult concern. The first section of the Recommendations section should include the reason for the consult, which may be the most important part of the consultation process.^1,2 It is important to recognize that an unclear consult question may be a sign of the primary team’s knowledge gap in psychiatry. The role of the C-L psychiatrist is to help the primary team organize their thoughts and concerns regarding their patient to decide on the final consult question.¹ The active consult question may change as clinical issues evolve.

2. Safety and critical issues. Include an assessment of or recommendation on safety and critical issues. An important consideration is whether to recommend a patient sitter and to provide a reason for this recommendation. Occasionally, critical issues are more pressing than the primary consult concern. For example, there are several situations in which abnormal laboratory values and acute medical issues manifest as psychiatric symptoms, including hyponatremia, hypoglycemia, hypotension, low oxygen saturation, or infection. The connection between the 2 may not be clear to the primary treatment team; thus, include a statement to draw their attention to this.

3. Nonpharmacologic recommendations. To provide comprehensive care, consider all treatment modalities, and consider recruiting additional clinical disciplines, as appropriate. Patients may have complex medical and psychiatric presentations that are difficult to differentiate; therefore, C-L psychiatrists should not hesitate to recommend consults from other medical specialists as needed. Likewise, dealing with psychiatric concerns often is difficult for clinicians in other specialties. When possible, it may be helpful to provide brief recommendations about how to approach the patient to diffuse negative emotions and reactions among the treatment team.

4. Psychopharmacology. In this section, the C-L psychiatrist should provide information on the use of any psychotropic medications and an explanation of their indications. If there are discrepancies between a patient’s home and hospital-ordered medications, clarify which medications the patient should be taking while hospitalized. If the C-L treatment team recommends initiating a new medication, provide details regarding the specific medication, dose, route, administration time, and titration schedule, as well as the specific situation for any as-needed medications. It is important to include the indication for any recommended medications, as well as any potential adverse effects. If psychotropic medications are not indicated, add a statement to emphasize this.

5. Social work support. Document any issues that need to be clarified by social work. This might include clarification of a patient’s insurance coverage, current living situation, or durable power of attorney. Also, document how the treatment team would prefer social work to assist with the patient’s care by (for example) providing the patient with resources for outpatient mental health and/or substance abuse treatment or housing options.

Continue to: Disposition

6. Disposition. Finally, include a recommendation regarding disposition. If transfer to a psychiatric facility is not indicated, provide a statement to affirm this. If transfer to a psychiatric facility is recommended, include a discussion of the patient’s appropriateness in the assessment and recommendations. It is helpful to inform the primary team of criteria that may or may not allow the patient to transfer to or be accepted by a psychiatry unit (eg, the patient will need to be off IV medications and able to tolerate oral intake prior to transfer). When transfer is not possible, communicate the reason to the primary treatment team and other ancillary staff.

Communicating responsibilities and expectations

After concluding the Recommendations section, end the consultation note with a brief sentence of gratitude (eg, “Thank you for this consultation and allowing us to assist in the care of your patient.”) and a comment regarding the C-L treatment team’s plan for follow-up. Also, include your contact information in case the primary treatment team has any questions or concerns.

The Recommendations section of a psychiatric consultation note is vital to convey current physician-to-physician recommendations. With the potential complexities in assessing and caring for a medically ill patient with comorbid psychiatric diagnoses, psychiatrists with less C-L experience may be unfamiliar with the essential elements of a consultation note. It is helpful to use a Template to ensure that the consultation and documentation are complete.

Written communication is an essential skill for a consultation-liaison (C-L) psychiatrist, but unfortunately, how to write a consultation note is not part of formal didactics in medical school or residency training.¹ Documentation of a consultation note is a permanent medical record entry that conveys current physician-to-physician information. While considerable literature describes the consultation process, little has been published about composing a consultation note.^1,2 Residents and clinicians who do not have frequent consultations may be unfamiliar with the consultation environment and their role as an expert consultant. Therefore, more explicit guidance on documentation and optimal formatting of the consultation note is needed.

The Box provides an outline for completing the Recommendations/Treatment Plan section of psychiatric consultation notes. When providing your recommendations, it is best to use bullet points, numbering, or bold text; do not bury the information in a dense paragraph.³ Be sure to address each of the following 6 elements.

1. Primary consult concern. The first section of the Recommendations section should include the reason for the consult, which may be the most important part of the consultation process.^1,2 It is important to recognize that an unclear consult question may be a sign of the primary team’s knowledge gap in psychiatry. The role of the C-L psychiatrist is to help the primary team organize their thoughts and concerns regarding their patient to decide on the final consult question.¹ The active consult question may change as clinical issues evolve.

2. Safety and critical issues. Include an assessment of or recommendation on safety and critical issues. An important consideration is whether to recommend a patient sitter and to provide a reason for this recommendation. Occasionally, critical issues are more pressing than the primary consult concern. For example, there are several situations in which abnormal laboratory values and acute medical issues manifest as psychiatric symptoms, including hyponatremia, hypoglycemia, hypotension, low oxygen saturation, or infection. The connection between the 2 may not be clear to the primary treatment team; thus, include a statement to draw their attention to this.

3. Nonpharmacologic recommendations. To provide comprehensive care, consider all treatment modalities, and consider recruiting additional clinical disciplines, as appropriate. Patients may have complex medical and psychiatric presentations that are difficult to differentiate; therefore, C-L psychiatrists should not hesitate to recommend consults from other medical specialists as needed. Likewise, dealing with psychiatric concerns often is difficult for clinicians in other specialties. When possible, it may be helpful to provide brief recommendations about how to approach the patient to diffuse negative emotions and reactions among the treatment team.

4. Psychopharmacology. In this section, the C-L psychiatrist should provide information on the use of any psychotropic medications and an explanation of their indications. If there are discrepancies between a patient’s home and hospital-ordered medications, clarify which medications the patient should be taking while hospitalized. If the C-L treatment team recommends initiating a new medication, provide details regarding the specific medication, dose, route, administration time, and titration schedule, as well as the specific situation for any as-needed medications. It is important to include the indication for any recommended medications, as well as any potential adverse effects. If psychotropic medications are not indicated, add a statement to emphasize this.

5. Social work support. Document any issues that need to be clarified by social work. This might include clarification of a patient’s insurance coverage, current living situation, or durable power of attorney. Also, document how the treatment team would prefer social work to assist with the patient’s care by (for example) providing the patient with resources for outpatient mental health and/or substance abuse treatment or housing options.

Continue to: Disposition

6. Disposition. Finally, include a recommendation regarding disposition. If transfer to a psychiatric facility is not indicated, provide a statement to affirm this. If transfer to a psychiatric facility is recommended, include a discussion of the patient’s appropriateness in the assessment and recommendations. It is helpful to inform the primary team of criteria that may or may not allow the patient to transfer to or be accepted by a psychiatry unit (eg, the patient will need to be off IV medications and able to tolerate oral intake prior to transfer). When transfer is not possible, communicate the reason to the primary treatment team and other ancillary staff.

Communicating responsibilities and expectations

After concluding the Recommendations section, end the consultation note with a brief sentence of gratitude (eg, “Thank you for this consultation and allowing us to assist in the care of your patient.”) and a comment regarding the C-L treatment team’s plan for follow-up. Also, include your contact information in case the primary treatment team has any questions or concerns.

The Recommendations section of a psychiatric consultation note is vital to convey current physician-to-physician recommendations. With the potential complexities in assessing and caring for a medically ill patient with comorbid psychiatric diagnoses, psychiatrists with less C-L experience may be unfamiliar with the essential elements of a consultation note. It is helpful to use a Template to ensure that the consultation and documentation are complete.

Written communication is an essential skill for a consultation-liaison (C-L) psychiatrist, but unfortunately, how to write a consultation note is not part of formal didactics in medical school or residency training.¹ Documentation of a consultation note is a permanent medical record entry that conveys current physician-to-physician information. While considerable literature describes the consultation process, little has been published about composing a consultation note.^1,2 Residents and clinicians who do not have frequent consultations may be unfamiliar with the consultation environment and their role as an expert consultant. Therefore, more explicit guidance on documentation and optimal formatting of the consultation note is needed.

The Box provides an outline for completing the Recommendations/Treatment Plan section of psychiatric consultation notes. When providing your recommendations, it is best to use bullet points, numbering, or bold text; do not bury the information in a dense paragraph.³ Be sure to address each of the following 6 elements.

1. Primary consult concern. The first section of the Recommendations section should include the reason for the consult, which may be the most important part of the consultation process.^1,2 It is important to recognize that an unclear consult question may be a sign of the primary team’s knowledge gap in psychiatry. The role of the C-L psychiatrist is to help the primary team organize their thoughts and concerns regarding their patient to decide on the final consult question.¹ The active consult question may change as clinical issues evolve.

2. Safety and critical issues. Include an assessment of or recommendation on safety and critical issues. An important consideration is whether to recommend a patient sitter and to provide a reason for this recommendation. Occasionally, critical issues are more pressing than the primary consult concern. For example, there are several situations in which abnormal laboratory values and acute medical issues manifest as psychiatric symptoms, including hyponatremia, hypoglycemia, hypotension, low oxygen saturation, or infection. The connection between the 2 may not be clear to the primary treatment team; thus, include a statement to draw their attention to this.

3. Nonpharmacologic recommendations. To provide comprehensive care, consider all treatment modalities, and consider recruiting additional clinical disciplines, as appropriate. Patients may have complex medical and psychiatric presentations that are difficult to differentiate; therefore, C-L psychiatrists should not hesitate to recommend consults from other medical specialists as needed. Likewise, dealing with psychiatric concerns often is difficult for clinicians in other specialties. When possible, it may be helpful to provide brief recommendations about how to approach the patient to diffuse negative emotions and reactions among the treatment team.

4. Psychopharmacology. In this section, the C-L psychiatrist should provide information on the use of any psychotropic medications and an explanation of their indications. If there are discrepancies between a patient’s home and hospital-ordered medications, clarify which medications the patient should be taking while hospitalized. If the C-L treatment team recommends initiating a new medication, provide details regarding the specific medication, dose, route, administration time, and titration schedule, as well as the specific situation for any as-needed medications. It is important to include the indication for any recommended medications, as well as any potential adverse effects. If psychotropic medications are not indicated, add a statement to emphasize this.

5. Social work support. Document any issues that need to be clarified by social work. This might include clarification of a patient’s insurance coverage, current living situation, or durable power of attorney. Also, document how the treatment team would prefer social work to assist with the patient’s care by (for example) providing the patient with resources for outpatient mental health and/or substance abuse treatment or housing options.

Continue to: Disposition

6. Disposition. Finally, include a recommendation regarding disposition. If transfer to a psychiatric facility is not indicated, provide a statement to affirm this. If transfer to a psychiatric facility is recommended, include a discussion of the patient’s appropriateness in the assessment and recommendations. It is helpful to inform the primary team of criteria that may or may not allow the patient to transfer to or be accepted by a psychiatry unit (eg, the patient will need to be off IV medications and able to tolerate oral intake prior to transfer). When transfer is not possible, communicate the reason to the primary treatment team and other ancillary staff.

Communicating responsibilities and expectations

After concluding the Recommendations section, end the consultation note with a brief sentence of gratitude (eg, “Thank you for this consultation and allowing us to assist in the care of your patient.”) and a comment regarding the C-L treatment team’s plan for follow-up. Also, include your contact information in case the primary treatment team has any questions or concerns.

The Recommendations section of a psychiatric consultation note is vital to convey current physician-to-physician recommendations. With the potential complexities in assessing and caring for a medically ill patient with comorbid psychiatric diagnoses, psychiatrists with less C-L experience may be unfamiliar with the essential elements of a consultation note. It is helpful to use a Template to ensure that the consultation and documentation are complete.

Tardive dyskinesia (TD) is an elusive-to-treat adverse effect of antipsychotics that has caused extreme discomfort (in a literal and figurative sense) for patients and their psychiatrists. In 2017, the prevalence of TD as a result of exposure to dopamine antagonists was approximately 30% with first-generation antipsychotics and 20% with second-generation antipsychotics.¹ There have been several effective attempts at reducing rates of TD, including lowering the dosing, shifting to second-generation antipsychotics, and using recently introduced pharmacologic treatments for TD. The past 2 years have seen increased efforts at treating this often-irreversible adverse effect with pharmacotherapy, such as the recently marketed vesicular monoamine transporter-2 (VMAT2) inhibitors valbenazine and deutetrabenazine, as well as the supplement Ginkgo biloba,² although issues with cost, adverse effects, or drug–drug interactions could limit the benefits of these agents.

Despite these strategies, one approach has been largely overlooked: prevention. Although it is included in many guidelines and literature reports, prevention has become less of a standard of practice and more of a cliché. Prevention is the key strategy for lowering the rate of TD, and it should be the assumed responsibility of each clinician in every prescription they write throughout the entire continuum of care. Here, we provide steps to take to help prevent TD, and what to consider when TD occurs.

1. Realize that we are all responsible for TD. We know TD exists, but we often feel that this adverse effect is not our fault. Avoid adapting a philosophy of “someone else caused it,” “they didn’t cause it yet,” or “it’s going to happen anyway.” We must remember that every unnecessary exposure to a dopamine antagonist increases the risk of TD, even if we don’t see the adverse effect firsthand.

2. Treat first-episode psychosis early and aggressively. Doing so may prevent chronicity of the illness, which would save a patient from long-term, high-dose exposure to antipsychotics. Lower the risk of TD with atypical antipsychotics and offer long-acting injectables when possible to improve medication adherence.

3. Treat both acute and chronic symptoms of psychosis throughout the continuum of care. The choice of medication and dose should be reevaluated at each interaction to enhance improvement of acute symptoms and to minimize chronic adverse effects. Always recognize the differences in aggressive treatment of an acute episode of psychosis vs maintenance treatment of baseline symptoms. Also, assess for TD by conducting abnormal involuntary movement scale (AIMS) examinations at baseline and at least biannually.

4. Use clozapine instead of 2 antipsychotics in chronic, refractory patients when possible. Clozapine is largely underutilized, despite continued evidence of its superiority in effectiveness and prevention of relapse³ vs other agents, and has a lower risk of TD. The use of polypharmacy, on the other hand, has continued to display a lack of added benefit in treating symptoms of psychosis, and an increase in adverse effects.⁴

5. Consider pharmacotherapy if TD has already occurred. Psychiatrists have been waiting for pharmacologic options for treating TD for quite some time. Explore using VMAT2 inhibitors and other agents when it is too late to implement prevention or when a patient’s symptoms are refractory to other treatments. However, avoid anticholinergic medications; there is insufficient data to support the use of these agents in the treatment of TD.⁵

Tardive dyskinesia (TD) is an elusive-to-treat adverse effect of antipsychotics that has caused extreme discomfort (in a literal and figurative sense) for patients and their psychiatrists. In 2017, the prevalence of TD as a result of exposure to dopamine antagonists was approximately 30% with first-generation antipsychotics and 20% with second-generation antipsychotics.¹ There have been several effective attempts at reducing rates of TD, including lowering the dosing, shifting to second-generation antipsychotics, and using recently introduced pharmacologic treatments for TD. The past 2 years have seen increased efforts at treating this often-irreversible adverse effect with pharmacotherapy, such as the recently marketed vesicular monoamine transporter-2 (VMAT2) inhibitors valbenazine and deutetrabenazine, as well as the supplement Ginkgo biloba,² although issues with cost, adverse effects, or drug–drug interactions could limit the benefits of these agents.

Despite these strategies, one approach has been largely overlooked: prevention. Although it is included in many guidelines and literature reports, prevention has become less of a standard of practice and more of a cliché. Prevention is the key strategy for lowering the rate of TD, and it should be the assumed responsibility of each clinician in every prescription they write throughout the entire continuum of care. Here, we provide steps to take to help prevent TD, and what to consider when TD occurs.

1. Realize that we are all responsible for TD. We know TD exists, but we often feel that this adverse effect is not our fault. Avoid adapting a philosophy of “someone else caused it,” “they didn’t cause it yet,” or “it’s going to happen anyway.” We must remember that every unnecessary exposure to a dopamine antagonist increases the risk of TD, even if we don’t see the adverse effect firsthand.

2. Treat first-episode psychosis early and aggressively. Doing so may prevent chronicity of the illness, which would save a patient from long-term, high-dose exposure to antipsychotics. Lower the risk of TD with atypical antipsychotics and offer long-acting injectables when possible to improve medication adherence.

3. Treat both acute and chronic symptoms of psychosis throughout the continuum of care. The choice of medication and dose should be reevaluated at each interaction to enhance improvement of acute symptoms and to minimize chronic adverse effects. Always recognize the differences in aggressive treatment of an acute episode of psychosis vs maintenance treatment of baseline symptoms. Also, assess for TD by conducting abnormal involuntary movement scale (AIMS) examinations at baseline and at least biannually.

4. Use clozapine instead of 2 antipsychotics in chronic, refractory patients when possible. Clozapine is largely underutilized, despite continued evidence of its superiority in effectiveness and prevention of relapse³ vs other agents, and has a lower risk of TD. The use of polypharmacy, on the other hand, has continued to display a lack of added benefit in treating symptoms of psychosis, and an increase in adverse effects.⁴

5. Consider pharmacotherapy if TD has already occurred. Psychiatrists have been waiting for pharmacologic options for treating TD for quite some time. Explore using VMAT2 inhibitors and other agents when it is too late to implement prevention or when a patient’s symptoms are refractory to other treatments. However, avoid anticholinergic medications; there is insufficient data to support the use of these agents in the treatment of TD.⁵

Tardive dyskinesia (TD) is an elusive-to-treat adverse effect of antipsychotics that has caused extreme discomfort (in a literal and figurative sense) for patients and their psychiatrists. In 2017, the prevalence of TD as a result of exposure to dopamine antagonists was approximately 30% with first-generation antipsychotics and 20% with second-generation antipsychotics.¹ There have been several effective attempts at reducing rates of TD, including lowering the dosing, shifting to second-generation antipsychotics, and using recently introduced pharmacologic treatments for TD. The past 2 years have seen increased efforts at treating this often-irreversible adverse effect with pharmacotherapy, such as the recently marketed vesicular monoamine transporter-2 (VMAT2) inhibitors valbenazine and deutetrabenazine, as well as the supplement Ginkgo biloba,² although issues with cost, adverse effects, or drug–drug interactions could limit the benefits of these agents.

Despite these strategies, one approach has been largely overlooked: prevention. Although it is included in many guidelines and literature reports, prevention has become less of a standard of practice and more of a cliché. Prevention is the key strategy for lowering the rate of TD, and it should be the assumed responsibility of each clinician in every prescription they write throughout the entire continuum of care. Here, we provide steps to take to help prevent TD, and what to consider when TD occurs.

1. Realize that we are all responsible for TD. We know TD exists, but we often feel that this adverse effect is not our fault. Avoid adapting a philosophy of “someone else caused it,” “they didn’t cause it yet,” or “it’s going to happen anyway.” We must remember that every unnecessary exposure to a dopamine antagonist increases the risk of TD, even if we don’t see the adverse effect firsthand.

2. Treat first-episode psychosis early and aggressively. Doing so may prevent chronicity of the illness, which would save a patient from long-term, high-dose exposure to antipsychotics. Lower the risk of TD with atypical antipsychotics and offer long-acting injectables when possible to improve medication adherence.

3. Treat both acute and chronic symptoms of psychosis throughout the continuum of care. The choice of medication and dose should be reevaluated at each interaction to enhance improvement of acute symptoms and to minimize chronic adverse effects. Always recognize the differences in aggressive treatment of an acute episode of psychosis vs maintenance treatment of baseline symptoms. Also, assess for TD by conducting abnormal involuntary movement scale (AIMS) examinations at baseline and at least biannually.

4. Use clozapine instead of 2 antipsychotics in chronic, refractory patients when possible. Clozapine is largely underutilized, despite continued evidence of its superiority in effectiveness and prevention of relapse³ vs other agents, and has a lower risk of TD. The use of polypharmacy, on the other hand, has continued to display a lack of added benefit in treating symptoms of psychosis, and an increase in adverse effects.⁴

5. Consider pharmacotherapy if TD has already occurred. Psychiatrists have been waiting for pharmacologic options for treating TD for quite some time. Explore using VMAT2 inhibitors and other agents when it is too late to implement prevention or when a patient’s symptoms are refractory to other treatments. However, avoid anticholinergic medications; there is insufficient data to support the use of these agents in the treatment of TD.⁵

Recently, I was talking with a colleague who works for a large hospital and health care system. While discussing his experiences over the past five years, he suddenly stopped and blurted out, “I don’t trust this organization. Nobody trusts this organization!”

Taken aback, I asked what made him say that.

