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Changes to the CPT code set and Medicare billing
The Current Procedural Terminology (CPT) code set for 2011 includes several changes of interest to ObGyns. These include 1) guideline clarifications regarding wound debridement and obstetric care codes; 2) new codes for subsequent observation care; micro-remodeling of the bladder neck; insertion of a vaginal after-loading device; and 3) a lab code for detecting amniotic fluid in cervicovaginal secretions (using the AmniSure kit).
There is also a new code for vaccine counseling that will have an impact on you if your practice offers the human papillomavirus (HPV) vaccine to patients younger than 19 years.
There are changes to Medicare this year that you should take note of if you care for these patients, particularly in the area of preventive visit billing.
CPT and Medicare changes both took effect on January 1. The Health Insurance Portability and Accountability Act (HIPAA) requires that insurers accepted the new codes on that date.
Changes to the CPT code set
OBSERVATION CARE
One of the biggest headaches for medical practices has been standardized coding and billing for observation care that lasts more than 1 day. In the past, payers accepted a problem E/M for Day 2 of observation care, or instructed practices to code an unlisted E/M service. Now, you may report all care rendered in the observation setting with the addition of three new codes for subsequent care:
99244 Subsequent observation care, per day, for the evaluation and management of a patient, which requires at least 2 of these 3 key components: problem focused interval history, problem focused examination; medical decision making that is straightforward or of low complexity. Counseling and/or coordination of care with other providers or agencies are provided consistent with the nature of the problem(s) and the patient’s and/or family’s needs. Usually, the patient is stable, recovering, or improving. Physicians typically spend 15 minutes at the bedside and on the patient’s hospital floor or unit.
99225 Subsequent observation care, per day, for the evaluation and management of a patient, which requires at least 2 of these 3 key components: an expanded problem focused interval history; an expanded problem focused examination; medical decision making of moderate complexity. Counseling and/or coordination of care with other providers or agencies are provided consistent with the nature of the problem(s) and the patient’s and/or family’s needs. Usually, the patient is responding inadequately to therapy or has developed a minor complication. Physicians typically spend 25 minutes at the bedside and on the patient’s hospital floor or unit.
99226 Subsequent observation care, per day, for the evaluation and management of a patient, which requires at least 2 of these 3 key components: a detailed interval history; a detailed examination; medical decision making of high complexity. Counseling and/or coordination of care with other providers or agencies are provided consistent with the nature of the problem(s) and the patient’s and/or family’s needs. Usually, the patient is unstable or has developed a significant complication or a significant new problem. Physicians typically spend 35 minutes at the bedside and on the patient’s hospital floor or unit.
Note that each of these codes 1) “suggests” the status of the patient for each level of billing, and 2) includes a typical time. This means that, unlike the observation care admission codes or the observation admission/same-day discharge codes, time that is spent with the patient, or on the unit, may be used to select the code—if you document 1) the requirement that more than 50% of the typical time was spent on counseling or coordination of care, or both, and 2) a detailed description of this activity.
Codes for wound debridement were given a facelift with the addition of a new guideline that addresses both surgical and medical debridement. The surgical debridement codes, (11042–11047) are now reported on the basis of the depth of tissue removed and the surface area of the wound. This means that codes 11040 and 11041 were deleted to make room for new and revised codes.
This change will mean that, when you report these codes, you will need to document more information to bill. It’s also understood that coding separately for debridement of dermis or epidermis at the same time you code for debriding underlying structures would be inappropriate.
CPT has also indicated that active wound management codes 97597 and 97598 can now be reported by physicians or nonphysician providers as long as the provider has direct (one-on-one) contact. These codes should be reported for skin-surface debridement only.
The new and revised codes (some of which have been published in CPT in nonsequential order) are:
11042 Debridement, subcutaneous tissue (includes epidermis and dermis, if performed); first 20 sq cm or less
+11045 (new add-on code reported with 11042 only) each additional 20 sq cm or part thereof
11043 Debridement, muscle and/or facia (includes epidermis, dermis, and subcutaneous tissue, if performed); first 20 sq cm or less
+11046 (new add-on code reported with 11043 only) each additional 20 sq cm or part thereof
11044 Debridement, bone (includes epidermis, dermis, subcutaneous tissue, muscle and/or fascia, if performed); first 20 sq cm or less
+11047 (new add-on code reported with 11044 only) each additional 20 sq cm or part thereof
97597 Debridement (e.g., high pressure waterjet with/without suction, sharp selective debridement with scissors, scalpel and forceps), open wound, (e.g., fibrin, devitalized epidermis and/or dermis, exudate, debris, biofilm), including topical application(s), wound assessment, use of a whirlpool, when performed and instruction(s) for ongoing care, per session, total wound(s) surface area; first 20 sq cm or less
+95798 (add-on code reported with 97597 only) Each additional 20 sq cm, or part thereof.
TRANSURETHRAL RADIOFREQUENCY
Category III code 0193T, which described transurethral radiofrequency micro-remodeling for stress urinary incontinence, has been deleted and converted to a Category I CPT code, 53860 (Transurethral radiofrequency micro-remodeling of the female bladder neck and proximal urethra for stress urinary incontinence). The procedure includes a periurethral block and flushing the bladder with a lidocaine slurry, and can be performed in the office.
In all, the procedure requires nine treatment cycles during the session, but the code is billed only once. Catheterization and measurement of a voiding sample after the procedure are included in the code.
AFTERLOADING DEVICES FOR CLINICAL BRACHYTHERAPY
CPT revised—slightly—existing code 57155, and added code 57156 (Insertion of a vaginal radiation afterloading apparatus for clinical brachytherapy).
- Code 57155 was revised to clarify that only a single tandem is inserted into the uterus. There had been confusion earlier in this regard.
- The new code describes a procedure that may also include dilation of the vaginal canal to remove postradiation adhesions. That procedure also involves 1) placement of bladder and rectal catheters and 2) radiographic imaging to confirm placement, which are not coded separately.
CLARIFICATION OF OBSTETRIC GUIDELINES
Been having problems with payers and their interpretation of the delivery only, postpartum only, and delivery with postpartum care codes? CPT has, at last, clarified what you can, and cannot, bill in those circumstances. (Keep in mind, however, that you may not unbundle these procedures if more extensive care is provided: Most payers want you to bill the global OB care code that includes antepartum, intrapartum, and postpartum care.)
In some cases (such as Medicaid), the payer stipulates that only the physician who actually performed the delivery may bill for it, even if the delivering physician is covering for, or is a member of, the same group practice as the primary attending of record. The “delivery-only” codes should be reported when 1) an unaffiliated physician has delivered the baby but will not be providing any outpatient postpartum care or 2) the payer has specified this method of billing for the covering or affiliated provider.
CPT has clarified that delivery-only codes (59409, 59514, or 59612, 59620) include admission to the hospital, the admission history and physical exam, uncomplicated labor and delivery (including delivery of the placenta, or use of forceps or vacuum extraction). These codes do not include inpatient rounding or discharge day care after delivery (and, of course, include no outpatient postpartum care). When, as the delivering physician, you also provide inpatient postdelivery care, therefore, you may additionally bill subsequent hospital care codes and discharge day management codes (99231-99233, 99238-99239).
If the unaffiliated physician performs the delivery and also intends on providing outpatient postpartum care, the CPT codes for delivery with postpartum are to be reported (59410, 59515, 59614, 59622). In addition to the delivery, these codes include all inpatient and outpatient postpartum care. And finally, for those physicians who are only providing outpatient postpartum care, the code 59430, Postpartum care only, should be reported.
PLACENTAL ALPHA MICROGLOBULIN-1
A new code, 84112 (Placental alpha microglobulin-1 [PAMG-11], cervicovaginal secretion, qualitative), has been added to allow the clinical laboratory to bill for this immunoassay that detects amniotic fluid in the secretions. Physician work involves collection of the specimen but, under CPT rules, collection is included as part of any E/M service.
Note: An existing code for this test that is used by Blue Cross/Blue Shield payers (S3628) remains valid in 2011.
HPV VACCINE COUNSELING
Before January 1, 2011, if you counseled a patient about the HPV vaccine, you could report preventive counseling codes, such as 99401–99404, in addition to the vaccine administration code, 90471 (Immunization administration, 1 vaccine). Now, however, you have a new code for counseling and vaccine administration for a patient who is younger than 19 years—the age group most likely to be counseled about this vaccine. When you see, and counsel, such a patient before administering the vaccine, on the same date of service, code 90460 (Immunization administration through 18 years of age via any route of administration, with counseling by physician or other qualified health care profession; first vaccine/toxoid component), and 90649 for the quadrivalent or 90650 for the bivalent HPV vaccine.
If your patient is 19 years or older and requires counseling, continue to bill 99401– 99404 for counseling, with 90471 for immunization and 90649 or 90650 for the vaccine. Keep in mind: Whether you report 90460 or the 9940X codes, you are required to document the content of the counseling. Codes 9940X also require documentation of the duration of counseling.
INFLUENZA VACCINE
New codes have been established for the flu vaccine, but you won’t be using them: They are intended to address future pandemic strains of influenza. This year’s vaccine contains the H1N1 strain, but is coded as the normal seasonal flu vaccine, based on the type given:
90656 (preservative-free)
90658 (split virus)
90660 (intranasal)
90662 (enhanced vaccine for patients older than 65 years).
Changes to Medicare billing
Some of the coding and billing changes this year that have an impact on ObGyn practice come from the Centers of Medicare and Medicaid Services (CMS) and the Affordable Care Act.
TIMELY FILING
The Affordable Care Act calls for a reduction in the maximum time period for submission of Medicare fee-for-service claims. Before January 1, a provider had 15 to 27 months to submit first-time claims to Medicare. Now, these claims must be filed within a calendar year of the date of service. Exceptions can be made for retroactive entitlement or in situations in which there is a secondary payer.
PAYMENTS TO CERTIFIED NURSE MIDWIVES
Next, more good news—if you employ a certified nurse midwife (CNM) in your practice. Before January 1, Medicare reimbursed direct billing from a CNM at only 65% of the Medicare Physician Fee Schedule. Now, a CNM is paid the same as a physician when she (he) bills under her own number.
In the past, some practices billed for the services of a CNM under “incident to” rules, to capture the physician payment—but this also meant that the CNM could not see a new patient. Under the change I’m describing, all CNMs can bill Medicare directly; see new patients; and be paid the same as the physician is paid. In addition, CNMs are no longer required to be supervised by a physician when they perform diagnostic tests that fall under the scope of their practice.
ANNUAL WELLNESS VISIT
The Affordable Care Act extended preventive coverage to Medicare beneficiaries in the form of an annual wellness visit. The two new codes here have been valued based on a level 4-problem new and established E/M service:
G0438 Annual wellness visit, including personalized prevention plan services, first visit
G0439 Annual wellness visit, including personalized prevention plan services, subsequent visit
Payment for the initial visit is made only beginning the second year the patient is eligible for Medicare Part B—during the first year of coverage, only the Initial Preventive Physical Examination (IPPE) (the “Welcome to Medicare”) exam will be covered.
CMS has stated that only one physician will be paid for the initial visit; when the patient returns to the same or a new physician in the third year, only a subsequent visit will be paid. It is, therefore, important that this information be conveyed to any new physician who sees the patient.
The annual codes can be billed in addition to any other preventive service, such as G0101 or Q0091; no modifier is needed for this combination. Medicare has waived both the copayment and the deductible for the annual wellness visit, as well as all Medicare-covered preventive services that have been recommended with a grade of “A” (“strongly recommends”) or “B” (“recommends”) by the US Preventive Services Task Force.
The annual wellness visit requires seven elements at a minimum (i.e., you may document and perform more elements than this, but not fewer):
- Establish or update the patient’s medical and family history
- List her current medical providers and suppliers and all prescribed medications
- Record measurements of height, weight, body mass index (initial visit only), blood pressure, and other routine measurements
- Detect any cognitive impairment
- Establish or update a screening schedule for the next 5 to 10 years, including screenings appropriate for the general population, and any additional screenings that may be appropriate because of her particular risk factors
- Review the patient’s 1) potential (i.e., risk factors) for depression, based on use of an appropriate screening instrument, and 2) functional ability and level of safety based on direct observation or screening questions
- Furnish 1) personalized health advice and 2) refer her appropriately to health education or preventive services.
CMS has also indicated that, although they will pay for a problem E/M service and the annual wellness visit on the same date of service with a modifier -25 added to the E/M service, they expect this type of billing to be rare—because of the nature of the wellness visit, which is time-intensive. They also expect that, given these requirements, the patient will not be billed additionally for a noncovered preventive service.
We want to hear from you! Tell us what you think.
The Current Procedural Terminology (CPT) code set for 2011 includes several changes of interest to ObGyns. These include 1) guideline clarifications regarding wound debridement and obstetric care codes; 2) new codes for subsequent observation care; micro-remodeling of the bladder neck; insertion of a vaginal after-loading device; and 3) a lab code for detecting amniotic fluid in cervicovaginal secretions (using the AmniSure kit).
There is also a new code for vaccine counseling that will have an impact on you if your practice offers the human papillomavirus (HPV) vaccine to patients younger than 19 years.
There are changes to Medicare this year that you should take note of if you care for these patients, particularly in the area of preventive visit billing.
CPT and Medicare changes both took effect on January 1. The Health Insurance Portability and Accountability Act (HIPAA) requires that insurers accepted the new codes on that date.
Changes to the CPT code set
OBSERVATION CARE
One of the biggest headaches for medical practices has been standardized coding and billing for observation care that lasts more than 1 day. In the past, payers accepted a problem E/M for Day 2 of observation care, or instructed practices to code an unlisted E/M service. Now, you may report all care rendered in the observation setting with the addition of three new codes for subsequent care:
99244 Subsequent observation care, per day, for the evaluation and management of a patient, which requires at least 2 of these 3 key components: problem focused interval history, problem focused examination; medical decision making that is straightforward or of low complexity. Counseling and/or coordination of care with other providers or agencies are provided consistent with the nature of the problem(s) and the patient’s and/or family’s needs. Usually, the patient is stable, recovering, or improving. Physicians typically spend 15 minutes at the bedside and on the patient’s hospital floor or unit.
99225 Subsequent observation care, per day, for the evaluation and management of a patient, which requires at least 2 of these 3 key components: an expanded problem focused interval history; an expanded problem focused examination; medical decision making of moderate complexity. Counseling and/or coordination of care with other providers or agencies are provided consistent with the nature of the problem(s) and the patient’s and/or family’s needs. Usually, the patient is responding inadequately to therapy or has developed a minor complication. Physicians typically spend 25 minutes at the bedside and on the patient’s hospital floor or unit.
99226 Subsequent observation care, per day, for the evaluation and management of a patient, which requires at least 2 of these 3 key components: a detailed interval history; a detailed examination; medical decision making of high complexity. Counseling and/or coordination of care with other providers or agencies are provided consistent with the nature of the problem(s) and the patient’s and/or family’s needs. Usually, the patient is unstable or has developed a significant complication or a significant new problem. Physicians typically spend 35 minutes at the bedside and on the patient’s hospital floor or unit.
Note that each of these codes 1) “suggests” the status of the patient for each level of billing, and 2) includes a typical time. This means that, unlike the observation care admission codes or the observation admission/same-day discharge codes, time that is spent with the patient, or on the unit, may be used to select the code—if you document 1) the requirement that more than 50% of the typical time was spent on counseling or coordination of care, or both, and 2) a detailed description of this activity.
Codes for wound debridement were given a facelift with the addition of a new guideline that addresses both surgical and medical debridement. The surgical debridement codes, (11042–11047) are now reported on the basis of the depth of tissue removed and the surface area of the wound. This means that codes 11040 and 11041 were deleted to make room for new and revised codes.
This change will mean that, when you report these codes, you will need to document more information to bill. It’s also understood that coding separately for debridement of dermis or epidermis at the same time you code for debriding underlying structures would be inappropriate.
CPT has also indicated that active wound management codes 97597 and 97598 can now be reported by physicians or nonphysician providers as long as the provider has direct (one-on-one) contact. These codes should be reported for skin-surface debridement only.
The new and revised codes (some of which have been published in CPT in nonsequential order) are:
11042 Debridement, subcutaneous tissue (includes epidermis and dermis, if performed); first 20 sq cm or less
+11045 (new add-on code reported with 11042 only) each additional 20 sq cm or part thereof
11043 Debridement, muscle and/or facia (includes epidermis, dermis, and subcutaneous tissue, if performed); first 20 sq cm or less
+11046 (new add-on code reported with 11043 only) each additional 20 sq cm or part thereof
11044 Debridement, bone (includes epidermis, dermis, subcutaneous tissue, muscle and/or fascia, if performed); first 20 sq cm or less
+11047 (new add-on code reported with 11044 only) each additional 20 sq cm or part thereof
97597 Debridement (e.g., high pressure waterjet with/without suction, sharp selective debridement with scissors, scalpel and forceps), open wound, (e.g., fibrin, devitalized epidermis and/or dermis, exudate, debris, biofilm), including topical application(s), wound assessment, use of a whirlpool, when performed and instruction(s) for ongoing care, per session, total wound(s) surface area; first 20 sq cm or less
+95798 (add-on code reported with 97597 only) Each additional 20 sq cm, or part thereof.
TRANSURETHRAL RADIOFREQUENCY
Category III code 0193T, which described transurethral radiofrequency micro-remodeling for stress urinary incontinence, has been deleted and converted to a Category I CPT code, 53860 (Transurethral radiofrequency micro-remodeling of the female bladder neck and proximal urethra for stress urinary incontinence). The procedure includes a periurethral block and flushing the bladder with a lidocaine slurry, and can be performed in the office.
In all, the procedure requires nine treatment cycles during the session, but the code is billed only once. Catheterization and measurement of a voiding sample after the procedure are included in the code.
AFTERLOADING DEVICES FOR CLINICAL BRACHYTHERAPY
CPT revised—slightly—existing code 57155, and added code 57156 (Insertion of a vaginal radiation afterloading apparatus for clinical brachytherapy).
- Code 57155 was revised to clarify that only a single tandem is inserted into the uterus. There had been confusion earlier in this regard.
- The new code describes a procedure that may also include dilation of the vaginal canal to remove postradiation adhesions. That procedure also involves 1) placement of bladder and rectal catheters and 2) radiographic imaging to confirm placement, which are not coded separately.
CLARIFICATION OF OBSTETRIC GUIDELINES
Been having problems with payers and their interpretation of the delivery only, postpartum only, and delivery with postpartum care codes? CPT has, at last, clarified what you can, and cannot, bill in those circumstances. (Keep in mind, however, that you may not unbundle these procedures if more extensive care is provided: Most payers want you to bill the global OB care code that includes antepartum, intrapartum, and postpartum care.)
In some cases (such as Medicaid), the payer stipulates that only the physician who actually performed the delivery may bill for it, even if the delivering physician is covering for, or is a member of, the same group practice as the primary attending of record. The “delivery-only” codes should be reported when 1) an unaffiliated physician has delivered the baby but will not be providing any outpatient postpartum care or 2) the payer has specified this method of billing for the covering or affiliated provider.
CPT has clarified that delivery-only codes (59409, 59514, or 59612, 59620) include admission to the hospital, the admission history and physical exam, uncomplicated labor and delivery (including delivery of the placenta, or use of forceps or vacuum extraction). These codes do not include inpatient rounding or discharge day care after delivery (and, of course, include no outpatient postpartum care). When, as the delivering physician, you also provide inpatient postdelivery care, therefore, you may additionally bill subsequent hospital care codes and discharge day management codes (99231-99233, 99238-99239).
