Q. My patient delivered the first of her twins vaginally but is still carrying the second fetus. When we report our services, how should we code for both the first and (eventual) second delivery? I know that I will be billing 59409 (vaginal delivery only [with or without episiotomy and/or forceps]) for the first delivery and 59400 (Routine obstetric care including antepartum care, vaginal delivery [with or without episiotomy, and/or forceps] and postpartum care) for the second—assuming that a cesarean section is not required. But can I use the diagnosis code 761.5 (multiple pregnancy) with these codes, as well?

A. Here is one of those situations that ICD9 was not constructed to handle! You may not report 761.5 on the mother’s record because this is still one pregnancy for both events. Code 761.5 can only be reported on the baby’s record once he or she is receiving direct care. Therefore, report the twin diagnosis code 651.01 for both deliveries. However, consider waiting and billing the deliveries together, on the same claim, with the different delivery dates specified (as so: “4/21: 59409, 651.01”; then “5/xx: 59400, 651.01”), and include an explanation with the claim to ensure payment for both deliveries.

In-office lab test is not an occasion for a modifier

Q. We billed an office visit and a wet mount (87210 [smear, primary source with interpretation; wet mount for infectious agents (eg, saline, India ink, KOH preps)]). The lab service was determined to be global by the insurance company and was denied. What is the appropriate code for the wet mount?

A. The A modifier is usually unnecessary for a laboratory test with an office visit. The closest modifier that would apply is -25 (significant, separately identifiable evaluation and management service by the same physician on the same day of a procedure).

I suspect that your problem may not be a global issue, but one of coverage for a lab test performed by your practice under CLIA (Clinical Laboratory Improvement Amendments). [Editor’s note: Details about coding for office lab tests (eg, wet mounts and KOH preps) in relation to CLIA certificate requirements were discussed in Reimbursement Adviser in the August 2006 issue of OBG Management. Read this installment at obgmanagement.com by linking to “Past Issues” on the top navigation bar of the home page.]

To sort out this situation, you first need to contact the payer to find out whether it considers a lab test global to an office visit, which should never be the case. Perhaps your billing staff misinterpreted the denial message. Or maybe this payer does, in fact, require a modifier for any service billed at the same time as an office visit.

On the other hand, it could also be that you do not have the required CLIA certificate to bill for the wet mount using code 87210.

Payer may balk at modified biophysical profile

Q. We are performing a limited ultrasonography to evaluate amniotic fluid volume and a fetal non-stress test at the same time on our pregnant patient. How can we best code this evaluation to ensure proper reimbursement?

A. No single code describes this modified (so to speak) biophysical profile. Instead, you have 2 coding options, either of which may cause a headache with the payer:

• Code for the complete biophysical profile (76818) but add a modifier -52 for a reduced service. The problem? Not all payers permit use of this modifier with an imaging code.
  
• Itemize your services by reporting 59025 for the fetal non-stress test and 76815 (limited pelvic ultrasound) for evaluation of amniotic fluid volume. The problem here? Code 59025 is bundled into code 76815; although you are allowed to use the modifier -59 (distinct procedural service) to bypass the edit, you can only do so if you can meet the criteria for doing so (eg, care involves a different incision or excision, a different patient encounter, or a different injury or site). Some payers may not accept that you’ve met those requirements, although I would disagree with that decision: Each test is performed independently and measures different things. So, to bill this combination of tests, add modifier -59 to the bundled code: 76815, 59025-59.
  

Hysteroscopy before but not during thermoablation

Q. Please clarify: How do we correctly report a thermoablation procedure when hysteroscopy is performed before the procedure but not for guidance during the procedure? Are 58353 (endometrial ablation, thermal, without hysteroscopic guidance) and 58555-51 (Hysteroscopy, diagnostic [separate procedure]; multiple procedure) appropriate codes?

A. The problem is that code 58555 is bundled into 58353 under National Correct Coding Initiative (NCCI) rules. Because of this, the modifier -51 (multiple procedures) cannot be used. Although this bundled code allows the use of a modifier -59 (distinct procedure), meeting the criteria for using it is almost impossible.

Modifier -59 is defined as follows in CPT: “…used to identify procedures/services that are not normally reported together, but are appropriate under the circumstances. This may represent a different session or patient encounter, different procedure or surgery, different site or organ system, separate incision/excision, separate lesion, or separate injury (or area of injury in extensive injuries) not ordinarily encountered or performed on the same day by the same physician.”

In the situation that you describe, the hysteroscope was inserted in the same area as the ablation, not at a different site; no separate excision or incision was made when inserting the hysteroscope; this was not a different surgical session; and, last, although hysteroscopy might, technically, be a distinct procedure from the ablation, it was directly related to the performance of the ablation in that it represented initial “exploration.”

I believe, therefore, that correct coding in this case is to report the all-inclusive 58563 (Hysteroscopy, surgical; with endometrial ablation [eg, endometrial resection, electrosurgical ablation, thermoablation]). Support for this opinion is found in ACOG’s Ob/GYN Coding Manual: Components of Correct Procedural Coding 2007. A comment included with code 58353 states: “If hysteroscopy is also performed, report code 58563 instead.”

Q. My patient delivered the first of her twins vaginally but is still carrying the second fetus. When we report our services, how should we code for both the first and (eventual) second delivery? I know that I will be billing 59409 (vaginal delivery only [with or without episiotomy and/or forceps]) for the first delivery and 59400 (Routine obstetric care including antepartum care, vaginal delivery [with or without episiotomy, and/or forceps] and postpartum care) for the second—assuming that a cesarean section is not required. But can I use the diagnosis code 761.5 (multiple pregnancy) with these codes, as well?

A. Here is one of those situations that ICD9 was not constructed to handle! You may not report 761.5 on the mother’s record because this is still one pregnancy for both events. Code 761.5 can only be reported on the baby’s record once he or she is receiving direct care. Therefore, report the twin diagnosis code 651.01 for both deliveries. However, consider waiting and billing the deliveries together, on the same claim, with the different delivery dates specified (as so: “4/21: 59409, 651.01”; then “5/xx: 59400, 651.01”), and include an explanation with the claim to ensure payment for both deliveries.

In-office lab test is not an occasion for a modifier

Q. We billed an office visit and a wet mount (87210 [smear, primary source with interpretation; wet mount for infectious agents (eg, saline, India ink, KOH preps)]). The lab service was determined to be global by the insurance company and was denied. What is the appropriate code for the wet mount?

A. The A modifier is usually unnecessary for a laboratory test with an office visit. The closest modifier that would apply is -25 (significant, separately identifiable evaluation and management service by the same physician on the same day of a procedure).

I suspect that your problem may not be a global issue, but one of coverage for a lab test performed by your practice under CLIA (Clinical Laboratory Improvement Amendments). [Editor’s note: Details about coding for office lab tests (eg, wet mounts and KOH preps) in relation to CLIA certificate requirements were discussed in Reimbursement Adviser in the August 2006 issue of OBG Management. Read this installment at obgmanagement.com by linking to “Past Issues” on the top navigation bar of the home page.]