First of all, he explained, there is a complete and pervasive lack of transparency as to both short- and long-term goals for the organization. Information is treated as proprietary thinking by nonclinical “corporate folks” and not released to the boots-on-the-ground clinician—which makes it difficult to work toward goals efficiently.

Furthermore, he related, there is consistent failure to provide accurate financial data or any plans to improve the organization’s financial position in the marketplace. This prevents providers from making a positive impact on cost containment. No one is invested. Provider compensation packages are neither universal nor simple. The financial folks devise complex formulas that do not account for the vagaries and complexities of health care. This health care organization views every patient as a Financial Information Number and makes no allowance for the fact that many have complex illnesses requiring significant time and attention.

Lastly, he described a systematic and insidious elimination of support staff at all levels—but particularly bedside nurses. The traditional “nursing safety net”—especially relevant in academic institutions—is in tatters, which threatens to undermine day-to-day success in patient care. Staffing of ancillary providers (those in physical, occupational, or speech-language therapy) has been cut back, which means patients wait longer to see these specialists and primary medical providers are frustrated by the lack of progress their patients make.

Stunned by his comments, I started thinking: How many of us recognize some or all of this description? How many trust the organization we work for? Realizing that a huge percentage of NPs, PAs, and physicians work for large entities, these are important questions.

Trust is central to human interaction on both personal and professional levels. Tschannen-Moran defines it as “one’s willingness to be vulnerable to another, based on the confidence that the other is ben­evolent, honest, open, reliable, and com­petent.”¹

Continue to: A more focused definition of organizational trust

Organizational trust may require a broader and yet more focused definition—such as that of Cummings and Bromley, who stipulate that trust is a belief, held by an individual or groups of individuals, that another individual or group

• Makes a good faith effort to behave in accordance with any (explicit or implicit) commitments
• Is honest
• Does not take excessive advantage of another, even when the opportunity to do so exists.²

Thus, organizational (or collective) trust refers to the propensity of workgroups, administrators, and employees to trust others within the organization.

But does it really matter if we experience this kind of trust for our employer? Can’t we just show up and do our jobs? Frankly, no (at least, if we truly care about the work that we do).

Research has demonstrated that trust is a critical part of creating a shared vision; employees tend to help one another and work collaboratively when trust is present.^3,4 Trust is also the foundation for flexibility and innovation.⁵ Employees are generally happier, more satisfied, and less stressed in high-trust organizations—and it has been shown that organizations benefit, too.⁶

By contrast, low-trust organizations usually create barriers to effective performance. In the absence of trust, people create rules and restrictions that mandate how others should act.⁴ Valuable time is then spent studying, enforcing, discussing, and rewriting rules. This yields low-flexibility results and leaves employees to simply follow and enforce policies. Another outcome is high transaction costs and less efficient work—meaning that processes become slower and more restricted by policies and paperwork.⁴ Low trust is also a barrier to change.⁷

Although we recognize organizational trust as an essential component of effective leadership, it remains an issue—one that can make or break an organization’s culture. Lack of trust, particularly between management and employees, creates a hostile work environment in which stress levels are high and productivity is reduced.

Continue to: Three dimensions of trust

There are three dimensions of trust, according to the Grunig Relationship Instrument:

Competence: The belief that an organization has the ability to do what it says it will do (this includes effectiveness and survivability in the marketplace).

Integrity: The belief that an organization is fair and just.

Dependability/reliability: The belief that an organization will do what it says it will do (ie, acts consistently and dependably).⁸

These concepts have been integrated into a “trust measurement questionnaire” that assists in the assessment of an organization’s trustworthiness. While this tool has been used in a variety of industries and has even been used to assess business-to-business relationships, some of the most relevant items for individual employees are outlined in the Table.⁸

But measuring trust is only effective if it leads to action. Once you’ve realized you don’t trust your employer, what should you do about it? Unfortunately, the answer is often “push for change or leave!” Aside from voicing your concerns or requesting more information (or leaving), the onus is really on the leaders of the organization to improve communication (among other things).

Continue to: 7 ways leaders can improve trust within their organization

According to Gleeson, there are seven ways leaders can improve trust within their organization, which include

• Having the right people in the right job, since trust must be demonstrated from top to bottom and vice versa
• Being transparent
• Sharing information with all vested parties, from industry partners to customers to employees
• Providing resources to all parties in an equitable manner
• Offering feedback to employees at all levels, perhaps through regular “status update” meetings
• Facing challenges head-on, using teamwork to promote trust and positive attitudes
• Leading by example—the organization’s values and mission should be exemplified by everyone.⁹

If we want to be leaders, not only within our professions but within our workplaces, we must nurture the ideas of trust, transparency, and communication. I am very interested in hearing from you about organizations that you feel are trustworthy and what makes them so—and what experiences you’ve had that led you to avoid or leave employment situations (you need not “name names,” of course). You can reach me at [email protected].

Recently, I was talking with a colleague who works for a large hospital and health care system. While discussing his experiences over the past five years, he suddenly stopped and blurted out, “I don’t trust this organization. Nobody trusts this organization!”

Taken aback, I asked what made him say that.

First of all, he explained, there is a complete and pervasive lack of transparency as to both short- and long-term goals for the organization. Information is treated as proprietary thinking by nonclinical “corporate folks” and not released to the boots-on-the-ground clinician—which makes it difficult to work toward goals efficiently.

Furthermore, he related, there is consistent failure to provide accurate financial data or any plans to improve the organization’s financial position in the marketplace. This prevents providers from making a positive impact on cost containment. No one is invested. Provider compensation packages are neither universal nor simple. The financial folks devise complex formulas that do not account for the vagaries and complexities of health care. This health care organization views every patient as a Financial Information Number and makes no allowance for the fact that many have complex illnesses requiring significant time and attention.

Lastly, he described a systematic and insidious elimination of support staff at all levels—but particularly bedside nurses. The traditional “nursing safety net”—especially relevant in academic institutions—is in tatters, which threatens to undermine day-to-day success in patient care. Staffing of ancillary providers (those in physical, occupational, or speech-language therapy) has been cut back, which means patients wait longer to see these specialists and primary medical providers are frustrated by the lack of progress their patients make.

Stunned by his comments, I started thinking: How many of us recognize some or all of this description? How many trust the organization we work for? Realizing that a huge percentage of NPs, PAs, and physicians work for large entities, these are important questions.

Trust is central to human interaction on both personal and professional levels. Tschannen-Moran defines it as “one’s willingness to be vulnerable to another, based on the confidence that the other is ben­evolent, honest, open, reliable, and com­petent.”¹

Continue to: A more focused definition of organizational trust

Organizational trust may require a broader and yet more focused definition—such as that of Cummings and Bromley, who stipulate that trust is a belief, held by an individual or groups of individuals, that another individual or group

• Makes a good faith effort to behave in accordance with any (explicit or implicit) commitments
• Is honest
• Does not take excessive advantage of another, even when the opportunity to do so exists.²

Thus, organizational (or collective) trust refers to the propensity of workgroups, administrators, and employees to trust others within the organization.

But does it really matter if we experience this kind of trust for our employer? Can’t we just show up and do our jobs? Frankly, no (at least, if we truly care about the work that we do).

Research has demonstrated that trust is a critical part of creating a shared vision; employees tend to help one another and work collaboratively when trust is present.^3,4 Trust is also the foundation for flexibility and innovation.⁵ Employees are generally happier, more satisfied, and less stressed in high-trust organizations—and it has been shown that organizations benefit, too.⁶

By contrast, low-trust organizations usually create barriers to effective performance. In the absence of trust, people create rules and restrictions that mandate how others should act.⁴ Valuable time is then spent studying, enforcing, discussing, and rewriting rules. This yields low-flexibility results and leaves employees to simply follow and enforce policies. Another outcome is high transaction costs and less efficient work—meaning that processes become slower and more restricted by policies and paperwork.⁴ Low trust is also a barrier to change.⁷

Although we recognize organizational trust as an essential component of effective leadership, it remains an issue—one that can make or break an organization’s culture. Lack of trust, particularly between management and employees, creates a hostile work environment in which stress levels are high and productivity is reduced.

Continue to: Three dimensions of trust

There are three dimensions of trust, according to the Grunig Relationship Instrument:

Competence: The belief that an organization has the ability to do what it says it will do (this includes effectiveness and survivability in the marketplace).

Integrity: The belief that an organization is fair and just.

Dependability/reliability: The belief that an organization will do what it says it will do (ie, acts consistently and dependably).⁸

These concepts have been integrated into a “trust measurement questionnaire” that assists in the assessment of an organization’s trustworthiness. While this tool has been used in a variety of industries and has even been used to assess business-to-business relationships, some of the most relevant items for individual employees are outlined in the Table.⁸

But measuring trust is only effective if it leads to action. Once you’ve realized you don’t trust your employer, what should you do about it? Unfortunately, the answer is often “push for change or leave!” Aside from voicing your concerns or requesting more information (or leaving), the onus is really on the leaders of the organization to improve communication (among other things).

Continue to: 7 ways leaders can improve trust within their organization

According to Gleeson, there are seven ways leaders can improve trust within their organization, which include

• Having the right people in the right job, since trust must be demonstrated from top to bottom and vice versa
• Being transparent
• Sharing information with all vested parties, from industry partners to customers to employees
• Providing resources to all parties in an equitable manner
• Offering feedback to employees at all levels, perhaps through regular “status update” meetings
• Facing challenges head-on, using teamwork to promote trust and positive attitudes
• Leading by example—the organization’s values and mission should be exemplified by everyone.⁹

If we want to be leaders, not only within our professions but within our workplaces, we must nurture the ideas of trust, transparency, and communication. I am very interested in hearing from you about organizations that you feel are trustworthy and what makes them so—and what experiences you’ve had that led you to avoid or leave employment situations (you need not “name names,” of course). You can reach me at [email protected].

Recently, I was talking with a colleague who works for a large hospital and health care system. While discussing his experiences over the past five years, he suddenly stopped and blurted out, “I don’t trust this organization. Nobody trusts this organization!”

Taken aback, I asked what made him say that.

First of all, he explained, there is a complete and pervasive lack of transparency as to both short- and long-term goals for the organization. Information is treated as proprietary thinking by nonclinical “corporate folks” and not released to the boots-on-the-ground clinician—which makes it difficult to work toward goals efficiently.

Furthermore, he related, there is consistent failure to provide accurate financial data or any plans to improve the organization’s financial position in the marketplace. This prevents providers from making a positive impact on cost containment. No one is invested. Provider compensation packages are neither universal nor simple. The financial folks devise complex formulas that do not account for the vagaries and complexities of health care. This health care organization views every patient as a Financial Information Number and makes no allowance for the fact that many have complex illnesses requiring significant time and attention.

Lastly, he described a systematic and insidious elimination of support staff at all levels—but particularly bedside nurses. The traditional “nursing safety net”—especially relevant in academic institutions—is in tatters, which threatens to undermine day-to-day success in patient care. Staffing of ancillary providers (those in physical, occupational, or speech-language therapy) has been cut back, which means patients wait longer to see these specialists and primary medical providers are frustrated by the lack of progress their patients make.

Stunned by his comments, I started thinking: How many of us recognize some or all of this description? How many trust the organization we work for? Realizing that a huge percentage of NPs, PAs, and physicians work for large entities, these are important questions.

Trust is central to human interaction on both personal and professional levels. Tschannen-Moran defines it as “one’s willingness to be vulnerable to another, based on the confidence that the other is ben­evolent, honest, open, reliable, and com­petent.”¹

Continue to: A more focused definition of organizational trust

Organizational trust may require a broader and yet more focused definition—such as that of Cummings and Bromley, who stipulate that trust is a belief, held by an individual or groups of individuals, that another individual or group

• Makes a good faith effort to behave in accordance with any (explicit or implicit) commitments
• Is honest
• Does not take excessive advantage of another, even when the opportunity to do so exists.²

Thus, organizational (or collective) trust refers to the propensity of workgroups, administrators, and employees to trust others within the organization.

But does it really matter if we experience this kind of trust for our employer? Can’t we just show up and do our jobs? Frankly, no (at least, if we truly care about the work that we do).

Research has demonstrated that trust is a critical part of creating a shared vision; employees tend to help one another and work collaboratively when trust is present.^3,4 Trust is also the foundation for flexibility and innovation.⁵ Employees are generally happier, more satisfied, and less stressed in high-trust organizations—and it has been shown that organizations benefit, too.⁶

By contrast, low-trust organizations usually create barriers to effective performance. In the absence of trust, people create rules and restrictions that mandate how others should act.⁴ Valuable time is then spent studying, enforcing, discussing, and rewriting rules. This yields low-flexibility results and leaves employees to simply follow and enforce policies. Another outcome is high transaction costs and less efficient work—meaning that processes become slower and more restricted by policies and paperwork.⁴ Low trust is also a barrier to change.⁷

Although we recognize organizational trust as an essential component of effective leadership, it remains an issue—one that can make or break an organization’s culture. Lack of trust, particularly between management and employees, creates a hostile work environment in which stress levels are high and productivity is reduced.

Continue to: Three dimensions of trust

There are three dimensions of trust, according to the Grunig Relationship Instrument:

Competence: The belief that an organization has the ability to do what it says it will do (this includes effectiveness and survivability in the marketplace).

Integrity: The belief that an organization is fair and just.

Dependability/reliability: The belief that an organization will do what it says it will do (ie, acts consistently and dependably).⁸

These concepts have been integrated into a “trust measurement questionnaire” that assists in the assessment of an organization’s trustworthiness. While this tool has been used in a variety of industries and has even been used to assess business-to-business relationships, some of the most relevant items for individual employees are outlined in the Table.⁸

But measuring trust is only effective if it leads to action. Once you’ve realized you don’t trust your employer, what should you do about it? Unfortunately, the answer is often “push for change or leave!” Aside from voicing your concerns or requesting more information (or leaving), the onus is really on the leaders of the organization to improve communication (among other things).

Continue to: 7 ways leaders can improve trust within their organization

According to Gleeson, there are seven ways leaders can improve trust within their organization, which include

• Having the right people in the right job, since trust must be demonstrated from top to bottom and vice versa
• Being transparent
• Sharing information with all vested parties, from industry partners to customers to employees
• Providing resources to all parties in an equitable manner
• Offering feedback to employees at all levels, perhaps through regular “status update” meetings
• Facing challenges head-on, using teamwork to promote trust and positive attitudes
• Leading by example—the organization’s values and mission should be exemplified by everyone.⁹

If we want to be leaders, not only within our professions but within our workplaces, we must nurture the ideas of trust, transparency, and communication. I am very interested in hearing from you about organizations that you feel are trustworthy and what makes them so—and what experiences you’ve had that led you to avoid or leave employment situations (you need not “name names,” of course). You can reach me at [email protected].

Caring for a newborn can be a source of joy for family physicians (FPs). In this article, we examine care provided in the first month of life, including a thorough physical examination, safe hospital discharge procedures, assessment of neonatal feeding, evaluation of jaundice and fever, and prevention of sudden infant death syndrome (SIDS). In addition, we describe how FPs can support women of childbearing age between pregnancies, with the goal of reducing the risk of adverse outcomes in future pregnancies. (See “Your role in risk assessment and interventions during the interconception period.”)

 

 

Ensuring a thorough exam, making use of a discharge checklist

Before parents leave the hospital with their newborn, it is essential that they receive written and verbal counseling on important issues in neonatal care. A discharge checklist can help make sure all topics have been covered.¹ A hearing screen and pulse oximetry before discharge are required for all newborns in most states, in addition to important preventive counseling for parents. TABLE 1² and TABLE 2² summarize important newborn physical exam findings and common skin conditions. Parents should be given additional written information regarding prevention of SIDS and proper use of car seats.

Hospital physicians should assess maternal medical and psychosocial readiness for discharge. Through shared decision-making with the newborn’s parents, physicians should create a plan for outpatient follow-up. Assessment through a physician home visit can provide safe and effective care similar to what is provided at a visit to an office medical practice.^3-7 A follow-up appointment should be made 2 to 5 days before discharge, preferably connecting the newborn to a medical home where comprehensive health care services are offered.^1,5,6,8

Age, gestational age, risk factors for hyperbilirubinemia, and the timing and level of bilirubin testing should be considered when establishing a follow-up interval. Most newborns who are discharged before 72 hours of age should have a follow-up visit in 2 days; a newborn who has a recognized risk factor for a health problem should be seen sooner. Newborns in the “low-risk zone” (ie, no recognized risk factors) should be seen based on age at discharge or need for breastfeeding support.⁹

Tracking baby’s weight, ensuring proper feeding

A newborn who is discharged at 24 hours of life, or sooner, should be seen in the office within 2 days of discharge to 1) ensure that he (she) is getting proper nutrition and 2) monitor his weight^1,3,5 (TABLE 3^10-13). All newborns should be seen again at 2 weeks of life, with additional visits more frequently if there are concerns about nutrition.¹

Recording an accurate weight is critical; the newborn should be weighed completely undressed and without a diaper. Healthy newborns can safely lose up to 10% of birth weight within the first week of life; they should be back to their birth weight by approximately 2 weeks of life.^10,11 A healthy newborn loses approximately 0.5 to 1 oz a day;¹¹ greater than 10% loss of birth weight should trigger a thorough medical work-up and feeding assessment.

Breastfeeding. For breastfeeding mothers, physicians should recommend on-demand feeding or a feeding at least every 2 or 3 hours. Adequate intake in breastfed infants can be intimidating for new parents to monitor, but they can use a written chart or any of several available smartphone applications to document length and timing of feeds and frequency of urination and bowel movements. By the fifth day of life, a newborn should be having at least 6 voids and 3 or 4 stools a day.^10-12

In addition, physicians can counsel parents on what to look for—in the mother and the newborn—to confirm that breastfeeding is successful, with adequate nutritional intake (TABLE 3^10-13). Physicians should recommend against providing a pacifier to breastfeeding infants during the first several weeks of life—or until breastfeeding is well established (usually at 3 or 4 weeks of age). The World Health Organization (WHO) recommends against providing bottles, pacifiers, and artificial nipples to breastfeeding newborns.¹⁴ Liquids other than colostrum or breast milk should not be given unless there is a documented medical need, such as inadequate weight gain or feeding difficulty.¹⁵ If the newborn experiences early latch difficulties, supplementation with expressed breast milk is preferable to supplementation with formula. Assistance from a trained lactation consultant is a key element in the support of the breastfeeding dyad.^11,12,16

Breastfeeding optimizes development of the newborn’s immune system, thus bolstering disease prevention; it also assists with maternal postpartum weight loss and psychological well-being. Exclusively or primarily formula-fed newborns are at increased risk of gastrointestinal, ear, and respiratory infections throughout infancy and childhood; type 1 diabetes mellitus; asthma; childhood and adult obesity; and leukemia.^17,18 Mothers who feed their newborn primarily formula increase their own risk of obesity, type 2 diabetes mellitus, ovarian and breast cancer, and depression.^17-22

Infant feeding is a personal and family choice but, in the absence of medical contraindications—such as maternal human immunodeficiency virus infection and galactosemia—exclusive breastfeeding should be recommended.^17,18 FPs are well suited to support the mother–infant breastfeeding dyad in the neonatal period, based on expert recommendations. Specifically, the American Academy of Family Physicians (AAFP) and American Academy of Pediatrics (AAP) recommend that all infants be exclusively breastfed for the first 6 months of life and continue some breastfeeding through the first year or longer.^17,18 WHO recommends breastfeeding until 24 months of age—longer if mother and infant want to, unless breastfeeding is contraindicated.^14,17,18

Physicians should provide up-to-date information to parents regarding the risks and benefits of feeding choices. Support for breastfeeding mothers postnatally has been shown to be helpful in lengthening the time of exclusive breastfeeding.¹² Certain medications pass through breast milk, and updated guides to medication cautions can be found at the National Institutes of Health’s LACTMED Web site (https://toxnet.nlm.nih.gov/newtoxnet/lactmed.htm).¹³ In many cases, when a maternal medication is incompatible with breastfeeding, the family physician can consider substituting another appropriate medication that is compatible.

Physician recommendation and support improves the rate of breastfeeding, but many mother–infant dyads require additional support to maintain breastfeeding for the recommended duration; such support can take the form of a certified lactation consultant or counselor, doula, or peer counselor.^23-25 Although structured breastfeeding education in the antenatal period has been demonstrated to be effective in improving breastfeeding initiation and duration, recent research shows that support groups and assistance from the professionals previously mentioned also improve the breastfeeding rate.^26-28

Adequate intake in breastfed infants can be intimidating for new parents to monitor, but they can use a written chart or any of several available smartphone applications.