If the unaffiliated physician performs the delivery and also intends on providing outpatient postpartum care, the CPT codes for delivery with postpartum are to be reported (59410, 59515, 59614, 59622). In addition to the delivery, these codes include all inpatient and outpatient postpartum care. And finally, for those physicians who are only providing outpatient postpartum care, the code 59430, Postpartum care only, should be reported.
PLACENTAL ALPHA MICROGLOBULIN-1
A new code, 84112 (Placental alpha microglobulin-1 [PAMG-11], cervicovaginal secretion, qualitative), has been added to allow the clinical laboratory to bill for this immunoassay that detects amniotic fluid in the secretions. Physician work involves collection of the specimen but, under CPT rules, collection is included as part of any E/M service.
Note: An existing code for this test that is used by Blue Cross/Blue Shield payers (S3628) remains valid in 2011.
HPV VACCINE COUNSELING
Before January 1, 2011, if you counseled a patient about the HPV vaccine, you could report preventive counseling codes, such as 99401–99404, in addition to the vaccine administration code, 90471 (Immunization administration, 1 vaccine). Now, however, you have a new code for counseling and vaccine administration for a patient who is younger than 19 years—the age group most likely to be counseled about this vaccine. When you see, and counsel, such a patient before administering the vaccine, on the same date of service, code 90460 (Immunization administration through 18 years of age via any route of administration, with counseling by physician or other qualified health care profession; first vaccine/toxoid component), and 90649 for the quadrivalent or 90650 for the bivalent HPV vaccine.
If your patient is 19 years or older and requires counseling, continue to bill 99401– 99404 for counseling, with 90471 for immunization and 90649 or 90650 for the vaccine. Keep in mind: Whether you report 90460 or the 9940X codes, you are required to document the content of the counseling. Codes 9940X also require documentation of the duration of counseling.
INFLUENZA VACCINE
New codes have been established for the flu vaccine, but you won’t be using them: They are intended to address future pandemic strains of influenza. This year’s vaccine contains the H1N1 strain, but is coded as the normal seasonal flu vaccine, based on the type given:
90656 (preservative-free)
90658 (split virus)
90660 (intranasal)
90662 (enhanced vaccine for patients older than 65 years).
Changes to Medicare billing
Some of the coding and billing changes this year that have an impact on ObGyn practice come from the Centers of Medicare and Medicaid Services (CMS) and the Affordable Care Act.
TIMELY FILING
The Affordable Care Act calls for a reduction in the maximum time period for submission of Medicare fee-for-service claims. Before January 1, a provider had 15 to 27 months to submit first-time claims to Medicare. Now, these claims must be filed within a calendar year of the date of service. Exceptions can be made for retroactive entitlement or in situations in which there is a secondary payer.
PAYMENTS TO CERTIFIED NURSE MIDWIVES
Next, more good news—if you employ a certified nurse midwife (CNM) in your practice. Before January 1, Medicare reimbursed direct billing from a CNM at only 65% of the Medicare Physician Fee Schedule. Now, a CNM is paid the same as a physician when she (he) bills under her own number.
In the past, some practices billed for the services of a CNM under “incident to” rules, to capture the physician payment—but this also meant that the CNM could not see a new patient. Under the change I’m describing, all CNMs can bill Medicare directly; see new patients; and be paid the same as the physician is paid. In addition, CNMs are no longer required to be supervised by a physician when they perform diagnostic tests that fall under the scope of their practice.
ANNUAL WELLNESS VISIT
The Affordable Care Act extended preventive coverage to Medicare beneficiaries in the form of an annual wellness visit. The two new codes here have been valued based on a level 4-problem new and established E/M service:
G0438 Annual wellness visit, including personalized prevention plan services, first visit
G0439 Annual wellness visit, including personalized prevention plan services, subsequent visit
Payment for the initial visit is made only beginning the second year the patient is eligible for Medicare Part B—during the first year of coverage, only the Initial Preventive Physical Examination (IPPE) (the “Welcome to Medicare”) exam will be covered.
CMS has stated that only one physician will be paid for the initial visit; when the patient returns to the same or a new physician in the third year, only a subsequent visit will be paid. It is, therefore, important that this information be conveyed to any new physician who sees the patient.
The annual codes can be billed in addition to any other preventive service, such as G0101 or Q0091; no modifier is needed for this combination. Medicare has waived both the copayment and the deductible for the annual wellness visit, as well as all Medicare-covered preventive services that have been recommended with a grade of “A” (“strongly recommends”) or “B” (“recommends”) by the US Preventive Services Task Force.
The annual wellness visit requires seven elements at a minimum (i.e., you may document and perform more elements than this, but not fewer):
- Establish or update the patient’s medical and family history
- List her current medical providers and suppliers and all prescribed medications
- Record measurements of height, weight, body mass index (initial visit only), blood pressure, and other routine measurements
- Detect any cognitive impairment
- Establish or update a screening schedule for the next 5 to 10 years, including screenings appropriate for the general population, and any additional screenings that may be appropriate because of her particular risk factors
- Review the patient’s 1) potential (i.e., risk factors) for depression, based on use of an appropriate screening instrument, and 2) functional ability and level of safety based on direct observation or screening questions
- Furnish 1) personalized health advice and 2) refer her appropriately to health education or preventive services.
CMS has also indicated that, although they will pay for a problem E/M service and the annual wellness visit on the same date of service with a modifier -25 added to the E/M service, they expect this type of billing to be rare—because of the nature of the wellness visit, which is time-intensive. They also expect that, given these requirements, the patient will not be billed additionally for a noncovered preventive service.
We want to hear from you! Tell us what you think.
The Current Procedural Terminology (CPT) code set for 2011 includes several changes of interest to ObGyns. These include 1) guideline clarifications regarding wound debridement and obstetric care codes; 2) new codes for subsequent observation care; micro-remodeling of the bladder neck; insertion of a vaginal after-loading device; and 3) a lab code for detecting amniotic fluid in cervicovaginal secretions (using the AmniSure kit).
There is also a new code for vaccine counseling that will have an impact on you if your practice offers the human papillomavirus (HPV) vaccine to patients younger than 19 years.
There are changes to Medicare this year that you should take note of if you care for these patients, particularly in the area of preventive visit billing.
CPT and Medicare changes both took effect on January 1. The Health Insurance Portability and Accountability Act (HIPAA) requires that insurers accepted the new codes on that date.
Changes to the CPT code set
OBSERVATION CARE
One of the biggest headaches for medical practices has been standardized coding and billing for observation care that lasts more than 1 day. In the past, payers accepted a problem E/M for Day 2 of observation care, or instructed practices to code an unlisted E/M service. Now, you may report all care rendered in the observation setting with the addition of three new codes for subsequent care:
99244 Subsequent observation care, per day, for the evaluation and management of a patient, which requires at least 2 of these 3 key components: problem focused interval history, problem focused examination; medical decision making that is straightforward or of low complexity. Counseling and/or coordination of care with other providers or agencies are provided consistent with the nature of the problem(s) and the patient’s and/or family’s needs. Usually, the patient is stable, recovering, or improving. Physicians typically spend 15 minutes at the bedside and on the patient’s hospital floor or unit.
99225 Subsequent observation care, per day, for the evaluation and management of a patient, which requires at least 2 of these 3 key components: an expanded problem focused interval history; an expanded problem focused examination; medical decision making of moderate complexity. Counseling and/or coordination of care with other providers or agencies are provided consistent with the nature of the problem(s) and the patient’s and/or family’s needs. Usually, the patient is responding inadequately to therapy or has developed a minor complication. Physicians typically spend 25 minutes at the bedside and on the patient’s hospital floor or unit.
99226 Subsequent observation care, per day, for the evaluation and management of a patient, which requires at least 2 of these 3 key components: a detailed interval history; a detailed examination; medical decision making of high complexity. Counseling and/or coordination of care with other providers or agencies are provided consistent with the nature of the problem(s) and the patient’s and/or family’s needs. Usually, the patient is unstable or has developed a significant complication or a significant new problem. Physicians typically spend 35 minutes at the bedside and on the patient’s hospital floor or unit.
Note that each of these codes 1) “suggests” the status of the patient for each level of billing, and 2) includes a typical time. This means that, unlike the observation care admission codes or the observation admission/same-day discharge codes, time that is spent with the patient, or on the unit, may be used to select the code—if you document 1) the requirement that more than 50% of the typical time was spent on counseling or coordination of care, or both, and 2) a detailed description of this activity.
Codes for wound debridement were given a facelift with the addition of a new guideline that addresses both surgical and medical debridement. The surgical debridement codes, (11042–11047) are now reported on the basis of the depth of tissue removed and the surface area of the wound. This means that codes 11040 and 11041 were deleted to make room for new and revised codes.
This change will mean that, when you report these codes, you will need to document more information to bill. It’s also understood that coding separately for debridement of dermis or epidermis at the same time you code for debriding underlying structures would be inappropriate.
CPT has also indicated that active wound management codes 97597 and 97598 can now be reported by physicians or nonphysician providers as long as the provider has direct (one-on-one) contact. These codes should be reported for skin-surface debridement only.
The new and revised codes (some of which have been published in CPT in nonsequential order) are:
11042 Debridement, subcutaneous tissue (includes epidermis and dermis, if performed); first 20 sq cm or less
+11045 (new add-on code reported with 11042 only) each additional 20 sq cm or part thereof
11043 Debridement, muscle and/or facia (includes epidermis, dermis, and subcutaneous tissue, if performed); first 20 sq cm or less
+11046 (new add-on code reported with 11043 only) each additional 20 sq cm or part thereof
11044 Debridement, bone (includes epidermis, dermis, subcutaneous tissue, muscle and/or fascia, if performed); first 20 sq cm or less
+11047 (new add-on code reported with 11044 only) each additional 20 sq cm or part thereof
97597 Debridement (e.g., high pressure waterjet with/without suction, sharp selective debridement with scissors, scalpel and forceps), open wound, (e.g., fibrin, devitalized epidermis and/or dermis, exudate, debris, biofilm), including topical application(s), wound assessment, use of a whirlpool, when performed and instruction(s) for ongoing care, per session, total wound(s) surface area; first 20 sq cm or less
+95798 (add-on code reported with 97597 only) Each additional 20 sq cm, or part thereof.
TRANSURETHRAL RADIOFREQUENCY
Category III code 0193T, which described transurethral radiofrequency micro-remodeling for stress urinary incontinence, has been deleted and converted to a Category I CPT code, 53860 (Transurethral radiofrequency micro-remodeling of the female bladder neck and proximal urethra for stress urinary incontinence). The procedure includes a periurethral block and flushing the bladder with a lidocaine slurry, and can be performed in the office.
In all, the procedure requires nine treatment cycles during the session, but the code is billed only once. Catheterization and measurement of a voiding sample after the procedure are included in the code.
AFTERLOADING DEVICES FOR CLINICAL BRACHYTHERAPY
CPT revised—slightly—existing code 57155, and added code 57156 (Insertion of a vaginal radiation afterloading apparatus for clinical brachytherapy).
- Code 57155 was revised to clarify that only a single tandem is inserted into the uterus. There had been confusion earlier in this regard.
- The new code describes a procedure that may also include dilation of the vaginal canal to remove postradiation adhesions. That procedure also involves 1) placement of bladder and rectal catheters and 2) radiographic imaging to confirm placement, which are not coded separately.
CLARIFICATION OF OBSTETRIC GUIDELINES
Been having problems with payers and their interpretation of the delivery only, postpartum only, and delivery with postpartum care codes? CPT has, at last, clarified what you can, and cannot, bill in those circumstances. (Keep in mind, however, that you may not unbundle these procedures if more extensive care is provided: Most payers want you to bill the global OB care code that includes antepartum, intrapartum, and postpartum care.)
In some cases (such as Medicaid), the payer stipulates that only the physician who actually performed the delivery may bill for it, even if the delivering physician is covering for, or is a member of, the same group practice as the primary attending of record. The “delivery-only” codes should be reported when 1) an unaffiliated physician has delivered the baby but will not be providing any outpatient postpartum care or 2) the payer has specified this method of billing for the covering or affiliated provider.
CPT has clarified that delivery-only codes (59409, 59514, or 59612, 59620) include admission to the hospital, the admission history and physical exam, uncomplicated labor and delivery (including delivery of the placenta, or use of forceps or vacuum extraction). These codes do not include inpatient rounding or discharge day care after delivery (and, of course, include no outpatient postpartum care). When, as the delivering physician, you also provide inpatient postdelivery care, therefore, you may additionally bill subsequent hospital care codes and discharge day management codes (99231-99233, 99238-99239).
If the unaffiliated physician performs the delivery and also intends on providing outpatient postpartum care, the CPT codes for delivery with postpartum are to be reported (59410, 59515, 59614, 59622). In addition to the delivery, these codes include all inpatient and outpatient postpartum care. And finally, for those physicians who are only providing outpatient postpartum care, the code 59430, Postpartum care only, should be reported.
PLACENTAL ALPHA MICROGLOBULIN-1
A new code, 84112 (Placental alpha microglobulin-1 [PAMG-11], cervicovaginal secretion, qualitative), has been added to allow the clinical laboratory to bill for this immunoassay that detects amniotic fluid in the secretions. Physician work involves collection of the specimen but, under CPT rules, collection is included as part of any E/M service.
Note: An existing code for this test that is used by Blue Cross/Blue Shield payers (S3628) remains valid in 2011.
HPV VACCINE COUNSELING
Before January 1, 2011, if you counseled a patient about the HPV vaccine, you could report preventive counseling codes, such as 99401–99404, in addition to the vaccine administration code, 90471 (Immunization administration, 1 vaccine). Now, however, you have a new code for counseling and vaccine administration for a patient who is younger than 19 years—the age group most likely to be counseled about this vaccine. When you see, and counsel, such a patient before administering the vaccine, on the same date of service, code 90460 (Immunization administration through 18 years of age via any route of administration, with counseling by physician or other qualified health care profession; first vaccine/toxoid component), and 90649 for the quadrivalent or 90650 for the bivalent HPV vaccine.
If your patient is 19 years or older and requires counseling, continue to bill 99401– 99404 for counseling, with 90471 for immunization and 90649 or 90650 for the vaccine. Keep in mind: Whether you report 90460 or the 9940X codes, you are required to document the content of the counseling. Codes 9940X also require documentation of the duration of counseling.
INFLUENZA VACCINE
New codes have been established for the flu vaccine, but you won’t be using them: They are intended to address future pandemic strains of influenza. This year’s vaccine contains the H1N1 strain, but is coded as the normal seasonal flu vaccine, based on the type given:
90656 (preservative-free)
90658 (split virus)
90660 (intranasal)
90662 (enhanced vaccine for patients older than 65 years).
Changes to Medicare billing
Some of the coding and billing changes this year that have an impact on ObGyn practice come from the Centers of Medicare and Medicaid Services (CMS) and the Affordable Care Act.
TIMELY FILING
The Affordable Care Act calls for a reduction in the maximum time period for submission of Medicare fee-for-service claims. Before January 1, a provider had 15 to 27 months to submit first-time claims to Medicare. Now, these claims must be filed within a calendar year of the date of service. Exceptions can be made for retroactive entitlement or in situations in which there is a secondary payer.
PAYMENTS TO CERTIFIED NURSE MIDWIVES
Next, more good news—if you employ a certified nurse midwife (CNM) in your practice. Before January 1, Medicare reimbursed direct billing from a CNM at only 65% of the Medicare Physician Fee Schedule. Now, a CNM is paid the same as a physician when she (he) bills under her own number.
In the past, some practices billed for the services of a CNM under “incident to” rules, to capture the physician payment—but this also meant that the CNM could not see a new patient. Under the change I’m describing, all CNMs can bill Medicare directly; see new patients; and be paid the same as the physician is paid. In addition, CNMs are no longer required to be supervised by a physician when they perform diagnostic tests that fall under the scope of their practice.
ANNUAL WELLNESS VISIT
The Affordable Care Act extended preventive coverage to Medicare beneficiaries in the form of an annual wellness visit. The two new codes here have been valued based on a level 4-problem new and established E/M service:
G0438 Annual wellness visit, including personalized prevention plan services, first visit
G0439 Annual wellness visit, including personalized prevention plan services, subsequent visit
Payment for the initial visit is made only beginning the second year the patient is eligible for Medicare Part B—during the first year of coverage, only the Initial Preventive Physical Examination (IPPE) (the “Welcome to Medicare”) exam will be covered.
CMS has stated that only one physician will be paid for the initial visit; when the patient returns to the same or a new physician in the third year, only a subsequent visit will be paid. It is, therefore, important that this information be conveyed to any new physician who sees the patient.
The annual codes can be billed in addition to any other preventive service, such as G0101 or Q0091; no modifier is needed for this combination. Medicare has waived both the copayment and the deductible for the annual wellness visit, as well as all Medicare-covered preventive services that have been recommended with a grade of “A” (“strongly recommends”) or “B” (“recommends”) by the US Preventive Services Task Force.
The annual wellness visit requires seven elements at a minimum (i.e., you may document and perform more elements than this, but not fewer):
- Establish or update the patient’s medical and family history
- List her current medical providers and suppliers and all prescribed medications
- Record measurements of height, weight, body mass index (initial visit only), blood pressure, and other routine measurements
- Detect any cognitive impairment
- Establish or update a screening schedule for the next 5 to 10 years, including screenings appropriate for the general population, and any additional screenings that may be appropriate because of her particular risk factors
- Review the patient’s 1) potential (i.e., risk factors) for depression, based on use of an appropriate screening instrument, and 2) functional ability and level of safety based on direct observation or screening questions
- Furnish 1) personalized health advice and 2) refer her appropriately to health education or preventive services.
CMS has also indicated that, although they will pay for a problem E/M service and the annual wellness visit on the same date of service with a modifier -25 added to the E/M service, they expect this type of billing to be rare—because of the nature of the wellness visit, which is time-intensive. They also expect that, given these requirements, the patient will not be billed additionally for a noncovered preventive service.
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IN THIS ARTICLE
Would a colonoscopy have made a difference? ... Suicide blamed on failure to diagnose bipolar disorder
Would a colonoscopy have made a difference?
ABDOMINAL PAIN, BURNING AND CRAMPING, and inability to eat led a 31-year-old man to visit his primary care physician. A nurse practitioner (NP) examined the man, prescribed ranitidine, and gave him an appointment for a complete physical the following month.
The patient’s history, as provided during the physical exam, included tobacco chewing, high coffee intake, and occasional abdominal pain and increased stools. He said that his mother had been diagnosed with colon cancer at 54 years of age. Neither a rectal exam nor colonoscopy was performed.
The NP substituted pantoprazole for ranitidine and ordered an upper gastrointestinal series with contrast to rule out gastritis or an ulcer. The results were negative. They were given to the primary care physician, who never saw the patient or reviewed his chart.
A month later, the patient saw a nurse for continued problems eating, despite symptom relief on pantoprazole. The nurse stuck with a diagnosis of gastritis and told the patient to follow up in 6 months and to call if problems arose.
Four months later, the patient returned complaining of worsening stomach cramps and burning. The NP changed his medication to lansoprazole and set up an appointment in 3 months with a gastroenterologist.
The patient returned a month afterward reporting increasing pain and loose stools. The GI consult was moved to an earlier date after discussion with the primary care physician, but the patient went to an emergency room before the scheduled consultation.
An abdominal computed tomography scan and colonoscopy revealed near obstruction of the right side of the colon by a stage IV tumor and metastasis to the peritoneum and lymph nodes. The patient underwent immediate surgery, followed by chemotherapy, more surgery, and a cingulotomy for pain relief. He died about 2 years later.