To sort out this situation, you first need to contact the payer to find out whether it considers a lab test global to an office visit, which should never be the case. Perhaps your billing staff misinterpreted the denial message. Or maybe this payer does, in fact, require a modifier for any service billed at the same time as an office visit.

On the other hand, it could also be that you do not have the required CLIA certificate to bill for the wet mount using code 87210.

Payer may balk at modified biophysical profile

Q. We are performing a limited ultrasonography to evaluate amniotic fluid volume and a fetal non-stress test at the same time on our pregnant patient. How can we best code this evaluation to ensure proper reimbursement?

A. No single code describes this modified (so to speak) biophysical profile. Instead, you have 2 coding options, either of which may cause a headache with the payer:

• Code for the complete biophysical profile (76818) but add a modifier -52 for a reduced service. The problem? Not all payers permit use of this modifier with an imaging code.
  
• Itemize your services by reporting 59025 for the fetal non-stress test and 76815 (limited pelvic ultrasound) for evaluation of amniotic fluid volume. The problem here? Code 59025 is bundled into code 76815; although you are allowed to use the modifier -59 (distinct procedural service) to bypass the edit, you can only do so if you can meet the criteria for doing so (eg, care involves a different incision or excision, a different patient encounter, or a different injury or site). Some payers may not accept that you’ve met those requirements, although I would disagree with that decision: Each test is performed independently and measures different things. So, to bill this combination of tests, add modifier -59 to the bundled code: 76815, 59025-59.
  

Hysteroscopy before but not during thermoablation

Q. Please clarify: How do we correctly report a thermoablation procedure when hysteroscopy is performed before the procedure but not for guidance during the procedure? Are 58353 (endometrial ablation, thermal, without hysteroscopic guidance) and 58555-51 (Hysteroscopy, diagnostic [separate procedure]; multiple procedure) appropriate codes?

A. The problem is that code 58555 is bundled into 58353 under National Correct Coding Initiative (NCCI) rules. Because of this, the modifier -51 (multiple procedures) cannot be used. Although this bundled code allows the use of a modifier -59 (distinct procedure), meeting the criteria for using it is almost impossible.

Modifier -59 is defined as follows in CPT: “…used to identify procedures/services that are not normally reported together, but are appropriate under the circumstances. This may represent a different session or patient encounter, different procedure or surgery, different site or organ system, separate incision/excision, separate lesion, or separate injury (or area of injury in extensive injuries) not ordinarily encountered or performed on the same day by the same physician.”

In the situation that you describe, the hysteroscope was inserted in the same area as the ablation, not at a different site; no separate excision or incision was made when inserting the hysteroscope; this was not a different surgical session; and, last, although hysteroscopy might, technically, be a distinct procedure from the ablation, it was directly related to the performance of the ablation in that it represented initial “exploration.”

I believe, therefore, that correct coding in this case is to report the all-inclusive 58563 (Hysteroscopy, surgical; with endometrial ablation [eg, endometrial resection, electrosurgical ablation, thermoablation]). Support for this opinion is found in ACOG’s Ob/GYN Coding Manual: Components of Correct Procedural Coding 2007. A comment included with code 58353 states: “If hysteroscopy is also performed, report code 58563 instead.”

Q. My patient delivered the first of her twins vaginally but is still carrying the second fetus. When we report our services, how should we code for both the first and (eventual) second delivery? I know that I will be billing 59409 (vaginal delivery only [with or without episiotomy and/or forceps]) for the first delivery and 59400 (Routine obstetric care including antepartum care, vaginal delivery [with or without episiotomy, and/or forceps] and postpartum care) for the second—assuming that a cesarean section is not required. But can I use the diagnosis code 761.5 (multiple pregnancy) with these codes, as well?

A. Here is one of those situations that ICD9 was not constructed to handle! You may not report 761.5 on the mother’s record because this is still one pregnancy for both events. Code 761.5 can only be reported on the baby’s record once he or she is receiving direct care. Therefore, report the twin diagnosis code 651.01 for both deliveries. However, consider waiting and billing the deliveries together, on the same claim, with the different delivery dates specified (as so: “4/21: 59409, 651.01”; then “5/xx: 59400, 651.01”), and include an explanation with the claim to ensure payment for both deliveries.

In-office lab test is not an occasion for a modifier

Q. We billed an office visit and a wet mount (87210 [smear, primary source with interpretation; wet mount for infectious agents (eg, saline, India ink, KOH preps)]). The lab service was determined to be global by the insurance company and was denied. What is the appropriate code for the wet mount?

A. The A modifier is usually unnecessary for a laboratory test with an office visit. The closest modifier that would apply is -25 (significant, separately identifiable evaluation and management service by the same physician on the same day of a procedure).

I suspect that your problem may not be a global issue, but one of coverage for a lab test performed by your practice under CLIA (Clinical Laboratory Improvement Amendments). [Editor’s note: Details about coding for office lab tests (eg, wet mounts and KOH preps) in relation to CLIA certificate requirements were discussed in Reimbursement Adviser in the August 2006 issue of OBG Management. Read this installment at obgmanagement.com by linking to “Past Issues” on the top navigation bar of the home page.]

To sort out this situation, you first need to contact the payer to find out whether it considers a lab test global to an office visit, which should never be the case. Perhaps your billing staff misinterpreted the denial message. Or maybe this payer does, in fact, require a modifier for any service billed at the same time as an office visit.

On the other hand, it could also be that you do not have the required CLIA certificate to bill for the wet mount using code 87210.

Payer may balk at modified biophysical profile

Q. We are performing a limited ultrasonography to evaluate amniotic fluid volume and a fetal non-stress test at the same time on our pregnant patient. How can we best code this evaluation to ensure proper reimbursement?

A. No single code describes this modified (so to speak) biophysical profile. Instead, you have 2 coding options, either of which may cause a headache with the payer:

• Code for the complete biophysical profile (76818) but add a modifier -52 for a reduced service. The problem? Not all payers permit use of this modifier with an imaging code.
  
• Itemize your services by reporting 59025 for the fetal non-stress test and 76815 (limited pelvic ultrasound) for evaluation of amniotic fluid volume. The problem here? Code 59025 is bundled into code 76815; although you are allowed to use the modifier -59 (distinct procedural service) to bypass the edit, you can only do so if you can meet the criteria for doing so (eg, care involves a different incision or excision, a different patient encounter, or a different injury or site). Some payers may not accept that you’ve met those requirements, although I would disagree with that decision: Each test is performed independently and measures different things. So, to bill this combination of tests, add modifier -59 to the bundled code: 76815, 59025-59.
  

Hysteroscopy before but not during thermoablation

Q. Please clarify: How do we correctly report a thermoablation procedure when hysteroscopy is performed before the procedure but not for guidance during the procedure? Are 58353 (endometrial ablation, thermal, without hysteroscopic guidance) and 58555-51 (Hysteroscopy, diagnostic [separate procedure]; multiple procedure) appropriate codes?

A. The problem is that code 58555 is bundled into 58353 under National Correct Coding Initiative (NCCI) rules. Because of this, the modifier -51 (multiple procedures) cannot be used. Although this bundled code allows the use of a modifier -59 (distinct procedure), meeting the criteria for using it is almost impossible.