The AAFP recommends that FPs’ offices adopt specific, evidence-based practices that can have an impact on breastfeeding initiation and duration. Such practices include phone and in-person breastfeeding support from nursing staff and removing any formula advertisements from the office.¹⁷

Formula feeding. When parents choose formula feeding, most infants tolerate cow’s milk-based formula.²⁹ For healthy term infants, differences between brands of formula are generally insignificant. Soy-protein formulas are of value only if lactose intolerance is strongly suspected, such as after prolonged episodes of loose stools. Even then, intolerance is usually transient and cow’s milk-based formula can be tried again in 2 to 4 weeks.

Physicians should recommend 20 kcal/oz of iron-fortified formula for infants who are fed formula—except in special circumstances, such as premature newborns, who may require a more calorie-dense formula. Parents should pay special attention to the manufacturer’s instructions for mixing formula with water because overdilution can cause hyponatremia. Typical volume for newborns should be at least 15 to 30 mL/feed for the first few days; newborns should not go more than 4 hours between feedings. Within the first week, newborns will start taking 60 to 90 mL/feed and increase that gradually to approximately 120 mL/feed by the end of the first month of life. On average, infants need a little more than 100 kcal/kg of body weight a day; for a 3.5-kg infant, that is at least 500 mL of formula over the course of a day.^17,22

Because formula does not contain fluoride, physicians should recommend that parents mix formula that is provided as a powder with fluoridated water. Low-iron formula offers no advantage; feeding with it will cause iron-deficiency anemia in most infants.

When tongue-tie interferes with feeding

Tongue-tie—or ankyloglossia, an atypically short or thick lingual frenulum—is present in 3% to 16% of all births. The condition can make breastfeeding difficult; result in poor neonatal weight gain; and cause sore nipples in 25% to 44% of cases.³⁰ Once tongue-tie is noted, the physician should talk to the mother about the history of feeding success, including whether her nipples are sore and whether the newborn is having difficulty feeding (ie, transferring milk). The Hazelbaker Assessment Tool for Lingual Frenulum Function and the simpler Bristol Tongue Assessment Tool can be used to assess the severity of tongue-tie.^30-35

When tongue-tie interferes with feeding, a physician who is not trained in treatment can refer the mother and infant to a specialist in the community. Frenotomy has been used for many years as a treatment for tongue-tie; improvement in nipple pain and the mother-reported breastfeeding score have been reported postoperatively in several studies.^30-33

Ensure proper vitamin D intake through supplementation

Newborns should consume 400 IU/d of supplemental vitamin D to prevent deficiency and its clinical manifestation, rickets, or other associated abnormalities of calcium metabolism. Deficiency of vitamin D has also been linked to a number of other conditions, including developmental delay and, possibly, type 1 diabetes mellitus in childhood and cardiovascular disease later in life.³⁶

Newborns should consume 400 IU/d of supplemental vitamin D to prevent deficiency and its clinical manifestation, rickets, or other associated abnormalities of calcium metabolism.

In the first months of life, few infants who are solely formula-fed will consume a full liter daily; for them, supplementation of vitamin D for at least one month should be prescribed.³⁵ For breastfed infants, high-dosage maternal vitamin D supplementation may be effective, precluding infant oral vitamin D supplementation³⁶; however, neither the AAFP nor the AAP has issued guidance promoting maternal supplementation in lieu of direct oral infant supplementation.³⁷

Jaundice prevention—and recognition

An elevated bilirubin level is seen in most newborns in the first days of life because of increased production and decreased clearance of bilirubin—a condition known as physiologic jaundice. Conditions that aggravate physiologic hyperbilirubinemia include inborn errors of metabolism, ABO blood-group incompatibility, hemoglobin variants, and inflammatory states such as sepsis. It is important to distinguish physiologic jaundice from exaggerated physiologic and pathologic forms of hyperbilirubinemia; the latter is a medical emergency. Before we get to that, a word about prevention.

Prevention. Because poor caloric intake and dehydration are associated with hyperbilirubinemia, physicians should advise breastfeeding mothers to feed their newborn at least 8 to 12 times daily during the first week of life. However, routine supplementation of liquids other than breast milk should be discouraged in newborns who are not dehydrated.³⁸

The total serum bilirubin level should be tested in every newborn who has clinical jaundice in the first 24 hours of life.

All pregnant women should be tested for ABO and Rh (D) blood types and undergo serum screening for isoimmune antibodies. Randomized trials have demonstrated that the incidence of significant hyperbilirubinemia can be reduced if, for Rh-negative mothers and those who did not undergo prenatal blood-group testing, infant cord blood is tested for 1) ABO and Rh (D) types and 2) direct antibody (Coombs’ test).^38,39

Screening and assessment. It is recommended that all newborns be screened for jaundice before discharge by 1) assessment of clinical risk factors or 2) testing of transcutaneous bilirubin (TcB) or total serum bilirubin (TSB). Furthermore, because evidence shows that treating clinical jaundice can improve outcomes and rehospitalization, TSB should be measured in every newborn who has clinical jaundice in the first 24 hours of life. Measurement of TcB or TSB should also be performed on all infants in whom there appears to be clinical jaundice that is excessive for age.^38,39

During routine clinical care, TcB measurement provides a reasonable estimate of the TSB level in healthy newborns at levels less than 15 mg/dL,⁴⁰ although TcB testing might not be available in the outpatient office. An AAP management algorithm can help determine when a newborn should be seen for outpatient follow-up based on risk of hyperbilirubinemia; higher-risk newborns should be reevaluated in 24 hours.⁹ Outpatient visual assessment of jaundice for cephalocaudal progression—in a well-lit room, with a fully undressed newborn—correlates well with TSB test results. However, visual assessment should not be used alone to screen for hyperbilirubinemia; recent studies have demonstrated that such assessment lacks clinical reliability.⁴⁰

Laboratory assessment. All bilirubin levels should be interpreted based on the newborn’s age in hours. The need for phototherapy should be based on the zone (low, low-intermediate, high-intermediate, or high, as categorized in the AAP nomogram³⁸ in which the TSB level falls. TABLE 4^38-40 provides recommendations for laboratory studies based on risk factors. Standard curves for risk stratification have been developed by the AAP.^37,38

Treatment. Decisions to initiate treatment should be based on the AAP algorithm.³⁸ When initiating phototherapy, precautions include ensuring adequate fluid intake, patching eyes, and monitoring temperature. Phototherapy can generally be stopped when the TSB level falls by 5 mg/dL or below 14 mg/dL. Home phototherapy, using a fiberoptic blanket, for uncomplicated jaundice (in carefully selected newborns with reliable parents) allows continued breastfeeding and bonding with the family, and can significantly decrease the rate of rehospitalization for infants older than 34 weeks.⁴¹

Breastfeeding is often associated with a higher bilirubin level than is seen in infants fed formula exclusively; increasing the frequency of feeding usually reduces the bilirubin level. So-called breast-milk jaundice is a delayed, but common, form of jaundice that is usually diagnosed in the second week of life and peaks by the end of the second week, resolving gradually over one to 4 months. If evaluation reveals no pathologic source, breastfeeding can generally be continued. Temporary discontinuation of breastfeeding to consider a diagnosis of breast-milk jaundice or other reasons for an elevated bilirubin level increases the risk of breastfeeding failure and is usually unnecessary.^12,37,39

Fever—a full work-up, thorough history are key

Concern about serious bacterial illness (SBI) makes the evaluation of fever critical for those who care for newborns. Many studies have attempted to identify which newborns might be able to be cared for safely as outpatients to prevent unnecessary testing and antibiotics.^5,42 Regrettably, SBI in infants remains difficult to predict, and protocols that have been developed may miss as many as 1 of every 10 newborns who has SBI.⁴³ Initial management of all infants 28 days old or younger with fever must therefore include a full work-up, including lumbar puncture and empiric antibiotics.⁴⁴

Evaluation. When an infant younger than 28 days has a fever, the physician should first verify that the temperature was taken rectally and how it was documented. In an infant who has a history of prematurity, it is crucial to correct for chronological age when deciding on proper evaluation.

Additional important findings in the history include a significant change in behavior, associated symptoms, and exposure to sick contacts. The maternal and birth history, including prolonged rupture of membranes, colonization with group B Streptococcus, administration of antibiotics at delivery, and genital herpes simplex virus (HSV) infection may suggest a cause for fever.⁴⁵

The evaluation of fever might include the white blood cell (WBC) count, blood culture, measurement of markers of inflammation, urine studies, lumbar puncture, stool culture, and chest radiograph. Traditionally, the WBC count has been utilized as a standard marker for sepsis, although it has a low sensitivity and specificity for SBI, especially in newborns.⁴⁶ Blood cultures should be obtained routinely in the newborn with fever, and before antibiotics are administered in older infants.

Procalcitonin (PCT; a calcitonin precursor) and the inflammatory marker C-reactive protein (CRP) have been shown, in several large studies, to have relatively high sensitivity and specificity for SBI; measurement of these constituents may enhance detection of serious illness.^46-49 In a large study of 2047 febrile infants older than 30 months, the PCT level was determined to be more accurate than the CRP level, the WBC count, and the absolute neutrophil count in predicting SBI.^48,49 PCT shows the most promise for preventing a full fever work-up and empiric antibiotics. It has not yet been widely translated into practice, however, because of a lack of clear guidance on how to combine PCT levels with other laboratory markers and clinical decision-making.^48-50

Urinalysis (UA) should be obtained for all newborns who present with fever. Traditionally, it was recommended that urine should be cultured for all newborns with fever; however, more recent data show that the initial urinalysis is much more sensitive than once thought. In a study, UA was positive (defined as pyuria or a positive leukocyte esterase test, or both) in all but 1 of 203 infants who had bacteremic UTI (sensitivity, 99.5%).⁵¹

The procalcitonin level was determined to be more accurate than the C-reactive protein level, the white blood cell count, and the absolute neutrophil count in predicting serious bacterial illness.

Stool culture is necessary in newborns only when they present with blood or mucus in diarrhea. Lumbar puncture should be performed in all febrile newborns and all newborns for whom empiric antibiotics have been prescribed.^43,44 A chest radiograph may be useful in diagnosis when a newborn has any other sign of pulmonary disease: respiratory rate >50/min, retractions, wheezing, grunting, stridor, nasal flaring, cough, and positive findings on lung examination.^43,44

Treatment. Management for all newborns who have a rectal temperature ≥38° C includes admission to the hospital and empiric antibiotics; guidance is based primarily on expert consensus. Common pathogens for SBI include group B Strep, Escherichia coli, Enterococcus spp., and Listeria monocytogenes.^43,44 Empiric antibiotics, including ampicillin (to cover L monocytogenes) and cefotaxime or gentamicin should be started immediately after sending for blood, urine, and cerebrospinal fluid (CSF) cultures.^43-45

Management for all newborns who have rectal temperature ≥38° C includes admission to the hospital and empiric antibiotics.

All infants who are ill-appearing or have vesicles, seizures, or a maternal history of genital HSV infection should also be started on empiric acyclovir. Vesicles should be cultured and CSF should be sent for HSV DNA polymerase chain reaction before acyclovir is administered.^43-45

Sudden infant death syndrome: Steps to take to minimize risk

SIDS is defined as the sudden death of a child younger than 1 year that remains unexplained after a thorough case investigation and comprehensive review of the clinical history. The risk of SIDS in the United States is less than 1 for every 1000 live births; incidence peaks between 2 and 4 months of age.⁵² In the United States, SIDS and other sleep-related infant deaths, such as strangulation in bed or accidental suffocation, account for more than 4000 deaths a year.⁵³ The incidence of SIDS declined markedly after the “Back to Sleep” campaign was launched in 2003, but has leveled off since 2005.^53-55

Numerous risk factors for SIDS have been identified, including maternal factors (young maternal age, maternal smoking during pregnancy, late or no prenatal care) and infant and environmental factors (prematurity, low birth weight, male gender, prone sleeping position, sleeping on a soft surface or with bedding accessories, bed-sharing (ie, sleeping in the parents’ bed), and overheating. In many cases, the risk factors are modifiable; sleeping in the prone position is the most meaningful modifiable risk factor.

Home monitors have not been proven to reduce the incidence of SIDS and are not recommended for that purpose.

To minimize the risk for SIDS, parents should be educated on the risk factors—prenatally as well as at each infant well visit. Home monitors have not been proven to reduce the incidence of SIDS and are not recommended for that purpose.^54-57 Although evidence is strongest for supine positioning as a preventive intervention for SIDS, other evidence-based recommendations include use of a firm sleep surface; breastfeeding; use of a pacifier; room-sharing with parents without bed-sharing; routine immunization; avoidance of overheating; avoiding falling asleep with the infant on a chair or couch; and avoiding exposure to tobacco smoke, alcohol, and drugs of abuse.^55,56 A recent systematic review showed that large-scale community interventions and education campaigns can play a significant role in parental and community adoption of safe sleep recommendations; however, families and communities rarely exhibit complete adherence to safe sleep practices.⁵⁷

Other concerns in the first month of life and immediately beyond

In TABLE 5,² we list additional common newborn problems not reviewed in the text of this article and summarize evidence-based treatment strategies.

CORRESPONDENCE
Scott Hartman, MD, Associate Professor, Department of Family Medicine, University of Rochester Medical Center, 777 South Clinton Avenue, Rochester, NY 14620; [email protected].

Acknowledgement
We thank Nancy Phillips for her assistance in the preparation of this article.

Caring for a newborn can be a source of joy for family physicians (FPs). In this article, we examine care provided in the first month of life, including a thorough physical examination, safe hospital discharge procedures, assessment of neonatal feeding, evaluation of jaundice and fever, and prevention of sudden infant death syndrome (SIDS). In addition, we describe how FPs can support women of childbearing age between pregnancies, with the goal of reducing the risk of adverse outcomes in future pregnancies. (See “Your role in risk assessment and interventions during the interconception period.”)

 

 

Ensuring a thorough exam, making use of a discharge checklist

Before parents leave the hospital with their newborn, it is essential that they receive written and verbal counseling on important issues in neonatal care. A discharge checklist can help make sure all topics have been covered.¹ A hearing screen and pulse oximetry before discharge are required for all newborns in most states, in addition to important preventive counseling for parents. TABLE 1² and TABLE 2² summarize important newborn physical exam findings and common skin conditions. Parents should be given additional written information regarding prevention of SIDS and proper use of car seats.

Hospital physicians should assess maternal medical and psychosocial readiness for discharge. Through shared decision-making with the newborn’s parents, physicians should create a plan for outpatient follow-up. Assessment through a physician home visit can provide safe and effective care similar to what is provided at a visit to an office medical practice.^3-7 A follow-up appointment should be made 2 to 5 days before discharge, preferably connecting the newborn to a medical home where comprehensive health care services are offered.^1,5,6,8

Age, gestational age, risk factors for hyperbilirubinemia, and the timing and level of bilirubin testing should be considered when establishing a follow-up interval. Most newborns who are discharged before 72 hours of age should have a follow-up visit in 2 days; a newborn who has a recognized risk factor for a health problem should be seen sooner. Newborns in the “low-risk zone” (ie, no recognized risk factors) should be seen based on age at discharge or need for breastfeeding support.⁹

Tracking baby’s weight, ensuring proper feeding

A newborn who is discharged at 24 hours of life, or sooner, should be seen in the office within 2 days of discharge to 1) ensure that he (she) is getting proper nutrition and 2) monitor his weight^1,3,5 (TABLE 3^10-13). All newborns should be seen again at 2 weeks of life, with additional visits more frequently if there are concerns about nutrition.¹

Recording an accurate weight is critical; the newborn should be weighed completely undressed and without a diaper. Healthy newborns can safely lose up to 10% of birth weight within the first week of life; they should be back to their birth weight by approximately 2 weeks of life.^10,11 A healthy newborn loses approximately 0.5 to 1 oz a day;¹¹ greater than 10% loss of birth weight should trigger a thorough medical work-up and feeding assessment.

Breastfeeding. For breastfeeding mothers, physicians should recommend on-demand feeding or a feeding at least every 2 or 3 hours. Adequate intake in breastfed infants can be intimidating for new parents to monitor, but they can use a written chart or any of several available smartphone applications to document length and timing of feeds and frequency of urination and bowel movements. By the fifth day of life, a newborn should be having at least 6 voids and 3 or 4 stools a day.^10-12

In addition, physicians can counsel parents on what to look for—in the mother and the newborn—to confirm that breastfeeding is successful, with adequate nutritional intake (TABLE 3^10-13). Physicians should recommend against providing a pacifier to breastfeeding infants during the first several weeks of life—or until breastfeeding is well established (usually at 3 or 4 weeks of age). The World Health Organization (WHO) recommends against providing bottles, pacifiers, and artificial nipples to breastfeeding newborns.¹⁴ Liquids other than colostrum or breast milk should not be given unless there is a documented medical need, such as inadequate weight gain or feeding difficulty.¹⁵ If the newborn experiences early latch difficulties, supplementation with expressed breast milk is preferable to supplementation with formula. Assistance from a trained lactation consultant is a key element in the support of the breastfeeding dyad.^11,12,16

Breastfeeding optimizes development of the newborn’s immune system, thus bolstering disease prevention; it also assists with maternal postpartum weight loss and psychological well-being. Exclusively or primarily formula-fed newborns are at increased risk of gastrointestinal, ear, and respiratory infections throughout infancy and childhood; type 1 diabetes mellitus; asthma; childhood and adult obesity; and leukemia.^17,18 Mothers who feed their newborn primarily formula increase their own risk of obesity, type 2 diabetes mellitus, ovarian and breast cancer, and depression.^17-22

Infant feeding is a personal and family choice but, in the absence of medical contraindications—such as maternal human immunodeficiency virus infection and galactosemia—exclusive breastfeeding should be recommended.^17,18 FPs are well suited to support the mother–infant breastfeeding dyad in the neonatal period, based on expert recommendations. Specifically, the American Academy of Family Physicians (AAFP) and American Academy of Pediatrics (AAP) recommend that all infants be exclusively breastfed for the first 6 months of life and continue some breastfeeding through the first year or longer.^17,18 WHO recommends breastfeeding until 24 months of age—longer if mother and infant want to, unless breastfeeding is contraindicated.^14,17,18

Physicians should provide up-to-date information to parents regarding the risks and benefits of feeding choices. Support for breastfeeding mothers postnatally has been shown to be helpful in lengthening the time of exclusive breastfeeding.¹² Certain medications pass through breast milk, and updated guides to medication cautions can be found at the National Institutes of Health’s LACTMED Web site (https://toxnet.nlm.nih.gov/newtoxnet/lactmed.htm).¹³ In many cases, when a maternal medication is incompatible with breastfeeding, the family physician can consider substituting another appropriate medication that is compatible.

Physician recommendation and support improves the rate of breastfeeding, but many mother–infant dyads require additional support to maintain breastfeeding for the recommended duration; such support can take the form of a certified lactation consultant or counselor, doula, or peer counselor.^23-25 Although structured breastfeeding education in the antenatal period has been demonstrated to be effective in improving breastfeeding initiation and duration, recent research shows that support groups and assistance from the professionals previously mentioned also improve the breastfeeding rate.^26-28

Adequate intake in breastfed infants can be intimidating for new parents to monitor, but they can use a written chart or any of several available smartphone applications.

The AAFP recommends that FPs’ offices adopt specific, evidence-based practices that can have an impact on breastfeeding initiation and duration. Such practices include phone and in-person breastfeeding support from nursing staff and removing any formula advertisements from the office.¹⁷

Formula feeding. When parents choose formula feeding, most infants tolerate cow’s milk-based formula.²⁹ For healthy term infants, differences between brands of formula are generally insignificant. Soy-protein formulas are of value only if lactose intolerance is strongly suspected, such as after prolonged episodes of loose stools. Even then, intolerance is usually transient and cow’s milk-based formula can be tried again in 2 to 4 weeks.

Physicians should recommend 20 kcal/oz of iron-fortified formula for infants who are fed formula—except in special circumstances, such as premature newborns, who may require a more calorie-dense formula. Parents should pay special attention to the manufacturer’s instructions for mixing formula with water because overdilution can cause hyponatremia. Typical volume for newborns should be at least 15 to 30 mL/feed for the first few days; newborns should not go more than 4 hours between feedings. Within the first week, newborns will start taking 60 to 90 mL/feed and increase that gradually to approximately 120 mL/feed by the end of the first month of life. On average, infants need a little more than 100 kcal/kg of body weight a day; for a 3.5-kg infant, that is at least 500 mL of formula over the course of a day.^17,22

Because formula does not contain fluoride, physicians should recommend that parents mix formula that is provided as a powder with fluoridated water. Low-iron formula offers no advantage; feeding with it will cause iron-deficiency anemia in most infants.