PLAINTIFF’S CLAIM The NP should have performed a rectal exam, obtained stool for occult blood tests, or ordered a colonoscopy. The patient’s chances of survival would have been better if he’d been diagnosed and treated earlier.
THE DEFENSE The patient didn’t need a colonoscopy; his tobacco chewing and excessive coffee drinking explained his eating difficulties. The NP was properly supervised and there was no independent duty to review individual patient charts and sign off on them regularly. The patient was already at stage IV when he was seen initially; nothing could have changed the treatment or outcome.
VERDICT $4.65 million Massachusetts verdict.
COMMENT Regardless of the medical facts of this case, supervision of staff and other health professionals is tricky. Clear job descriptions, protocols for care, and expectations for consultation will help avoid legal pitfalls.
Suicide blamed on failure to diagnose bipolar disorder
A 29-YEAR-OLD WOMAN spent about 6 months under the care of a psychiatrist, during which time she was diagnosed with severe depression. The psychiatrist prescribed a series of selective serotonin reuptake inhibitors (SSRIs). The patient took the medications as prescribed but eventually committed suicide.
PLAINTIFF’S CLAIM The psychiatrist misdiagnosed the patient; the patient’s depression was one symptom of bipolar disorder. The US Food and Drug Administration has warned that SSRIs increase the risk of suicide in patients with bipolar disorder.
THE DEFENSE The last time the psychiatrist saw the patient was more than 30 days before her death; the diagnosis of depression was correct.
VERDICT $175,000 Michigan settlement.
COMMENT Every patient with depressive features should be screened for bipolar disorder. As this case illustrates, the medical and legal consequences can be profound.
Would a colonoscopy have made a difference?
ABDOMINAL PAIN, BURNING AND CRAMPING, and inability to eat led a 31-year-old man to visit his primary care physician. A nurse practitioner (NP) examined the man, prescribed ranitidine, and gave him an appointment for a complete physical the following month.
The patient’s history, as provided during the physical exam, included tobacco chewing, high coffee intake, and occasional abdominal pain and increased stools. He said that his mother had been diagnosed with colon cancer at 54 years of age. Neither a rectal exam nor colonoscopy was performed.
The NP substituted pantoprazole for ranitidine and ordered an upper gastrointestinal series with contrast to rule out gastritis or an ulcer. The results were negative. They were given to the primary care physician, who never saw the patient or reviewed his chart.
A month later, the patient saw a nurse for continued problems eating, despite symptom relief on pantoprazole. The nurse stuck with a diagnosis of gastritis and told the patient to follow up in 6 months and to call if problems arose.
Four months later, the patient returned complaining of worsening stomach cramps and burning. The NP changed his medication to lansoprazole and set up an appointment in 3 months with a gastroenterologist.
The patient returned a month afterward reporting increasing pain and loose stools. The GI consult was moved to an earlier date after discussion with the primary care physician, but the patient went to an emergency room before the scheduled consultation.
An abdominal computed tomography scan and colonoscopy revealed near obstruction of the right side of the colon by a stage IV tumor and metastasis to the peritoneum and lymph nodes. The patient underwent immediate surgery, followed by chemotherapy, more surgery, and a cingulotomy for pain relief. He died about 2 years later.
PLAINTIFF’S CLAIM The NP should have performed a rectal exam, obtained stool for occult blood tests, or ordered a colonoscopy. The patient’s chances of survival would have been better if he’d been diagnosed and treated earlier.
THE DEFENSE The patient didn’t need a colonoscopy; his tobacco chewing and excessive coffee drinking explained his eating difficulties. The NP was properly supervised and there was no independent duty to review individual patient charts and sign off on them regularly. The patient was already at stage IV when he was seen initially; nothing could have changed the treatment or outcome.
VERDICT $4.65 million Massachusetts verdict.
COMMENT Regardless of the medical facts of this case, supervision of staff and other health professionals is tricky. Clear job descriptions, protocols for care, and expectations for consultation will help avoid legal pitfalls.
Suicide blamed on failure to diagnose bipolar disorder
A 29-YEAR-OLD WOMAN spent about 6 months under the care of a psychiatrist, during which time she was diagnosed with severe depression. The psychiatrist prescribed a series of selective serotonin reuptake inhibitors (SSRIs). The patient took the medications as prescribed but eventually committed suicide.
PLAINTIFF’S CLAIM The psychiatrist misdiagnosed the patient; the patient’s depression was one symptom of bipolar disorder. The US Food and Drug Administration has warned that SSRIs increase the risk of suicide in patients with bipolar disorder.
THE DEFENSE The last time the psychiatrist saw the patient was more than 30 days before her death; the diagnosis of depression was correct.
VERDICT $175,000 Michigan settlement.
COMMENT Every patient with depressive features should be screened for bipolar disorder. As this case illustrates, the medical and legal consequences can be profound.
Would a colonoscopy have made a difference?
ABDOMINAL PAIN, BURNING AND CRAMPING, and inability to eat led a 31-year-old man to visit his primary care physician. A nurse practitioner (NP) examined the man, prescribed ranitidine, and gave him an appointment for a complete physical the following month.
The patient’s history, as provided during the physical exam, included tobacco chewing, high coffee intake, and occasional abdominal pain and increased stools. He said that his mother had been diagnosed with colon cancer at 54 years of age. Neither a rectal exam nor colonoscopy was performed.
The NP substituted pantoprazole for ranitidine and ordered an upper gastrointestinal series with contrast to rule out gastritis or an ulcer. The results were negative. They were given to the primary care physician, who never saw the patient or reviewed his chart.
A month later, the patient saw a nurse for continued problems eating, despite symptom relief on pantoprazole. The nurse stuck with a diagnosis of gastritis and told the patient to follow up in 6 months and to call if problems arose.
Four months later, the patient returned complaining of worsening stomach cramps and burning. The NP changed his medication to lansoprazole and set up an appointment in 3 months with a gastroenterologist.
The patient returned a month afterward reporting increasing pain and loose stools. The GI consult was moved to an earlier date after discussion with the primary care physician, but the patient went to an emergency room before the scheduled consultation.
An abdominal computed tomography scan and colonoscopy revealed near obstruction of the right side of the colon by a stage IV tumor and metastasis to the peritoneum and lymph nodes. The patient underwent immediate surgery, followed by chemotherapy, more surgery, and a cingulotomy for pain relief. He died about 2 years later.
PLAINTIFF’S CLAIM The NP should have performed a rectal exam, obtained stool for occult blood tests, or ordered a colonoscopy. The patient’s chances of survival would have been better if he’d been diagnosed and treated earlier.
THE DEFENSE The patient didn’t need a colonoscopy; his tobacco chewing and excessive coffee drinking explained his eating difficulties. The NP was properly supervised and there was no independent duty to review individual patient charts and sign off on them regularly. The patient was already at stage IV when he was seen initially; nothing could have changed the treatment or outcome.
VERDICT $4.65 million Massachusetts verdict.
COMMENT Regardless of the medical facts of this case, supervision of staff and other health professionals is tricky. Clear job descriptions, protocols for care, and expectations for consultation will help avoid legal pitfalls.
Suicide blamed on failure to diagnose bipolar disorder
A 29-YEAR-OLD WOMAN spent about 6 months under the care of a psychiatrist, during which time she was diagnosed with severe depression. The psychiatrist prescribed a series of selective serotonin reuptake inhibitors (SSRIs). The patient took the medications as prescribed but eventually committed suicide.
PLAINTIFF’S CLAIM The psychiatrist misdiagnosed the patient; the patient’s depression was one symptom of bipolar disorder. The US Food and Drug Administration has warned that SSRIs increase the risk of suicide in patients with bipolar disorder.
THE DEFENSE The last time the psychiatrist saw the patient was more than 30 days before her death; the diagnosis of depression was correct.
VERDICT $175,000 Michigan settlement.
COMMENT Every patient with depressive features should be screened for bipolar disorder. As this case illustrates, the medical and legal consequences can be profound.
Traumatic brain injury: Pharmacotherapy options for cognitive deficits
Mr. A, age 45, presents to the psychiatry clinic complaining of “ADHD.” He says he is not able to sit through movies and often gets distracted while on his computer at work. He also is having problems in his relationship with his wife; she says having a conversation with him is difficult. He has seen a psychiatrist for depression, which is currently managed by his primary care physician (PCP), who prescribed sertraline, 100 mg/d. Mr. A feels that although his depression is now under control, the medication has had limited effect on improving his concentration.
With further discussion, Mr. A reveals that 6 months ago he was involved in a car accident and suffered a mild traumatic brain injury (TBI). He was hospitalized overnight and was encouraged to follow up with his PCP. During his only follow-up visit, Mr. A told his PCP that he was having difficulty concentrating since the accident. However, because Mr. A has a remote history of alcohol abuse, his physician was reluctant to give him additional medication and referred him to a psychiatrist.
TBI is increasingly common but often overlooked or not treated in the emergency room (ER). Each year at least 1.7 million people experience a TBI; 275,000 are hospitalized and 52,000 die.1 The true incidence likely is greater because patients who do not present to the ER or hospital are not included in most studies, and the often-subtle psychiatric sequelae may preclude patients from seeking mental health treatment.
Psychiatric disorders are common among those who sustain a TBI (Table 1).2 One prospective cohort study found that patients with mild TBI are 2.8 times more likely than other patients to develop a psychiatric disorder.3 Statistics regarding TBI and psychiatric illness often are limited because they rely on self-reports, chart review, or retrospective studies.4
TBI severity can be classified on the basis of Glasgow Coma Scale score and other factors (Table 2).5 The correlation between severity of injury and resulting psychiatric illness or post-concussive symptoms is unclear.6 There is evidence that cognitive defects are associated with decreased function. Cognitive dysfunction also has been associated with disability 10 years after moderate to severe TBI.7 The association between cognitive dysfunction and outcome is more strongly correlated with moderate to severe TBI; there is no clear association in mild TBI.7 Additionally, compared with patients with severe TBI, those with mild TBI were more likely to be employed. At all severity levels, function improves over time. Mild, moderate, and severe TBI have a similar recovery curve.7
Table 1
Psychiatric symptoms: Common among TBI patients
| Psychiatric symptom | Incidence |
|---|---|
| Aggression | 30% |
| Anxiety | 10% to 70% |
| Apathy | 10% |
| Cognitive impairment | 25% to 70% |
| Depression | 25% to 50% |
| Mania | 1% to 10% |
| Psychosis | 3% to 8% |
| TBI: traumatic brain injury | |
| Source: Adapted from reference 2 | |
Table 2
Classifying severity of traumatic brain injury
| Severity | GCS score | LOC duration | PTA* |
|---|---|---|---|
| Mild | 13 to 15 | <30 minutes | <1 hour |
| Moderate | 9 to 12 | 1 to 24 hours | 1 to 24 hours |
| Severe | <8 | >24 hours | >24 hours |
| *Includes loss of memory immediately before or after the accident | |||
| GCS: Glasgow Coma Scale; LOC: loss of consciousness; PTA: posttraumatic amnesia | |||
| Source: Reference 5 | |||
Cognitive dysfunction and TBI
Cognitive dysfunction can be split into 3 categories:
- executive function
- memory
- processing speed.
The incidence of cognitive dysfunction after TBI is unclear. Several methods are used to quantify cognitive dysfunction in TBI patients; it is widely regarded that the Mini-Mental State Exam is not adequate to screen for subtle cognitive deficits.6 However, there is no clear consensus on which tool should be used.5
Off-label pharmacotherapy
There are no FDA-approved medications for treating neuropsychiatric sequelae of TBI. Treatment should be symptom-based and employ the “start low, go slow” approach. Compared with patients without brain injury, TBI patients may experience increased adverse effects from psychotropics but may require standard doses. These patients also may have comorbidities such as seizure disorders, substance abuse, and depression that will affect treatment.2 Different areas of cognitive function respond to different medication classes. Suggested medications include stimulant and nonstimulant catecholaminergic agents and cholinesterase inhibitors (Table 3).8
Executive function responds to non-stimulant catecholaminergics. In a review, Writer and Schillerstrom5 found that TBI patients who received catecholaminergic augmentation showed improved function in 6 of 7 studies. In 2 randomized controlled trials (RCTs) and 4 nonrandomized, placebo-controlled trials, patients with mild to severe TBI showed improved executive function, attention, global cognitive function, memory, language, and/ or arousal with use of bromocriptine, pramipexole, carbidopa/levodopa, or amantadine.5 The greatest improvements were found in executive function. In 1 RCT, 10 patients with mild to severe TBI showed no functional improvement after 2 weeks of treatment.
Amantadine, 200 to 400 mg/d, has been shown to safely improve arousal and cognitive function in patients with moderate to severe TBI when started 3 days to 5 months after injury.9 Amantadine, 400 mg/d, also improves executive function measures without significant benefit in attention or memory in patients with mild to severe TBI 6 months post-injury.10
Memory responds to cholinesterase inhibitors. Memory deficits secondary to TBI affect immediate and delayed memory. The cholinesterase inhibitor donepezil is approved for treating Alzheimer’s disease (AD) in the United States and Canada, and research suggests memory deficits after TBI may be similar to those seen in AD.11 This includes deficits in long-term memory storage, which likely is associated with the cholinergic system.11 Post-mortem studies have found similarities in traumatically injured brains and those of AD patients.11
Three small prospective studies of done-pezil have shown improved memory and attention in TBI patients when cognition is the primary outcome, with 1 small negative open-label trial.7 In a study of 53 patients, Whelan et al12 found that donepezil improved patients’ intelligence quotient and clinician-based assessment of cognition over 2 years. Taverni et al13 found memory improvement in 2 TBI patients within 3 weeks of starting donepezil. These results suggest that donepezil may be used in acute and late phases of memory deficits following mild, moderate, or severe TBI.6 All studies titrated donepezil from 5 to 10 mg/d over several weeks. Dosing guidelines for donepezil in AD suggest 5 mg/d for 4 to 6 weeks, which may be increased to 10 mg/d if needed.8
Rivastigmine (3 to 6 mg/d) has been shown to be effective in mild TBI when started 1 year after injury and safe for 12 to 38 weeks of treatment.14,15 One retrospective cohort study of 111 patients with chronic TBI found no difference among donepezil, rivastigmine, or galantamine, with mean doses of 7.2 mg/d, 10 mg/d, and 2.3 mg/d, respectively.16 Sixty-one percent of patients showed improvement and the remainder had modest or no response. This study suggests that positive response on cognition may be similar among cholinesterase inhibitors. In case reports, physostigmine has offered some benefit17,18; however, cardiovascular and autonomic side effects restrict its use.11 Tacrine is associated with problematic gastrointestinal and hepatic side effects.11
Processing speed responds to stimulant catecholaminergics. Although the incidence of psychiatric illness is not correlated with TBI severity, evidence suggests that speed of processing mediates the relationship between injury severity and functional decline.19 Therefore, aggressively treating these deficits may help improve function.
Methylphenidate improves attention and processing speed after TBI. A review of 7 randomized trials and 2 nonrandomized trials indicated that patients with mild to severe, chronic TBI experienced significantly improved cognitive function after methylphenidate treatment.5 Willmott and Ponsford20 found significant enhancement in information processing speed within 2 weeks of methylphenidate treatment in 40 patients with moderate or severe TBI. Methylphenidate increased the rate of recovery and led to improvement in acute21 and post-acute phases.22 In addition, methylphenidate may improve processing speed even in the absence of significant changes in attention.23
The standard methylphenidate dose used in most studies, 0.3 mg/kg twice daily, is safe and effective. Dosing usually is started at 5 mg/d and titrated to symptomatic relief. Because methylphenidate does not lower the seizure threshold, it is safe for patients at high risk for seizure.24 Methylphenidate also significantly improves attention and speed of processing in pediatric head trauma.25,26
Dextroamphetamine also is used to treat speed of processing dysfunction after TBI, but is less studied than methylphenidate. Dextroamphetamine, 5 to 30 mg/d, was found to effectively treat attention problems that interfered with rehabilitation in patients with severe TBI.27
Table 3
Recommended treatments for mild TBI-related cognitive deficits
| Deficit | First-line medication | Side effects | Contraindications | Other treatments |
|---|---|---|---|---|
| Memory | Donepezil (5 to 10 mg/d) | Diarrhea, nausea, vomiting, muscle cramps, fatigue, anorexia | Hypersensitivity to donepezil or piperidine derivatives | Rivastigmine, galantamine, physostigmine, CDP-choline |
| Speed of processing | Methylphenidate (0.3 mg/kg twice daily) | Headache, insomnia, decreased appetite, nausea, vomiting, anxiety, irritability | Hypersensitivity to methylphenidate, glaucoma, history of Tourette syndrome or tics, use of MAOI within 14 days | Dextroamphetamine |
| Executive function | Amantadine (200 to 400 mg/d) | CNS depression, orthostatic hypotension, peripheral edema, agitation, nausea, anorexia | Hypersensitivity to amantadine | Bromocriptine, pramipexole, carbidopa/levodopa |
| CDP-choline: cytidinediphosphocholine; MAOI: monoamine oxidase inhibitor | ||||
| Source: Reference 8 | ||||
Nonpharmacologic treatments
In addition to pharmacotherapy, nonpharmacologic interventions also should be a mainstay of treatment. Compensatory training and cognitive exercise may improve patients’ cognitive deficits and return some sense of control. Individual and family psychotherapy, including cognitive-behavioral therapy, also may be beneficial.2 Review sources have identified the importance of validating patients’ symptoms and developing a goal-based treatment plan.6
CASE CONTINUED: Improvement with stimulants
Unlike many TBI patients who do not recognize the often-subtle psychiatric sequelae of their injury, Mr. A is aware of his difficulty concentrating, which is temporally linked with his accident. After exploring the association between Mr. A’s symptoms and his injury, his psychiatrist concludes that Mr. A’s cognitive deficits likely are associated with his TBI. Mr. A’s history of alcohol abuse raises concerns about prescribing stimulants. However, after assuring that Mr. A’s depression is well controlled and addressing his risk of substance abuse, his psychiatrist prescribes methylphenidate titrated to 30 mg/d. When he returns to the clinic several weeks later, Mr. A reports improved attention and functioning at work, and continues to follow up with the psychiatrist without requiring changes to his medication regimen.
Related Resource
- Konrad C, Geburek AJ, Rist F, et al. Long-term cognitive and emotional consequences of mild traumatic brain injury. Psychol Med. 2010;22:1-15.
Drug Brand Names
- Amantadine • Symadine, Symmetrel
- Bromocriptine • Parlodel
- Carbidopa/levodopa • Sinemet
- Dextroamphetamine • Dexedrine
- Donepezil • Aricept
- Galantamine • Razadyne
- Methylphenidate • Ritalin, Methylin, others
- Physostigmine • Antilirium
- Pramipexole • Mirapex
- Rivastigmine • Exelon
- Sertraline • Zoloft
- Tacrine • Cognex
Disclosures
Dr. Scher and Ms. Loomis report no financial relationship with any company whose products mentioned in this article or with the manufacturers of competing products.
Dr. McCarron is a speaker for Eli Lilly and Company.
1. Faul M, Xu L, Wald MM, et al. Traumatic brain injury in the United States; emergency department visits, hospitalizations, and deaths, 2002-2006. Atlanta, GA: Centers for Disease Control and Prevention; 2010. Available at: http://www.cdc.gov/traumaticbraininjury/tbi_ed.html. Accessed December 1, 2010.
2. Vaishnavi S, Rao V, Fann JR. Neuropsychiatric problems after traumatic brain injury: unraveling the silent epidemic. Psychosomatics. 2009;50(3):198-205.