Modifier -59 is defined as follows in CPT: “…used to identify procedures/services that are not normally reported together, but are appropriate under the circumstances. This may represent a different session or patient encounter, different procedure or surgery, different site or organ system, separate incision/excision, separate lesion, or separate injury (or area of injury in extensive injuries) not ordinarily encountered or performed on the same day by the same physician.”

In the situation that you describe, the hysteroscope was inserted in the same area as the ablation, not at a different site; no separate excision or incision was made when inserting the hysteroscope; this was not a different surgical session; and, last, although hysteroscopy might, technically, be a distinct procedure from the ablation, it was directly related to the performance of the ablation in that it represented initial “exploration.”

I believe, therefore, that correct coding in this case is to report the all-inclusive 58563 (Hysteroscopy, surgical; with endometrial ablation [eg, endometrial resection, electrosurgical ablation, thermoablation]). Support for this opinion is found in ACOG’s Ob/GYN Coding Manual: Components of Correct Procedural Coding 2007. A comment included with code 58353 states: “If hysteroscopy is also performed, report code 58563 instead.”

Q. Recently, we were denied a claim for hospital care related to a patient’s premature labor. She was admitted to stop labor at 30 weeks but delivered 5 days after admission. The reason for denial? “Invalid ICD9 code.” But the code we used, 644.03 (threatened premature labor), appears to be correct. We also reported 644.21 (early onset of delivery) with the delivery code. Should we appeal, given that care prior to delivery is well documented?

A. I believe that your denial is based on incorrect use of the fifth digit on the reported diagnosis codes, not on refusal to reimburse separately for additional care before delivery. ICD9 guidelines related to fifth-digit coding for obstetric cases state:

“The fifth-digits, which are appropriate for each code number, are listed in brackets under each code. The fifth digits on each code should all be consistent with each other. That is, should a delivery occur all of the fifth digits should indicate the delivery.”

In this case, although the patient was still in the antepartum period during initial care, she did deliver during that hospitalization. That means a fifth digit of “3” (antepartum condition or complication) is incompatible with a fifth digit of “1” (delivered, with or without mention of antepartum condition), which is probably what generated the denial message. You have 2 choices:

• Resubmit a corrected claim, indicating a fifth digit of “1” for both diagnostic codes
  
• Appeal the denial, indicating the diagnostic correction and supplying information regarding the additional care for this patient.
  

Bundle codes for repair of a pelvic floor defect?

Q. To treat a patient who has a pelvic floor defect, we performed an anterior repair, a posterior repair, and an enterocele repair, using mesh—plus cystoscopy. Does one code capture all these procedures?

A. I assume that you used mesh to augment the anterior and posterior repairs. A single CPT code, 57265 (combined anteroposterior colporrhaphy; with enterocele repair) captures the first 3 procedures, and CPT allows the addon mesh code 57267 (insertion of mesh or other prosthesis for repair of pelvic floor defect, each site [anterior, posterior compartment], vaginal approach) to be reported with 57265.

Based on the definition of the addon mesh code, it is appropriate for you to bill for a quantity of 2: 1 for the anterior compartment repair and 1 for the posterior compartment repair, which includes the rectocele and enterocele.

As for reporting the cystoscopy (with 52000 [cystourethroscopy (separate procedure)]), the reason that you provide for the procedure will determine whether you are reimbursed. There must be a medical indication for cystoscopy beyond your simply checking your work, which is considered a standard of surgical care by most payers.

Q. Recently, we were denied a claim for hospital care related to a patient’s premature labor. She was admitted to stop labor at 30 weeks but delivered 5 days after admission. The reason for denial? “Invalid ICD9 code.” But the code we used, 644.03 (threatened premature labor), appears to be correct. We also reported 644.21 (early onset of delivery) with the delivery code. Should we appeal, given that care prior to delivery is well documented?

A. I believe that your denial is based on incorrect use of the fifth digit on the reported diagnosis codes, not on refusal to reimburse separately for additional care before delivery. ICD9 guidelines related to fifth-digit coding for obstetric cases state:

“The fifth-digits, which are appropriate for each code number, are listed in brackets under each code. The fifth digits on each code should all be consistent with each other. That is, should a delivery occur all of the fifth digits should indicate the delivery.”

In this case, although the patient was still in the antepartum period during initial care, she did deliver during that hospitalization. That means a fifth digit of “3” (antepartum condition or complication) is incompatible with a fifth digit of “1” (delivered, with or without mention of antepartum condition), which is probably what generated the denial message. You have 2 choices:

• Resubmit a corrected claim, indicating a fifth digit of “1” for both diagnostic codes
  
• Appeal the denial, indicating the diagnostic correction and supplying information regarding the additional care for this patient.
  

Bundle codes for repair of a pelvic floor defect?

Q. To treat a patient who has a pelvic floor defect, we performed an anterior repair, a posterior repair, and an enterocele repair, using mesh—plus cystoscopy. Does one code capture all these procedures?

A. I assume that you used mesh to augment the anterior and posterior repairs. A single CPT code, 57265 (combined anteroposterior colporrhaphy; with enterocele repair) captures the first 3 procedures, and CPT allows the addon mesh code 57267 (insertion of mesh or other prosthesis for repair of pelvic floor defect, each site [anterior, posterior compartment], vaginal approach) to be reported with 57265.

Based on the definition of the addon mesh code, it is appropriate for you to bill for a quantity of 2: 1 for the anterior compartment repair and 1 for the posterior compartment repair, which includes the rectocele and enterocele.

As for reporting the cystoscopy (with 52000 [cystourethroscopy (separate procedure)]), the reason that you provide for the procedure will determine whether you are reimbursed. There must be a medical indication for cystoscopy beyond your simply checking your work, which is considered a standard of surgical care by most payers.

Q. Recently, we were denied a claim for hospital care related to a patient’s premature labor. She was admitted to stop labor at 30 weeks but delivered 5 days after admission. The reason for denial? “Invalid ICD9 code.” But the code we used, 644.03 (threatened premature labor), appears to be correct. We also reported 644.21 (early onset of delivery) with the delivery code. Should we appeal, given that care prior to delivery is well documented?

A. I believe that your denial is based on incorrect use of the fifth digit on the reported diagnosis codes, not on refusal to reimburse separately for additional care before delivery. ICD9 guidelines related to fifth-digit coding for obstetric cases state:

“The fifth-digits, which are appropriate for each code number, are listed in brackets under each code. The fifth digits on each code should all be consistent with each other. That is, should a delivery occur all of the fifth digits should indicate the delivery.”

In this case, although the patient was still in the antepartum period during initial care, she did deliver during that hospitalization. That means a fifth digit of “3” (antepartum condition or complication) is incompatible with a fifth digit of “1” (delivered, with or without mention of antepartum condition), which is probably what generated the denial message. You have 2 choices:

• Resubmit a corrected claim, indicating a fifth digit of “1” for both diagnostic codes
  
• Appeal the denial, indicating the diagnostic correction and supplying information regarding the additional care for this patient.
  