When tongue-tie interferes with feeding

Tongue-tie—or ankyloglossia, an atypically short or thick lingual frenulum—is present in 3% to 16% of all births. The condition can make breastfeeding difficult; result in poor neonatal weight gain; and cause sore nipples in 25% to 44% of cases.³⁰ Once tongue-tie is noted, the physician should talk to the mother about the history of feeding success, including whether her nipples are sore and whether the newborn is having difficulty feeding (ie, transferring milk). The Hazelbaker Assessment Tool for Lingual Frenulum Function and the simpler Bristol Tongue Assessment Tool can be used to assess the severity of tongue-tie.^30-35

When tongue-tie interferes with feeding, a physician who is not trained in treatment can refer the mother and infant to a specialist in the community. Frenotomy has been used for many years as a treatment for tongue-tie; improvement in nipple pain and the mother-reported breastfeeding score have been reported postoperatively in several studies.^30-33

Ensure proper vitamin D intake through supplementation

Newborns should consume 400 IU/d of supplemental vitamin D to prevent deficiency and its clinical manifestation, rickets, or other associated abnormalities of calcium metabolism. Deficiency of vitamin D has also been linked to a number of other conditions, including developmental delay and, possibly, type 1 diabetes mellitus in childhood and cardiovascular disease later in life.³⁶

Newborns should consume 400 IU/d of supplemental vitamin D to prevent deficiency and its clinical manifestation, rickets, or other associated abnormalities of calcium metabolism.

In the first months of life, few infants who are solely formula-fed will consume a full liter daily; for them, supplementation of vitamin D for at least one month should be prescribed.³⁵ For breastfed infants, high-dosage maternal vitamin D supplementation may be effective, precluding infant oral vitamin D supplementation³⁶; however, neither the AAFP nor the AAP has issued guidance promoting maternal supplementation in lieu of direct oral infant supplementation.³⁷

Jaundice prevention—and recognition

An elevated bilirubin level is seen in most newborns in the first days of life because of increased production and decreased clearance of bilirubin—a condition known as physiologic jaundice. Conditions that aggravate physiologic hyperbilirubinemia include inborn errors of metabolism, ABO blood-group incompatibility, hemoglobin variants, and inflammatory states such as sepsis. It is important to distinguish physiologic jaundice from exaggerated physiologic and pathologic forms of hyperbilirubinemia; the latter is a medical emergency. Before we get to that, a word about prevention.

Prevention. Because poor caloric intake and dehydration are associated with hyperbilirubinemia, physicians should advise breastfeeding mothers to feed their newborn at least 8 to 12 times daily during the first week of life. However, routine supplementation of liquids other than breast milk should be discouraged in newborns who are not dehydrated.³⁸

The total serum bilirubin level should be tested in every newborn who has clinical jaundice in the first 24 hours of life.

All pregnant women should be tested for ABO and Rh (D) blood types and undergo serum screening for isoimmune antibodies. Randomized trials have demonstrated that the incidence of significant hyperbilirubinemia can be reduced if, for Rh-negative mothers and those who did not undergo prenatal blood-group testing, infant cord blood is tested for 1) ABO and Rh (D) types and 2) direct antibody (Coombs’ test).^38,39

Screening and assessment. It is recommended that all newborns be screened for jaundice before discharge by 1) assessment of clinical risk factors or 2) testing of transcutaneous bilirubin (TcB) or total serum bilirubin (TSB). Furthermore, because evidence shows that treating clinical jaundice can improve outcomes and rehospitalization, TSB should be measured in every newborn who has clinical jaundice in the first 24 hours of life. Measurement of TcB or TSB should also be performed on all infants in whom there appears to be clinical jaundice that is excessive for age.^38,39

During routine clinical care, TcB measurement provides a reasonable estimate of the TSB level in healthy newborns at levels less than 15 mg/dL,⁴⁰ although TcB testing might not be available in the outpatient office. An AAP management algorithm can help determine when a newborn should be seen for outpatient follow-up based on risk of hyperbilirubinemia; higher-risk newborns should be reevaluated in 24 hours.⁹ Outpatient visual assessment of jaundice for cephalocaudal progression—in a well-lit room, with a fully undressed newborn—correlates well with TSB test results. However, visual assessment should not be used alone to screen for hyperbilirubinemia; recent studies have demonstrated that such assessment lacks clinical reliability.⁴⁰

Laboratory assessment. All bilirubin levels should be interpreted based on the newborn’s age in hours. The need for phototherapy should be based on the zone (low, low-intermediate, high-intermediate, or high, as categorized in the AAP nomogram³⁸ in which the TSB level falls. TABLE 4^38-40 provides recommendations for laboratory studies based on risk factors. Standard curves for risk stratification have been developed by the AAP.^37,38

Treatment. Decisions to initiate treatment should be based on the AAP algorithm.³⁸ When initiating phototherapy, precautions include ensuring adequate fluid intake, patching eyes, and monitoring temperature. Phototherapy can generally be stopped when the TSB level falls by 5 mg/dL or below 14 mg/dL. Home phototherapy, using a fiberoptic blanket, for uncomplicated jaundice (in carefully selected newborns with reliable parents) allows continued breastfeeding and bonding with the family, and can significantly decrease the rate of rehospitalization for infants older than 34 weeks.⁴¹

Breastfeeding is often associated with a higher bilirubin level than is seen in infants fed formula exclusively; increasing the frequency of feeding usually reduces the bilirubin level. So-called breast-milk jaundice is a delayed, but common, form of jaundice that is usually diagnosed in the second week of life and peaks by the end of the second week, resolving gradually over one to 4 months. If evaluation reveals no pathologic source, breastfeeding can generally be continued. Temporary discontinuation of breastfeeding to consider a diagnosis of breast-milk jaundice or other reasons for an elevated bilirubin level increases the risk of breastfeeding failure and is usually unnecessary.^12,37,39

Fever—a full work-up, thorough history are key

Concern about serious bacterial illness (SBI) makes the evaluation of fever critical for those who care for newborns. Many studies have attempted to identify which newborns might be able to be cared for safely as outpatients to prevent unnecessary testing and antibiotics.^5,42 Regrettably, SBI in infants remains difficult to predict, and protocols that have been developed may miss as many as 1 of every 10 newborns who has SBI.⁴³ Initial management of all infants 28 days old or younger with fever must therefore include a full work-up, including lumbar puncture and empiric antibiotics.⁴⁴

Evaluation. When an infant younger than 28 days has a fever, the physician should first verify that the temperature was taken rectally and how it was documented. In an infant who has a history of prematurity, it is crucial to correct for chronological age when deciding on proper evaluation.

Additional important findings in the history include a significant change in behavior, associated symptoms, and exposure to sick contacts. The maternal and birth history, including prolonged rupture of membranes, colonization with group B Streptococcus, administration of antibiotics at delivery, and genital herpes simplex virus (HSV) infection may suggest a cause for fever.⁴⁵

The evaluation of fever might include the white blood cell (WBC) count, blood culture, measurement of markers of inflammation, urine studies, lumbar puncture, stool culture, and chest radiograph. Traditionally, the WBC count has been utilized as a standard marker for sepsis, although it has a low sensitivity and specificity for SBI, especially in newborns.⁴⁶ Blood cultures should be obtained routinely in the newborn with fever, and before antibiotics are administered in older infants.

Procalcitonin (PCT; a calcitonin precursor) and the inflammatory marker C-reactive protein (CRP) have been shown, in several large studies, to have relatively high sensitivity and specificity for SBI; measurement of these constituents may enhance detection of serious illness.^46-49 In a large study of 2047 febrile infants older than 30 months, the PCT level was determined to be more accurate than the CRP level, the WBC count, and the absolute neutrophil count in predicting SBI.^48,49 PCT shows the most promise for preventing a full fever work-up and empiric antibiotics. It has not yet been widely translated into practice, however, because of a lack of clear guidance on how to combine PCT levels with other laboratory markers and clinical decision-making.^48-50

Urinalysis (UA) should be obtained for all newborns who present with fever. Traditionally, it was recommended that urine should be cultured for all newborns with fever; however, more recent data show that the initial urinalysis is much more sensitive than once thought. In a study, UA was positive (defined as pyuria or a positive leukocyte esterase test, or both) in all but 1 of 203 infants who had bacteremic UTI (sensitivity, 99.5%).⁵¹

The procalcitonin level was determined to be more accurate than the C-reactive protein level, the white blood cell count, and the absolute neutrophil count in predicting serious bacterial illness.

Stool culture is necessary in newborns only when they present with blood or mucus in diarrhea. Lumbar puncture should be performed in all febrile newborns and all newborns for whom empiric antibiotics have been prescribed.^43,44 A chest radiograph may be useful in diagnosis when a newborn has any other sign of pulmonary disease: respiratory rate >50/min, retractions, wheezing, grunting, stridor, nasal flaring, cough, and positive findings on lung examination.^43,44

Treatment. Management for all newborns who have a rectal temperature ≥38° C includes admission to the hospital and empiric antibiotics; guidance is based primarily on expert consensus. Common pathogens for SBI include group B Strep, Escherichia coli, Enterococcus spp., and Listeria monocytogenes.^43,44 Empiric antibiotics, including ampicillin (to cover L monocytogenes) and cefotaxime or gentamicin should be started immediately after sending for blood, urine, and cerebrospinal fluid (CSF) cultures.^43-45

Management for all newborns who have rectal temperature ≥38° C includes admission to the hospital and empiric antibiotics.

All infants who are ill-appearing or have vesicles, seizures, or a maternal history of genital HSV infection should also be started on empiric acyclovir. Vesicles should be cultured and CSF should be sent for HSV DNA polymerase chain reaction before acyclovir is administered.^43-45

Sudden infant death syndrome: Steps to take to minimize risk

SIDS is defined as the sudden death of a child younger than 1 year that remains unexplained after a thorough case investigation and comprehensive review of the clinical history. The risk of SIDS in the United States is less than 1 for every 1000 live births; incidence peaks between 2 and 4 months of age.⁵² In the United States, SIDS and other sleep-related infant deaths, such as strangulation in bed or accidental suffocation, account for more than 4000 deaths a year.⁵³ The incidence of SIDS declined markedly after the “Back to Sleep” campaign was launched in 2003, but has leveled off since 2005.^53-55

Numerous risk factors for SIDS have been identified, including maternal factors (young maternal age, maternal smoking during pregnancy, late or no prenatal care) and infant and environmental factors (prematurity, low birth weight, male gender, prone sleeping position, sleeping on a soft surface or with bedding accessories, bed-sharing (ie, sleeping in the parents’ bed), and overheating. In many cases, the risk factors are modifiable; sleeping in the prone position is the most meaningful modifiable risk factor.

Home monitors have not been proven to reduce the incidence of SIDS and are not recommended for that purpose.

To minimize the risk for SIDS, parents should be educated on the risk factors—prenatally as well as at each infant well visit. Home monitors have not been proven to reduce the incidence of SIDS and are not recommended for that purpose.^54-57 Although evidence is strongest for supine positioning as a preventive intervention for SIDS, other evidence-based recommendations include use of a firm sleep surface; breastfeeding; use of a pacifier; room-sharing with parents without bed-sharing; routine immunization; avoidance of overheating; avoiding falling asleep with the infant on a chair or couch; and avoiding exposure to tobacco smoke, alcohol, and drugs of abuse.^55,56 A recent systematic review showed that large-scale community interventions and education campaigns can play a significant role in parental and community adoption of safe sleep recommendations; however, families and communities rarely exhibit complete adherence to safe sleep practices.⁵⁷

Other concerns in the first month of life and immediately beyond

In TABLE 5,² we list additional common newborn problems not reviewed in the text of this article and summarize evidence-based treatment strategies.

CORRESPONDENCE
Scott Hartman, MD, Associate Professor, Department of Family Medicine, University of Rochester Medical Center, 777 South Clinton Avenue, Rochester, NY 14620; [email protected].

Acknowledgement
We thank Nancy Phillips for her assistance in the preparation of this article.

Caring for a newborn can be a source of joy for family physicians (FPs). In this article, we examine care provided in the first month of life, including a thorough physical examination, safe hospital discharge procedures, assessment of neonatal feeding, evaluation of jaundice and fever, and prevention of sudden infant death syndrome (SIDS). In addition, we describe how FPs can support women of childbearing age between pregnancies, with the goal of reducing the risk of adverse outcomes in future pregnancies. (See “Your role in risk assessment and interventions during the interconception period.”)

 

 

Ensuring a thorough exam, making use of a discharge checklist

Before parents leave the hospital with their newborn, it is essential that they receive written and verbal counseling on important issues in neonatal care. A discharge checklist can help make sure all topics have been covered.¹ A hearing screen and pulse oximetry before discharge are required for all newborns in most states, in addition to important preventive counseling for parents. TABLE 1² and TABLE 2² summarize important newborn physical exam findings and common skin conditions. Parents should be given additional written information regarding prevention of SIDS and proper use of car seats.

Hospital physicians should assess maternal medical and psychosocial readiness for discharge. Through shared decision-making with the newborn’s parents, physicians should create a plan for outpatient follow-up. Assessment through a physician home visit can provide safe and effective care similar to what is provided at a visit to an office medical practice.^3-7 A follow-up appointment should be made 2 to 5 days before discharge, preferably connecting the newborn to a medical home where comprehensive health care services are offered.^1,5,6,8

Age, gestational age, risk factors for hyperbilirubinemia, and the timing and level of bilirubin testing should be considered when establishing a follow-up interval. Most newborns who are discharged before 72 hours of age should have a follow-up visit in 2 days; a newborn who has a recognized risk factor for a health problem should be seen sooner. Newborns in the “low-risk zone” (ie, no recognized risk factors) should be seen based on age at discharge or need for breastfeeding support.⁹

Tracking baby’s weight, ensuring proper feeding

A newborn who is discharged at 24 hours of life, or sooner, should be seen in the office within 2 days of discharge to 1) ensure that he (she) is getting proper nutrition and 2) monitor his weight^1,3,5 (TABLE 3^10-13). All newborns should be seen again at 2 weeks of life, with additional visits more frequently if there are concerns about nutrition.¹

Recording an accurate weight is critical; the newborn should be weighed completely undressed and without a diaper. Healthy newborns can safely lose up to 10% of birth weight within the first week of life; they should be back to their birth weight by approximately 2 weeks of life.^10,11 A healthy newborn loses approximately 0.5 to 1 oz a day;¹¹ greater than 10% loss of birth weight should trigger a thorough medical work-up and feeding assessment.

Breastfeeding. For breastfeeding mothers, physicians should recommend on-demand feeding or a feeding at least every 2 or 3 hours. Adequate intake in breastfed infants can be intimidating for new parents to monitor, but they can use a written chart or any of several available smartphone applications to document length and timing of feeds and frequency of urination and bowel movements. By the fifth day of life, a newborn should be having at least 6 voids and 3 or 4 stools a day.^10-12

In addition, physicians can counsel parents on what to look for—in the mother and the newborn—to confirm that breastfeeding is successful, with adequate nutritional intake (TABLE 3^10-13). Physicians should recommend against providing a pacifier to breastfeeding infants during the first several weeks of life—or until breastfeeding is well established (usually at 3 or 4 weeks of age). The World Health Organization (WHO) recommends against providing bottles, pacifiers, and artificial nipples to breastfeeding newborns.¹⁴ Liquids other than colostrum or breast milk should not be given unless there is a documented medical need, such as inadequate weight gain or feeding difficulty.¹⁵ If the newborn experiences early latch difficulties, supplementation with expressed breast milk is preferable to supplementation with formula. Assistance from a trained lactation consultant is a key element in the support of the breastfeeding dyad.^11,12,16

Breastfeeding optimizes development of the newborn’s immune system, thus bolstering disease prevention; it also assists with maternal postpartum weight loss and psychological well-being. Exclusively or primarily formula-fed newborns are at increased risk of gastrointestinal, ear, and respiratory infections throughout infancy and childhood; type 1 diabetes mellitus; asthma; childhood and adult obesity; and leukemia.^17,18 Mothers who feed their newborn primarily formula increase their own risk of obesity, type 2 diabetes mellitus, ovarian and breast cancer, and depression.^17-22

Infant feeding is a personal and family choice but, in the absence of medical contraindications—such as maternal human immunodeficiency virus infection and galactosemia—exclusive breastfeeding should be recommended.^17,18 FPs are well suited to support the mother–infant breastfeeding dyad in the neonatal period, based on expert recommendations. Specifically, the American Academy of Family Physicians (AAFP) and American Academy of Pediatrics (AAP) recommend that all infants be exclusively breastfed for the first 6 months of life and continue some breastfeeding through the first year or longer.^17,18 WHO recommends breastfeeding until 24 months of age—longer if mother and infant want to, unless breastfeeding is contraindicated.^14,17,18

Physicians should provide up-to-date information to parents regarding the risks and benefits of feeding choices. Support for breastfeeding mothers postnatally has been shown to be helpful in lengthening the time of exclusive breastfeeding.¹² Certain medications pass through breast milk, and updated guides to medication cautions can be found at the National Institutes of Health’s LACTMED Web site (https://toxnet.nlm.nih.gov/newtoxnet/lactmed.htm).¹³ In many cases, when a maternal medication is incompatible with breastfeeding, the family physician can consider substituting another appropriate medication that is compatible.

Physician recommendation and support improves the rate of breastfeeding, but many mother–infant dyads require additional support to maintain breastfeeding for the recommended duration; such support can take the form of a certified lactation consultant or counselor, doula, or peer counselor.^23-25 Although structured breastfeeding education in the antenatal period has been demonstrated to be effective in improving breastfeeding initiation and duration, recent research shows that support groups and assistance from the professionals previously mentioned also improve the breastfeeding rate.^26-28

Adequate intake in breastfed infants can be intimidating for new parents to monitor, but they can use a written chart or any of several available smartphone applications.

The AAFP recommends that FPs’ offices adopt specific, evidence-based practices that can have an impact on breastfeeding initiation and duration. Such practices include phone and in-person breastfeeding support from nursing staff and removing any formula advertisements from the office.¹⁷

Formula feeding. When parents choose formula feeding, most infants tolerate cow’s milk-based formula.²⁹ For healthy term infants, differences between brands of formula are generally insignificant. Soy-protein formulas are of value only if lactose intolerance is strongly suspected, such as after prolonged episodes of loose stools. Even then, intolerance is usually transient and cow’s milk-based formula can be tried again in 2 to 4 weeks.

Physicians should recommend 20 kcal/oz of iron-fortified formula for infants who are fed formula—except in special circumstances, such as premature newborns, who may require a more calorie-dense formula. Parents should pay special attention to the manufacturer’s instructions for mixing formula with water because overdilution can cause hyponatremia. Typical volume for newborns should be at least 15 to 30 mL/feed for the first few days; newborns should not go more than 4 hours between feedings. Within the first week, newborns will start taking 60 to 90 mL/feed and increase that gradually to approximately 120 mL/feed by the end of the first month of life. On average, infants need a little more than 100 kcal/kg of body weight a day; for a 3.5-kg infant, that is at least 500 mL of formula over the course of a day.^17,22

Because formula does not contain fluoride, physicians should recommend that parents mix formula that is provided as a powder with fluoridated water. Low-iron formula offers no advantage; feeding with it will cause iron-deficiency anemia in most infants.

When tongue-tie interferes with feeding

Tongue-tie—or ankyloglossia, an atypically short or thick lingual frenulum—is present in 3% to 16% of all births. The condition can make breastfeeding difficult; result in poor neonatal weight gain; and cause sore nipples in 25% to 44% of cases.³⁰ Once tongue-tie is noted, the physician should talk to the mother about the history of feeding success, including whether her nipples are sore and whether the newborn is having difficulty feeding (ie, transferring milk). The Hazelbaker Assessment Tool for Lingual Frenulum Function and the simpler Bristol Tongue Assessment Tool can be used to assess the severity of tongue-tie.^30-35

When tongue-tie interferes with feeding, a physician who is not trained in treatment can refer the mother and infant to a specialist in the community. Frenotomy has been used for many years as a treatment for tongue-tie; improvement in nipple pain and the mother-reported breastfeeding score have been reported postoperatively in several studies.^30-33

Ensure proper vitamin D intake through supplementation

Newborns should consume 400 IU/d of supplemental vitamin D to prevent deficiency and its clinical manifestation, rickets, or other associated abnormalities of calcium metabolism. Deficiency of vitamin D has also been linked to a number of other conditions, including developmental delay and, possibly, type 1 diabetes mellitus in childhood and cardiovascular disease later in life.³⁶

Newborns should consume 400 IU/d of supplemental vitamin D to prevent deficiency and its clinical manifestation, rickets, or other associated abnormalities of calcium metabolism.