3. Fann JR, Burington B, Leonetti A, et al. Psychiatric illness following traumatic brain injury in an adult health maintenance organization population. Arch Gen Psychiatry. 2004;61(1):53-61.
4. Bryant RA, O’Donnell ML, Creamer M, et al. The psychiatric sequelae of traumatic injury. Am J Psychiatry. 2010;167(3):312-320.
5. Writer BW, Schillerstrom JE. Psychopharmacological treatment for cognitive impairment in survivors of traumatic brain injury: a critical review. J Neuropsychiatry Clin Neurosci. 2009;21(4):362-370.
6. Arciniegas DB, Anderson CA, Topkoff J, et al. Mild traumatic brain injury: a neuropsychiatric approach to diagnosis, evaluation, and treatment. Neuropsychiatr Dis Treat. 2005;1(4):311-327.
7. Sigurdardottir S, Andelic N, Roe C, et al. Cognitive recovery and predictors of functional outcome 1 year after traumatic brain injury. J Int Neuropsychol Soc. 2009;15(5):740-750.
8. Physicians’ desk reference 64th ed. Montvale, NJ: Thomson Reuters; 2010.
9. Sawyer E Mauro LS, Mauro LS, Ohlinger MJ. Amantadine enhancement of arousal and cognition after traumatic brain injury. Ann Pharmacother. 2008;42(2):247-252.
10. Kraus MF, Smith GS, Butters M, et al. Effects of the dopaminergic agent and NMDA receptor antagonist amantadine on cognitive function, cerebral glucose metabolism and D2 receptor availability in chronic traumatic brain injury: a study using positron emission tomography (PET). Brain Inj. 2005;19(7):471-479.
11. Griffin SL, van Reekum R, Masanic C. A review of cholinergic agents in the treatment of neurobehavioral deficits following traumatic brain injury. J Neuropsychiatry Clin Neurosci. 2003;15(1):17-26.
12. Whelan FJ, Walker MS, Schultz SK. Donepezil in the treatment of cognitive dysfunction associated with traumatic brain injury. Ann Clin Psychiatry. 2000;12(3):131-135.
13. Taverni JP, Seliger G, Lichtman SW. Donepezil medicated memory improvement in traumatic brain injury during post acute rehabilitation. Brain Inj. 1998;12(1):77-80.
14. Silver JM, McAllister TW, Arciniegas DB. Depression and cognitive complaints following mild traumatic brain injury. Am J Psychiatry. 2009;166(6):653-661.
15. Silver JM, Koumaras B, Chen M, et al. Effects of rivastigmine on cognitive function in patients with traumatic brain injury. Neurology. 2006;67(5):748-755.
16. Tenovuo O. Central acetylcholinesterase inhibitors in the treatment of chronic traumatic brain injury—clinical experience in 111 patients. Prog Neuropsychopharmacol Biol Psychiatry. 2005;29(1):61-67.
17. Goldberg E, Gerstman LJ, Mattis S, et al. Selective effects of cholinergic treatment on verbal memory in posttraumatic amnesia. J Clin Neuropsychol. 1982;4(3):219-234.
18. Eames P, Sutton A. Protracted post-traumatic confusional state treated with physostigmine. Brain Inj. 1995;9(7):729-734.
19. Rassovsky Y, Satz P, Alfano MS, et al. Functional outcome in TBI II: verbal memory and information processing speed mediators. J Clin Exp Neuropsychol. 2006;28(4):581-591.
20. Willmott C, Ponsford J. Efficacy of methylphenidate in the rehabilitation of attention following traumatic brain injury: a randomised, crossover, double blind, placebo controlled inpatient trial. J Neurol Neurosurg Psychiatry. 2009;80(5):552-557.
20. Kaelin DL, Cifu DX, Matthies B. Methylphenidate effect on attention deficit in the acutely brain-injured adult. Arch Phys Med Rehabil. 1996;77(1):6-9.
22. Whyte J, Hart T, Vaccaro M, et al. Effects of methylphenidate on attention deficits after traumatic brain injury: a multidimensional, randomized, controlled trial. Am J Phys Med Rehabil. 2004;83(6):401-420.
23. Whyte J, Hart T, Schuster K, et al. Effects of methylphenidate on attentional function after traumatic brain injury. A randomized, placebo-controlled trial. Am J Phys Med Rehabil. 1997;76(6):440-450.
24. Wroblewski BA, Leary JM, Phelan AM, et al. Methylphenidate and seizure frequency in brain injured patients with seizure disorders. J Clin Psychiatry. 1992;53(3):86-89.
25. Mahalick DM, Carmel PW, Greenberg JP, et al. Psychopharmacologic treatment of acquired attention disorders in children with brain injury. Pediatr Neurosurg. 1998;29(3):121-126.
26. Hornyak JE, Nelson VS, Hurvitz EA. The use of methylphenidate in paediatric traumatic brain injury. Pediatr Rehabil. 1997;1(1):15-17.
27. Hornstein A, Lennihan L, Seliger G. Amphetamine in recovery from brain injury. Brain Inj. 1996;10(2):145-148.
Mr. A, age 45, presents to the psychiatry clinic complaining of “ADHD.” He says he is not able to sit through movies and often gets distracted while on his computer at work. He also is having problems in his relationship with his wife; she says having a conversation with him is difficult. He has seen a psychiatrist for depression, which is currently managed by his primary care physician (PCP), who prescribed sertraline, 100 mg/d. Mr. A feels that although his depression is now under control, the medication has had limited effect on improving his concentration.
With further discussion, Mr. A reveals that 6 months ago he was involved in a car accident and suffered a mild traumatic brain injury (TBI). He was hospitalized overnight and was encouraged to follow up with his PCP. During his only follow-up visit, Mr. A told his PCP that he was having difficulty concentrating since the accident. However, because Mr. A has a remote history of alcohol abuse, his physician was reluctant to give him additional medication and referred him to a psychiatrist.
TBI is increasingly common but often overlooked or not treated in the emergency room (ER). Each year at least 1.7 million people experience a TBI; 275,000 are hospitalized and 52,000 die.1 The true incidence likely is greater because patients who do not present to the ER or hospital are not included in most studies, and the often-subtle psychiatric sequelae may preclude patients from seeking mental health treatment.
Psychiatric disorders are common among those who sustain a TBI (Table 1).2 One prospective cohort study found that patients with mild TBI are 2.8 times more likely than other patients to develop a psychiatric disorder.3 Statistics regarding TBI and psychiatric illness often are limited because they rely on self-reports, chart review, or retrospective studies.4
TBI severity can be classified on the basis of Glasgow Coma Scale score and other factors (Table 2).5 The correlation between severity of injury and resulting psychiatric illness or post-concussive symptoms is unclear.6 There is evidence that cognitive defects are associated with decreased function. Cognitive dysfunction also has been associated with disability 10 years after moderate to severe TBI.7 The association between cognitive dysfunction and outcome is more strongly correlated with moderate to severe TBI; there is no clear association in mild TBI.7 Additionally, compared with patients with severe TBI, those with mild TBI were more likely to be employed. At all severity levels, function improves over time. Mild, moderate, and severe TBI have a similar recovery curve.7
Table 1
Psychiatric symptoms: Common among TBI patients
| Psychiatric symptom | Incidence |
|---|---|
| Aggression | 30% |
| Anxiety | 10% to 70% |
| Apathy | 10% |
| Cognitive impairment | 25% to 70% |
| Depression | 25% to 50% |
| Mania | 1% to 10% |
| Psychosis | 3% to 8% |
| TBI: traumatic brain injury | |
| Source: Adapted from reference 2 | |
Table 2
Classifying severity of traumatic brain injury
| Severity | GCS score | LOC duration | PTA* |
|---|---|---|---|
| Mild | 13 to 15 | <30 minutes | <1 hour |
| Moderate | 9 to 12 | 1 to 24 hours | 1 to 24 hours |
| Severe | <8 | >24 hours | >24 hours |
| *Includes loss of memory immediately before or after the accident | |||
| GCS: Glasgow Coma Scale; LOC: loss of consciousness; PTA: posttraumatic amnesia | |||
| Source: Reference 5 | |||
Cognitive dysfunction and TBI
Cognitive dysfunction can be split into 3 categories:
- executive function
- memory
- processing speed.
The incidence of cognitive dysfunction after TBI is unclear. Several methods are used to quantify cognitive dysfunction in TBI patients; it is widely regarded that the Mini-Mental State Exam is not adequate to screen for subtle cognitive deficits.6 However, there is no clear consensus on which tool should be used.5
Off-label pharmacotherapy
There are no FDA-approved medications for treating neuropsychiatric sequelae of TBI. Treatment should be symptom-based and employ the “start low, go slow” approach. Compared with patients without brain injury, TBI patients may experience increased adverse effects from psychotropics but may require standard doses. These patients also may have comorbidities such as seizure disorders, substance abuse, and depression that will affect treatment.2 Different areas of cognitive function respond to different medication classes. Suggested medications include stimulant and nonstimulant catecholaminergic agents and cholinesterase inhibitors (Table 3).8
Executive function responds to non-stimulant catecholaminergics. In a review, Writer and Schillerstrom5 found that TBI patients who received catecholaminergic augmentation showed improved function in 6 of 7 studies. In 2 randomized controlled trials (RCTs) and 4 nonrandomized, placebo-controlled trials, patients with mild to severe TBI showed improved executive function, attention, global cognitive function, memory, language, and/ or arousal with use of bromocriptine, pramipexole, carbidopa/levodopa, or amantadine.5 The greatest improvements were found in executive function. In 1 RCT, 10 patients with mild to severe TBI showed no functional improvement after 2 weeks of treatment.
Amantadine, 200 to 400 mg/d, has been shown to safely improve arousal and cognitive function in patients with moderate to severe TBI when started 3 days to 5 months after injury.9 Amantadine, 400 mg/d, also improves executive function measures without significant benefit in attention or memory in patients with mild to severe TBI 6 months post-injury.10
Memory responds to cholinesterase inhibitors. Memory deficits secondary to TBI affect immediate and delayed memory. The cholinesterase inhibitor donepezil is approved for treating Alzheimer’s disease (AD) in the United States and Canada, and research suggests memory deficits after TBI may be similar to those seen in AD.11 This includes deficits in long-term memory storage, which likely is associated with the cholinergic system.11 Post-mortem studies have found similarities in traumatically injured brains and those of AD patients.11
Three small prospective studies of done-pezil have shown improved memory and attention in TBI patients when cognition is the primary outcome, with 1 small negative open-label trial.7 In a study of 53 patients, Whelan et al12 found that donepezil improved patients’ intelligence quotient and clinician-based assessment of cognition over 2 years. Taverni et al13 found memory improvement in 2 TBI patients within 3 weeks of starting donepezil. These results suggest that donepezil may be used in acute and late phases of memory deficits following mild, moderate, or severe TBI.6 All studies titrated donepezil from 5 to 10 mg/d over several weeks. Dosing guidelines for donepezil in AD suggest 5 mg/d for 4 to 6 weeks, which may be increased to 10 mg/d if needed.8
Rivastigmine (3 to 6 mg/d) has been shown to be effective in mild TBI when started 1 year after injury and safe for 12 to 38 weeks of treatment.14,15 One retrospective cohort study of 111 patients with chronic TBI found no difference among donepezil, rivastigmine, or galantamine, with mean doses of 7.2 mg/d, 10 mg/d, and 2.3 mg/d, respectively.16 Sixty-one percent of patients showed improvement and the remainder had modest or no response. This study suggests that positive response on cognition may be similar among cholinesterase inhibitors. In case reports, physostigmine has offered some benefit17,18; however, cardiovascular and autonomic side effects restrict its use.11 Tacrine is associated with problematic gastrointestinal and hepatic side effects.11
Processing speed responds to stimulant catecholaminergics. Although the incidence of psychiatric illness is not correlated with TBI severity, evidence suggests that speed of processing mediates the relationship between injury severity and functional decline.19 Therefore, aggressively treating these deficits may help improve function.
Methylphenidate improves attention and processing speed after TBI. A review of 7 randomized trials and 2 nonrandomized trials indicated that patients with mild to severe, chronic TBI experienced significantly improved cognitive function after methylphenidate treatment.5 Willmott and Ponsford20 found significant enhancement in information processing speed within 2 weeks of methylphenidate treatment in 40 patients with moderate or severe TBI. Methylphenidate increased the rate of recovery and led to improvement in acute21 and post-acute phases.22 In addition, methylphenidate may improve processing speed even in the absence of significant changes in attention.23
The standard methylphenidate dose used in most studies, 0.3 mg/kg twice daily, is safe and effective. Dosing usually is started at 5 mg/d and titrated to symptomatic relief. Because methylphenidate does not lower the seizure threshold, it is safe for patients at high risk for seizure.24 Methylphenidate also significantly improves attention and speed of processing in pediatric head trauma.25,26
Dextroamphetamine also is used to treat speed of processing dysfunction after TBI, but is less studied than methylphenidate. Dextroamphetamine, 5 to 30 mg/d, was found to effectively treat attention problems that interfered with rehabilitation in patients with severe TBI.27
Table 3
Recommended treatments for mild TBI-related cognitive deficits
| Deficit | First-line medication | Side effects | Contraindications | Other treatments |
|---|---|---|---|---|
| Memory | Donepezil (5 to 10 mg/d) | Diarrhea, nausea, vomiting, muscle cramps, fatigue, anorexia | Hypersensitivity to donepezil or piperidine derivatives | Rivastigmine, galantamine, physostigmine, CDP-choline |
| Speed of processing | Methylphenidate (0.3 mg/kg twice daily) | Headache, insomnia, decreased appetite, nausea, vomiting, anxiety, irritability | Hypersensitivity to methylphenidate, glaucoma, history of Tourette syndrome or tics, use of MAOI within 14 days | Dextroamphetamine |
| Executive function | Amantadine (200 to 400 mg/d) | CNS depression, orthostatic hypotension, peripheral edema, agitation, nausea, anorexia | Hypersensitivity to amantadine | Bromocriptine, pramipexole, carbidopa/levodopa |
| CDP-choline: cytidinediphosphocholine; MAOI: monoamine oxidase inhibitor | ||||
| Source: Reference 8 | ||||
Nonpharmacologic treatments
In addition to pharmacotherapy, nonpharmacologic interventions also should be a mainstay of treatment. Compensatory training and cognitive exercise may improve patients’ cognitive deficits and return some sense of control. Individual and family psychotherapy, including cognitive-behavioral therapy, also may be beneficial.2 Review sources have identified the importance of validating patients’ symptoms and developing a goal-based treatment plan.6
CASE CONTINUED: Improvement with stimulants
Unlike many TBI patients who do not recognize the often-subtle psychiatric sequelae of their injury, Mr. A is aware of his difficulty concentrating, which is temporally linked with his accident. After exploring the association between Mr. A’s symptoms and his injury, his psychiatrist concludes that Mr. A’s cognitive deficits likely are associated with his TBI. Mr. A’s history of alcohol abuse raises concerns about prescribing stimulants. However, after assuring that Mr. A’s depression is well controlled and addressing his risk of substance abuse, his psychiatrist prescribes methylphenidate titrated to 30 mg/d. When he returns to the clinic several weeks later, Mr. A reports improved attention and functioning at work, and continues to follow up with the psychiatrist without requiring changes to his medication regimen.
Related Resource
- Konrad C, Geburek AJ, Rist F, et al. Long-term cognitive and emotional consequences of mild traumatic brain injury. Psychol Med. 2010;22:1-15.
Drug Brand Names
- Amantadine • Symadine, Symmetrel
- Bromocriptine • Parlodel
- Carbidopa/levodopa • Sinemet
- Dextroamphetamine • Dexedrine
- Donepezil • Aricept
- Galantamine • Razadyne
- Methylphenidate • Ritalin, Methylin, others
- Physostigmine • Antilirium
- Pramipexole • Mirapex
- Rivastigmine • Exelon
- Sertraline • Zoloft
- Tacrine • Cognex
Disclosures
Dr. Scher and Ms. Loomis report no financial relationship with any company whose products mentioned in this article or with the manufacturers of competing products.
Dr. McCarron is a speaker for Eli Lilly and Company.
Mr. A, age 45, presents to the psychiatry clinic complaining of “ADHD.” He says he is not able to sit through movies and often gets distracted while on his computer at work. He also is having problems in his relationship with his wife; she says having a conversation with him is difficult. He has seen a psychiatrist for depression, which is currently managed by his primary care physician (PCP), who prescribed sertraline, 100 mg/d. Mr. A feels that although his depression is now under control, the medication has had limited effect on improving his concentration.
With further discussion, Mr. A reveals that 6 months ago he was involved in a car accident and suffered a mild traumatic brain injury (TBI). He was hospitalized overnight and was encouraged to follow up with his PCP. During his only follow-up visit, Mr. A told his PCP that he was having difficulty concentrating since the accident. However, because Mr. A has a remote history of alcohol abuse, his physician was reluctant to give him additional medication and referred him to a psychiatrist.
TBI is increasingly common but often overlooked or not treated in the emergency room (ER). Each year at least 1.7 million people experience a TBI; 275,000 are hospitalized and 52,000 die.1 The true incidence likely is greater because patients who do not present to the ER or hospital are not included in most studies, and the often-subtle psychiatric sequelae may preclude patients from seeking mental health treatment.
Psychiatric disorders are common among those who sustain a TBI (Table 1).2 One prospective cohort study found that patients with mild TBI are 2.8 times more likely than other patients to develop a psychiatric disorder.3 Statistics regarding TBI and psychiatric illness often are limited because they rely on self-reports, chart review, or retrospective studies.4
TBI severity can be classified on the basis of Glasgow Coma Scale score and other factors (Table 2).5 The correlation between severity of injury and resulting psychiatric illness or post-concussive symptoms is unclear.6 There is evidence that cognitive defects are associated with decreased function. Cognitive dysfunction also has been associated with disability 10 years after moderate to severe TBI.7 The association between cognitive dysfunction and outcome is more strongly correlated with moderate to severe TBI; there is no clear association in mild TBI.7 Additionally, compared with patients with severe TBI, those with mild TBI were more likely to be employed. At all severity levels, function improves over time. Mild, moderate, and severe TBI have a similar recovery curve.7
Table 1
Psychiatric symptoms: Common among TBI patients
| Psychiatric symptom | Incidence |
|---|---|
| Aggression | 30% |
| Anxiety | 10% to 70% |
| Apathy | 10% |
| Cognitive impairment | 25% to 70% |
| Depression | 25% to 50% |
| Mania | 1% to 10% |
| Psychosis | 3% to 8% |
| TBI: traumatic brain injury | |
| Source: Adapted from reference 2 | |
Table 2
Classifying severity of traumatic brain injury
| Severity | GCS score | LOC duration | PTA* |
|---|---|---|---|
| Mild | 13 to 15 | <30 minutes | <1 hour |
| Moderate | 9 to 12 | 1 to 24 hours | 1 to 24 hours |
| Severe | <8 | >24 hours | >24 hours |
| *Includes loss of memory immediately before or after the accident | |||
| GCS: Glasgow Coma Scale; LOC: loss of consciousness; PTA: posttraumatic amnesia | |||
| Source: Reference 5 | |||
Cognitive dysfunction and TBI
Cognitive dysfunction can be split into 3 categories:
- executive function
- memory
- processing speed.