Bundle codes for repair of a pelvic floor defect?

Q. To treat a patient who has a pelvic floor defect, we performed an anterior repair, a posterior repair, and an enterocele repair, using mesh—plus cystoscopy. Does one code capture all these procedures?

A. I assume that you used mesh to augment the anterior and posterior repairs. A single CPT code, 57265 (combined anteroposterior colporrhaphy; with enterocele repair) captures the first 3 procedures, and CPT allows the addon mesh code 57267 (insertion of mesh or other prosthesis for repair of pelvic floor defect, each site [anterior, posterior compartment], vaginal approach) to be reported with 57265.

Based on the definition of the addon mesh code, it is appropriate for you to bill for a quantity of 2: 1 for the anterior compartment repair and 1 for the posterior compartment repair, which includes the rectocele and enterocele.

As for reporting the cystoscopy (with 52000 [cystourethroscopy (separate procedure)]), the reason that you provide for the procedure will determine whether you are reimbursed. There must be a medical indication for cystoscopy beyond your simply checking your work, which is considered a standard of surgical care by most payers.

Lisdexamfetamine—FDA-approved to treat attention-deficit/hyperactivity disorder (ADHD) in children ages 6 to 12 (Table 1)—reduces ADHD symptoms during and after school and may be less likely to be abused than other psychostimulants, particularly immediate-release preparations, clinical data suggest.

Table 1

Lisdexamfetamine: Fast facts

Clinical implications

Because it is effective for about 12 hours, lisdexamfetamine might improve the child’s ability to complete homework and participate in extracurricular activities, which in turn might enhance academic performance and/or socialization skills.

Lisdexamfetamine could help the child with ADHD who shows no contraindications to the drug —particularly if he or she needs daylong coverage.

How it works

Lisdexamfetamine—a dextroamphetamine derivative—is rapidly absorbed and converted to dextroamphetamine, which is believed to exert therapeutic effect by:

• blocking norepinephrine and dopamine reuptake into presynaptic neurons
• increasing the neurotransmitters’ release into the extraneuronal space.

The medication’s amphetamine release is highly predictable, which contributes to its therapeutic benefit in ADHD. Amphetamine is released through GI metabolism of lisdexamfetamine, which produces the active d-amphetamine moiety that reaches the bloodstream. The medication is derived from d-amphetamine, with negligible amounts of lysine cleaved.

Lisdexamfetamine requires in vivo metabolism (in the GI tract) to its active constituent d-amphetamine. As a result, the medication will not produce high d-amphetamine blood levels—and should not cause euphoria or other reinforcing effects—if injected or snorted. Its abuse potential is lower overall compared with immediate-release psychostimulant formulations.

Pharmacokinetics

Dextroamphetamine’s plasma elimination half-life is approximately 9½ hours—which accounts for lisdexamfetamine’s extended action. The drug reaches steady-state concentrations in 2 to 3 days.

Food does not affect absorption and delays maximum concentration by 1 hour or less, so taking lisdexamfetamine during breakfast should not slow its therapeutic effect. Because dextroamphetamine reaches maximum concentration in approximately 3½ hours, the medication should take effect by the time the child gets to school. In one randomized, phase-2 trial, children with ADHD who received lisdexamfetamine, 30 to 70 mg/d, showed overall improvement within 2 hours after dosing.¹

Efficacy

Lisdexamfetamine reduced ADHD symptoms in 2 double-blind studies: a phase-2 crossover study and a phase-3 random-dose trial.

Phase-2 crossover study.² Fifty-two children ages 6 to 12 with combined or hyperactive-impulsive type ADHD received extended-release mixed amphetamine salts (MAS) for 3 weeks. Subjects received 10 mg/d or dosages titrated to 20 or 30 mg/d based on response to medication.

The youths then were divided into 3 groups based on optimal MAS dosage and received 3 treatments for 1 week each:

• group 1: placebo; MAS, 10 mg/d; lisdexamfetamine, 30 mg/d
• group 2: placebo; MAS, 20 mg/d; lisdexamfetamine, 50 mg/d
• group 3: placebo; MAS, 30 mg/d; lisdexamfetamine, 70 mg/d.

While taking lisdexamfetamine or MAS, subjects showed similar improvement in behavior, based on Swanson, Kotkin, Agler, M-Flynn, and Pelham (SKAMP) scores, and inattention, based on SKAMP and Permanent Product Measure of Performance scores.

Both psychostimulants outperformed placebo in both measures, and both improved behavior more decisively than inattention. Based on post-hoc analysis, improvement 12 hours after dosing was more substantial with lisdexamfetamine than with MAS.

Phase-3 random-dose trial.³ A total of 290 children ages 6 to 12 with combined or hyperactive-impulsive type ADHD were “washed out” from prior medications over 1 week, then received lisdexamfetamine or placebo for 4 weeks. Treatment-group children were started at 30 mg/d; some received dosages titrated at random to 50 or 70 mg/d in weekly 20-mg increments.

Over 4 weeks, ADHD Rating Scale Version IV (ADHD-RS-IV) scores fell 50% to 59% among the 3 lisdexamfetamine dosage groups, compared with a 15% reduction in the placebo group. Substantial ADHD-RS-IV score improvements after 1 week of lisdexamfetamine were maintained throughout the trial, suggesting the medication sustains ADHD symptom improvement. Controlled trials have not addressed lisdexamfetamine use >4 weeks, however.

Based on parents’ and guardians’ reports, treatment-group patients’ ADHD symptoms were notably less severe at 10 AM, 2 PM, and 6 PM compared with placebo-group children.³ This suggests that lisdexamfetamine offers a daylong therapeutic effect.

Tolerability

In the phase-3 study,³ 162 of 218 (74%) children receiving any dosage of lisdexamfetamine reported an adverse event, compared with 34 of 72 (47%) children in the placebo group. Overall, 39% of lisdexamfetamine-group patients reported decreased appetite. Also common were insomnia, headaches, irritability, upper abdominal pain, vomiting, and weight loss (Table 2).

Although most adverse events were mild to moderate, 9.2% of treatment-group children dropped out because of intolerability, compared with 1.4% of the placebo group. The investigators increased dosages quickly, regardless of efficacy or tolerability,³ which might have increased side-effect incidence among the treatment groups.

In the phase-2 crossover trial,² adverse event rates were similar among the lisdexamfetamine, extended-release MAS, and placebo groups (15% to 18%). Among youths receiving lisdexamfetamine, 8% reported insomnia and 6% reported appetite loss, compared with 2% and 4% of the MAS group, respectively.

Table 2

Rates of commonly reported adverse effects
during phase-3 lisdexamfetamine (LDX) study

Safety

Findling et al⁴ found a larger change in corrected QT interval with lisdexamfetamine (7 to 14 msec) than with extended-release MAS (5 to 10 msec) 5 and 10½ hours after dosing. The authors reasoned that these findings are atypical, and no children suffered serious adverse events during the trial. Nonetheless, more research on whether lisdexamfetamine increases cardiac risk is needed.