In the first months of life, few infants who are solely formula-fed will consume a full liter daily; for them, supplementation of vitamin D for at least one month should be prescribed.³⁵ For breastfed infants, high-dosage maternal vitamin D supplementation may be effective, precluding infant oral vitamin D supplementation³⁶; however, neither the AAFP nor the AAP has issued guidance promoting maternal supplementation in lieu of direct oral infant supplementation.³⁷

Jaundice prevention—and recognition

An elevated bilirubin level is seen in most newborns in the first days of life because of increased production and decreased clearance of bilirubin—a condition known as physiologic jaundice. Conditions that aggravate physiologic hyperbilirubinemia include inborn errors of metabolism, ABO blood-group incompatibility, hemoglobin variants, and inflammatory states such as sepsis. It is important to distinguish physiologic jaundice from exaggerated physiologic and pathologic forms of hyperbilirubinemia; the latter is a medical emergency. Before we get to that, a word about prevention.

Prevention. Because poor caloric intake and dehydration are associated with hyperbilirubinemia, physicians should advise breastfeeding mothers to feed their newborn at least 8 to 12 times daily during the first week of life. However, routine supplementation of liquids other than breast milk should be discouraged in newborns who are not dehydrated.³⁸

The total serum bilirubin level should be tested in every newborn who has clinical jaundice in the first 24 hours of life.

All pregnant women should be tested for ABO and Rh (D) blood types and undergo serum screening for isoimmune antibodies. Randomized trials have demonstrated that the incidence of significant hyperbilirubinemia can be reduced if, for Rh-negative mothers and those who did not undergo prenatal blood-group testing, infant cord blood is tested for 1) ABO and Rh (D) types and 2) direct antibody (Coombs’ test).^38,39

Screening and assessment. It is recommended that all newborns be screened for jaundice before discharge by 1) assessment of clinical risk factors or 2) testing of transcutaneous bilirubin (TcB) or total serum bilirubin (TSB). Furthermore, because evidence shows that treating clinical jaundice can improve outcomes and rehospitalization, TSB should be measured in every newborn who has clinical jaundice in the first 24 hours of life. Measurement of TcB or TSB should also be performed on all infants in whom there appears to be clinical jaundice that is excessive for age.^38,39

During routine clinical care, TcB measurement provides a reasonable estimate of the TSB level in healthy newborns at levels less than 15 mg/dL,⁴⁰ although TcB testing might not be available in the outpatient office. An AAP management algorithm can help determine when a newborn should be seen for outpatient follow-up based on risk of hyperbilirubinemia; higher-risk newborns should be reevaluated in 24 hours.⁹ Outpatient visual assessment of jaundice for cephalocaudal progression—in a well-lit room, with a fully undressed newborn—correlates well with TSB test results. However, visual assessment should not be used alone to screen for hyperbilirubinemia; recent studies have demonstrated that such assessment lacks clinical reliability.⁴⁰

Laboratory assessment. All bilirubin levels should be interpreted based on the newborn’s age in hours. The need for phototherapy should be based on the zone (low, low-intermediate, high-intermediate, or high, as categorized in the AAP nomogram³⁸ in which the TSB level falls. TABLE 4^38-40 provides recommendations for laboratory studies based on risk factors. Standard curves for risk stratification have been developed by the AAP.^37,38

Treatment. Decisions to initiate treatment should be based on the AAP algorithm.³⁸ When initiating phototherapy, precautions include ensuring adequate fluid intake, patching eyes, and monitoring temperature. Phototherapy can generally be stopped when the TSB level falls by 5 mg/dL or below 14 mg/dL. Home phototherapy, using a fiberoptic blanket, for uncomplicated jaundice (in carefully selected newborns with reliable parents) allows continued breastfeeding and bonding with the family, and can significantly decrease the rate of rehospitalization for infants older than 34 weeks.⁴¹

Breastfeeding is often associated with a higher bilirubin level than is seen in infants fed formula exclusively; increasing the frequency of feeding usually reduces the bilirubin level. So-called breast-milk jaundice is a delayed, but common, form of jaundice that is usually diagnosed in the second week of life and peaks by the end of the second week, resolving gradually over one to 4 months. If evaluation reveals no pathologic source, breastfeeding can generally be continued. Temporary discontinuation of breastfeeding to consider a diagnosis of breast-milk jaundice or other reasons for an elevated bilirubin level increases the risk of breastfeeding failure and is usually unnecessary.^12,37,39

Fever—a full work-up, thorough history are key

Concern about serious bacterial illness (SBI) makes the evaluation of fever critical for those who care for newborns. Many studies have attempted to identify which newborns might be able to be cared for safely as outpatients to prevent unnecessary testing and antibiotics.^5,42 Regrettably, SBI in infants remains difficult to predict, and protocols that have been developed may miss as many as 1 of every 10 newborns who has SBI.⁴³ Initial management of all infants 28 days old or younger with fever must therefore include a full work-up, including lumbar puncture and empiric antibiotics.⁴⁴

Evaluation. When an infant younger than 28 days has a fever, the physician should first verify that the temperature was taken rectally and how it was documented. In an infant who has a history of prematurity, it is crucial to correct for chronological age when deciding on proper evaluation.

Additional important findings in the history include a significant change in behavior, associated symptoms, and exposure to sick contacts. The maternal and birth history, including prolonged rupture of membranes, colonization with group B Streptococcus, administration of antibiotics at delivery, and genital herpes simplex virus (HSV) infection may suggest a cause for fever.⁴⁵

The evaluation of fever might include the white blood cell (WBC) count, blood culture, measurement of markers of inflammation, urine studies, lumbar puncture, stool culture, and chest radiograph. Traditionally, the WBC count has been utilized as a standard marker for sepsis, although it has a low sensitivity and specificity for SBI, especially in newborns.⁴⁶ Blood cultures should be obtained routinely in the newborn with fever, and before antibiotics are administered in older infants.

Procalcitonin (PCT; a calcitonin precursor) and the inflammatory marker C-reactive protein (CRP) have been shown, in several large studies, to have relatively high sensitivity and specificity for SBI; measurement of these constituents may enhance detection of serious illness.^46-49 In a large study of 2047 febrile infants older than 30 months, the PCT level was determined to be more accurate than the CRP level, the WBC count, and the absolute neutrophil count in predicting SBI.^48,49 PCT shows the most promise for preventing a full fever work-up and empiric antibiotics. It has not yet been widely translated into practice, however, because of a lack of clear guidance on how to combine PCT levels with other laboratory markers and clinical decision-making.^48-50

Urinalysis (UA) should be obtained for all newborns who present with fever. Traditionally, it was recommended that urine should be cultured for all newborns with fever; however, more recent data show that the initial urinalysis is much more sensitive than once thought. In a study, UA was positive (defined as pyuria or a positive leukocyte esterase test, or both) in all but 1 of 203 infants who had bacteremic UTI (sensitivity, 99.5%).⁵¹

The procalcitonin level was determined to be more accurate than the C-reactive protein level, the white blood cell count, and the absolute neutrophil count in predicting serious bacterial illness.

Stool culture is necessary in newborns only when they present with blood or mucus in diarrhea. Lumbar puncture should be performed in all febrile newborns and all newborns for whom empiric antibiotics have been prescribed.^43,44 A chest radiograph may be useful in diagnosis when a newborn has any other sign of pulmonary disease: respiratory rate >50/min, retractions, wheezing, grunting, stridor, nasal flaring, cough, and positive findings on lung examination.^43,44

Treatment. Management for all newborns who have a rectal temperature ≥38° C includes admission to the hospital and empiric antibiotics; guidance is based primarily on expert consensus. Common pathogens for SBI include group B Strep, Escherichia coli, Enterococcus spp., and Listeria monocytogenes.^43,44 Empiric antibiotics, including ampicillin (to cover L monocytogenes) and cefotaxime or gentamicin should be started immediately after sending for blood, urine, and cerebrospinal fluid (CSF) cultures.^43-45

Management for all newborns who have rectal temperature ≥38° C includes admission to the hospital and empiric antibiotics.

All infants who are ill-appearing or have vesicles, seizures, or a maternal history of genital HSV infection should also be started on empiric acyclovir. Vesicles should be cultured and CSF should be sent for HSV DNA polymerase chain reaction before acyclovir is administered.^43-45

Sudden infant death syndrome: Steps to take to minimize risk

SIDS is defined as the sudden death of a child younger than 1 year that remains unexplained after a thorough case investigation and comprehensive review of the clinical history. The risk of SIDS in the United States is less than 1 for every 1000 live births; incidence peaks between 2 and 4 months of age.⁵² In the United States, SIDS and other sleep-related infant deaths, such as strangulation in bed or accidental suffocation, account for more than 4000 deaths a year.⁵³ The incidence of SIDS declined markedly after the “Back to Sleep” campaign was launched in 2003, but has leveled off since 2005.^53-55

Numerous risk factors for SIDS have been identified, including maternal factors (young maternal age, maternal smoking during pregnancy, late or no prenatal care) and infant and environmental factors (prematurity, low birth weight, male gender, prone sleeping position, sleeping on a soft surface or with bedding accessories, bed-sharing (ie, sleeping in the parents’ bed), and overheating. In many cases, the risk factors are modifiable; sleeping in the prone position is the most meaningful modifiable risk factor.

Home monitors have not been proven to reduce the incidence of SIDS and are not recommended for that purpose.

To minimize the risk for SIDS, parents should be educated on the risk factors—prenatally as well as at each infant well visit. Home monitors have not been proven to reduce the incidence of SIDS and are not recommended for that purpose.^54-57 Although evidence is strongest for supine positioning as a preventive intervention for SIDS, other evidence-based recommendations include use of a firm sleep surface; breastfeeding; use of a pacifier; room-sharing with parents without bed-sharing; routine immunization; avoidance of overheating; avoiding falling asleep with the infant on a chair or couch; and avoiding exposure to tobacco smoke, alcohol, and drugs of abuse.^55,56 A recent systematic review showed that large-scale community interventions and education campaigns can play a significant role in parental and community adoption of safe sleep recommendations; however, families and communities rarely exhibit complete adherence to safe sleep practices.⁵⁷

Other concerns in the first month of life and immediately beyond

In TABLE 5,² we list additional common newborn problems not reviewed in the text of this article and summarize evidence-based treatment strategies.

CORRESPONDENCE
Scott Hartman, MD, Associate Professor, Department of Family Medicine, University of Rochester Medical Center, 777 South Clinton Avenue, Rochester, NY 14620; [email protected].

Acknowledgement
We thank Nancy Phillips for her assistance in the preparation of this article.

THE CASE

A 67-year-old woman presented to our orthopaedic clinic with a 2-year history of bilateral thigh and knee pain and weakness of her legs. She had no history of trauma, and the pain, which was localized to the distal anterior thighs and patellofemoral area, was 7/10 at rest and worse with standing and walking.

Her medical history was significant for osteoporosis (diagnosed in 2004), hypertension, hypothyroidism, gastroesophageal reflux disease, and menopause (age 54). Her original dual-energy x-ray absorptiometry (DEXA) scan did not reveal the presence of any previous fractures. She was started on calcium and vitamin D supplementation and oral alendronate (70 mg once a week). She took alendronate for 4 years until 2008, when it was stopped due to nausea. She was then started on zoledronic acid (5 mg IV annually). She received 5 infusions of zoledronic acid between 2008 and 2013; she did not have an infusion in 2012. Her medication list also included lisinopril, omeprazole, naproxen, cyclobenzaprine, and a multivitamin. She had normal renal function (estimated glomerular filtration rate >60 mL/min/1.73 m²) and she did not drink alcohol or use tobacco.

In the 2 years prior to her visit to our clinic, she had been evaluated by her primary care provider, an orthopedic sports medicine specialist, 2 spinal surgeons, and a physiatrist. She had also undergone 30 physical therapy sessions. Bilateral femur radiographs (FIGURE 1) ordered by her orthopedist 6 months earlier demonstrated no evidence of fracture, but did show an incidental enchondroma in the right distal diaphysis and bilateral thickening of the lateral femoral cortices.

Finally, with no relief in sight, her obstetrician suggested that she might be experiencing myalgias attributable to her zoledronic acid infusions. She was subsequently referred to us.

The physical exam revealed a thin female with a body mass index of 21. She had mild tenderness on palpation of the bilateral anterior thighs and knees. There was no pain with hip or knee range of motion and minimal pain in the bilateral lower extremities with axial loading. The patient had normal sensation, did not have an antalgic gait, and exhibited 5/5 strength bilaterally in all distributions of the lower extremities.

THE DIAGNOSIS

Due to continued pain despite negative x-rays, we obtained a 3-phase bone scan of the pelvis and bilateral femurs. Delayed images showed moderately increased activity in the mid-right and mid-left lateral femoral diaphyses at the cortex and confirmed stress fractures (FIGURE 2).

DISCUSSION

Bisphosphonates are considered first-line therapy for osteoporosis, according to current evidence-based guidelines.¹ These medications inhibit osteoclast activity and can bind to the bone for more than 10 years.^2,3 (In women with bone mineral density scores ≤ –2.5, the number needed to treat is 21.^1,4)

If radiographs are negative, but suspicion remains, an MRI or a bone scan should be ordered.

Patients taking bisphosphonates, however, are susceptible to atypical femoral fractures (AFFs), which are stress or insufficiency fractures associated with minimal or no trauma.⁵ The pathophysiology remains unknown at this time, but AFFs may result from changes in bone remodeling that occur when a bone experiences repetitive microtrauma, leading to lateral cortical thickening of the femur.^6,7 Incidence of AFFs in patients taking bisphosphonates is estimated to be between 3.2 and 50 cases per 100,000 person-years; however, this risk increases to approximately 100 per 100,000 person-years with long-term use.⁵ Other risk factors include low body weight, advancing age, rheumatoid arthritis, long-term glucocorticoid therapy, and excessive alcohol and cigarette use.⁸

 

 

What you’ll see

Symptoms typically include unilateral or bilateral prodromal pain with a sharp or achy character that is localized to the mid-thigh, upper thigh, or groin.⁹ If an AFF is suspected, we recommend performing a bilateral exam and obtaining radiographs.

If characteristic features are found (eg, signs of focal cortical thickening or beaking) and pain arises in the opposite limb, obtain a radiograph of the contralateral femur. If radiographs are negative but suspicion remains, order magnetic resonance imaging or a bone scan, to identify a cortical fracture line, bone and marrow edema, or hyperemia.⁵

Begin treatment by discontinuing bisphosphonates

Upon identification of an AFF, discontinue bisphosphonates and initiate calcium and vitamin D supplementation.⁵ Prophylactic surgical fixation may also be necessary to accelerate healing and prevent fracture propagation and further pain.

Our patient. Due to the longevity of the symptoms and the bilateral stress fractures noted on the bone scan, our patient chose to proceed with intramedullary nailing of the bilateral femurs (FIGURES 3 and 4). On postop Day 1, she was able to ambulate using a walker and to participate in bilateral weight-bearing (as tolerated). She was discharged to a skilled nursing facility, where she progressed to full weight-bearing without aid. On follow-up (one year postop), the patient reported no residual leg pain and was able to work out 5 days per week. Radiographs of her femurs demonstrated healed fractures and stable position of the intramedullary nails.

THE TAKEAWAY

An increased suspicion for AFFs due to bisphosphonate use can lead to earlier diagnosis and decreased morbidity for patients. Use of femoral imaging can promote detection and reduce financial burden.

To help prevent AFFs from occurring, we recommend reevaluating the need for continued bisphosphonate therapy after 2 to 5 years of treatment. Continued surveillance is also advisable throughout the duration of their use.

ACKNOWLEDGMENT
The authors wish to acknowledge Dr. Maurice Manring for his help in preparing this manuscript.

THE CASE

A 67-year-old woman presented to our orthopaedic clinic with a 2-year history of bilateral thigh and knee pain and weakness of her legs. She had no history of trauma, and the pain, which was localized to the distal anterior thighs and patellofemoral area, was 7/10 at rest and worse with standing and walking.

Her medical history was significant for osteoporosis (diagnosed in 2004), hypertension, hypothyroidism, gastroesophageal reflux disease, and menopause (age 54). Her original dual-energy x-ray absorptiometry (DEXA) scan did not reveal the presence of any previous fractures. She was started on calcium and vitamin D supplementation and oral alendronate (70 mg once a week). She took alendronate for 4 years until 2008, when it was stopped due to nausea. She was then started on zoledronic acid (5 mg IV annually). She received 5 infusions of zoledronic acid between 2008 and 2013; she did not have an infusion in 2012. Her medication list also included lisinopril, omeprazole, naproxen, cyclobenzaprine, and a multivitamin. She had normal renal function (estimated glomerular filtration rate >60 mL/min/1.73 m²) and she did not drink alcohol or use tobacco.

In the 2 years prior to her visit to our clinic, she had been evaluated by her primary care provider, an orthopedic sports medicine specialist, 2 spinal surgeons, and a physiatrist. She had also undergone 30 physical therapy sessions. Bilateral femur radiographs (FIGURE 1) ordered by her orthopedist 6 months earlier demonstrated no evidence of fracture, but did show an incidental enchondroma in the right distal diaphysis and bilateral thickening of the lateral femoral cortices.

Finally, with no relief in sight, her obstetrician suggested that she might be experiencing myalgias attributable to her zoledronic acid infusions. She was subsequently referred to us.

The physical exam revealed a thin female with a body mass index of 21. She had mild tenderness on palpation of the bilateral anterior thighs and knees. There was no pain with hip or knee range of motion and minimal pain in the bilateral lower extremities with axial loading. The patient had normal sensation, did not have an antalgic gait, and exhibited 5/5 strength bilaterally in all distributions of the lower extremities.

THE DIAGNOSIS

Due to continued pain despite negative x-rays, we obtained a 3-phase bone scan of the pelvis and bilateral femurs. Delayed images showed moderately increased activity in the mid-right and mid-left lateral femoral diaphyses at the cortex and confirmed stress fractures (FIGURE 2).

DISCUSSION

Bisphosphonates are considered first-line therapy for osteoporosis, according to current evidence-based guidelines.¹ These medications inhibit osteoclast activity and can bind to the bone for more than 10 years.^2,3 (In women with bone mineral density scores ≤ –2.5, the number needed to treat is 21.^1,4)

If radiographs are negative, but suspicion remains, an MRI or a bone scan should be ordered.

Patients taking bisphosphonates, however, are susceptible to atypical femoral fractures (AFFs), which are stress or insufficiency fractures associated with minimal or no trauma.⁵ The pathophysiology remains unknown at this time, but AFFs may result from changes in bone remodeling that occur when a bone experiences repetitive microtrauma, leading to lateral cortical thickening of the femur.^6,7 Incidence of AFFs in patients taking bisphosphonates is estimated to be between 3.2 and 50 cases per 100,000 person-years; however, this risk increases to approximately 100 per 100,000 person-years with long-term use.⁵ Other risk factors include low body weight, advancing age, rheumatoid arthritis, long-term glucocorticoid therapy, and excessive alcohol and cigarette use.⁸

 

 

What you’ll see

Symptoms typically include unilateral or bilateral prodromal pain with a sharp or achy character that is localized to the mid-thigh, upper thigh, or groin.⁹ If an AFF is suspected, we recommend performing a bilateral exam and obtaining radiographs.

If characteristic features are found (eg, signs of focal cortical thickening or beaking) and pain arises in the opposite limb, obtain a radiograph of the contralateral femur. If radiographs are negative but suspicion remains, order magnetic resonance imaging or a bone scan, to identify a cortical fracture line, bone and marrow edema, or hyperemia.⁵

Begin treatment by discontinuing bisphosphonates

Upon identification of an AFF, discontinue bisphosphonates and initiate calcium and vitamin D supplementation.⁵ Prophylactic surgical fixation may also be necessary to accelerate healing and prevent fracture propagation and further pain.

Our patient. Due to the longevity of the symptoms and the bilateral stress fractures noted on the bone scan, our patient chose to proceed with intramedullary nailing of the bilateral femurs (FIGURES 3 and 4). On postop Day 1, she was able to ambulate using a walker and to participate in bilateral weight-bearing (as tolerated). She was discharged to a skilled nursing facility, where she progressed to full weight-bearing without aid. On follow-up (one year postop), the patient reported no residual leg pain and was able to work out 5 days per week. Radiographs of her femurs demonstrated healed fractures and stable position of the intramedullary nails.

THE TAKEAWAY

An increased suspicion for AFFs due to bisphosphonate use can lead to earlier diagnosis and decreased morbidity for patients. Use of femoral imaging can promote detection and reduce financial burden.

To help prevent AFFs from occurring, we recommend reevaluating the need for continued bisphosphonate therapy after 2 to 5 years of treatment. Continued surveillance is also advisable throughout the duration of their use.

ACKNOWLEDGMENT
The authors wish to acknowledge Dr. Maurice Manring for his help in preparing this manuscript.