The incidence of cognitive dysfunction after TBI is unclear. Several methods are used to quantify cognitive dysfunction in TBI patients; it is widely regarded that the Mini-Mental State Exam is not adequate to screen for subtle cognitive deficits.6 However, there is no clear consensus on which tool should be used.5
Off-label pharmacotherapy
There are no FDA-approved medications for treating neuropsychiatric sequelae of TBI. Treatment should be symptom-based and employ the “start low, go slow” approach. Compared with patients without brain injury, TBI patients may experience increased adverse effects from psychotropics but may require standard doses. These patients also may have comorbidities such as seizure disorders, substance abuse, and depression that will affect treatment.2 Different areas of cognitive function respond to different medication classes. Suggested medications include stimulant and nonstimulant catecholaminergic agents and cholinesterase inhibitors (Table 3).8
Executive function responds to non-stimulant catecholaminergics. In a review, Writer and Schillerstrom5 found that TBI patients who received catecholaminergic augmentation showed improved function in 6 of 7 studies. In 2 randomized controlled trials (RCTs) and 4 nonrandomized, placebo-controlled trials, patients with mild to severe TBI showed improved executive function, attention, global cognitive function, memory, language, and/ or arousal with use of bromocriptine, pramipexole, carbidopa/levodopa, or amantadine.5 The greatest improvements were found in executive function. In 1 RCT, 10 patients with mild to severe TBI showed no functional improvement after 2 weeks of treatment.
Amantadine, 200 to 400 mg/d, has been shown to safely improve arousal and cognitive function in patients with moderate to severe TBI when started 3 days to 5 months after injury.9 Amantadine, 400 mg/d, also improves executive function measures without significant benefit in attention or memory in patients with mild to severe TBI 6 months post-injury.10
Memory responds to cholinesterase inhibitors. Memory deficits secondary to TBI affect immediate and delayed memory. The cholinesterase inhibitor donepezil is approved for treating Alzheimer’s disease (AD) in the United States and Canada, and research suggests memory deficits after TBI may be similar to those seen in AD.11 This includes deficits in long-term memory storage, which likely is associated with the cholinergic system.11 Post-mortem studies have found similarities in traumatically injured brains and those of AD patients.11
Three small prospective studies of done-pezil have shown improved memory and attention in TBI patients when cognition is the primary outcome, with 1 small negative open-label trial.7 In a study of 53 patients, Whelan et al12 found that donepezil improved patients’ intelligence quotient and clinician-based assessment of cognition over 2 years. Taverni et al13 found memory improvement in 2 TBI patients within 3 weeks of starting donepezil. These results suggest that donepezil may be used in acute and late phases of memory deficits following mild, moderate, or severe TBI.6 All studies titrated donepezil from 5 to 10 mg/d over several weeks. Dosing guidelines for donepezil in AD suggest 5 mg/d for 4 to 6 weeks, which may be increased to 10 mg/d if needed.8
Rivastigmine (3 to 6 mg/d) has been shown to be effective in mild TBI when started 1 year after injury and safe for 12 to 38 weeks of treatment.14,15 One retrospective cohort study of 111 patients with chronic TBI found no difference among donepezil, rivastigmine, or galantamine, with mean doses of 7.2 mg/d, 10 mg/d, and 2.3 mg/d, respectively.16 Sixty-one percent of patients showed improvement and the remainder had modest or no response. This study suggests that positive response on cognition may be similar among cholinesterase inhibitors. In case reports, physostigmine has offered some benefit17,18; however, cardiovascular and autonomic side effects restrict its use.11 Tacrine is associated with problematic gastrointestinal and hepatic side effects.11
Processing speed responds to stimulant catecholaminergics. Although the incidence of psychiatric illness is not correlated with TBI severity, evidence suggests that speed of processing mediates the relationship between injury severity and functional decline.19 Therefore, aggressively treating these deficits may help improve function.
Methylphenidate improves attention and processing speed after TBI. A review of 7 randomized trials and 2 nonrandomized trials indicated that patients with mild to severe, chronic TBI experienced significantly improved cognitive function after methylphenidate treatment.5 Willmott and Ponsford20 found significant enhancement in information processing speed within 2 weeks of methylphenidate treatment in 40 patients with moderate or severe TBI. Methylphenidate increased the rate of recovery and led to improvement in acute21 and post-acute phases.22 In addition, methylphenidate may improve processing speed even in the absence of significant changes in attention.23
The standard methylphenidate dose used in most studies, 0.3 mg/kg twice daily, is safe and effective. Dosing usually is started at 5 mg/d and titrated to symptomatic relief. Because methylphenidate does not lower the seizure threshold, it is safe for patients at high risk for seizure.24 Methylphenidate also significantly improves attention and speed of processing in pediatric head trauma.25,26
Dextroamphetamine also is used to treat speed of processing dysfunction after TBI, but is less studied than methylphenidate. Dextroamphetamine, 5 to 30 mg/d, was found to effectively treat attention problems that interfered with rehabilitation in patients with severe TBI.27
Table 3
Recommended treatments for mild TBI-related cognitive deficits
| Deficit | First-line medication | Side effects | Contraindications | Other treatments |
|---|---|---|---|---|
| Memory | Donepezil (5 to 10 mg/d) | Diarrhea, nausea, vomiting, muscle cramps, fatigue, anorexia | Hypersensitivity to donepezil or piperidine derivatives | Rivastigmine, galantamine, physostigmine, CDP-choline |
| Speed of processing | Methylphenidate (0.3 mg/kg twice daily) | Headache, insomnia, decreased appetite, nausea, vomiting, anxiety, irritability | Hypersensitivity to methylphenidate, glaucoma, history of Tourette syndrome or tics, use of MAOI within 14 days | Dextroamphetamine |
| Executive function | Amantadine (200 to 400 mg/d) | CNS depression, orthostatic hypotension, peripheral edema, agitation, nausea, anorexia | Hypersensitivity to amantadine | Bromocriptine, pramipexole, carbidopa/levodopa |
| CDP-choline: cytidinediphosphocholine; MAOI: monoamine oxidase inhibitor | ||||
| Source: Reference 8 | ||||
Nonpharmacologic treatments
In addition to pharmacotherapy, nonpharmacologic interventions also should be a mainstay of treatment. Compensatory training and cognitive exercise may improve patients’ cognitive deficits and return some sense of control. Individual and family psychotherapy, including cognitive-behavioral therapy, also may be beneficial.2 Review sources have identified the importance of validating patients’ symptoms and developing a goal-based treatment plan.6
CASE CONTINUED: Improvement with stimulants
Unlike many TBI patients who do not recognize the often-subtle psychiatric sequelae of their injury, Mr. A is aware of his difficulty concentrating, which is temporally linked with his accident. After exploring the association between Mr. A’s symptoms and his injury, his psychiatrist concludes that Mr. A’s cognitive deficits likely are associated with his TBI. Mr. A’s history of alcohol abuse raises concerns about prescribing stimulants. However, after assuring that Mr. A’s depression is well controlled and addressing his risk of substance abuse, his psychiatrist prescribes methylphenidate titrated to 30 mg/d. When he returns to the clinic several weeks later, Mr. A reports improved attention and functioning at work, and continues to follow up with the psychiatrist without requiring changes to his medication regimen.
Related Resource
- Konrad C, Geburek AJ, Rist F, et al. Long-term cognitive and emotional consequences of mild traumatic brain injury. Psychol Med. 2010;22:1-15.
Drug Brand Names
- Amantadine • Symadine, Symmetrel
- Bromocriptine • Parlodel
- Carbidopa/levodopa • Sinemet
- Dextroamphetamine • Dexedrine
- Donepezil • Aricept
- Galantamine • Razadyne
- Methylphenidate • Ritalin, Methylin, others
- Physostigmine • Antilirium
- Pramipexole • Mirapex
- Rivastigmine • Exelon
- Sertraline • Zoloft
- Tacrine • Cognex
Disclosures
Dr. Scher and Ms. Loomis report no financial relationship with any company whose products mentioned in this article or with the manufacturers of competing products.
Dr. McCarron is a speaker for Eli Lilly and Company.
1. Faul M, Xu L, Wald MM, et al. Traumatic brain injury in the United States; emergency department visits, hospitalizations, and deaths, 2002-2006. Atlanta, GA: Centers for Disease Control and Prevention; 2010. Available at: http://www.cdc.gov/traumaticbraininjury/tbi_ed.html. Accessed December 1, 2010.
2. Vaishnavi S, Rao V, Fann JR. Neuropsychiatric problems after traumatic brain injury: unraveling the silent epidemic. Psychosomatics. 2009;50(3):198-205.
3. Fann JR, Burington B, Leonetti A, et al. Psychiatric illness following traumatic brain injury in an adult health maintenance organization population. Arch Gen Psychiatry. 2004;61(1):53-61.
4. Bryant RA, O’Donnell ML, Creamer M, et al. The psychiatric sequelae of traumatic injury. Am J Psychiatry. 2010;167(3):312-320.
5. Writer BW, Schillerstrom JE. Psychopharmacological treatment for cognitive impairment in survivors of traumatic brain injury: a critical review. J Neuropsychiatry Clin Neurosci. 2009;21(4):362-370.
6. Arciniegas DB, Anderson CA, Topkoff J, et al. Mild traumatic brain injury: a neuropsychiatric approach to diagnosis, evaluation, and treatment. Neuropsychiatr Dis Treat. 2005;1(4):311-327.
7. Sigurdardottir S, Andelic N, Roe C, et al. Cognitive recovery and predictors of functional outcome 1 year after traumatic brain injury. J Int Neuropsychol Soc. 2009;15(5):740-750.
8. Physicians’ desk reference 64th ed. Montvale, NJ: Thomson Reuters; 2010.
9. Sawyer E Mauro LS, Mauro LS, Ohlinger MJ. Amantadine enhancement of arousal and cognition after traumatic brain injury. Ann Pharmacother. 2008;42(2):247-252.
10. Kraus MF, Smith GS, Butters M, et al. Effects of the dopaminergic agent and NMDA receptor antagonist amantadine on cognitive function, cerebral glucose metabolism and D2 receptor availability in chronic traumatic brain injury: a study using positron emission tomography (PET). Brain Inj. 2005;19(7):471-479.
11. Griffin SL, van Reekum R, Masanic C. A review of cholinergic agents in the treatment of neurobehavioral deficits following traumatic brain injury. J Neuropsychiatry Clin Neurosci. 2003;15(1):17-26.
12. Whelan FJ, Walker MS, Schultz SK. Donepezil in the treatment of cognitive dysfunction associated with traumatic brain injury. Ann Clin Psychiatry. 2000;12(3):131-135.
13. Taverni JP, Seliger G, Lichtman SW. Donepezil medicated memory improvement in traumatic brain injury during post acute rehabilitation. Brain Inj. 1998;12(1):77-80.
14. Silver JM, McAllister TW, Arciniegas DB. Depression and cognitive complaints following mild traumatic brain injury. Am J Psychiatry. 2009;166(6):653-661.
15. Silver JM, Koumaras B, Chen M, et al. Effects of rivastigmine on cognitive function in patients with traumatic brain injury. Neurology. 2006;67(5):748-755.
16. Tenovuo O. Central acetylcholinesterase inhibitors in the treatment of chronic traumatic brain injury—clinical experience in 111 patients. Prog Neuropsychopharmacol Biol Psychiatry. 2005;29(1):61-67.
17. Goldberg E, Gerstman LJ, Mattis S, et al. Selective effects of cholinergic treatment on verbal memory in posttraumatic amnesia. J Clin Neuropsychol. 1982;4(3):219-234.
18. Eames P, Sutton A. Protracted post-traumatic confusional state treated with physostigmine. Brain Inj. 1995;9(7):729-734.
19. Rassovsky Y, Satz P, Alfano MS, et al. Functional outcome in TBI II: verbal memory and information processing speed mediators. J Clin Exp Neuropsychol. 2006;28(4):581-591.
20. Willmott C, Ponsford J. Efficacy of methylphenidate in the rehabilitation of attention following traumatic brain injury: a randomised, crossover, double blind, placebo controlled inpatient trial. J Neurol Neurosurg Psychiatry. 2009;80(5):552-557.
20. Kaelin DL, Cifu DX, Matthies B. Methylphenidate effect on attention deficit in the acutely brain-injured adult. Arch Phys Med Rehabil. 1996;77(1):6-9.
22. Whyte J, Hart T, Vaccaro M, et al. Effects of methylphenidate on attention deficits after traumatic brain injury: a multidimensional, randomized, controlled trial. Am J Phys Med Rehabil. 2004;83(6):401-420.
23. Whyte J, Hart T, Schuster K, et al. Effects of methylphenidate on attentional function after traumatic brain injury. A randomized, placebo-controlled trial. Am J Phys Med Rehabil. 1997;76(6):440-450.
24. Wroblewski BA, Leary JM, Phelan AM, et al. Methylphenidate and seizure frequency in brain injured patients with seizure disorders. J Clin Psychiatry. 1992;53(3):86-89.
25. Mahalick DM, Carmel PW, Greenberg JP, et al. Psychopharmacologic treatment of acquired attention disorders in children with brain injury. Pediatr Neurosurg. 1998;29(3):121-126.
26. Hornyak JE, Nelson VS, Hurvitz EA. The use of methylphenidate in paediatric traumatic brain injury. Pediatr Rehabil. 1997;1(1):15-17.
27. Hornstein A, Lennihan L, Seliger G. Amphetamine in recovery from brain injury. Brain Inj. 1996;10(2):145-148.
1. Faul M, Xu L, Wald MM, et al. Traumatic brain injury in the United States; emergency department visits, hospitalizations, and deaths, 2002-2006. Atlanta, GA: Centers for Disease Control and Prevention; 2010. Available at: http://www.cdc.gov/traumaticbraininjury/tbi_ed.html. Accessed December 1, 2010.
2. Vaishnavi S, Rao V, Fann JR. Neuropsychiatric problems after traumatic brain injury: unraveling the silent epidemic. Psychosomatics. 2009;50(3):198-205.
3. Fann JR, Burington B, Leonetti A, et al. Psychiatric illness following traumatic brain injury in an adult health maintenance organization population. Arch Gen Psychiatry. 2004;61(1):53-61.
4. Bryant RA, O’Donnell ML, Creamer M, et al. The psychiatric sequelae of traumatic injury. Am J Psychiatry. 2010;167(3):312-320.
5. Writer BW, Schillerstrom JE. Psychopharmacological treatment for cognitive impairment in survivors of traumatic brain injury: a critical review. J Neuropsychiatry Clin Neurosci. 2009;21(4):362-370.
6. Arciniegas DB, Anderson CA, Topkoff J, et al. Mild traumatic brain injury: a neuropsychiatric approach to diagnosis, evaluation, and treatment. Neuropsychiatr Dis Treat. 2005;1(4):311-327.
7. Sigurdardottir S, Andelic N, Roe C, et al. Cognitive recovery and predictors of functional outcome 1 year after traumatic brain injury. J Int Neuropsychol Soc. 2009;15(5):740-750.
8. Physicians’ desk reference 64th ed. Montvale, NJ: Thomson Reuters; 2010.
9. Sawyer E Mauro LS, Mauro LS, Ohlinger MJ. Amantadine enhancement of arousal and cognition after traumatic brain injury. Ann Pharmacother. 2008;42(2):247-252.
10. Kraus MF, Smith GS, Butters M, et al. Effects of the dopaminergic agent and NMDA receptor antagonist amantadine on cognitive function, cerebral glucose metabolism and D2 receptor availability in chronic traumatic brain injury: a study using positron emission tomography (PET). Brain Inj. 2005;19(7):471-479.
11. Griffin SL, van Reekum R, Masanic C. A review of cholinergic agents in the treatment of neurobehavioral deficits following traumatic brain injury. J Neuropsychiatry Clin Neurosci. 2003;15(1):17-26.
12. Whelan FJ, Walker MS, Schultz SK. Donepezil in the treatment of cognitive dysfunction associated with traumatic brain injury. Ann Clin Psychiatry. 2000;12(3):131-135.
13. Taverni JP, Seliger G, Lichtman SW. Donepezil medicated memory improvement in traumatic brain injury during post acute rehabilitation. Brain Inj. 1998;12(1):77-80.
14. Silver JM, McAllister TW, Arciniegas DB. Depression and cognitive complaints following mild traumatic brain injury. Am J Psychiatry. 2009;166(6):653-661.
15. Silver JM, Koumaras B, Chen M, et al. Effects of rivastigmine on cognitive function in patients with traumatic brain injury. Neurology. 2006;67(5):748-755.
16. Tenovuo O. Central acetylcholinesterase inhibitors in the treatment of chronic traumatic brain injury—clinical experience in 111 patients. Prog Neuropsychopharmacol Biol Psychiatry. 2005;29(1):61-67.
17. Goldberg E, Gerstman LJ, Mattis S, et al. Selective effects of cholinergic treatment on verbal memory in posttraumatic amnesia. J Clin Neuropsychol. 1982;4(3):219-234.
18. Eames P, Sutton A. Protracted post-traumatic confusional state treated with physostigmine. Brain Inj. 1995;9(7):729-734.
19. Rassovsky Y, Satz P, Alfano MS, et al. Functional outcome in TBI II: verbal memory and information processing speed mediators. J Clin Exp Neuropsychol. 2006;28(4):581-591.
20. Willmott C, Ponsford J. Efficacy of methylphenidate in the rehabilitation of attention following traumatic brain injury: a randomised, crossover, double blind, placebo controlled inpatient trial. J Neurol Neurosurg Psychiatry. 2009;80(5):552-557.
20. Kaelin DL, Cifu DX, Matthies B. Methylphenidate effect on attention deficit in the acutely brain-injured adult. Arch Phys Med Rehabil. 1996;77(1):6-9.
22. Whyte J, Hart T, Vaccaro M, et al. Effects of methylphenidate on attention deficits after traumatic brain injury: a multidimensional, randomized, controlled trial. Am J Phys Med Rehabil. 2004;83(6):401-420.
23. Whyte J, Hart T, Schuster K, et al. Effects of methylphenidate on attentional function after traumatic brain injury. A randomized, placebo-controlled trial. Am J Phys Med Rehabil. 1997;76(6):440-450.
24. Wroblewski BA, Leary JM, Phelan AM, et al. Methylphenidate and seizure frequency in brain injured patients with seizure disorders. J Clin Psychiatry. 1992;53(3):86-89.
25. Mahalick DM, Carmel PW, Greenberg JP, et al. Psychopharmacologic treatment of acquired attention disorders in children with brain injury. Pediatr Neurosurg. 1998;29(3):121-126.
26. Hornyak JE, Nelson VS, Hurvitz EA. The use of methylphenidate in paediatric traumatic brain injury. Pediatr Rehabil. 1997;1(1):15-17.
27. Hornstein A, Lennihan L, Seliger G. Amphetamine in recovery from brain injury. Brain Inj. 1996;10(2):145-148.
Genetic Evaluation of Children
Genetic testing has entered a new era in the past few years. Our ability to perform DNA-based tests and identify an individual's susceptibility to cancer, heart disease, diabetes, and so many other conditions is beginning to have a major impact on our practice of medicine.
Experts predict – thanks to advances in technology we already have – that in a few years we will be able to screen during the newborn period and identify every mutation and polymorphism present. This screening will permit us to predict a child's “medical life” through identification of individual susceptibilities to disease likely to develop during his or her lifetime. Although still in its infancy, this technology would revolutionize pediatrics from a field in which we wait for the child to develop symptoms and signs of disease and then react with medication and other treatments, to one where we can predict disease. This will give us the opportunity to help our patients in a whole new way: to prevent the symptoms and signs from arising in the first place.