In a lethal-dose study in rats,⁵ oral lisdexamfetamine doses up to 1,000 mg/kg did not result in death, suggesting the medication might undergo saturation kinetics in the GI tract that may protect against overdose or abuse at higher dosages. By comparison, the median lethal oral dosage of d-amphetamine in rats was 96.8 mg/kg.⁵

Abuse potential

As with other psychostimulants indicated for ADHD, the Drug Enforcement Administration has classified lisdexamfetamine as a schedule II drug, which applies to addictive prescription-only medications with an accepted medical use.

Clinical data suggest, however, that lisdexamfetamine might be less “enjoyable”—and less likely to be abused intravenously, orally, or intranasally—than equipotent d-amphetamine. In an abuse liability study,⁶ 12 adults with histories of stimulant abuse received intravenous immediate-release (IR) d-amphetamine, 10 or 20 mg. Two days later, they received a comparable dose of IV lisdexamfetamine, 25 or 50 mg. The researchers found that:

• Plasma d-amphetamine peaked within 5 minutes after injection, compared with 2 to 3 hours after lisdexamfetamine dosing.
• Subjects who received IR d-amphetamine said they felt euphoria within 15 minutes of injection. By contrast, no one reported euphoria or amphetamine-like subjective effects after receiving lisdexamfetamine.

When asked which medication they would try again, 9 of 12 subjects chose IR d-amphetamine and 1 chose lisdexamfetamine.

In a double-blind, randomized, placebo-controlled study,⁷ oral lisdexamfetamine, 50 or 100 mg, was not more “likeable” than placebo. Subjects reported “liking” effects with 150 mg of lisdexamfetamine, however, suggesting the medication could be misused or abused at higher-than-therapeutic dosages.

Contraindications

As with other psychostimulants, do not give lisdexamfetamine to youths with preexisting serious structural cardiac abnormalities or other heart problems. Assess patient and family history of heart disease before prescribing this medication.

Do not prescribe lisdexamfetamine to patients taking a monoamine oxidase inhibitor (MAOI). By slowing amphetamine metabolism, these antidepressants intensify amphetamines’ effect on monoamine release, which can cause headaches and lead to hypertensive crisis. Before starting lisdexamfetamine, ask if the patient is taking an MAOI or has taken one within 2 weeks of presentation.

Use caution when prescribing lisdexamfetamine to patients with:

• a comorbid eating disorder or sleep disturbance. Determine whether to address the comorbidity before treating ADHD symptoms, and make sure lisdexamfetamine is not worsening the comorbid symptoms.
• untreated hypertension or other cardiovascular conditions, as stimulant medications can increase blood pressure and heart rate. Watch for significant heart rate and blood pressure changes in patients taking lisdexamfetamine, which probably would not cause sustained blood pressure increase in patients taking antihypertensives.⁸

Related resources

• Lisdexamfetamine Web site. www.vyvanse.com.

Drug brand names

• Extended-release mixed amphetamine salts • Adderall XR
• Lisdexamfetamine • Vyvanse

Disclosure

Dr. Wilens receives research/grant support from Abbott Laboratories, Eli Lilly and Company, National Institute on Drug Abuse, NeuroSearch, Ortho-McNeil, and Shire; is a speaker for Novartis Pharmaceuticals Corp., Ortho-McNeil, and Shire; and is a consultant to Abbott Laboratories, Eli Lilly and Company, GlaxoSmithKline, National Institute on Drug Abuse, Novartis Pharmaceuticals Corp., Ortho-McNeil, Pfizer, and Shire.

Lisdexamfetamine—FDA-approved to treat attention-deficit/hyperactivity disorder (ADHD) in children ages 6 to 12 (Table 1)—reduces ADHD symptoms during and after school and may be less likely to be abused than other psychostimulants, particularly immediate-release preparations, clinical data suggest.

Table 1

Lisdexamfetamine: Fast facts

Clinical implications

Because it is effective for about 12 hours, lisdexamfetamine might improve the child’s ability to complete homework and participate in extracurricular activities, which in turn might enhance academic performance and/or socialization skills.

Lisdexamfetamine could help the child with ADHD who shows no contraindications to the drug —particularly if he or she needs daylong coverage.

How it works

Lisdexamfetamine—a dextroamphetamine derivative—is rapidly absorbed and converted to dextroamphetamine, which is believed to exert therapeutic effect by:

• blocking norepinephrine and dopamine reuptake into presynaptic neurons
• increasing the neurotransmitters’ release into the extraneuronal space.

The medication’s amphetamine release is highly predictable, which contributes to its therapeutic benefit in ADHD. Amphetamine is released through GI metabolism of lisdexamfetamine, which produces the active d-amphetamine moiety that reaches the bloodstream. The medication is derived from d-amphetamine, with negligible amounts of lysine cleaved.

Lisdexamfetamine requires in vivo metabolism (in the GI tract) to its active constituent d-amphetamine. As a result, the medication will not produce high d-amphetamine blood levels—and should not cause euphoria or other reinforcing effects—if injected or snorted. Its abuse potential is lower overall compared with immediate-release psychostimulant formulations.

Pharmacokinetics

Dextroamphetamine’s plasma elimination half-life is approximately 9½ hours—which accounts for lisdexamfetamine’s extended action. The drug reaches steady-state concentrations in 2 to 3 days.

Food does not affect absorption and delays maximum concentration by 1 hour or less, so taking lisdexamfetamine during breakfast should not slow its therapeutic effect. Because dextroamphetamine reaches maximum concentration in approximately 3½ hours, the medication should take effect by the time the child gets to school. In one randomized, phase-2 trial, children with ADHD who received lisdexamfetamine, 30 to 70 mg/d, showed overall improvement within 2 hours after dosing.¹

Efficacy

Lisdexamfetamine reduced ADHD symptoms in 2 double-blind studies: a phase-2 crossover study and a phase-3 random-dose trial.

Phase-2 crossover study.² Fifty-two children ages 6 to 12 with combined or hyperactive-impulsive type ADHD received extended-release mixed amphetamine salts (MAS) for 3 weeks. Subjects received 10 mg/d or dosages titrated to 20 or 30 mg/d based on response to medication.

The youths then were divided into 3 groups based on optimal MAS dosage and received 3 treatments for 1 week each:

• group 1: placebo; MAS, 10 mg/d; lisdexamfetamine, 30 mg/d
• group 2: placebo; MAS, 20 mg/d; lisdexamfetamine, 50 mg/d
• group 3: placebo; MAS, 30 mg/d; lisdexamfetamine, 70 mg/d.

While taking lisdexamfetamine or MAS, subjects showed similar improvement in behavior, based on Swanson, Kotkin, Agler, M-Flynn, and Pelham (SKAMP) scores, and inattention, based on SKAMP and Permanent Product Measure of Performance scores.

Both psychostimulants outperformed placebo in both measures, and both improved behavior more decisively than inattention. Based on post-hoc analysis, improvement 12 hours after dosing was more substantial with lisdexamfetamine than with MAS.