THE CASE

A 67-year-old woman presented to our orthopaedic clinic with a 2-year history of bilateral thigh and knee pain and weakness of her legs. She had no history of trauma, and the pain, which was localized to the distal anterior thighs and patellofemoral area, was 7/10 at rest and worse with standing and walking.

Her medical history was significant for osteoporosis (diagnosed in 2004), hypertension, hypothyroidism, gastroesophageal reflux disease, and menopause (age 54). Her original dual-energy x-ray absorptiometry (DEXA) scan did not reveal the presence of any previous fractures. She was started on calcium and vitamin D supplementation and oral alendronate (70 mg once a week). She took alendronate for 4 years until 2008, when it was stopped due to nausea. She was then started on zoledronic acid (5 mg IV annually). She received 5 infusions of zoledronic acid between 2008 and 2013; she did not have an infusion in 2012. Her medication list also included lisinopril, omeprazole, naproxen, cyclobenzaprine, and a multivitamin. She had normal renal function (estimated glomerular filtration rate >60 mL/min/1.73 m²) and she did not drink alcohol or use tobacco.

In the 2 years prior to her visit to our clinic, she had been evaluated by her primary care provider, an orthopedic sports medicine specialist, 2 spinal surgeons, and a physiatrist. She had also undergone 30 physical therapy sessions. Bilateral femur radiographs (FIGURE 1) ordered by her orthopedist 6 months earlier demonstrated no evidence of fracture, but did show an incidental enchondroma in the right distal diaphysis and bilateral thickening of the lateral femoral cortices.

Finally, with no relief in sight, her obstetrician suggested that she might be experiencing myalgias attributable to her zoledronic acid infusions. She was subsequently referred to us.

The physical exam revealed a thin female with a body mass index of 21. She had mild tenderness on palpation of the bilateral anterior thighs and knees. There was no pain with hip or knee range of motion and minimal pain in the bilateral lower extremities with axial loading. The patient had normal sensation, did not have an antalgic gait, and exhibited 5/5 strength bilaterally in all distributions of the lower extremities.

THE DIAGNOSIS

Due to continued pain despite negative x-rays, we obtained a 3-phase bone scan of the pelvis and bilateral femurs. Delayed images showed moderately increased activity in the mid-right and mid-left lateral femoral diaphyses at the cortex and confirmed stress fractures (FIGURE 2).

DISCUSSION

Bisphosphonates are considered first-line therapy for osteoporosis, according to current evidence-based guidelines.¹ These medications inhibit osteoclast activity and can bind to the bone for more than 10 years.^2,3 (In women with bone mineral density scores ≤ –2.5, the number needed to treat is 21.^1,4)

If radiographs are negative, but suspicion remains, an MRI or a bone scan should be ordered.

Patients taking bisphosphonates, however, are susceptible to atypical femoral fractures (AFFs), which are stress or insufficiency fractures associated with minimal or no trauma.⁵ The pathophysiology remains unknown at this time, but AFFs may result from changes in bone remodeling that occur when a bone experiences repetitive microtrauma, leading to lateral cortical thickening of the femur.^6,7 Incidence of AFFs in patients taking bisphosphonates is estimated to be between 3.2 and 50 cases per 100,000 person-years; however, this risk increases to approximately 100 per 100,000 person-years with long-term use.⁵ Other risk factors include low body weight, advancing age, rheumatoid arthritis, long-term glucocorticoid therapy, and excessive alcohol and cigarette use.⁸

 

 

What you’ll see

Symptoms typically include unilateral or bilateral prodromal pain with a sharp or achy character that is localized to the mid-thigh, upper thigh, or groin.⁹ If an AFF is suspected, we recommend performing a bilateral exam and obtaining radiographs.

If characteristic features are found (eg, signs of focal cortical thickening or beaking) and pain arises in the opposite limb, obtain a radiograph of the contralateral femur. If radiographs are negative but suspicion remains, order magnetic resonance imaging or a bone scan, to identify a cortical fracture line, bone and marrow edema, or hyperemia.⁵

Begin treatment by discontinuing bisphosphonates

Upon identification of an AFF, discontinue bisphosphonates and initiate calcium and vitamin D supplementation.⁵ Prophylactic surgical fixation may also be necessary to accelerate healing and prevent fracture propagation and further pain.

Our patient. Due to the longevity of the symptoms and the bilateral stress fractures noted on the bone scan, our patient chose to proceed with intramedullary nailing of the bilateral femurs (FIGURES 3 and 4). On postop Day 1, she was able to ambulate using a walker and to participate in bilateral weight-bearing (as tolerated). She was discharged to a skilled nursing facility, where she progressed to full weight-bearing without aid. On follow-up (one year postop), the patient reported no residual leg pain and was able to work out 5 days per week. Radiographs of her femurs demonstrated healed fractures and stable position of the intramedullary nails.

THE TAKEAWAY

An increased suspicion for AFFs due to bisphosphonate use can lead to earlier diagnosis and decreased morbidity for patients. Use of femoral imaging can promote detection and reduce financial burden.

To help prevent AFFs from occurring, we recommend reevaluating the need for continued bisphosphonate therapy after 2 to 5 years of treatment. Continued surveillance is also advisable throughout the duration of their use.

ACKNOWLEDGMENT
The authors wish to acknowledge Dr. Maurice Manring for his help in preparing this manuscript.

EVIDENCE SUMMARY

The POLST form offers choices within 4 treatment areas: “attempt CPR” or “allow natural death” if the patient is in cardiopulmonary arrest; “comfort,” “limited,” or “full” medical interventions if pulse or breathing is present; choices of additional orders, including intravenous fluids, feeding tubes, and antibiotics; and additional written orders. Most POLST studies used cross-sectional and retrospective cohort designs and assessed whether CPR was attempted. Fewer studies also evaluated adherence to orders in the other treatment areas.

Community settings: Patients with POLST more likely to die out of hospital

The largest study of POLST use in community settings evaluated deaths in Oregon over one year.¹ It found that patients who indicated “do not attempt CPR” on a POLST form were 6 times more likely to die a natural, out-of-hospital death than those who had no POLST form (TABLE^1-10).

A West Virginia study found that patients with POLST forms had 30% higher out-of-hospital death rates than those with traditional advanced directives and no POLST.² In a Wisconsin study, no decedents who indicated DNR on their POLST forms received CPR.³

One study that evaluated the consistency of actual medical interventions with POLST orders in all 4 treatment areas found it to be good in most areas (“feeding tubes,” “attempting CPR.” “antibiotics,” and “IV fluids”) except “additional written orders.⁴

 

 

Skilled nursing facilities: Generally high adherence to POLST orders

The largest study to evaluate the consistency of treatments with POLST orders among nursing home residents found high adherence overall (94%).⁵ Caregivers performed CPR on none of 299 residents who selected “DNR.” However, they did not administer CPR to 6 of 7 who chose “attempt CPR” and administered antibiotics to 32% of patients who specified “no antibiotics” on their POLST forms.⁵

A second study of nursing home residents who selected “comfort measures only” also found high consistency for attempting CPR, intensive care admission, and ventilator support, although physicians hospitalized 2% of patients to extend life.⁶ Similarly, treatments matched POLST orders well overall in a Washington state study, although one patient got a feeding tube against orders.⁷

POLST adherence is good, but can EMS workers find the form?

A study comparing emergency medical services (EMS) management with POLST orders in an Oregon registry found good consistency.⁸ EMS providers didn’t attempt or halted CPR in most patients with DNR orders who were found in cardiac arrest and initiated CPR in most patients who chose “attempt CPR.” EMS providers initiated CPR in the field on 11 patients (22%) with a DNR order but discontinued resuscitation en route to the hospital.

In a smaller study, EMS providers never located paper POLST forms at the scene in most cases.⁹

Hospice: POLST orders prevent unwanted Tx, except maybe antibiotics

A study evaluating management in hospice programs in 3 states found that care providers followed POLST orders for limited treatment in 98% of cases.¹⁰ No patients received unwanted CPR, intubation, or feeding tubes. POLST orders didn’t predict whether patients were treated with antibiotics, however.

EVIDENCE SUMMARY

The POLST form offers choices within 4 treatment areas: “attempt CPR” or “allow natural death” if the patient is in cardiopulmonary arrest; “comfort,” “limited,” or “full” medical interventions if pulse or breathing is present; choices of additional orders, including intravenous fluids, feeding tubes, and antibiotics; and additional written orders. Most POLST studies used cross-sectional and retrospective cohort designs and assessed whether CPR was attempted. Fewer studies also evaluated adherence to orders in the other treatment areas.

Community settings: Patients with POLST more likely to die out of hospital

The largest study of POLST use in community settings evaluated deaths in Oregon over one year.¹ It found that patients who indicated “do not attempt CPR” on a POLST form were 6 times more likely to die a natural, out-of-hospital death than those who had no POLST form (TABLE^1-10).

A West Virginia study found that patients with POLST forms had 30% higher out-of-hospital death rates than those with traditional advanced directives and no POLST.² In a Wisconsin study, no decedents who indicated DNR on their POLST forms received CPR.³

One study that evaluated the consistency of actual medical interventions with POLST orders in all 4 treatment areas found it to be good in most areas (“feeding tubes,” “attempting CPR.” “antibiotics,” and “IV fluids”) except “additional written orders.⁴

 

 

Skilled nursing facilities: Generally high adherence to POLST orders

The largest study to evaluate the consistency of treatments with POLST orders among nursing home residents found high adherence overall (94%).⁵ Caregivers performed CPR on none of 299 residents who selected “DNR.” However, they did not administer CPR to 6 of 7 who chose “attempt CPR” and administered antibiotics to 32% of patients who specified “no antibiotics” on their POLST forms.⁵

A second study of nursing home residents who selected “comfort measures only” also found high consistency for attempting CPR, intensive care admission, and ventilator support, although physicians hospitalized 2% of patients to extend life.⁶ Similarly, treatments matched POLST orders well overall in a Washington state study, although one patient got a feeding tube against orders.⁷

POLST adherence is good, but can EMS workers find the form?

A study comparing emergency medical services (EMS) management with POLST orders in an Oregon registry found good consistency.⁸ EMS providers didn’t attempt or halted CPR in most patients with DNR orders who were found in cardiac arrest and initiated CPR in most patients who chose “attempt CPR.” EMS providers initiated CPR in the field on 11 patients (22%) with a DNR order but discontinued resuscitation en route to the hospital.

In a smaller study, EMS providers never located paper POLST forms at the scene in most cases.⁹

Hospice: POLST orders prevent unwanted Tx, except maybe antibiotics

A study evaluating management in hospice programs in 3 states found that care providers followed POLST orders for limited treatment in 98% of cases.¹⁰ No patients received unwanted CPR, intubation, or feeding tubes. POLST orders didn’t predict whether patients were treated with antibiotics, however.

EVIDENCE SUMMARY

The POLST form offers choices within 4 treatment areas: “attempt CPR” or “allow natural death” if the patient is in cardiopulmonary arrest; “comfort,” “limited,” or “full” medical interventions if pulse or breathing is present; choices of additional orders, including intravenous fluids, feeding tubes, and antibiotics; and additional written orders. Most POLST studies used cross-sectional and retrospective cohort designs and assessed whether CPR was attempted. Fewer studies also evaluated adherence to orders in the other treatment areas.

Community settings: Patients with POLST more likely to die out of hospital

The largest study of POLST use in community settings evaluated deaths in Oregon over one year.¹ It found that patients who indicated “do not attempt CPR” on a POLST form were 6 times more likely to die a natural, out-of-hospital death than those who had no POLST form (TABLE^1-10).

A West Virginia study found that patients with POLST forms had 30% higher out-of-hospital death rates than those with traditional advanced directives and no POLST.² In a Wisconsin study, no decedents who indicated DNR on their POLST forms received CPR.³

One study that evaluated the consistency of actual medical interventions with POLST orders in all 4 treatment areas found it to be good in most areas (“feeding tubes,” “attempting CPR.” “antibiotics,” and “IV fluids”) except “additional written orders.⁴

 

 

Skilled nursing facilities: Generally high adherence to POLST orders

The largest study to evaluate the consistency of treatments with POLST orders among nursing home residents found high adherence overall (94%).⁵ Caregivers performed CPR on none of 299 residents who selected “DNR.” However, they did not administer CPR to 6 of 7 who chose “attempt CPR” and administered antibiotics to 32% of patients who specified “no antibiotics” on their POLST forms.⁵

A second study of nursing home residents who selected “comfort measures only” also found high consistency for attempting CPR, intensive care admission, and ventilator support, although physicians hospitalized 2% of patients to extend life.⁶ Similarly, treatments matched POLST orders well overall in a Washington state study, although one patient got a feeding tube against orders.⁷

POLST adherence is good, but can EMS workers find the form?

A study comparing emergency medical services (EMS) management with POLST orders in an Oregon registry found good consistency.⁸ EMS providers didn’t attempt or halted CPR in most patients with DNR orders who were found in cardiac arrest and initiated CPR in most patients who chose “attempt CPR.” EMS providers initiated CPR in the field on 11 patients (22%) with a DNR order but discontinued resuscitation en route to the hospital.

In a smaller study, EMS providers never located paper POLST forms at the scene in most cases.⁹

Hospice: POLST orders prevent unwanted Tx, except maybe antibiotics

A study evaluating management in hospice programs in 3 states found that care providers followed POLST orders for limited treatment in 98% of cases.¹⁰ No patients received unwanted CPR, intubation, or feeding tubes. POLST orders didn’t predict whether patients were treated with antibiotics, however.

EVIDENCE SUMMARY

A 2013 systematic review of RCTs, systematic reviews, and meta-analyses examined the prophylactic use of low-dose aspirin for the primary prevention of cardiovascular disease (CVD) among adults 18 years and older.¹ Twenty-seven papers met inclusion criteria; the total number of patients wasn’t reported.

A composite finding of nonfatal MI, nonfatal stroke, and CVD death indicated a number needed to treat (NNT) of 138 over 10 years of therapy (relative risk [RR]=0.90; 95% confidence interval [CI], 0.85-0.96). CVD death wasn’t disaggregated from this composite, but an analysis of all-cause mortality didn’t reach statistical significance (RR=0.94; 95% CI, 0.88-1.00). RR for nonfatal stroke alone also wasn’t disaggregated.

Risk of gastrointestinal (GI) bleeding was found to be a number needed to harm (NNH) of 108 over 10 years (RR=1.37; 95% CI, 1.15-1.62) whereas risk of hemorrhagic stroke didn’t reach statistical significance (RR=1.32; 95% CI, 1.00-1.74). This population-level review didn’t report disaggregated findings by age or baseline atherosclerotic cardiovascular disease (ASCVD) risk.

Another review finds benefit only for prevention of nonfatal MI

A 2016 systematic review included 2 good-quality and 9 fair-quality RCTs evaluating the benefits of low-dose aspirin compared with placebo or no treatment for primary prevention of CVD events in 118,445 patients ages 40 years and older.² The review found benefit only for nonfatal MI, with an NNT of 126 over 10 years (RR=0.78; 95% CI, 0.71-0.87). There was no change in RR for nonfatal stroke (RR=0.95; 95% CI, 0.85-1.06); negligible impact on all-cause mortality (RR=0.95; 95% CI, 0.89-0.99); and no statistically significant benefit for CVD-specific mortality (RR=0.94; 95% CI, 0.86-1.03).

 

 

Aspirin carries risk of GI hemorrhage, but not hemorrhagic stroke

A companion 2016 systematic review of 16 RCTs, cohort studies, and meta-analyses evaluated the risk of serious bleeding in patients using low-dose aspirin for primary prevention of either CVD or cancer.³ The review (number of patients not reported) found that estimated excess bleeding events differed substantially depending on varying sources for baseline bleeding rates in aspirin nonusers.

The most conservative comparison yielded an NNH of 72 over 10 years of therapy (1.39 excess major GI bleeding events per 1000 person-years, 95% CI, 0.70-2.28). Comparison with other baseline bleeding rates in trial data yielded less risk of harm, with an NNH of 357 over 10 years (0.28 excess major GI bleeding events per 1000 person-years; 95% CI, 0.14-0.46). Excess risk for hemorrhagic stroke was not statistically significant (0.32 excess events per 1000 person-years; 95% CI, −0.05 to 0.82).

RECOMMENDATIONS

The US Preventive Services Task Force gives a Grade B recommendation (recommended, based on moderate to substantial benefit) to the use of aspirin to prevent CVD among adults ages 50 to 59 years with an ASCVD risk ≥10% who don’t have increased bleeding risk and are capable of 10 years of pharmacologic adherence with a similar expected longevity.⁴ The Task Force assigns a Grade C recommendation (individual and professional choice) to patients 60 to 69 years of age with the same constellation of risk factors and health status. Insufficient evidence was available to make recommendations for other age cohorts.

The American College of Chest Physicians recommends 75 to 100 mg of aspirin daily for adults 50 years or older who have moderate to high CV risk, defined as ≥10%.⁵

A working group of the European Society of Cardiology (ESC) released a statement in 2014 recommending aspirin for primary prevention in adults with a CV risk ≥20% and no risk factors for bleeding. For patients with a CVD risk between 10% and 20%, the ESC recommends deferring to patient preference.⁶

EVIDENCE SUMMARY

A 2013 systematic review of RCTs, systematic reviews, and meta-analyses examined the prophylactic use of low-dose aspirin for the primary prevention of cardiovascular disease (CVD) among adults 18 years and older.¹ Twenty-seven papers met inclusion criteria; the total number of patients wasn’t reported.

A composite finding of nonfatal MI, nonfatal stroke, and CVD death indicated a number needed to treat (NNT) of 138 over 10 years of therapy (relative risk [RR]=0.90; 95% confidence interval [CI], 0.85-0.96). CVD death wasn’t disaggregated from this composite, but an analysis of all-cause mortality didn’t reach statistical significance (RR=0.94; 95% CI, 0.88-1.00). RR for nonfatal stroke alone also wasn’t disaggregated.

Risk of gastrointestinal (GI) bleeding was found to be a number needed to harm (NNH) of 108 over 10 years (RR=1.37; 95% CI, 1.15-1.62) whereas risk of hemorrhagic stroke didn’t reach statistical significance (RR=1.32; 95% CI, 1.00-1.74). This population-level review didn’t report disaggregated findings by age or baseline atherosclerotic cardiovascular disease (ASCVD) risk.

Another review finds benefit only for prevention of nonfatal MI

A 2016 systematic review included 2 good-quality and 9 fair-quality RCTs evaluating the benefits of low-dose aspirin compared with placebo or no treatment for primary prevention of CVD events in 118,445 patients ages 40 years and older.² The review found benefit only for nonfatal MI, with an NNT of 126 over 10 years (RR=0.78; 95% CI, 0.71-0.87). There was no change in RR for nonfatal stroke (RR=0.95; 95% CI, 0.85-1.06); negligible impact on all-cause mortality (RR=0.95; 95% CI, 0.89-0.99); and no statistically significant benefit for CVD-specific mortality (RR=0.94; 95% CI, 0.86-1.03).

 

 

Aspirin carries risk of GI hemorrhage, but not hemorrhagic stroke

A companion 2016 systematic review of 16 RCTs, cohort studies, and meta-analyses evaluated the risk of serious bleeding in patients using low-dose aspirin for primary prevention of either CVD or cancer.³ The review (number of patients not reported) found that estimated excess bleeding events differed substantially depending on varying sources for baseline bleeding rates in aspirin nonusers.

The most conservative comparison yielded an NNH of 72 over 10 years of therapy (1.39 excess major GI bleeding events per 1000 person-years, 95% CI, 0.70-2.28). Comparison with other baseline bleeding rates in trial data yielded less risk of harm, with an NNH of 357 over 10 years (0.28 excess major GI bleeding events per 1000 person-years; 95% CI, 0.14-0.46). Excess risk for hemorrhagic stroke was not statistically significant (0.32 excess events per 1000 person-years; 95% CI, −0.05 to 0.82).

RECOMMENDATIONS

The US Preventive Services Task Force gives a Grade B recommendation (recommended, based on moderate to substantial benefit) to the use of aspirin to prevent CVD among adults ages 50 to 59 years with an ASCVD risk ≥10% who don’t have increased bleeding risk and are capable of 10 years of pharmacologic adherence with a similar expected longevity.⁴ The Task Force assigns a Grade C recommendation (individual and professional choice) to patients 60 to 69 years of age with the same constellation of risk factors and health status. Insufficient evidence was available to make recommendations for other age cohorts.