With the good comes the bad, as with any new technology. For example, interpretation of results with this advanced testing will require special expertise in genetics and genomics. Unfortunately, interpretation of genetic findings often is not as “black and white” as diagnosis of anemia based on serum hemoglobin and hematocrit levels. Genetic test results often include polymorphisms, and most of these variations of normal are benign and not associated with disease. Subspecialist consultation may be needed to make these important distinctions.
General pediatricians play an essential role in interpretation of newborn screening tests. Fortunately, results are normal for the majority of children and no further follow-up is indicated. However, if an abnormality is detected, referral to a specialist is warranted to facilitate an early intervention that, in some cases, can make a difference in the long-term health of the child. You also can refer families who request consultation with a geneticist to discuss recurrence risk in future progeny and for additional genetic testing, as indicated.
Beyond standard newborn genetic screening, the role of the pediatrician is somewhat limited regarding the screening and testing for specific genetic disorders. However, there are situations in which the pediatrician should feel comfortable in ordering and interpreting genetic tests.
For example, testing in children with intellectual disabilities and autism spectrum disorder has become standard. As tier 1 testing in such children, I usually order a microarray-based comparative genomic hybridization (array CGH), a test that has largely replaced high-resolution chromosome analysis in this population. I also perform DNA testing for fragile X syndrome, the most common inherited cause of intellectual disabilities. Because the results of this testing will be normal in 80%–90% of these children, I encourage pediatricians to order these tests themselves. I then make myself available if genetic evaluation reveals an abnormality.
Another factor to consider is the recent direct-to-consumer marketing of genetic testing that expands standard newborn screening or uses genetic markers to predict susceptibility to specific conditions. These tests often require the family, with or without the assistance of the pediatrician, to send a sample of DNA to a reference lab. The lab returns the results directly to the family. Again, the laboratory results are difficult to interpret, and you may be called on to provide guidance. Sometimes interpretation is straightforward, but in other cases it can be tricky, and if you are uncomfortable you might want to refer them to a medical geneticist or genetic counselor.
When you refer a child to a geneticist, include all results of your previous testing, those performed by other specialists, and newborn screening. Genetic tests performed on the mother during the pregnancy (for example, amniocentesis, chorionic villus sampling, sonograms, and/or biochemical screening tests) also are important. Provide any imaging findings, including MRIs or CT scans.
Proceed cautiously when counseling families regarding results of genetic testing. It can be trickier than you might think. For example, results of a test for a single gene disorder might uncover a previously unknown change in the child's DNA. The finding could be a benign polymorphism that has no clinical consequences or it could be a pathogenic mutation responsible for the child's signs and symptoms.
Simply informing the family about this finding is inadequate. To be certain, the parents need to be tested. If one or both of them has the same genetic change, the polymorphism might be benign. In contrast, if neither parent has the mutation, the child's test result might reflect a spontaneous genetic change and increase the likelihood you have discovered the cause of the clinical condition.
In general, there are three categories of children who may require genetic testing. First, there are those children who have multiple congenital anomalies or dysmorphic features. These findings could be caused by chromosome abnormalities, single gene mutations, or teratogenic agents. In these children, in order to ensure that the appropriate tests are ordered, a genetic consultation is important.
A second group of children who may require genetic testing are those in whom deviation from typical development or “normal” growth parameters occur during the first few years of life. Such children may have chromosome abnormalities, single gene mutations, and/or an underlying metabolic disorder. Keep in mind seizures, developmental regression, failure to thrive, and respiratory disturbances can bolster the likelihood of a genetic or metabolic etiology.
Before ordering any genetic testing, it is essential to take a complete patient and family history and to perform a complete physical exam. Children with a family history of a first- or second-degree family member with a genetic disorder also might benefit from genetic evaluation, comprising the third group. For example, even before symptoms are present, testing a child who has a brother with Duchenne muscular dystrophy or a relative with cystic fibrosis may prove life saving if it uncovers a similar diagnosis.
Genetic testing has entered a new era in the past few years. Our ability to perform DNA-based tests and identify an individual's susceptibility to cancer, heart disease, diabetes, and so many other conditions is beginning to have a major impact on our practice of medicine.
Experts predict – thanks to advances in technology we already have – that in a few years we will be able to screen during the newborn period and identify every mutation and polymorphism present. This screening will permit us to predict a child's “medical life” through identification of individual susceptibilities to disease likely to develop during his or her lifetime. Although still in its infancy, this technology would revolutionize pediatrics from a field in which we wait for the child to develop symptoms and signs of disease and then react with medication and other treatments, to one where we can predict disease. This will give us the opportunity to help our patients in a whole new way: to prevent the symptoms and signs from arising in the first place.
With the good comes the bad, as with any new technology. For example, interpretation of results with this advanced testing will require special expertise in genetics and genomics. Unfortunately, interpretation of genetic findings often is not as “black and white” as diagnosis of anemia based on serum hemoglobin and hematocrit levels. Genetic test results often include polymorphisms, and most of these variations of normal are benign and not associated with disease. Subspecialist consultation may be needed to make these important distinctions.
General pediatricians play an essential role in interpretation of newborn screening tests. Fortunately, results are normal for the majority of children and no further follow-up is indicated. However, if an abnormality is detected, referral to a specialist is warranted to facilitate an early intervention that, in some cases, can make a difference in the long-term health of the child. You also can refer families who request consultation with a geneticist to discuss recurrence risk in future progeny and for additional genetic testing, as indicated.
Beyond standard newborn genetic screening, the role of the pediatrician is somewhat limited regarding the screening and testing for specific genetic disorders. However, there are situations in which the pediatrician should feel comfortable in ordering and interpreting genetic tests.
For example, testing in children with intellectual disabilities and autism spectrum disorder has become standard. As tier 1 testing in such children, I usually order a microarray-based comparative genomic hybridization (array CGH), a test that has largely replaced high-resolution chromosome analysis in this population. I also perform DNA testing for fragile X syndrome, the most common inherited cause of intellectual disabilities. Because the results of this testing will be normal in 80%–90% of these children, I encourage pediatricians to order these tests themselves. I then make myself available if genetic evaluation reveals an abnormality.
Another factor to consider is the recent direct-to-consumer marketing of genetic testing that expands standard newborn screening or uses genetic markers to predict susceptibility to specific conditions. These tests often require the family, with or without the assistance of the pediatrician, to send a sample of DNA to a reference lab. The lab returns the results directly to the family. Again, the laboratory results are difficult to interpret, and you may be called on to provide guidance. Sometimes interpretation is straightforward, but in other cases it can be tricky, and if you are uncomfortable you might want to refer them to a medical geneticist or genetic counselor.
When you refer a child to a geneticist, include all results of your previous testing, those performed by other specialists, and newborn screening. Genetic tests performed on the mother during the pregnancy (for example, amniocentesis, chorionic villus sampling, sonograms, and/or biochemical screening tests) also are important. Provide any imaging findings, including MRIs or CT scans.
Proceed cautiously when counseling families regarding results of genetic testing. It can be trickier than you might think. For example, results of a test for a single gene disorder might uncover a previously unknown change in the child's DNA. The finding could be a benign polymorphism that has no clinical consequences or it could be a pathogenic mutation responsible for the child's signs and symptoms.
Simply informing the family about this finding is inadequate. To be certain, the parents need to be tested. If one or both of them has the same genetic change, the polymorphism might be benign. In contrast, if neither parent has the mutation, the child's test result might reflect a spontaneous genetic change and increase the likelihood you have discovered the cause of the clinical condition.
In general, there are three categories of children who may require genetic testing. First, there are those children who have multiple congenital anomalies or dysmorphic features. These findings could be caused by chromosome abnormalities, single gene mutations, or teratogenic agents. In these children, in order to ensure that the appropriate tests are ordered, a genetic consultation is important.
A second group of children who may require genetic testing are those in whom deviation from typical development or “normal” growth parameters occur during the first few years of life. Such children may have chromosome abnormalities, single gene mutations, and/or an underlying metabolic disorder. Keep in mind seizures, developmental regression, failure to thrive, and respiratory disturbances can bolster the likelihood of a genetic or metabolic etiology.
Before ordering any genetic testing, it is essential to take a complete patient and family history and to perform a complete physical exam. Children with a family history of a first- or second-degree family member with a genetic disorder also might benefit from genetic evaluation, comprising the third group. For example, even before symptoms are present, testing a child who has a brother with Duchenne muscular dystrophy or a relative with cystic fibrosis may prove life saving if it uncovers a similar diagnosis.
Genetic testing has entered a new era in the past few years. Our ability to perform DNA-based tests and identify an individual's susceptibility to cancer, heart disease, diabetes, and so many other conditions is beginning to have a major impact on our practice of medicine.
Experts predict – thanks to advances in technology we already have – that in a few years we will be able to screen during the newborn period and identify every mutation and polymorphism present. This screening will permit us to predict a child's “medical life” through identification of individual susceptibilities to disease likely to develop during his or her lifetime. Although still in its infancy, this technology would revolutionize pediatrics from a field in which we wait for the child to develop symptoms and signs of disease and then react with medication and other treatments, to one where we can predict disease. This will give us the opportunity to help our patients in a whole new way: to prevent the symptoms and signs from arising in the first place.
With the good comes the bad, as with any new technology. For example, interpretation of results with this advanced testing will require special expertise in genetics and genomics. Unfortunately, interpretation of genetic findings often is not as “black and white” as diagnosis of anemia based on serum hemoglobin and hematocrit levels. Genetic test results often include polymorphisms, and most of these variations of normal are benign and not associated with disease. Subspecialist consultation may be needed to make these important distinctions.
General pediatricians play an essential role in interpretation of newborn screening tests. Fortunately, results are normal for the majority of children and no further follow-up is indicated. However, if an abnormality is detected, referral to a specialist is warranted to facilitate an early intervention that, in some cases, can make a difference in the long-term health of the child. You also can refer families who request consultation with a geneticist to discuss recurrence risk in future progeny and for additional genetic testing, as indicated.
Beyond standard newborn genetic screening, the role of the pediatrician is somewhat limited regarding the screening and testing for specific genetic disorders. However, there are situations in which the pediatrician should feel comfortable in ordering and interpreting genetic tests.
For example, testing in children with intellectual disabilities and autism spectrum disorder has become standard. As tier 1 testing in such children, I usually order a microarray-based comparative genomic hybridization (array CGH), a test that has largely replaced high-resolution chromosome analysis in this population. I also perform DNA testing for fragile X syndrome, the most common inherited cause of intellectual disabilities. Because the results of this testing will be normal in 80%–90% of these children, I encourage pediatricians to order these tests themselves. I then make myself available if genetic evaluation reveals an abnormality.
Another factor to consider is the recent direct-to-consumer marketing of genetic testing that expands standard newborn screening or uses genetic markers to predict susceptibility to specific conditions. These tests often require the family, with or without the assistance of the pediatrician, to send a sample of DNA to a reference lab. The lab returns the results directly to the family. Again, the laboratory results are difficult to interpret, and you may be called on to provide guidance. Sometimes interpretation is straightforward, but in other cases it can be tricky, and if you are uncomfortable you might want to refer them to a medical geneticist or genetic counselor.
When you refer a child to a geneticist, include all results of your previous testing, those performed by other specialists, and newborn screening. Genetic tests performed on the mother during the pregnancy (for example, amniocentesis, chorionic villus sampling, sonograms, and/or biochemical screening tests) also are important. Provide any imaging findings, including MRIs or CT scans.
Proceed cautiously when counseling families regarding results of genetic testing. It can be trickier than you might think. For example, results of a test for a single gene disorder might uncover a previously unknown change in the child's DNA. The finding could be a benign polymorphism that has no clinical consequences or it could be a pathogenic mutation responsible for the child's signs and symptoms.
Simply informing the family about this finding is inadequate. To be certain, the parents need to be tested. If one or both of them has the same genetic change, the polymorphism might be benign. In contrast, if neither parent has the mutation, the child's test result might reflect a spontaneous genetic change and increase the likelihood you have discovered the cause of the clinical condition.
In general, there are three categories of children who may require genetic testing. First, there are those children who have multiple congenital anomalies or dysmorphic features. These findings could be caused by chromosome abnormalities, single gene mutations, or teratogenic agents. In these children, in order to ensure that the appropriate tests are ordered, a genetic consultation is important.
A second group of children who may require genetic testing are those in whom deviation from typical development or “normal” growth parameters occur during the first few years of life. Such children may have chromosome abnormalities, single gene mutations, and/or an underlying metabolic disorder. Keep in mind seizures, developmental regression, failure to thrive, and respiratory disturbances can bolster the likelihood of a genetic or metabolic etiology.
Before ordering any genetic testing, it is essential to take a complete patient and family history and to perform a complete physical exam. Children with a family history of a first- or second-degree family member with a genetic disorder also might benefit from genetic evaluation, comprising the third group. For example, even before symptoms are present, testing a child who has a brother with Duchenne muscular dystrophy or a relative with cystic fibrosis may prove life saving if it uncovers a similar diagnosis.
Helping Children With PTSD
Different forms of trauma can cause posttraumatic stress disorder in children, whether from an objective event like a car crash or sports injury to trauma involving loved ones, such as domestic violence, abuse, or neglect.
Pediatricians can help by routinely screening for dysfunction and by asking questions at annual well-child visits. Overt symptoms include fear related to the trauma such as avoiding the traumatic setting or activity. Less specific symptoms include anxiety, avoidance, social isolation, depression, and low self-esteem.
If a standard screen such as the Pediatric Symptom Checklist or another instrument reveals psychosocial dysfunction, you have to determine the cause of dysfunction, and PTSD should certainly be considered.
Is there family discord leading to violence in the home? If you suspect PTSD, ask a child what happened and why he or she thinks it happened. Determine if the child is blaming himself or herself in any way. Is the child grieving following a permanent injury and/or loss of a loved one? How have the parents discussed any traumatic event with the child? Do the parents feel traumatized by the child's experience?
If PTSD is a possibility, ask if the child is experiencing flashbacks, intrusive thoughts, and/or any related anxiety.
Some symptoms are expected after a traumatic event or following cancer or critical care treatment experienced as traumatic. Most children and adolescents overcome the fear of riding in a car or playing the sport that resulted in the trauma.
However, symptoms that persist for a month or more, with avoidance and associated anxiety, are core to the diagnosis of PTSD. The anxiety can build and be self-reinforcing so as to interfere with daily functioning. At this point, consider referral to a mental health specialist, preferably one with some experience in PTSD treatment. A specialist can help the patient overcome his or her anxiety and return to functioning through cognitive and behavioral techniques such as reframing the events, dealing with any guilt, and staged exposure to the anxiety.
If one of your patients experienced a car crash or other major trauma, you will likely know about it, already be treating the child, and should be planning to monitor them for signs of PTSD. In contrast, detection of subtle PTSD is more challenging, particularly if the trauma is unknown or occurred years ago. Trauma related to domestic violence or sexual abuse first requires consideration of this possibility and then gentle, empathic, and persistent questioning.
Triggers for reliving/reexperiencing the trauma also can be straightforward. For example, a child who gets into a car with a similar interior design years after a crash can immediately experience and emotionally return to the trauma. Other triggers are less obvious, such as a teenage girl who was held down and forced to have sex against her will, who later feels constrained by tight clothing and immediately relives the fear and anguish.
Like many presentations in pediatrics, management of PTSD depends on the developmental stage of the child, including his or her cognitive abilities and emotional state. For example, infants or toddlers might not be able to make much sense of what is happening when they witness domestic violence. Terror, fear, and confusion are their most likely reactions.
School-age children aged 5–8 years would not fully understand either, but they will try to make some sense of the domestic violence. Assuming no one reassures them otherwise, they also may feel that something they did sparked or contributed to the violence. For example, if they overhear arguments around issues in the family and hear their name mentioned, they may quickly assume that they are the cause of the domestic violence. This can lead to feelings of guilt, self-criticism, and unworthiness.
Adolescents will experience some of the same reactions as younger children. They will still experience shock, even if they are better equipped to conceptualize the domestic violence. Some will feel powerless because they cannot end the strife, particularly at a time when they are supposed to have more control over the real world. Teens might feel they have not lived up to expectations and perceive some blame. Others may choose to flee, find support through friends, and/or may deal with their feelings using substances.
Act when you encounter a patient who feels very guilty about parental fighting or who justifies abuse because he feels worthless or was told repeatedly he was a bad child. Help him realize he was not responsible for the conflict and that no one deserves abuse. Discuss other, more realistic possibilities for the family paradigm.
These are not easy conversations. Some pediatricians will feel comfortable working at this depth, others will prefer to refer.
Healing from PTSD related to family violence, sexual abuse, or criminal activity is a several-step process. As one's sense of guilt diminishes, other emotions such as anger at not being better protected or valued need to be addressed. Finally, there needs to be some grieving for what was lacking and some acceptance of what was possible. This is not a simple process; however, it is worthwhile because if their PTSD remains untreated, there is a greater likelihood they will continue to relive traumatic memories as adults.
There is some controversy as to whether talking through the traumatic event over and over truly helps. Some clinicians feel that a certain amount of supportive discussion in a calm way makes sense, especially early. But solely repeating the details of the event may re-traumatize the child and intensify negative feelings, especially if the memories are very vivid.
Cognitive and behavioral approaches can help the child reframe their trauma. An example is exposure therapy, where the child is carefully reexposed to the trauma in stages while they learn to reframe and diminish the intensity of the experience. Often, ideas about the trauma come out that can be examined objectively to try to lessen some of those traumatic feelings.
Exposure therapy also can incorporate gradual steps to help the child overcome their fear. If a person survived a plane crash, the first step might be to take him or her to the airport, then to board an airplane without taking off, and so forth. This approach reintroduces the trauma without eliciting a full response. You don't want the brain to go on “red alert” again. In a state of hyperarousal, reliving the trauma may do more harm than good.
The terrified moments that children experience during a traumatic sequence tend to get burned into their memories much more strongly than everyday events. A school-age child might remember nothing about an uneventful trip in the car, but if a traumatic accident happens, often she remembers almost every detail. She recalls descriptive elements of what happened as well as the emotional fright or anguish very vividly.
Sometimes vivid, traumatic memories will enter your patient's mind spontaneously without him knowing why. In other cases, there are triggers. Sometimes these flashbacks arise shortly following trauma and sometimes they take years.
Pediatricians can do their patients and families a service if they are aware of PTSD either after an overt event like a car accident or by considering trauma in an anxious or dysfunctional child.
Different forms of trauma can cause posttraumatic stress disorder in children, whether from an objective event like a car crash or sports injury to trauma involving loved ones, such as domestic violence, abuse, or neglect.
Pediatricians can help by routinely screening for dysfunction and by asking questions at annual well-child visits. Overt symptoms include fear related to the trauma such as avoiding the traumatic setting or activity. Less specific symptoms include anxiety, avoidance, social isolation, depression, and low self-esteem.
If a standard screen such as the Pediatric Symptom Checklist or another instrument reveals psychosocial dysfunction, you have to determine the cause of dysfunction, and PTSD should certainly be considered.
Is there family discord leading to violence in the home? If you suspect PTSD, ask a child what happened and why he or she thinks it happened. Determine if the child is blaming himself or herself in any way. Is the child grieving following a permanent injury and/or loss of a loved one? How have the parents discussed any traumatic event with the child? Do the parents feel traumatized by the child's experience?
If PTSD is a possibility, ask if the child is experiencing flashbacks, intrusive thoughts, and/or any related anxiety.
Some symptoms are expected after a traumatic event or following cancer or critical care treatment experienced as traumatic. Most children and adolescents overcome the fear of riding in a car or playing the sport that resulted in the trauma.