Phase-3 random-dose trial.³ A total of 290 children ages 6 to 12 with combined or hyperactive-impulsive type ADHD were “washed out” from prior medications over 1 week, then received lisdexamfetamine or placebo for 4 weeks. Treatment-group children were started at 30 mg/d; some received dosages titrated at random to 50 or 70 mg/d in weekly 20-mg increments.

Over 4 weeks, ADHD Rating Scale Version IV (ADHD-RS-IV) scores fell 50% to 59% among the 3 lisdexamfetamine dosage groups, compared with a 15% reduction in the placebo group. Substantial ADHD-RS-IV score improvements after 1 week of lisdexamfetamine were maintained throughout the trial, suggesting the medication sustains ADHD symptom improvement. Controlled trials have not addressed lisdexamfetamine use >4 weeks, however.

Based on parents’ and guardians’ reports, treatment-group patients’ ADHD symptoms were notably less severe at 10 AM, 2 PM, and 6 PM compared with placebo-group children.³ This suggests that lisdexamfetamine offers a daylong therapeutic effect.

Tolerability

In the phase-3 study,³ 162 of 218 (74%) children receiving any dosage of lisdexamfetamine reported an adverse event, compared with 34 of 72 (47%) children in the placebo group. Overall, 39% of lisdexamfetamine-group patients reported decreased appetite. Also common were insomnia, headaches, irritability, upper abdominal pain, vomiting, and weight loss (Table 2).

Although most adverse events were mild to moderate, 9.2% of treatment-group children dropped out because of intolerability, compared with 1.4% of the placebo group. The investigators increased dosages quickly, regardless of efficacy or tolerability,³ which might have increased side-effect incidence among the treatment groups.

In the phase-2 crossover trial,² adverse event rates were similar among the lisdexamfetamine, extended-release MAS, and placebo groups (15% to 18%). Among youths receiving lisdexamfetamine, 8% reported insomnia and 6% reported appetite loss, compared with 2% and 4% of the MAS group, respectively.

Table 2

Rates of commonly reported adverse effects
during phase-3 lisdexamfetamine (LDX) study

Safety

Findling et al⁴ found a larger change in corrected QT interval with lisdexamfetamine (7 to 14 msec) than with extended-release MAS (5 to 10 msec) 5 and 10½ hours after dosing. The authors reasoned that these findings are atypical, and no children suffered serious adverse events during the trial. Nonetheless, more research on whether lisdexamfetamine increases cardiac risk is needed.

In a lethal-dose study in rats,⁵ oral lisdexamfetamine doses up to 1,000 mg/kg did not result in death, suggesting the medication might undergo saturation kinetics in the GI tract that may protect against overdose or abuse at higher dosages. By comparison, the median lethal oral dosage of d-amphetamine in rats was 96.8 mg/kg.⁵

Abuse potential

As with other psychostimulants indicated for ADHD, the Drug Enforcement Administration has classified lisdexamfetamine as a schedule II drug, which applies to addictive prescription-only medications with an accepted medical use.

Clinical data suggest, however, that lisdexamfetamine might be less “enjoyable”—and less likely to be abused intravenously, orally, or intranasally—than equipotent d-amphetamine. In an abuse liability study,⁶ 12 adults with histories of stimulant abuse received intravenous immediate-release (IR) d-amphetamine, 10 or 20 mg. Two days later, they received a comparable dose of IV lisdexamfetamine, 25 or 50 mg. The researchers found that:

• Plasma d-amphetamine peaked within 5 minutes after injection, compared with 2 to 3 hours after lisdexamfetamine dosing.
• Subjects who received IR d-amphetamine said they felt euphoria within 15 minutes of injection. By contrast, no one reported euphoria or amphetamine-like subjective effects after receiving lisdexamfetamine.

When asked which medication they would try again, 9 of 12 subjects chose IR d-amphetamine and 1 chose lisdexamfetamine.

In a double-blind, randomized, placebo-controlled study,⁷ oral lisdexamfetamine, 50 or 100 mg, was not more “likeable” than placebo. Subjects reported “liking” effects with 150 mg of lisdexamfetamine, however, suggesting the medication could be misused or abused at higher-than-therapeutic dosages.

Contraindications

As with other psychostimulants, do not give lisdexamfetamine to youths with preexisting serious structural cardiac abnormalities or other heart problems. Assess patient and family history of heart disease before prescribing this medication.

Do not prescribe lisdexamfetamine to patients taking a monoamine oxidase inhibitor (MAOI). By slowing amphetamine metabolism, these antidepressants intensify amphetamines’ effect on monoamine release, which can cause headaches and lead to hypertensive crisis. Before starting lisdexamfetamine, ask if the patient is taking an MAOI or has taken one within 2 weeks of presentation.

Use caution when prescribing lisdexamfetamine to patients with:

• a comorbid eating disorder or sleep disturbance. Determine whether to address the comorbidity before treating ADHD symptoms, and make sure lisdexamfetamine is not worsening the comorbid symptoms.
• untreated hypertension or other cardiovascular conditions, as stimulant medications can increase blood pressure and heart rate. Watch for significant heart rate and blood pressure changes in patients taking lisdexamfetamine, which probably would not cause sustained blood pressure increase in patients taking antihypertensives.⁸

Related resources

• Lisdexamfetamine Web site. www.vyvanse.com.

Drug brand names

• Extended-release mixed amphetamine salts • Adderall XR
• Lisdexamfetamine • Vyvanse

Disclosure

Dr. Wilens receives research/grant support from Abbott Laboratories, Eli Lilly and Company, National Institute on Drug Abuse, NeuroSearch, Ortho-McNeil, and Shire; is a speaker for Novartis Pharmaceuticals Corp., Ortho-McNeil, and Shire; and is a consultant to Abbott Laboratories, Eli Lilly and Company, GlaxoSmithKline, National Institute on Drug Abuse, Novartis Pharmaceuticals Corp., Ortho-McNeil, Pfizer, and Shire.

Lisdexamfetamine—FDA-approved to treat attention-deficit/hyperactivity disorder (ADHD) in children ages 6 to 12 (Table 1)—reduces ADHD symptoms during and after school and may be less likely to be abused than other psychostimulants, particularly immediate-release preparations, clinical data suggest.

Table 1

Lisdexamfetamine: Fast facts

Clinical implications

Because it is effective for about 12 hours, lisdexamfetamine might improve the child’s ability to complete homework and participate in extracurricular activities, which in turn might enhance academic performance and/or socialization skills.

Lisdexamfetamine could help the child with ADHD who shows no contraindications to the drug —particularly if he or she needs daylong coverage.

How it works

Lisdexamfetamine—a dextroamphetamine derivative—is rapidly absorbed and converted to dextroamphetamine, which is believed to exert therapeutic effect by:

• blocking norepinephrine and dopamine reuptake into presynaptic neurons
• increasing the neurotransmitters’ release into the extraneuronal space.

The medication’s amphetamine release is highly predictable, which contributes to its therapeutic benefit in ADHD. Amphetamine is released through GI metabolism of lisdexamfetamine, which produces the active d-amphetamine moiety that reaches the bloodstream. The medication is derived from d-amphetamine, with negligible amounts of lysine cleaved.