The American College of Chest Physicians recommends 75 to 100 mg of aspirin daily for adults 50 years or older who have moderate to high CV risk, defined as ≥10%.⁵

A working group of the European Society of Cardiology (ESC) released a statement in 2014 recommending aspirin for primary prevention in adults with a CV risk ≥20% and no risk factors for bleeding. For patients with a CVD risk between 10% and 20%, the ESC recommends deferring to patient preference.⁶

EVIDENCE SUMMARY

A 2013 systematic review of RCTs, systematic reviews, and meta-analyses examined the prophylactic use of low-dose aspirin for the primary prevention of cardiovascular disease (CVD) among adults 18 years and older.¹ Twenty-seven papers met inclusion criteria; the total number of patients wasn’t reported.

A composite finding of nonfatal MI, nonfatal stroke, and CVD death indicated a number needed to treat (NNT) of 138 over 10 years of therapy (relative risk [RR]=0.90; 95% confidence interval [CI], 0.85-0.96). CVD death wasn’t disaggregated from this composite, but an analysis of all-cause mortality didn’t reach statistical significance (RR=0.94; 95% CI, 0.88-1.00). RR for nonfatal stroke alone also wasn’t disaggregated.

Risk of gastrointestinal (GI) bleeding was found to be a number needed to harm (NNH) of 108 over 10 years (RR=1.37; 95% CI, 1.15-1.62) whereas risk of hemorrhagic stroke didn’t reach statistical significance (RR=1.32; 95% CI, 1.00-1.74). This population-level review didn’t report disaggregated findings by age or baseline atherosclerotic cardiovascular disease (ASCVD) risk.

Another review finds benefit only for prevention of nonfatal MI

A 2016 systematic review included 2 good-quality and 9 fair-quality RCTs evaluating the benefits of low-dose aspirin compared with placebo or no treatment for primary prevention of CVD events in 118,445 patients ages 40 years and older.² The review found benefit only for nonfatal MI, with an NNT of 126 over 10 years (RR=0.78; 95% CI, 0.71-0.87). There was no change in RR for nonfatal stroke (RR=0.95; 95% CI, 0.85-1.06); negligible impact on all-cause mortality (RR=0.95; 95% CI, 0.89-0.99); and no statistically significant benefit for CVD-specific mortality (RR=0.94; 95% CI, 0.86-1.03).

 

 

Aspirin carries risk of GI hemorrhage, but not hemorrhagic stroke

A companion 2016 systematic review of 16 RCTs, cohort studies, and meta-analyses evaluated the risk of serious bleeding in patients using low-dose aspirin for primary prevention of either CVD or cancer.³ The review (number of patients not reported) found that estimated excess bleeding events differed substantially depending on varying sources for baseline bleeding rates in aspirin nonusers.

The most conservative comparison yielded an NNH of 72 over 10 years of therapy (1.39 excess major GI bleeding events per 1000 person-years, 95% CI, 0.70-2.28). Comparison with other baseline bleeding rates in trial data yielded less risk of harm, with an NNH of 357 over 10 years (0.28 excess major GI bleeding events per 1000 person-years; 95% CI, 0.14-0.46). Excess risk for hemorrhagic stroke was not statistically significant (0.32 excess events per 1000 person-years; 95% CI, −0.05 to 0.82).

RECOMMENDATIONS

The US Preventive Services Task Force gives a Grade B recommendation (recommended, based on moderate to substantial benefit) to the use of aspirin to prevent CVD among adults ages 50 to 59 years with an ASCVD risk ≥10% who don’t have increased bleeding risk and are capable of 10 years of pharmacologic adherence with a similar expected longevity.⁴ The Task Force assigns a Grade C recommendation (individual and professional choice) to patients 60 to 69 years of age with the same constellation of risk factors and health status. Insufficient evidence was available to make recommendations for other age cohorts.

The American College of Chest Physicians recommends 75 to 100 mg of aspirin daily for adults 50 years or older who have moderate to high CV risk, defined as ≥10%.⁵

A working group of the European Society of Cardiology (ESC) released a statement in 2014 recommending aspirin for primary prevention in adults with a CV risk ≥20% and no risk factors for bleeding. For patients with a CVD risk between 10% and 20%, the ESC recommends deferring to patient preference.⁶

In an interesting bit of timing, just one month before the tragic shooting at the Marjory Stoneman Douglas High School in Parkland, Florida, the AMA Journal of Ethics devoted its entire January issue to the role of physicians in preventing violence. Part of the discussion centered on the idea of treating gun violence as an infectious disease epidemic.¹

Dr. Gary Slutkin, an infectious disease specialist and former Centers for Disease Control and Prevention epidemiologist, is a proponent of this approach. His research has demonstrated that epidemic disease control measures are effective in reducing violence and violence-related deaths.^2-5

Just look at incidence. Violent deaths in the United States are at an epidemic proportion, just like deaths due to narcotic overdoses. In 2015, there were approximately 33,091 deaths due to narcotic overdoses and 36,252 deaths due to gun violence.^6,7

Imagine it—a day when violence goes the way of polio.

Geographic and social factors. Like infectious disease epidemics, violence tends to cluster in certain geographic areas and social networks. The cause of violence is multifactorial, just like other infectious disease epidemics, such as tuberculosis. Poverty, poor education, and inadequate family structure act as modulating factors that increase the rate of violence in those exposed to it.

Enlisting the community. This contagious disease prevention approach uses community health workers to map areas of high transmission, reach out to those exposed, and intervene to reduce risk factors. For example, gang-related deaths are often due to retaliation. A thorough investigation of a patient who arrives in the emergency department (ED) with a gunshot wound can reveal the next likely perpetrators and victims. Then community violence prevention workers can go directly to these people and others in their social networks, such as parents and friends, to attempt to prevent the next shooting. This approach, dubbed “Cure Violence” (CureViolence.org), has resulted in up to a 70% decrease in violence in some areas of Chicago.² Some neighborhoods of Baltimore and New York have seen similar reductions.^3-5

What can family practitioners do? Dr. Slutkin believes his approach could be expanded from EDs to other health care settings, like primary care, where we can identify people at risk and refer them to community violence prevention resources. Imagine it—a day when violence goes the way of polio.

In an interesting bit of timing, just one month before the tragic shooting at the Marjory Stoneman Douglas High School in Parkland, Florida, the AMA Journal of Ethics devoted its entire January issue to the role of physicians in preventing violence. Part of the discussion centered on the idea of treating gun violence as an infectious disease epidemic.¹

Dr. Gary Slutkin, an infectious disease specialist and former Centers for Disease Control and Prevention epidemiologist, is a proponent of this approach. His research has demonstrated that epidemic disease control measures are effective in reducing violence and violence-related deaths.^2-5

Just look at incidence. Violent deaths in the United States are at an epidemic proportion, just like deaths due to narcotic overdoses. In 2015, there were approximately 33,091 deaths due to narcotic overdoses and 36,252 deaths due to gun violence.^6,7

Imagine it—a day when violence goes the way of polio.

Geographic and social factors. Like infectious disease epidemics, violence tends to cluster in certain geographic areas and social networks. The cause of violence is multifactorial, just like other infectious disease epidemics, such as tuberculosis. Poverty, poor education, and inadequate family structure act as modulating factors that increase the rate of violence in those exposed to it.

Enlisting the community. This contagious disease prevention approach uses community health workers to map areas of high transmission, reach out to those exposed, and intervene to reduce risk factors. For example, gang-related deaths are often due to retaliation. A thorough investigation of a patient who arrives in the emergency department (ED) with a gunshot wound can reveal the next likely perpetrators and victims. Then community violence prevention workers can go directly to these people and others in their social networks, such as parents and friends, to attempt to prevent the next shooting. This approach, dubbed “Cure Violence” (CureViolence.org), has resulted in up to a 70% decrease in violence in some areas of Chicago.² Some neighborhoods of Baltimore and New York have seen similar reductions.^3-5

What can family practitioners do? Dr. Slutkin believes his approach could be expanded from EDs to other health care settings, like primary care, where we can identify people at risk and refer them to community violence prevention resources. Imagine it—a day when violence goes the way of polio.

In an interesting bit of timing, just one month before the tragic shooting at the Marjory Stoneman Douglas High School in Parkland, Florida, the AMA Journal of Ethics devoted its entire January issue to the role of physicians in preventing violence. Part of the discussion centered on the idea of treating gun violence as an infectious disease epidemic.¹

Dr. Gary Slutkin, an infectious disease specialist and former Centers for Disease Control and Prevention epidemiologist, is a proponent of this approach. His research has demonstrated that epidemic disease control measures are effective in reducing violence and violence-related deaths.^2-5

Just look at incidence. Violent deaths in the United States are at an epidemic proportion, just like deaths due to narcotic overdoses. In 2015, there were approximately 33,091 deaths due to narcotic overdoses and 36,252 deaths due to gun violence.^6,7

Imagine it—a day when violence goes the way of polio.

Geographic and social factors. Like infectious disease epidemics, violence tends to cluster in certain geographic areas and social networks. The cause of violence is multifactorial, just like other infectious disease epidemics, such as tuberculosis. Poverty, poor education, and inadequate family structure act as modulating factors that increase the rate of violence in those exposed to it.

Enlisting the community. This contagious disease prevention approach uses community health workers to map areas of high transmission, reach out to those exposed, and intervene to reduce risk factors. For example, gang-related deaths are often due to retaliation. A thorough investigation of a patient who arrives in the emergency department (ED) with a gunshot wound can reveal the next likely perpetrators and victims. Then community violence prevention workers can go directly to these people and others in their social networks, such as parents and friends, to attempt to prevent the next shooting. This approach, dubbed “Cure Violence” (CureViolence.org), has resulted in up to a 70% decrease in violence in some areas of Chicago.² Some neighborhoods of Baltimore and New York have seen similar reductions.^3-5

What can family practitioners do? Dr. Slutkin believes his approach could be expanded from EDs to other health care settings, like primary care, where we can identify people at risk and refer them to community violence prevention resources. Imagine it—a day when violence goes the way of polio.

A 60-year-old African American woman who had congestive heart failure (CHF) with reduced ejection fraction, untreated hepatitis C virus infection, and chronic kidney disease presented to the emergency department (ED) with a 6-month history of bilateral lower extremity edema. Use of diuretics and antibiotic therapy for suspected CHF exacerbation and cellulitis, directed by her primary care physician, had no effect. In the month prior to presenting to the ED, the patient took 2 different antibiotics, each for 10 days: clindamycin 300 mg every 6 hours and doxycycline 100 mg every 12 hours. Additionally, she was taking furosemide 40 mg/d with good urine output, but no appreciable improvement in lower extremity edema.

The physical examination revealed bilateral nonpitting edema. Weeping pearly papules, xerotic skin, and a cobblestone appearance extended from the dorsa of the patient’s feet to her knees (FIGURES 1A and 1B). The patient underwent Doppler ultrasound of the lower extremities and a skin biopsy.

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

 

 

Diagnosis: Elephantiasis nostras verrucosa

The Doppler ultrasound was negative, and the biopsy ruled out malignancy and infection; however, the pathology report was histologically consistent with a diagnosis of elephantiasis nostras verrucosa (ENV).

ENV is a disfiguring, nonfilarial lymphedema that affects the lower extremities and is characterized by progressive cobblestoning and verrucous distortion of gravity-dependent areas.¹ The skin changes are caused by lymphatic damage and obstruction from an accumulation of protein-rich fluid in the dermis and subcutaneous tissues.^1,2

The term ENV was first coined by Aldo Castellani in 1934 to differentiate the condition from elephantiasis tropica (filariasis), which is caused by parasitic Wuchereria worms.³ ENV is also known as lymphangitis recurrens elephantogenica, elephantiasis verrucosa, elephantiasis nostra, mossy leg, and elephantiasis of the temperate zone.¹

While the diagnosis of elephantiasis nostras verrucosa can be made based on history and exam alone, a skin biopsy is warranted to rule out underlying malignancy or fungal infection.

ENV is notably uncommon; its exact incidence is unknown. The etiology is multifactorial but can include obesity, chronic lymphedema, CHF, and recurrent cellulitis (the latter 2 were noted in our patient’s history).¹

Although the diagnosis can be made based on patient history and physical examination alone, skin biopsy is warranted to rule out underlying malignancy or fungal infection.^1,4 Histologic findings suggestive of ENV include pseudoepitheliomatous hyperplasia, lymph channel dilation, widened tissue spaces, and loss of dermal papillae.¹ In our patient’s case, the pathology report revealed dermal fibrosis, dilated lymph channels, and a mixed inflammatory infiltrate. Her lab work, which included a complete blood count and basic metabolic panel, was significant for neutrophilic leukocytosis (white blood cell count, 30,000 cells/mcL), chronic kidney disease, and elevated inflammatory markers.

The differential includes other types of edema and infections

Several other diseases must be differentiated from ENV, including:

Venous stasis dermatitis. Unlike ENV, this condition involves pitting edema with erythema and does not have a verrucous appearance.^2,4

Lipedema. Histologically, lipedema shows no changes. It typically spares the feet, has an early age of onset, and is associated with a positive family history.^1,2,4

Lipodermatosclerosis. This condition is caused by venous stasis with swelling of the proximal lower extremity and fibrosis of the distal parts. The affected leg develops an “inverted wine bottle” appearance.^2,4

Pretibial myxedema. Patients with pretibial myxedema will have thyroid function test abnormalities and exhibit other signs of hyperthyroidism. If suspected, the laboratory evaluation should include thyroid-stimulating hormone levels.^2,4

Filariasis. Endemic to tropical regions, filariasis is a parasitic infection. A travel history helps to differentiate this from ENV. If suspected, include a Giemsa blood smear in the laboratory evaluation.²

Chromoblastomycosis. This chronic fungal infection is typically contracted in rural tropical or subtropical regions. The causative fungi, which are present in soil, enter the skin through minor wounds (eg, thorns or splinters). The wounds are typically forgotten by the time the patient seeks medical attention. Biopsy can effectively rule out this condition.^1,2,5

Treatment centers on preserving function, preventing complications

Currently, no standard treatment exists for ENV.^1,4 Therapies are aimed at treating the underlying cause, preserving function in the affected limb, and preventing complications. Conservative therapy includes elevation of the affected limb and use of compression devices for edema. Antibiotics can be administered for associated cellulitis. There have been few case reports of successful treatment with oral retinoids. If medical therapy fails, surgical debridement serves as a last resort.^1,4,6

Our patient improved after a week with antibiotic therapy (IV piperacillin/tazobactam 3.375 g every 6 hours) and other conservative measures, such as leg elevation.

CORRESPONDENCE
Kavita Natrajan, MBBS, George Washington University/Medical Faculty Associates, Division of Hematology and Oncology, 2150 Pennsylvania Avenue NW, DC 20037; [email protected].

A 60-year-old African American woman who had congestive heart failure (CHF) with reduced ejection fraction, untreated hepatitis C virus infection, and chronic kidney disease presented to the emergency department (ED) with a 6-month history of bilateral lower extremity edema. Use of diuretics and antibiotic therapy for suspected CHF exacerbation and cellulitis, directed by her primary care physician, had no effect. In the month prior to presenting to the ED, the patient took 2 different antibiotics, each for 10 days: clindamycin 300 mg every 6 hours and doxycycline 100 mg every 12 hours. Additionally, she was taking furosemide 40 mg/d with good urine output, but no appreciable improvement in lower extremity edema.

The physical examination revealed bilateral nonpitting edema. Weeping pearly papules, xerotic skin, and a cobblestone appearance extended from the dorsa of the patient’s feet to her knees (FIGURES 1A and 1B). The patient underwent Doppler ultrasound of the lower extremities and a skin biopsy.

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

 

 

Diagnosis: Elephantiasis nostras verrucosa

The Doppler ultrasound was negative, and the biopsy ruled out malignancy and infection; however, the pathology report was histologically consistent with a diagnosis of elephantiasis nostras verrucosa (ENV).

ENV is a disfiguring, nonfilarial lymphedema that affects the lower extremities and is characterized by progressive cobblestoning and verrucous distortion of gravity-dependent areas.¹ The skin changes are caused by lymphatic damage and obstruction from an accumulation of protein-rich fluid in the dermis and subcutaneous tissues.^1,2

The term ENV was first coined by Aldo Castellani in 1934 to differentiate the condition from elephantiasis tropica (filariasis), which is caused by parasitic Wuchereria worms.³ ENV is also known as lymphangitis recurrens elephantogenica, elephantiasis verrucosa, elephantiasis nostra, mossy leg, and elephantiasis of the temperate zone.¹

While the diagnosis of elephantiasis nostras verrucosa can be made based on history and exam alone, a skin biopsy is warranted to rule out underlying malignancy or fungal infection.

ENV is notably uncommon; its exact incidence is unknown. The etiology is multifactorial but can include obesity, chronic lymphedema, CHF, and recurrent cellulitis (the latter 2 were noted in our patient’s history).¹

Although the diagnosis can be made based on patient history and physical examination alone, skin biopsy is warranted to rule out underlying malignancy or fungal infection.^1,4 Histologic findings suggestive of ENV include pseudoepitheliomatous hyperplasia, lymph channel dilation, widened tissue spaces, and loss of dermal papillae.¹ In our patient’s case, the pathology report revealed dermal fibrosis, dilated lymph channels, and a mixed inflammatory infiltrate. Her lab work, which included a complete blood count and basic metabolic panel, was significant for neutrophilic leukocytosis (white blood cell count, 30,000 cells/mcL), chronic kidney disease, and elevated inflammatory markers.

The differential includes other types of edema and infections

Several other diseases must be differentiated from ENV, including:

Venous stasis dermatitis. Unlike ENV, this condition involves pitting edema with erythema and does not have a verrucous appearance.^2,4

Lipedema. Histologically, lipedema shows no changes. It typically spares the feet, has an early age of onset, and is associated with a positive family history.^1,2,4

Lipodermatosclerosis. This condition is caused by venous stasis with swelling of the proximal lower extremity and fibrosis of the distal parts. The affected leg develops an “inverted wine bottle” appearance.^2,4

Pretibial myxedema. Patients with pretibial myxedema will have thyroid function test abnormalities and exhibit other signs of hyperthyroidism. If suspected, the laboratory evaluation should include thyroid-stimulating hormone levels.^2,4

Filariasis. Endemic to tropical regions, filariasis is a parasitic infection. A travel history helps to differentiate this from ENV. If suspected, include a Giemsa blood smear in the laboratory evaluation.²

Chromoblastomycosis. This chronic fungal infection is typically contracted in rural tropical or subtropical regions. The causative fungi, which are present in soil, enter the skin through minor wounds (eg, thorns or splinters). The wounds are typically forgotten by the time the patient seeks medical attention. Biopsy can effectively rule out this condition.^1,2,5

Treatment centers on preserving function, preventing complications

Currently, no standard treatment exists for ENV.^1,4 Therapies are aimed at treating the underlying cause, preserving function in the affected limb, and preventing complications. Conservative therapy includes elevation of the affected limb and use of compression devices for edema. Antibiotics can be administered for associated cellulitis. There have been few case reports of successful treatment with oral retinoids. If medical therapy fails, surgical debridement serves as a last resort.^1,4,6

Our patient improved after a week with antibiotic therapy (IV piperacillin/tazobactam 3.375 g every 6 hours) and other conservative measures, such as leg elevation.

CORRESPONDENCE
Kavita Natrajan, MBBS, George Washington University/Medical Faculty Associates, Division of Hematology and Oncology, 2150 Pennsylvania Avenue NW, DC 20037; [email protected].

A 60-year-old African American woman who had congestive heart failure (CHF) with reduced ejection fraction, untreated hepatitis C virus infection, and chronic kidney disease presented to the emergency department (ED) with a 6-month history of bilateral lower extremity edema. Use of diuretics and antibiotic therapy for suspected CHF exacerbation and cellulitis, directed by her primary care physician, had no effect. In the month prior to presenting to the ED, the patient took 2 different antibiotics, each for 10 days: clindamycin 300 mg every 6 hours and doxycycline 100 mg every 12 hours. Additionally, she was taking furosemide 40 mg/d with good urine output, but no appreciable improvement in lower extremity edema.

The physical examination revealed bilateral nonpitting edema. Weeping pearly papules, xerotic skin, and a cobblestone appearance extended from the dorsa of the patient’s feet to her knees (FIGURES 1A and 1B). The patient underwent Doppler ultrasound of the lower extremities and a skin biopsy.

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

 

 

Diagnosis: Elephantiasis nostras verrucosa

The Doppler ultrasound was negative, and the biopsy ruled out malignancy and infection; however, the pathology report was histologically consistent with a diagnosis of elephantiasis nostras verrucosa (ENV).