However, symptoms that persist for a month or more, with avoidance and associated anxiety, are core to the diagnosis of PTSD. The anxiety can build and be self-reinforcing so as to interfere with daily functioning. At this point, consider referral to a mental health specialist, preferably one with some experience in PTSD treatment. A specialist can help the patient overcome his or her anxiety and return to functioning through cognitive and behavioral techniques such as reframing the events, dealing with any guilt, and staged exposure to the anxiety.
If one of your patients experienced a car crash or other major trauma, you will likely know about it, already be treating the child, and should be planning to monitor them for signs of PTSD. In contrast, detection of subtle PTSD is more challenging, particularly if the trauma is unknown or occurred years ago. Trauma related to domestic violence or sexual abuse first requires consideration of this possibility and then gentle, empathic, and persistent questioning.
Triggers for reliving/reexperiencing the trauma also can be straightforward. For example, a child who gets into a car with a similar interior design years after a crash can immediately experience and emotionally return to the trauma. Other triggers are less obvious, such as a teenage girl who was held down and forced to have sex against her will, who later feels constrained by tight clothing and immediately relives the fear and anguish.
Like many presentations in pediatrics, management of PTSD depends on the developmental stage of the child, including his or her cognitive abilities and emotional state. For example, infants or toddlers might not be able to make much sense of what is happening when they witness domestic violence. Terror, fear, and confusion are their most likely reactions.
School-age children aged 5–8 years would not fully understand either, but they will try to make some sense of the domestic violence. Assuming no one reassures them otherwise, they also may feel that something they did sparked or contributed to the violence. For example, if they overhear arguments around issues in the family and hear their name mentioned, they may quickly assume that they are the cause of the domestic violence. This can lead to feelings of guilt, self-criticism, and unworthiness.
Adolescents will experience some of the same reactions as younger children. They will still experience shock, even if they are better equipped to conceptualize the domestic violence. Some will feel powerless because they cannot end the strife, particularly at a time when they are supposed to have more control over the real world. Teens might feel they have not lived up to expectations and perceive some blame. Others may choose to flee, find support through friends, and/or may deal with their feelings using substances.
Act when you encounter a patient who feels very guilty about parental fighting or who justifies abuse because he feels worthless or was told repeatedly he was a bad child. Help him realize he was not responsible for the conflict and that no one deserves abuse. Discuss other, more realistic possibilities for the family paradigm.
These are not easy conversations. Some pediatricians will feel comfortable working at this depth, others will prefer to refer.
Healing from PTSD related to family violence, sexual abuse, or criminal activity is a several-step process. As one's sense of guilt diminishes, other emotions such as anger at not being better protected or valued need to be addressed. Finally, there needs to be some grieving for what was lacking and some acceptance of what was possible. This is not a simple process; however, it is worthwhile because if their PTSD remains untreated, there is a greater likelihood they will continue to relive traumatic memories as adults.
There is some controversy as to whether talking through the traumatic event over and over truly helps. Some clinicians feel that a certain amount of supportive discussion in a calm way makes sense, especially early. But solely repeating the details of the event may re-traumatize the child and intensify negative feelings, especially if the memories are very vivid.
Cognitive and behavioral approaches can help the child reframe their trauma. An example is exposure therapy, where the child is carefully reexposed to the trauma in stages while they learn to reframe and diminish the intensity of the experience. Often, ideas about the trauma come out that can be examined objectively to try to lessen some of those traumatic feelings.
Exposure therapy also can incorporate gradual steps to help the child overcome their fear. If a person survived a plane crash, the first step might be to take him or her to the airport, then to board an airplane without taking off, and so forth. This approach reintroduces the trauma without eliciting a full response. You don't want the brain to go on “red alert” again. In a state of hyperarousal, reliving the trauma may do more harm than good.
The terrified moments that children experience during a traumatic sequence tend to get burned into their memories much more strongly than everyday events. A school-age child might remember nothing about an uneventful trip in the car, but if a traumatic accident happens, often she remembers almost every detail. She recalls descriptive elements of what happened as well as the emotional fright or anguish very vividly.
Sometimes vivid, traumatic memories will enter your patient's mind spontaneously without him knowing why. In other cases, there are triggers. Sometimes these flashbacks arise shortly following trauma and sometimes they take years.
Pediatricians can do their patients and families a service if they are aware of PTSD either after an overt event like a car accident or by considering trauma in an anxious or dysfunctional child.
Different forms of trauma can cause posttraumatic stress disorder in children, whether from an objective event like a car crash or sports injury to trauma involving loved ones, such as domestic violence, abuse, or neglect.
Pediatricians can help by routinely screening for dysfunction and by asking questions at annual well-child visits. Overt symptoms include fear related to the trauma such as avoiding the traumatic setting or activity. Less specific symptoms include anxiety, avoidance, social isolation, depression, and low self-esteem.
If a standard screen such as the Pediatric Symptom Checklist or another instrument reveals psychosocial dysfunction, you have to determine the cause of dysfunction, and PTSD should certainly be considered.
Is there family discord leading to violence in the home? If you suspect PTSD, ask a child what happened and why he or she thinks it happened. Determine if the child is blaming himself or herself in any way. Is the child grieving following a permanent injury and/or loss of a loved one? How have the parents discussed any traumatic event with the child? Do the parents feel traumatized by the child's experience?
If PTSD is a possibility, ask if the child is experiencing flashbacks, intrusive thoughts, and/or any related anxiety.
Some symptoms are expected after a traumatic event or following cancer or critical care treatment experienced as traumatic. Most children and adolescents overcome the fear of riding in a car or playing the sport that resulted in the trauma.
However, symptoms that persist for a month or more, with avoidance and associated anxiety, are core to the diagnosis of PTSD. The anxiety can build and be self-reinforcing so as to interfere with daily functioning. At this point, consider referral to a mental health specialist, preferably one with some experience in PTSD treatment. A specialist can help the patient overcome his or her anxiety and return to functioning through cognitive and behavioral techniques such as reframing the events, dealing with any guilt, and staged exposure to the anxiety.
If one of your patients experienced a car crash or other major trauma, you will likely know about it, already be treating the child, and should be planning to monitor them for signs of PTSD. In contrast, detection of subtle PTSD is more challenging, particularly if the trauma is unknown or occurred years ago. Trauma related to domestic violence or sexual abuse first requires consideration of this possibility and then gentle, empathic, and persistent questioning.
Triggers for reliving/reexperiencing the trauma also can be straightforward. For example, a child who gets into a car with a similar interior design years after a crash can immediately experience and emotionally return to the trauma. Other triggers are less obvious, such as a teenage girl who was held down and forced to have sex against her will, who later feels constrained by tight clothing and immediately relives the fear and anguish.
Like many presentations in pediatrics, management of PTSD depends on the developmental stage of the child, including his or her cognitive abilities and emotional state. For example, infants or toddlers might not be able to make much sense of what is happening when they witness domestic violence. Terror, fear, and confusion are their most likely reactions.
School-age children aged 5–8 years would not fully understand either, but they will try to make some sense of the domestic violence. Assuming no one reassures them otherwise, they also may feel that something they did sparked or contributed to the violence. For example, if they overhear arguments around issues in the family and hear their name mentioned, they may quickly assume that they are the cause of the domestic violence. This can lead to feelings of guilt, self-criticism, and unworthiness.
Adolescents will experience some of the same reactions as younger children. They will still experience shock, even if they are better equipped to conceptualize the domestic violence. Some will feel powerless because they cannot end the strife, particularly at a time when they are supposed to have more control over the real world. Teens might feel they have not lived up to expectations and perceive some blame. Others may choose to flee, find support through friends, and/or may deal with their feelings using substances.
Act when you encounter a patient who feels very guilty about parental fighting or who justifies abuse because he feels worthless or was told repeatedly he was a bad child. Help him realize he was not responsible for the conflict and that no one deserves abuse. Discuss other, more realistic possibilities for the family paradigm.
These are not easy conversations. Some pediatricians will feel comfortable working at this depth, others will prefer to refer.
Healing from PTSD related to family violence, sexual abuse, or criminal activity is a several-step process. As one's sense of guilt diminishes, other emotions such as anger at not being better protected or valued need to be addressed. Finally, there needs to be some grieving for what was lacking and some acceptance of what was possible. This is not a simple process; however, it is worthwhile because if their PTSD remains untreated, there is a greater likelihood they will continue to relive traumatic memories as adults.
There is some controversy as to whether talking through the traumatic event over and over truly helps. Some clinicians feel that a certain amount of supportive discussion in a calm way makes sense, especially early. But solely repeating the details of the event may re-traumatize the child and intensify negative feelings, especially if the memories are very vivid.
Cognitive and behavioral approaches can help the child reframe their trauma. An example is exposure therapy, where the child is carefully reexposed to the trauma in stages while they learn to reframe and diminish the intensity of the experience. Often, ideas about the trauma come out that can be examined objectively to try to lessen some of those traumatic feelings.
Exposure therapy also can incorporate gradual steps to help the child overcome their fear. If a person survived a plane crash, the first step might be to take him or her to the airport, then to board an airplane without taking off, and so forth. This approach reintroduces the trauma without eliciting a full response. You don't want the brain to go on “red alert” again. In a state of hyperarousal, reliving the trauma may do more harm than good.
The terrified moments that children experience during a traumatic sequence tend to get burned into their memories much more strongly than everyday events. A school-age child might remember nothing about an uneventful trip in the car, but if a traumatic accident happens, often she remembers almost every detail. She recalls descriptive elements of what happened as well as the emotional fright or anguish very vividly.
Sometimes vivid, traumatic memories will enter your patient's mind spontaneously without him knowing why. In other cases, there are triggers. Sometimes these flashbacks arise shortly following trauma and sometimes they take years.
Pediatricians can do their patients and families a service if they are aware of PTSD either after an overt event like a car accident or by considering trauma in an anxious or dysfunctional child.
FDA warns of possible link between breast implants and ALCL
The Food and Drug Administration (FDA), after a review of reported cases of anaplastic large-cell lymphoma (ALCL), warns that there may be a link between silicone and saline breast implants and the rare cancer.
People with breast implants “may have a very small but significant risk of ALCL in the scar capsule adjacent to the implant,” according to the agency.
The FDA based its announcement on a review of literature published between January 1997 and May 2010 that identified 34 unique cases of ALCL in women with either type of breast implant.
William Maisel, MD, chief scientist and deputy director for science in the FDA’s Center for Devices and Radiological Health, said, “We need more data and are asking that healthcare professionals tell us about any confirmed cases they identify.”
Of the 34 unique ALCL cases reviewed, 24 had silicone and 7 had saline implants; 3 implants did not have the type specified. The women ranged in age from 28 to 87 years, with a median age of 51 years.
ALCL occurred in 19 women who received implants for aesthetic augmentation, 11 for reconstruction, and 4 had no reason recorded for the implant.
The women developed ALCL in a median of 8 years from time of implant, ranging from 1 year to 23 years. Most of the patients were diagnosed because they had implant-related symptoms, such as seromas, capsular contractures, or peri-implant masses that needed implant revision surgery.
Physicians found lymphoma cells in the seroma surrounding the implant, in the fibrous capsule, or within a peri-implant mass in all of the ALCL cases.
According to the FDA report, CD30 status was positive in all 29 of the cases that included this information, which is consistent with an ALCL diagnosis. ALCL cases in the rest of the body can be either ALK-positive or ALK-negative. The 26 reports of ALCL in women with breast implants that included ALK status were all ALK-negative.
The FDA recommends that physicians consider an ALCL diagnosis if patients present with capsular contracture or masses adjacent to the breast implant. Physicians should report all confirmed cases of ALCL in people with breast implants to Medwatch.
The FDA does not recommend removing breast implants in patients without symptoms, which include pain, lumps, swelllng, or asymmetry that develop after the surgical site is fully healed. The agency plans to update its review of silicone breast implants in spring 2011.
ALCL occurs in about 1 in 500,000 women each year in the United States, according to the Surveillance, Epidemiology, and End Results (SEER) Program of the National Cancer Institute. In the breast, ALCL occurs in approximately 3 in 100,000,000 women annually in the US. 
The Food and Drug Administration (FDA), after a review of reported cases of anaplastic large-cell lymphoma (ALCL), warns that there may be a link between silicone and saline breast implants and the rare cancer.
People with breast implants “may have a very small but significant risk of ALCL in the scar capsule adjacent to the implant,” according to the agency.
The FDA based its announcement on a review of literature published between January 1997 and May 2010 that identified 34 unique cases of ALCL in women with either type of breast implant.
William Maisel, MD, chief scientist and deputy director for science in the FDA’s Center for Devices and Radiological Health, said, “We need more data and are asking that healthcare professionals tell us about any confirmed cases they identify.”
Of the 34 unique ALCL cases reviewed, 24 had silicone and 7 had saline implants; 3 implants did not have the type specified. The women ranged in age from 28 to 87 years, with a median age of 51 years.
ALCL occurred in 19 women who received implants for aesthetic augmentation, 11 for reconstruction, and 4 had no reason recorded for the implant.
The women developed ALCL in a median of 8 years from time of implant, ranging from 1 year to 23 years. Most of the patients were diagnosed because they had implant-related symptoms, such as seromas, capsular contractures, or peri-implant masses that needed implant revision surgery.
Physicians found lymphoma cells in the seroma surrounding the implant, in the fibrous capsule, or within a peri-implant mass in all of the ALCL cases.
According to the FDA report, CD30 status was positive in all 29 of the cases that included this information, which is consistent with an ALCL diagnosis. ALCL cases in the rest of the body can be either ALK-positive or ALK-negative. The 26 reports of ALCL in women with breast implants that included ALK status were all ALK-negative.
The FDA recommends that physicians consider an ALCL diagnosis if patients present with capsular contracture or masses adjacent to the breast implant. Physicians should report all confirmed cases of ALCL in people with breast implants to Medwatch.
The FDA does not recommend removing breast implants in patients without symptoms, which include pain, lumps, swelllng, or asymmetry that develop after the surgical site is fully healed. The agency plans to update its review of silicone breast implants in spring 2011.
ALCL occurs in about 1 in 500,000 women each year in the United States, according to the Surveillance, Epidemiology, and End Results (SEER) Program of the National Cancer Institute. In the breast, ALCL occurs in approximately 3 in 100,000,000 women annually in the US.
The Food and Drug Administration (FDA), after a review of reported cases of anaplastic large-cell lymphoma (ALCL), warns that there may be a link between silicone and saline breast implants and the rare cancer.
People with breast implants “may have a very small but significant risk of ALCL in the scar capsule adjacent to the implant,” according to the agency.
The FDA based its announcement on a review of literature published between January 1997 and May 2010 that identified 34 unique cases of ALCL in women with either type of breast implant.
William Maisel, MD, chief scientist and deputy director for science in the FDA’s Center for Devices and Radiological Health, said, “We need more data and are asking that healthcare professionals tell us about any confirmed cases they identify.”
Of the 34 unique ALCL cases reviewed, 24 had silicone and 7 had saline implants; 3 implants did not have the type specified. The women ranged in age from 28 to 87 years, with a median age of 51 years.
ALCL occurred in 19 women who received implants for aesthetic augmentation, 11 for reconstruction, and 4 had no reason recorded for the implant.
The women developed ALCL in a median of 8 years from time of implant, ranging from 1 year to 23 years. Most of the patients were diagnosed because they had implant-related symptoms, such as seromas, capsular contractures, or peri-implant masses that needed implant revision surgery.
Physicians found lymphoma cells in the seroma surrounding the implant, in the fibrous capsule, or within a peri-implant mass in all of the ALCL cases.
According to the FDA report, CD30 status was positive in all 29 of the cases that included this information, which is consistent with an ALCL diagnosis. ALCL cases in the rest of the body can be either ALK-positive or ALK-negative. The 26 reports of ALCL in women with breast implants that included ALK status were all ALK-negative.
The FDA recommends that physicians consider an ALCL diagnosis if patients present with capsular contracture or masses adjacent to the breast implant. Physicians should report all confirmed cases of ALCL in people with breast implants to Medwatch.
The FDA does not recommend removing breast implants in patients without symptoms, which include pain, lumps, swelllng, or asymmetry that develop after the surgical site is fully healed. The agency plans to update its review of silicone breast implants in spring 2011.
ALCL occurs in about 1 in 500,000 women each year in the United States, according to the Surveillance, Epidemiology, and End Results (SEER) Program of the National Cancer Institute. In the breast, ALCL occurs in approximately 3 in 100,000,000 women annually in the US.
When Opportunity Knocks
News that domestic spending on healthcare grew at the lowest rate in recorded history could be viewed as trouble for HM leaders negotiating new contracts—or it could be the chance for a new generation of hospitalists to prove their worth.
"This is an opportunity for people who can do good clinical integration. … You can have gainsharing and actually still make physicians win financially but still deliver the right care for patients," says Steven Deitelzweig, MD, MMM, SFHM, chair of SHM's Practice Management Committee and chair of hospital medicine for Ochsner Health System in New Orleans.
According to the report "Recession Contributes To Slowest Annual Rate Of Increase In Health Spending In Five Decades" (doi:10.1377/hlthaff.2010.1032), healthcare spending in 2009 grew just 4%, to $2.5 trillion, the lowest growth rate since the federal government began tracking the data 50 years ago.
The impact of a record slowing in healthcare spending is particularly germane to HM group negotiators, considering they find themselves in talks at a unique time, according to an article in this month’s issue of The Hospitalist. Industry participants say that between stimulus money for quality reforms, the worst economic downturn since the Great Depression, and healthcare reform, hospitals have to do the proverbial more with less.
Dr. Deitelzweig urges hospitalists to promote their quality initiatives and take charge of processes that can save their institutions money. A hospital administration that saves money by eliminating unnecessary procedures and smoothing transitions of care, for example, can argue it deserves a piece of those savings, he says.
"The pie will be shrinking," he adds. "But that doesn't mean you can't figure a way to provide the right care in a less expensive way."
News that domestic spending on healthcare grew at the lowest rate in recorded history could be viewed as trouble for HM leaders negotiating new contracts—or it could be the chance for a new generation of hospitalists to prove their worth.
"This is an opportunity for people who can do good clinical integration. … You can have gainsharing and actually still make physicians win financially but still deliver the right care for patients," says Steven Deitelzweig, MD, MMM, SFHM, chair of SHM's Practice Management Committee and chair of hospital medicine for Ochsner Health System in New Orleans.
According to the report "Recession Contributes To Slowest Annual Rate Of Increase In Health Spending In Five Decades" (doi:10.1377/hlthaff.2010.1032), healthcare spending in 2009 grew just 4%, to $2.5 trillion, the lowest growth rate since the federal government began tracking the data 50 years ago.
The impact of a record slowing in healthcare spending is particularly germane to HM group negotiators, considering they find themselves in talks at a unique time, according to an article in this month’s issue of The Hospitalist. Industry participants say that between stimulus money for quality reforms, the worst economic downturn since the Great Depression, and healthcare reform, hospitals have to do the proverbial more with less.
Dr. Deitelzweig urges hospitalists to promote their quality initiatives and take charge of processes that can save their institutions money. A hospital administration that saves money by eliminating unnecessary procedures and smoothing transitions of care, for example, can argue it deserves a piece of those savings, he says.
"The pie will be shrinking," he adds. "But that doesn't mean you can't figure a way to provide the right care in a less expensive way."
News that domestic spending on healthcare grew at the lowest rate in recorded history could be viewed as trouble for HM leaders negotiating new contracts—or it could be the chance for a new generation of hospitalists to prove their worth.