Lisdexamfetamine requires in vivo metabolism (in the GI tract) to its active constituent d-amphetamine. As a result, the medication will not produce high d-amphetamine blood levels—and should not cause euphoria or other reinforcing effects—if injected or snorted. Its abuse potential is lower overall compared with immediate-release psychostimulant formulations.

Pharmacokinetics

Dextroamphetamine’s plasma elimination half-life is approximately 9½ hours—which accounts for lisdexamfetamine’s extended action. The drug reaches steady-state concentrations in 2 to 3 days.

Food does not affect absorption and delays maximum concentration by 1 hour or less, so taking lisdexamfetamine during breakfast should not slow its therapeutic effect. Because dextroamphetamine reaches maximum concentration in approximately 3½ hours, the medication should take effect by the time the child gets to school. In one randomized, phase-2 trial, children with ADHD who received lisdexamfetamine, 30 to 70 mg/d, showed overall improvement within 2 hours after dosing.¹

Efficacy

Lisdexamfetamine reduced ADHD symptoms in 2 double-blind studies: a phase-2 crossover study and a phase-3 random-dose trial.

Phase-2 crossover study.² Fifty-two children ages 6 to 12 with combined or hyperactive-impulsive type ADHD received extended-release mixed amphetamine salts (MAS) for 3 weeks. Subjects received 10 mg/d or dosages titrated to 20 or 30 mg/d based on response to medication.

The youths then were divided into 3 groups based on optimal MAS dosage and received 3 treatments for 1 week each:

• group 1: placebo; MAS, 10 mg/d; lisdexamfetamine, 30 mg/d
• group 2: placebo; MAS, 20 mg/d; lisdexamfetamine, 50 mg/d
• group 3: placebo; MAS, 30 mg/d; lisdexamfetamine, 70 mg/d.

While taking lisdexamfetamine or MAS, subjects showed similar improvement in behavior, based on Swanson, Kotkin, Agler, M-Flynn, and Pelham (SKAMP) scores, and inattention, based on SKAMP and Permanent Product Measure of Performance scores.

Both psychostimulants outperformed placebo in both measures, and both improved behavior more decisively than inattention. Based on post-hoc analysis, improvement 12 hours after dosing was more substantial with lisdexamfetamine than with MAS.

Phase-3 random-dose trial.³ A total of 290 children ages 6 to 12 with combined or hyperactive-impulsive type ADHD were “washed out” from prior medications over 1 week, then received lisdexamfetamine or placebo for 4 weeks. Treatment-group children were started at 30 mg/d; some received dosages titrated at random to 50 or 70 mg/d in weekly 20-mg increments.

Over 4 weeks, ADHD Rating Scale Version IV (ADHD-RS-IV) scores fell 50% to 59% among the 3 lisdexamfetamine dosage groups, compared with a 15% reduction in the placebo group. Substantial ADHD-RS-IV score improvements after 1 week of lisdexamfetamine were maintained throughout the trial, suggesting the medication sustains ADHD symptom improvement. Controlled trials have not addressed lisdexamfetamine use >4 weeks, however.

Based on parents’ and guardians’ reports, treatment-group patients’ ADHD symptoms were notably less severe at 10 AM, 2 PM, and 6 PM compared with placebo-group children.³ This suggests that lisdexamfetamine offers a daylong therapeutic effect.

Tolerability

In the phase-3 study,³ 162 of 218 (74%) children receiving any dosage of lisdexamfetamine reported an adverse event, compared with 34 of 72 (47%) children in the placebo group. Overall, 39% of lisdexamfetamine-group patients reported decreased appetite. Also common were insomnia, headaches, irritability, upper abdominal pain, vomiting, and weight loss (Table 2).

Although most adverse events were mild to moderate, 9.2% of treatment-group children dropped out because of intolerability, compared with 1.4% of the placebo group. The investigators increased dosages quickly, regardless of efficacy or tolerability,³ which might have increased side-effect incidence among the treatment groups.

In the phase-2 crossover trial,² adverse event rates were similar among the lisdexamfetamine, extended-release MAS, and placebo groups (15% to 18%). Among youths receiving lisdexamfetamine, 8% reported insomnia and 6% reported appetite loss, compared with 2% and 4% of the MAS group, respectively.

Table 2

Rates of commonly reported adverse effects
during phase-3 lisdexamfetamine (LDX) study

Safety

Findling et al⁴ found a larger change in corrected QT interval with lisdexamfetamine (7 to 14 msec) than with extended-release MAS (5 to 10 msec) 5 and 10½ hours after dosing. The authors reasoned that these findings are atypical, and no children suffered serious adverse events during the trial. Nonetheless, more research on whether lisdexamfetamine increases cardiac risk is needed.

In a lethal-dose study in rats,⁵ oral lisdexamfetamine doses up to 1,000 mg/kg did not result in death, suggesting the medication might undergo saturation kinetics in the GI tract that may protect against overdose or abuse at higher dosages. By comparison, the median lethal oral dosage of d-amphetamine in rats was 96.8 mg/kg.⁵

Abuse potential

As with other psychostimulants indicated for ADHD, the Drug Enforcement Administration has classified lisdexamfetamine as a schedule II drug, which applies to addictive prescription-only medications with an accepted medical use.

Clinical data suggest, however, that lisdexamfetamine might be less “enjoyable”—and less likely to be abused intravenously, orally, or intranasally—than equipotent d-amphetamine. In an abuse liability study,⁶ 12 adults with histories of stimulant abuse received intravenous immediate-release (IR) d-amphetamine, 10 or 20 mg. Two days later, they received a comparable dose of IV lisdexamfetamine, 25 or 50 mg. The researchers found that:

• Plasma d-amphetamine peaked within 5 minutes after injection, compared with 2 to 3 hours after lisdexamfetamine dosing.
• Subjects who received IR d-amphetamine said they felt euphoria within 15 minutes of injection. By contrast, no one reported euphoria or amphetamine-like subjective effects after receiving lisdexamfetamine.

When asked which medication they would try again, 9 of 12 subjects chose IR d-amphetamine and 1 chose lisdexamfetamine.

In a double-blind, randomized, placebo-controlled study,⁷ oral lisdexamfetamine, 50 or 100 mg, was not more “likeable” than placebo. Subjects reported “liking” effects with 150 mg of lisdexamfetamine, however, suggesting the medication could be misused or abused at higher-than-therapeutic dosages.

Contraindications

As with other psychostimulants, do not give lisdexamfetamine to youths with preexisting serious structural cardiac abnormalities or other heart problems. Assess patient and family history of heart disease before prescribing this medication.

Do not prescribe lisdexamfetamine to patients taking a monoamine oxidase inhibitor (MAOI). By slowing amphetamine metabolism, these antidepressants intensify amphetamines’ effect on monoamine release, which can cause headaches and lead to hypertensive crisis. Before starting lisdexamfetamine, ask if the patient is taking an MAOI or has taken one within 2 weeks of presentation.