ENV is a disfiguring, nonfilarial lymphedema that affects the lower extremities and is characterized by progressive cobblestoning and verrucous distortion of gravity-dependent areas.¹ The skin changes are caused by lymphatic damage and obstruction from an accumulation of protein-rich fluid in the dermis and subcutaneous tissues.^1,2

The term ENV was first coined by Aldo Castellani in 1934 to differentiate the condition from elephantiasis tropica (filariasis), which is caused by parasitic Wuchereria worms.³ ENV is also known as lymphangitis recurrens elephantogenica, elephantiasis verrucosa, elephantiasis nostra, mossy leg, and elephantiasis of the temperate zone.¹

While the diagnosis of elephantiasis nostras verrucosa can be made based on history and exam alone, a skin biopsy is warranted to rule out underlying malignancy or fungal infection.

ENV is notably uncommon; its exact incidence is unknown. The etiology is multifactorial but can include obesity, chronic lymphedema, CHF, and recurrent cellulitis (the latter 2 were noted in our patient’s history).¹

Although the diagnosis can be made based on patient history and physical examination alone, skin biopsy is warranted to rule out underlying malignancy or fungal infection.^1,4 Histologic findings suggestive of ENV include pseudoepitheliomatous hyperplasia, lymph channel dilation, widened tissue spaces, and loss of dermal papillae.¹ In our patient’s case, the pathology report revealed dermal fibrosis, dilated lymph channels, and a mixed inflammatory infiltrate. Her lab work, which included a complete blood count and basic metabolic panel, was significant for neutrophilic leukocytosis (white blood cell count, 30,000 cells/mcL), chronic kidney disease, and elevated inflammatory markers.

The differential includes other types of edema and infections

Several other diseases must be differentiated from ENV, including:

Venous stasis dermatitis. Unlike ENV, this condition involves pitting edema with erythema and does not have a verrucous appearance.^2,4

Lipedema. Histologically, lipedema shows no changes. It typically spares the feet, has an early age of onset, and is associated with a positive family history.^1,2,4

Lipodermatosclerosis. This condition is caused by venous stasis with swelling of the proximal lower extremity and fibrosis of the distal parts. The affected leg develops an “inverted wine bottle” appearance.^2,4

Pretibial myxedema. Patients with pretibial myxedema will have thyroid function test abnormalities and exhibit other signs of hyperthyroidism. If suspected, the laboratory evaluation should include thyroid-stimulating hormone levels.^2,4

Filariasis. Endemic to tropical regions, filariasis is a parasitic infection. A travel history helps to differentiate this from ENV. If suspected, include a Giemsa blood smear in the laboratory evaluation.²

Chromoblastomycosis. This chronic fungal infection is typically contracted in rural tropical or subtropical regions. The causative fungi, which are present in soil, enter the skin through minor wounds (eg, thorns or splinters). The wounds are typically forgotten by the time the patient seeks medical attention. Biopsy can effectively rule out this condition.^1,2,5

Treatment centers on preserving function, preventing complications

Currently, no standard treatment exists for ENV.^1,4 Therapies are aimed at treating the underlying cause, preserving function in the affected limb, and preventing complications. Conservative therapy includes elevation of the affected limb and use of compression devices for edema. Antibiotics can be administered for associated cellulitis. There have been few case reports of successful treatment with oral retinoids. If medical therapy fails, surgical debridement serves as a last resort.^1,4,6

Our patient improved after a week with antibiotic therapy (IV piperacillin/tazobactam 3.375 g every 6 hours) and other conservative measures, such as leg elevation.

CORRESPONDENCE
Kavita Natrajan, MBBS, George Washington University/Medical Faculty Associates, Division of Hematology and Oncology, 2150 Pennsylvania Avenue NW, DC 20037; [email protected].

ILLUSTRATIVE CASE

A 15-year-old girl presents to your clinic with poorly controlled chronic migraines that are preventing her from attending school 3 to 4 days per month. As part of her treatment regimen, you are considering migraine prevention strategies.

Should you prescribe amitriptyline or topiramate for preventive migraine therapy?

Migraine headaches are the most common reason for headache presentation in pediatric neurology outpatient clinics, affecting 5% to 10% of the pediatric population worldwide.² Current recommendations regarding prophylactic migraine therapy in childhood are based on consensus opinions.^3,4 And the US Food and Drug Administration (FDA) has not approved any medications for preventing migraines in children younger than 12 years of age. However, surveys of pediatric headache specialists suggest that amitriptyline and topiramate are among the most commonly prescribed medications for childhood migraine prophylaxis.^3,4

There is low-quality evidence from individual randomized controlled trials (RCTs) about the effectiveness of topiramate. A meta-analysis by El-Chammas and colleagues included 3 RCTs comparing topiramate to placebo for the prevention of episodic migraines (migraine headaches that occur <15 times/month) in a combined total of 283 children younger than 18 years of age.⁵ Topiramate demonstrated a nonclinically significant, but statistically significant, reduction of less than one headache per month (-0.71; 95% confidence interval [CI], -1.19 to -0.24). This is based on moderate quality evidence due to a high placebo response rate and study durations of only 12 weeks.⁵ The FDA has approved topiramate for migraine prevention in children ages 12 to 17 years.⁶

Adult guidelines. The findings described above are consistent with the most recent adult guidelines from the American Academy of Neurology and the American Headache Society.⁷ In a joint publication from 2012, these societies recommended both topiramate and amitriptyline for the prevention of migraines in adults based on high-quality (Level A evidence) and medium-quality evidence (Level B), respectively.⁷

[polldaddy:9973304]

 

 

STUDY SUMMARY

Both drugs are no better than placebo in children

A multicenter, double-blind RCT by Powers and colleagues compared the effectiveness of amitriptyline, topiramate, and placebo in the prevention of pediatric migraines.¹ Target dosing for amitriptyline and topiramate was set at 1 mg/kg/d and 2 mg/kg/d, respectively. Titration toward these doses occurred over an 8-week period based on reported adverse effects. Patients then continued their maximum tolerated dose for an additional 16 weeks.

Patients were predominantly white (70%), female (68%), and 8 to 17 years of age. They had at least 4 headache days over a prospective 28-day pre-treatment period and a Pediatric Migraine Disability Assessment Scale (PedMIDAS) score of 11 to 139 (mild to moderate disability=11-50; severe disability >50).^1,8 The primary endpoint consisted of at least a 50% relative reduction (RR) in the number of headache days over the 28-day pre-therapy (baseline) period compared with the final 28 days of the trial.¹

The authors of the study included 328 patients in the primary efficacy analysis and randomly assigned them in a 2:2:1 ratio to receive either amitriptyline (132 patients), topiramate (130 patients), or placebo (66 patients), respectively. After 24 weeks of therapy, there was no significant difference between the amitriptyline, topiramate, and placebo groups in the primary endpoint (52% amitriptyline, 55% topiramate, 61% placebo; adjusted odds ratio [OR]=0.71; 98% CI, 0.34-1.48; P=.26 between amitriptyline and placebo; OR=0.81; 98% CI, 0.39-1.68; P=.48 between topiramate and placebo; OR=0.88; 98% CI, 0.49-1.59; P=.49 between amitriptyline and topiramate).

There was also no difference in the secondary outcomes of absolute reduction in headache days and headache-related disability as determined by PedMIDAS. The study was stopped early for futility. Compared with placebo, amitriptyline significantly increased fatigue (number needed to harm [NNH]=8) and dry mouth (NNH=9) and was associated with 3 serious adverse events of altered mood. Compared with placebo, topiramate significantly increased paresthesia (NNH=4) and weight loss (NNH=13) and was associated with one serious adverse event—a suicide attempt.¹

 

 

WHAT’S NEW?

Higher-level evidence demonstrates lack of efficacy

This RCT provides new, higher-level evidence that demonstrates the lack of efficacy of amitriptyline and topiramate in the prevention of pediatric migraines. It also highlights the risk of increased adverse events with topiramate and amitriptyline.

After 24 weeks of therapy, there was no significant difference between amitriptyline, topiramate, and placebo in the primary or secondary outcomes.

Two of the 3 topiramate trials used in the older meta-analysis by El-Chammas and colleagues⁵ and this new RCT¹ were included in an updated meta-analysis by Le and colleagues (total participants 465) published in 2017.² This newer meta-analysis found no statistical benefit associated with the use of topiramate over placebo. It demonstrated a nonsignificant decrease in the number of patients with at least a 50% relative reduction in headache frequency (risk ratio = 1.26; 95% CI, 0.94-1.67) and in the overall number of headache days (mean difference = -0.77; 95% CI, -2.31 to 0.76) in patients younger than 18 years of age.² Both meta-analyses, however, showed an increase in the rate of adverse events in patients using topiramate vs placebo.^2,5

CAVEATS

Is there a gender predominance?

El-Chammas and colleagues⁵ describe male pediatric patients as being the predominant pediatric gender with migraines. However, they do not quote an incidence rate or cite the reference for this statement. No other reference to gender predominance was noted in the literature. The current study,¹ in addition to the total population of the meta-analysis by Le and colleagues,² included women as the predominant patient population. Hopefully, future studies will help to delineate if there is a gender predominance and, if so, whether the current treatment data apply to both genders.

CHALLENGES TO IMPLEMENTATION

None to speak of

There are no barriers to implementing this recommendation immediately in all primary care settings.

ACKNOWLEDGEMENT

The PURLs Surveillance System was supported in part by Grant Number UL1RR024999 from the National Center For Research Resources, a Clinical Translational Science Award to the University of Chicago. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Center For Research Resources or the National Institutes of Health.

ILLUSTRATIVE CASE

A 15-year-old girl presents to your clinic with poorly controlled chronic migraines that are preventing her from attending school 3 to 4 days per month. As part of her treatment regimen, you are considering migraine prevention strategies.

Should you prescribe amitriptyline or topiramate for preventive migraine therapy?

Migraine headaches are the most common reason for headache presentation in pediatric neurology outpatient clinics, affecting 5% to 10% of the pediatric population worldwide.² Current recommendations regarding prophylactic migraine therapy in childhood are based on consensus opinions.^3,4 And the US Food and Drug Administration (FDA) has not approved any medications for preventing migraines in children younger than 12 years of age. However, surveys of pediatric headache specialists suggest that amitriptyline and topiramate are among the most commonly prescribed medications for childhood migraine prophylaxis.^3,4

There is low-quality evidence from individual randomized controlled trials (RCTs) about the effectiveness of topiramate. A meta-analysis by El-Chammas and colleagues included 3 RCTs comparing topiramate to placebo for the prevention of episodic migraines (migraine headaches that occur <15 times/month) in a combined total of 283 children younger than 18 years of age.⁵ Topiramate demonstrated a nonclinically significant, but statistically significant, reduction of less than one headache per month (-0.71; 95% confidence interval [CI], -1.19 to -0.24). This is based on moderate quality evidence due to a high placebo response rate and study durations of only 12 weeks.⁵ The FDA has approved topiramate for migraine prevention in children ages 12 to 17 years.⁶

Adult guidelines. The findings described above are consistent with the most recent adult guidelines from the American Academy of Neurology and the American Headache Society.⁷ In a joint publication from 2012, these societies recommended both topiramate and amitriptyline for the prevention of migraines in adults based on high-quality (Level A evidence) and medium-quality evidence (Level B), respectively.⁷

[polldaddy:9973304]

 

 

STUDY SUMMARY

Both drugs are no better than placebo in children

A multicenter, double-blind RCT by Powers and colleagues compared the effectiveness of amitriptyline, topiramate, and placebo in the prevention of pediatric migraines.¹ Target dosing for amitriptyline and topiramate was set at 1 mg/kg/d and 2 mg/kg/d, respectively. Titration toward these doses occurred over an 8-week period based on reported adverse effects. Patients then continued their maximum tolerated dose for an additional 16 weeks.

Patients were predominantly white (70%), female (68%), and 8 to 17 years of age. They had at least 4 headache days over a prospective 28-day pre-treatment period and a Pediatric Migraine Disability Assessment Scale (PedMIDAS) score of 11 to 139 (mild to moderate disability=11-50; severe disability >50).^1,8 The primary endpoint consisted of at least a 50% relative reduction (RR) in the number of headache days over the 28-day pre-therapy (baseline) period compared with the final 28 days of the trial.¹

The authors of the study included 328 patients in the primary efficacy analysis and randomly assigned them in a 2:2:1 ratio to receive either amitriptyline (132 patients), topiramate (130 patients), or placebo (66 patients), respectively. After 24 weeks of therapy, there was no significant difference between the amitriptyline, topiramate, and placebo groups in the primary endpoint (52% amitriptyline, 55% topiramate, 61% placebo; adjusted odds ratio [OR]=0.71; 98% CI, 0.34-1.48; P=.26 between amitriptyline and placebo; OR=0.81; 98% CI, 0.39-1.68; P=.48 between topiramate and placebo; OR=0.88; 98% CI, 0.49-1.59; P=.49 between amitriptyline and topiramate).

There was also no difference in the secondary outcomes of absolute reduction in headache days and headache-related disability as determined by PedMIDAS. The study was stopped early for futility. Compared with placebo, amitriptyline significantly increased fatigue (number needed to harm [NNH]=8) and dry mouth (NNH=9) and was associated with 3 serious adverse events of altered mood. Compared with placebo, topiramate significantly increased paresthesia (NNH=4) and weight loss (NNH=13) and was associated with one serious adverse event—a suicide attempt.¹

 

 

WHAT’S NEW?

Higher-level evidence demonstrates lack of efficacy

This RCT provides new, higher-level evidence that demonstrates the lack of efficacy of amitriptyline and topiramate in the prevention of pediatric migraines. It also highlights the risk of increased adverse events with topiramate and amitriptyline.

After 24 weeks of therapy, there was no significant difference between amitriptyline, topiramate, and placebo in the primary or secondary outcomes.

Two of the 3 topiramate trials used in the older meta-analysis by El-Chammas and colleagues⁵ and this new RCT¹ were included in an updated meta-analysis by Le and colleagues (total participants 465) published in 2017.² This newer meta-analysis found no statistical benefit associated with the use of topiramate over placebo. It demonstrated a nonsignificant decrease in the number of patients with at least a 50% relative reduction in headache frequency (risk ratio = 1.26; 95% CI, 0.94-1.67) and in the overall number of headache days (mean difference = -0.77; 95% CI, -2.31 to 0.76) in patients younger than 18 years of age.² Both meta-analyses, however, showed an increase in the rate of adverse events in patients using topiramate vs placebo.^2,5

CAVEATS

Is there a gender predominance?

El-Chammas and colleagues⁵ describe male pediatric patients as being the predominant pediatric gender with migraines. However, they do not quote an incidence rate or cite the reference for this statement. No other reference to gender predominance was noted in the literature. The current study,¹ in addition to the total population of the meta-analysis by Le and colleagues,² included women as the predominant patient population. Hopefully, future studies will help to delineate if there is a gender predominance and, if so, whether the current treatment data apply to both genders.

CHALLENGES TO IMPLEMENTATION

None to speak of

There are no barriers to implementing this recommendation immediately in all primary care settings.

ACKNOWLEDGEMENT

The PURLs Surveillance System was supported in part by Grant Number UL1RR024999 from the National Center For Research Resources, a Clinical Translational Science Award to the University of Chicago. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Center For Research Resources or the National Institutes of Health.

ILLUSTRATIVE CASE

A 15-year-old girl presents to your clinic with poorly controlled chronic migraines that are preventing her from attending school 3 to 4 days per month. As part of her treatment regimen, you are considering migraine prevention strategies.

Should you prescribe amitriptyline or topiramate for preventive migraine therapy?

Migraine headaches are the most common reason for headache presentation in pediatric neurology outpatient clinics, affecting 5% to 10% of the pediatric population worldwide.² Current recommendations regarding prophylactic migraine therapy in childhood are based on consensus opinions.^3,4 And the US Food and Drug Administration (FDA) has not approved any medications for preventing migraines in children younger than 12 years of age. However, surveys of pediatric headache specialists suggest that amitriptyline and topiramate are among the most commonly prescribed medications for childhood migraine prophylaxis.^3,4

There is low-quality evidence from individual randomized controlled trials (RCTs) about the effectiveness of topiramate. A meta-analysis by El-Chammas and colleagues included 3 RCTs comparing topiramate to placebo for the prevention of episodic migraines (migraine headaches that occur <15 times/month) in a combined total of 283 children younger than 18 years of age.⁵ Topiramate demonstrated a nonclinically significant, but statistically significant, reduction of less than one headache per month (-0.71; 95% confidence interval [CI], -1.19 to -0.24). This is based on moderate quality evidence due to a high placebo response rate and study durations of only 12 weeks.⁵ The FDA has approved topiramate for migraine prevention in children ages 12 to 17 years.⁶

Adult guidelines. The findings described above are consistent with the most recent adult guidelines from the American Academy of Neurology and the American Headache Society.⁷ In a joint publication from 2012, these societies recommended both topiramate and amitriptyline for the prevention of migraines in adults based on high-quality (Level A evidence) and medium-quality evidence (Level B), respectively.⁷

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STUDY SUMMARY

Both drugs are no better than placebo in children

A multicenter, double-blind RCT by Powers and colleagues compared the effectiveness of amitriptyline, topiramate, and placebo in the prevention of pediatric migraines.¹ Target dosing for amitriptyline and topiramate was set at 1 mg/kg/d and 2 mg/kg/d, respectively. Titration toward these doses occurred over an 8-week period based on reported adverse effects. Patients then continued their maximum tolerated dose for an additional 16 weeks.

Patients were predominantly white (70%), female (68%), and 8 to 17 years of age. They had at least 4 headache days over a prospective 28-day pre-treatment period and a Pediatric Migraine Disability Assessment Scale (PedMIDAS) score of 11 to 139 (mild to moderate disability=11-50; severe disability >50).^1,8 The primary endpoint consisted of at least a 50% relative reduction (RR) in the number of headache days over the 28-day pre-therapy (baseline) period compared with the final 28 days of the trial.¹

The authors of the study included 328 patients in the primary efficacy analysis and randomly assigned them in a 2:2:1 ratio to receive either amitriptyline (132 patients), topiramate (130 patients), or placebo (66 patients), respectively. After 24 weeks of therapy, there was no significant difference between the amitriptyline, topiramate, and placebo groups in the primary endpoint (52% amitriptyline, 55% topiramate, 61% placebo; adjusted odds ratio [OR]=0.71; 98% CI, 0.34-1.48; P=.26 between amitriptyline and placebo; OR=0.81; 98% CI, 0.39-1.68; P=.48 between topiramate and placebo; OR=0.88; 98% CI, 0.49-1.59; P=.49 between amitriptyline and topiramate).

There was also no difference in the secondary outcomes of absolute reduction in headache days and headache-related disability as determined by PedMIDAS. The study was stopped early for futility. Compared with placebo, amitriptyline significantly increased fatigue (number needed to harm [NNH]=8) and dry mouth (NNH=9) and was associated with 3 serious adverse events of altered mood. Compared with placebo, topiramate significantly increased paresthesia (NNH=4) and weight loss (NNH=13) and was associated with one serious adverse event—a suicide attempt.¹

 

 

WHAT’S NEW?

Higher-level evidence demonstrates lack of efficacy

This RCT provides new, higher-level evidence that demonstrates the lack of efficacy of amitriptyline and topiramate in the prevention of pediatric migraines. It also highlights the risk of increased adverse events with topiramate and amitriptyline.

After 24 weeks of therapy, there was no significant difference between amitriptyline, topiramate, and placebo in the primary or secondary outcomes.

Two of the 3 topiramate trials used in the older meta-analysis by El-Chammas and colleagues⁵ and this new RCT¹ were included in an updated meta-analysis by Le and colleagues (total participants 465) published in 2017.² This newer meta-analysis found no statistical benefit associated with the use of topiramate over placebo. It demonstrated a nonsignificant decrease in the number of patients with at least a 50% relative reduction in headache frequency (risk ratio = 1.26; 95% CI, 0.94-1.67) and in the overall number of headache days (mean difference = -0.77; 95% CI, -2.31 to 0.76) in patients younger than 18 years of age.² Both meta-analyses, however, showed an increase in the rate of adverse events in patients using topiramate vs placebo.^2,5

CAVEATS

Is there a gender predominance?

El-Chammas and colleagues⁵ describe male pediatric patients as being the predominant pediatric gender with migraines. However, they do not quote an incidence rate or cite the reference for this statement. No other reference to gender predominance was noted in the literature. The current study,¹ in addition to the total population of the meta-analysis by Le and colleagues,² included women as the predominant patient population. Hopefully, future studies will help to delineate if there is a gender predominance and, if so, whether the current treatment data apply to both genders.

CHALLENGES TO IMPLEMENTATION

None to speak of

There are no barriers to implementing this recommendation immediately in all primary care settings.

ACKNOWLEDGEMENT

The PURLs Surveillance System was supported in part by Grant Number UL1RR024999 from the National Center For Research Resources, a Clinical Translational Science Award to the University of Chicago. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Center For Research Resources or the National Institutes of Health.