"This is an opportunity for people who can do good clinical integration. … You can have gainsharing and actually still make physicians win financially but still deliver the right care for patients," says Steven Deitelzweig, MD, MMM, SFHM, chair of SHM's Practice Management Committee and chair of hospital medicine for Ochsner Health System in New Orleans.
According to the report "Recession Contributes To Slowest Annual Rate Of Increase In Health Spending In Five Decades" (doi:10.1377/hlthaff.2010.1032), healthcare spending in 2009 grew just 4%, to $2.5 trillion, the lowest growth rate since the federal government began tracking the data 50 years ago.
The impact of a record slowing in healthcare spending is particularly germane to HM group negotiators, considering they find themselves in talks at a unique time, according to an article in this month’s issue of The Hospitalist. Industry participants say that between stimulus money for quality reforms, the worst economic downturn since the Great Depression, and healthcare reform, hospitals have to do the proverbial more with less.
Dr. Deitelzweig urges hospitalists to promote their quality initiatives and take charge of processes that can save their institutions money. A hospital administration that saves money by eliminating unnecessary procedures and smoothing transitions of care, for example, can argue it deserves a piece of those savings, he says.
"The pie will be shrinking," he adds. "But that doesn't mean you can't figure a way to provide the right care in a less expensive way."
A Perfect Fit
Sally Bullock, MD, medical director of the hospitalist program at Middle Tennessee Medical Center (MTMC) in Murfreesboro, Tenn., received the hospital’s 2011 Physician of the Year award at its annual Physician Christmas Reception in December. The award is voted on by hospital staff, and this is the first time it was given to a hospitalist.
“I’ve been here on staff for 26 years, mostly in private practice as an internist,” Dr. Bullock says. “Visiting the hospital was always a favorite part of my practice. In fact, I did not use hospitalists to care for my patients.”
However, family demands and time pressures of the practice led her to leave it for the flexibility of multiple part-time medical jobs, including HM shifts. In November of 2007, after repeated requests from Andy Brown, MD, MTMC's vice president of medical affairs, she accepted the hospitalist leadership position.
"I encouraged Dr. Bullock to take on this role because she genuinely cares about her patients. Sally is an excellent clinician and communicator who also leads by example," Dr. Brown says. "I knew that physicians would recognize these qualities and want to be part of the program."
The hospitalist program at MTMC started in 1999 with six physicians but experienced contraction in 2006. Under Dr. Bullock's leadership, it has grown to 22 physicians, with more expansion expected this year.
"I just jumped on it, and we got busy recruiting," Dr. Bullock says, adding that the award from her peers at MTMC reflects both her longevity in the medical community and appreciation for "taking the hospitalist program where it needs to be."
Currently, her position includes hospitalist shifts, both scheduled and fill-in, squeezing in administrative duties, and mentoring other physicians. "I'm sort of the program's surge protector," she says.
Sally Bullock, MD, medical director of the hospitalist program at Middle Tennessee Medical Center (MTMC) in Murfreesboro, Tenn., received the hospital’s 2011 Physician of the Year award at its annual Physician Christmas Reception in December. The award is voted on by hospital staff, and this is the first time it was given to a hospitalist.
“I’ve been here on staff for 26 years, mostly in private practice as an internist,” Dr. Bullock says. “Visiting the hospital was always a favorite part of my practice. In fact, I did not use hospitalists to care for my patients.”
However, family demands and time pressures of the practice led her to leave it for the flexibility of multiple part-time medical jobs, including HM shifts. In November of 2007, after repeated requests from Andy Brown, MD, MTMC's vice president of medical affairs, she accepted the hospitalist leadership position.
"I encouraged Dr. Bullock to take on this role because she genuinely cares about her patients. Sally is an excellent clinician and communicator who also leads by example," Dr. Brown says. "I knew that physicians would recognize these qualities and want to be part of the program."
The hospitalist program at MTMC started in 1999 with six physicians but experienced contraction in 2006. Under Dr. Bullock's leadership, it has grown to 22 physicians, with more expansion expected this year.
"I just jumped on it, and we got busy recruiting," Dr. Bullock says, adding that the award from her peers at MTMC reflects both her longevity in the medical community and appreciation for "taking the hospitalist program where it needs to be."
Currently, her position includes hospitalist shifts, both scheduled and fill-in, squeezing in administrative duties, and mentoring other physicians. "I'm sort of the program's surge protector," she says.
Sally Bullock, MD, medical director of the hospitalist program at Middle Tennessee Medical Center (MTMC) in Murfreesboro, Tenn., received the hospital’s 2011 Physician of the Year award at its annual Physician Christmas Reception in December. The award is voted on by hospital staff, and this is the first time it was given to a hospitalist.
“I’ve been here on staff for 26 years, mostly in private practice as an internist,” Dr. Bullock says. “Visiting the hospital was always a favorite part of my practice. In fact, I did not use hospitalists to care for my patients.”
However, family demands and time pressures of the practice led her to leave it for the flexibility of multiple part-time medical jobs, including HM shifts. In November of 2007, after repeated requests from Andy Brown, MD, MTMC's vice president of medical affairs, she accepted the hospitalist leadership position.
"I encouraged Dr. Bullock to take on this role because she genuinely cares about her patients. Sally is an excellent clinician and communicator who also leads by example," Dr. Brown says. "I knew that physicians would recognize these qualities and want to be part of the program."
The hospitalist program at MTMC started in 1999 with six physicians but experienced contraction in 2006. Under Dr. Bullock's leadership, it has grown to 22 physicians, with more expansion expected this year.
"I just jumped on it, and we got busy recruiting," Dr. Bullock says, adding that the award from her peers at MTMC reflects both her longevity in the medical community and appreciation for "taking the hospitalist program where it needs to be."
Currently, her position includes hospitalist shifts, both scheduled and fill-in, squeezing in administrative duties, and mentoring other physicians. "I'm sort of the program's surge protector," she says.
Why I like ham
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A New Year’s Resolution to Crack Down on Opioids?
Sometime early this year, after two years of controversy, the FDA might finally release its revised proposal for more stringent regulations on opioid pain relievers. The following are the key questions—and answers—surrounding new regulations, as well as a look at other recent FDA actions, including increased scrutiny of diabetes and obesity drugs due to heart concerns.
Question: What’s the latest on the FDA release of new regulations for prescription opioids?
Answer: First, the back story: The controversy concerns the creation of a Risk Evaluation and Mitigation Strategy (REMS) for opioid analgesics amid a troubling boom in prescription drug abuse, addiction, and overdose, and an accompanying spike in deaths from opioid overdoses. Under a 2007 law, the FDA can require drug and medical device manufacturers to adopt a REMS to ensure that the benefits outweigh the risks of continued use and that patients are adequately informed. In this case, the strategy could impact how nearly 4 million patients receive long-acting and extended-release opioids annually, according to FDA statistics.
In February 2009, the FDA sent a letter to manufacturers of opioid pain relievers, proposing a classwide REMS that would require certification by a physician or pharmacist and restrict distribution of the drugs, among other provisions. In response, many healthcare providers and medical organizations warned of an increased regulatory burden that would negatively impact patients. Among the concerns: fewer primary-care physicians (PCPs) willing to manage patients with chronic pain, reduced access to medically necessary drugs in underserved communities, undermedicated cancer patients, and increased use of other drugs with less stringent oversight.
In response, the FDA dropped its proposal for a prescriber accreditation program and another for a patient registry. But an FDA advisory panel soundly rejected a revised REMS proposal in July, by a vote of 25-10. The panel criticized the new plans as being too lax, lacking a formal requirement f
Q: What will the new REMS likely include?
A: Based on the criticisms of FDA panelists in July, the revised REMS could mandate a training requirement for all prescribers. The program would likely be created by the FDA and not by the drug industry, as had first been proposed (many doctors have agreed that a centralized, standardized program would be far preferable to dealing with programs set up independently by drug manufacturers). The strategy also might govern immediate-release opioids, in addition to extended-release and long-acting formulations. The FDA could propose linking doctor education to an existing Drug Enforcement Administration registration, but that would require congressional approval.
Q: What was the outcome of safety deliberations over the diabetes drug rosiglitazone (Avandia)?
A: After several years of concern over a heightened risk of heart attacks and other heart problems among patients taking rosiglitazone for type 2 diabetes mellitus, the FDA sharply restricted its availability in September and required the manufacturer, GlaxoSmithKline, to submit a REMS. When implemented, the REMS will limit new prescriptions to patients who cannot achieve glycemic control with other medications and decide not to take the alternative (pioglitazone) for medical reasons.1 Other diabetes drugs have faced similar scrutiny: In October, the FDA rejected an extended-release form of the diabetes drug exenatide (Bydureon) due to safety concerns, citing the need for more studies from manufacturer Eli Lilly about its effect on heart rate.
Q: What’s the upshot of recent FDA actions on weight-loss drugs and supplements?
A: The FDA also cracked down on weight-loss formulations in 2010, declining to approve several new drugs, overseeing the withdrawal of Abbott Laboratory’s Meridia in October, and announcing a December recall of capsules marketed online as Fruta Planta. Safety concerns over the latter two were linked to sibutramine, a drug that is “known to increase blood pressure and/or pulse rate in some patients and may present a serious risk for patients with a history of coronary artery disease, congestive heart failure, arrhythmias or stroke,” according to the FDA. Additionally, the drug can interact “in life-threatening ways” with other medications, reinforcing the idea that hospitalists and other doctors should delve into patients’ recent history of weight-loss drug or supplement use.
Q: What should we expect from the FDA in the next year?
A: Analysts will be keeping an eye on the number of new drugs approved in 2011 to discern any new trends. As reported by The Wall Street Journal and other publications, the FDA gave 21 drugs the go-ahead in 2010, down from 26 cleared in 2009 and 25 approved in 2008. The dip has concerned some drug industry representatives, who warn that an overly cautious approach could lead to more delays in new drugs reaching patients. Of course, the lower number also could reflect a continued dry spell in the pipelines of many pharmaceutical companies. On the flipside, consumer watchdogs have expressed optimism that the FDA might be devoting more attention to safety. In November, for example, the FDA oversaw the pulling of popular painkiller propoxyphene (marketed as Darvon and Darvocet) after evidence accumulated that the medication can cause potentially fatal heart damage and rhythm abnormalities.
Bryn Nelson is a freelance medical writer based in Seattle.
References
1. Woodcock J, Sharfstein JM, Hamburg M. Regulatory action on rosiglitazone by the U.S. Food and Drug Administration. N Engl J Med. 2010;363(16):1489-1491.
Sometime early this year, after two years of controversy, the FDA might finally release its revised proposal for more stringent regulations on opioid pain relievers. The following are the key questions—and answers—surrounding new regulations, as well as a look at other recent FDA actions, including increased scrutiny of diabetes and obesity drugs due to heart concerns.
Question: What’s the latest on the FDA release of new regulations for prescription opioids?
Answer: First, the back story: The controversy concerns the creation of a Risk Evaluation and Mitigation Strategy (REMS) for opioid analgesics amid a troubling boom in prescription drug abuse, addiction, and overdose, and an accompanying spike in deaths from opioid overdoses. Under a 2007 law, the FDA can require drug and medical device manufacturers to adopt a REMS to ensure that the benefits outweigh the risks of continued use and that patients are adequately informed. In this case, the strategy could impact how nearly 4 million patients receive long-acting and extended-release opioids annually, according to FDA statistics.
In February 2009, the FDA sent a letter to manufacturers of opioid pain relievers, proposing a classwide REMS that would require certification by a physician or pharmacist and restrict distribution of the drugs, among other provisions. In response, many healthcare providers and medical organizations warned of an increased regulatory burden that would negatively impact patients. Among the concerns: fewer primary-care physicians (PCPs) willing to manage patients with chronic pain, reduced access to medically necessary drugs in underserved communities, undermedicated cancer patients, and increased use of other drugs with less stringent oversight.
In response, the FDA dropped its proposal for a prescriber accreditation program and another for a patient registry. But an FDA advisory panel soundly rejected a revised REMS proposal in July, by a vote of 25-10. The panel criticized the new plans as being too lax, lacking a formal requirement f
Q: What will the new REMS likely include?
A: Based on the criticisms of FDA panelists in July, the revised REMS could mandate a training requirement for all prescribers. The program would likely be created by the FDA and not by the drug industry, as had first been proposed (many doctors have agreed that a centralized, standardized program would be far preferable to dealing with programs set up independently by drug manufacturers). The strategy also might govern immediate-release opioids, in addition to extended-release and long-acting formulations. The FDA could propose linking doctor education to an existing Drug Enforcement Administration registration, but that would require congressional approval.
Q: What was the outcome of safety deliberations over the diabetes drug rosiglitazone (Avandia)?
A: After several years of concern over a heightened risk of heart attacks and other heart problems among patients taking rosiglitazone for type 2 diabetes mellitus, the FDA sharply restricted its availability in September and required the manufacturer, GlaxoSmithKline, to submit a REMS. When implemented, the REMS will limit new prescriptions to patients who cannot achieve glycemic control with other medications and decide not to take the alternative (pioglitazone) for medical reasons.1 Other diabetes drugs have faced similar scrutiny: In October, the FDA rejected an extended-release form of the diabetes drug exenatide (Bydureon) due to safety concerns, citing the need for more studies from manufacturer Eli Lilly about its effect on heart rate.
Q: What’s the upshot of recent FDA actions on weight-loss drugs and supplements?
A: The FDA also cracked down on weight-loss formulations in 2010, declining to approve several new drugs, overseeing the withdrawal of Abbott Laboratory’s Meridia in October, and announcing a December recall of capsules marketed online as Fruta Planta. Safety concerns over the latter two were linked to sibutramine, a drug that is “known to increase blood pressure and/or pulse rate in some patients and may present a serious risk for patients with a history of coronary artery disease, congestive heart failure, arrhythmias or stroke,” according to the FDA. Additionally, the drug can interact “in life-threatening ways” with other medications, reinforcing the idea that hospitalists and other doctors should delve into patients’ recent history of weight-loss drug or supplement use.
Q: What should we expect from the FDA in the next year?
A: Analysts will be keeping an eye on the number of new drugs approved in 2011 to discern any new trends. As reported by The Wall Street Journal and other publications, the FDA gave 21 drugs the go-ahead in 2010, down from 26 cleared in 2009 and 25 approved in 2008. The dip has concerned some drug industry representatives, who warn that an overly cautious approach could lead to more delays in new drugs reaching patients. Of course, the lower number also could reflect a continued dry spell in the pipelines of many pharmaceutical companies. On the flipside, consumer watchdogs have expressed optimism that the FDA might be devoting more attention to safety. In November, for example, the FDA oversaw the pulling of popular painkiller propoxyphene (marketed as Darvon and Darvocet) after evidence accumulated that the medication can cause potentially fatal heart damage and rhythm abnormalities.
Bryn Nelson is a freelance medical writer based in Seattle.
References
1. Woodcock J, Sharfstein JM, Hamburg M. Regulatory action on rosiglitazone by the U.S. Food and Drug Administration. N Engl J Med. 2010;363(16):1489-1491.
Sometime early this year, after two years of controversy, the FDA might finally release its revised proposal for more stringent regulations on opioid pain relievers. The following are the key questions—and answers—surrounding new regulations, as well as a look at other recent FDA actions, including increased scrutiny of diabetes and obesity drugs due to heart concerns.
Question: What’s the latest on the FDA release of new regulations for prescription opioids?
Answer: First, the back story: The controversy concerns the creation of a Risk Evaluation and Mitigation Strategy (REMS) for opioid analgesics amid a troubling boom in prescription drug abuse, addiction, and overdose, and an accompanying spike in deaths from opioid overdoses. Under a 2007 law, the FDA can require drug and medical device manufacturers to adopt a REMS to ensure that the benefits outweigh the risks of continued use and that patients are adequately informed. In this case, the strategy could impact how nearly 4 million patients receive long-acting and extended-release opioids annually, according to FDA statistics.
In February 2009, the FDA sent a letter to manufacturers of opioid pain relievers, proposing a classwide REMS that would require certification by a physician or pharmacist and restrict distribution of the drugs, among other provisions. In response, many healthcare providers and medical organizations warned of an increased regulatory burden that would negatively impact patients. Among the concerns: fewer primary-care physicians (PCPs) willing to manage patients with chronic pain, reduced access to medically necessary drugs in underserved communities, undermedicated cancer patients, and increased use of other drugs with less stringent oversight.
In response, the FDA dropped its proposal for a prescriber accreditation program and another for a patient registry. But an FDA advisory panel soundly rejected a revised REMS proposal in July, by a vote of 25-10. The panel criticized the new plans as being too lax, lacking a formal requirement f
Q: What will the new REMS likely include?
A: Based on the criticisms of FDA panelists in July, the revised REMS could mandate a training requirement for all prescribers. The program would likely be created by the FDA and not by the drug industry, as had first been proposed (many doctors have agreed that a centralized, standardized program would be far preferable to dealing with programs set up independently by drug manufacturers). The strategy also might govern immediate-release opioids, in addition to extended-release and long-acting formulations. The FDA could propose linking doctor education to an existing Drug Enforcement Administration registration, but that would require congressional approval.
Q: What was the outcome of safety deliberations over the diabetes drug rosiglitazone (Avandia)?
A: After several years of concern over a heightened risk of heart attacks and other heart problems among patients taking rosiglitazone for type 2 diabetes mellitus, the FDA sharply restricted its availability in September and required the manufacturer, GlaxoSmithKline, to submit a REMS. When implemented, the REMS will limit new prescriptions to patients who cannot achieve glycemic control with other medications and decide not to take the alternative (pioglitazone) for medical reasons.1 Other diabetes drugs have faced similar scrutiny: In October, the FDA rejected an extended-release form of the diabetes drug exenatide (Bydureon) due to safety concerns, citing the need for more studies from manufacturer Eli Lilly about its effect on heart rate.
Q: What’s the upshot of recent FDA actions on weight-loss drugs and supplements?
A: The FDA also cracked down on weight-loss formulations in 2010, declining to approve several new drugs, overseeing the withdrawal of Abbott Laboratory’s Meridia in October, and announcing a December recall of capsules marketed online as Fruta Planta. Safety concerns over the latter two were linked to sibutramine, a drug that is “known to increase blood pressure and/or pulse rate in some patients and may present a serious risk for patients with a history of coronary artery disease, congestive heart failure, arrhythmias or stroke,” according to the FDA. Additionally, the drug can interact “in life-threatening ways” with other medications, reinforcing the idea that hospitalists and other doctors should delve into patients’ recent history of weight-loss drug or supplement use.
Q: What should we expect from the FDA in the next year?
A: Analysts will be keeping an eye on the number of new drugs approved in 2011 to discern any new trends. As reported by The Wall Street Journal and other publications, the FDA gave 21 drugs the go-ahead in 2010, down from 26 cleared in 2009 and 25 approved in 2008. The dip has concerned some drug industry representatives, who warn that an overly cautious approach could lead to more delays in new drugs reaching patients. Of course, the lower number also could reflect a continued dry spell in the pipelines of many pharmaceutical companies. On the flipside, consumer watchdogs have expressed optimism that the FDA might be devoting more attention to safety. In November, for example, the FDA oversaw the pulling of popular painkiller propoxyphene (marketed as Darvon and Darvocet) after evidence accumulated that the medication can cause potentially fatal heart damage and rhythm abnormalities.
Bryn Nelson is a freelance medical writer based in Seattle.
References
1. Woodcock J, Sharfstein JM, Hamburg M. Regulatory action on rosiglitazone by the U.S. Food and Drug Administration. N Engl J Med. 2010;363(16):1489-1491.