Use caution when prescribing lisdexamfetamine to patients with:

• a comorbid eating disorder or sleep disturbance. Determine whether to address the comorbidity before treating ADHD symptoms, and make sure lisdexamfetamine is not worsening the comorbid symptoms.
• untreated hypertension or other cardiovascular conditions, as stimulant medications can increase blood pressure and heart rate. Watch for significant heart rate and blood pressure changes in patients taking lisdexamfetamine, which probably would not cause sustained blood pressure increase in patients taking antihypertensives.⁸

Related resources

• Lisdexamfetamine Web site. www.vyvanse.com.

Drug brand names

• Extended-release mixed amphetamine salts • Adderall XR
• Lisdexamfetamine • Vyvanse

Disclosure

Dr. Wilens receives research/grant support from Abbott Laboratories, Eli Lilly and Company, National Institute on Drug Abuse, NeuroSearch, Ortho-McNeil, and Shire; is a speaker for Novartis Pharmaceuticals Corp., Ortho-McNeil, and Shire; and is a consultant to Abbott Laboratories, Eli Lilly and Company, GlaxoSmithKline, National Institute on Drug Abuse, Novartis Pharmaceuticals Corp., Ortho-McNeil, Pfizer, and Shire.

Patient commits suicide after 15-minute checks are stopped

Honolulu County (HI) Circuit Court

A patient was brought to a hospital and interviewed by a psychiatrist. She was found to be at moderate risk for suicide, was admitted, and ordered to be monitored every 15 minutes. The patient attempted suicide 2 days later by closing a drawer on her neck. She died from the injuries the following day.

The patient’s family claimed that a hospital nurse misread the psychiatrist’s instructions and stopped the 15-minute checks on the morning of the incident, believing that the order was limited to 15-minute checks for the first 24 hours, even though they had been done for almost 2 days. The patient refused medication on the first day of admission, and the psychiatrist had started the procedure to obtain a court order committing the patient and allowing injection of necessary medication. The claims against the hospital were settled for a confidential amount.

The patient’s family claimed the psychiatrist diagnosed the patient with major depression with recurrent suicide ideation but failed to properly assess her for suicide monitoring. The family also said the patient should have been determined to be at least at high risk and required to be within sight of staff.

The psychiatrist claimed to be unaware the 15-minute monitoring had ceased. The psychiatrist saw the patient 30 minutes before she was found collapsed with her head in the drawer. The hospital staff checked the patient approximately 15 to 30 minutes before she was found.

• A defense verdict was returned
  

Reduced observation blamed for suicide by hanging

Kings County (NY) Supreme Court

A 45-year-old police lieutenant who suffered from alcohol abuse and depression was admitted to a psychiatric care facility. He was classiffied “Q15,” a category assigned to patients who must be visually inspected every 15 minutes, cannot have access to sharp objects or any other material or object they can use to inflict bodily harm, and must request permission to use restrooms. The next day the psychiatrist examined the patient and moved him to a “Q30” status, which halved the frequency of visual inspections, gave him unrestricted access to restrooms, and allowed him to have a bathrobe with a belt. The patient hanged himself the next day, using a restroom door to support a noose he made from the bathrobe belt.

The patient’s family faulted the hospital and psychiatrist for prematurely advancing the patient to “Q30” status. The hospital and psychiatrist claimed the suicide could not have been predicted and argued that given his background as a police lieutenant, the patient would have interpreted more stringent restrictions as incarceration. The psychiatrist argued that such a perception would have impeded the patient’s progress.

• A $71,989 verdict was returned, apportioning fault 65% to the hospital and 35% to the psychiatrist
  

Dr. Grant’s observations

Constant patient observation—such as one-to-one staffing or 15-minute checks—is used to protect patients from harming themselves or others. One study of a psychiatric hospital¹ reported that 13% of psychiatric inpatients required constant observation.

Even 15 minutes is sufficient time to complete a suicide.³ Common methods of inpatient suicide include hanging, overdosing, and jumping from high places.^4,5 One study found that 73% of inpatient suicides in a psychiatric ward occurred after 28 days of admission.⁵

The cost of constant observation may account for as much as 20% of the total nursing budget at a psychiatric hospital and up to 10% at a long-term care facility or general hospital.⁶ The annual cost of constant observation can exceed $500,000, depending on the hospital’s size and monitoring frequency.⁶

Determining responsibility

The outcomes of these 2 cases may appear inconsistent. In the first, the psychiatrist who assessed the patient as a moderate suicide risk was not negligent, even though the family claimed the patient was at high risk. In the second case, the psychiatrist was found partly liable for not maintaining a higher vigilance of suicide risk assessment.

Physicians cannot put every patient on one-to-one monitoring or 15-minute checks because of fear of suicide and malpractice litigation. These 2 cases demonstrate that if a suicide occurs, the courts will look for clinical reasons for the level of observation. The level of suicide precautions—one-to-one vs 15-minute checks—should be based on the patient’s clinical presentation and supported by clinical rationale.⁷

Risk analysis

The courts look to see if the suicide assessment was “clinically reasonable”.⁸ To meet this standard, perform a “suicide risk-benefit analysis” each time you make a significant clinical decision, such as ordering 15-minute checks. The record should include information sources you used (such as family members or previous medical records), factors that entered the clinical decision, and how you balanced these factors in a risk-benefit assessment (Box 1).⁹

Document decisions. Mistakes in clinical judgment do not necessarily constitute negligence,⁸ but deviations in the standard of care cannot be adequately determined in a court of law unless the clinician had documented his or her thought processes at the time of the decision.

Predicting which patients will re-experience or deny suicidal ideation is impossible,⁷ but if the patient is determined to be at high risk for suicide, then implement and document a plan to address this risk. In addition, communicate information regarding the risk-benefit assessment to staff responsible for implementing these precautions.

Box 1

• a patient is admitted for inpatient treatment
  
• observation status changes
  
• a patient’s clinical condition changes substantially
  
• acute psychosocial stressors are discovered during the hospitalization.⁷
  

Patient commits suicide after 15-minute checks are stopped

Honolulu County (HI) Circuit Court

A patient was brought to a hospital and interviewed by a psychiatrist. She was found to be at moderate risk for suicide, was admitted, and ordered to be monitored every 15 minutes. The patient attempted suicide 2 days later by closing a drawer on her neck. She died from the injuries the following day.

The patient’s family claimed that a hospital nurse misread the psychiatrist’s instructions and stopped the 15-minute checks on the morning of the incident, believing that the order was limited to 15-minute checks for the first 24 hours, even though they had been done for almost 2 days. The patient refused medication on the first day of admission, and the psychiatrist had started the procedure to obtain a court order committing the patient and allowing injection of necessary medication. The claims against the hospital were settled for a confidential amount.

The patient’s family claimed the psychiatrist diagnosed the patient with major depression with recurrent suicide ideation but failed to properly assess her for suicide monitoring. The family also said the patient should have been determined to be at least at high risk and required to be within sight of staff.

The psychiatrist claimed to be unaware the 15-minute monitoring had ceased. The psychiatrist saw the patient 30 minutes before she was found collapsed with her head in the drawer. The hospital staff checked the patient approximately 15 to 30 minutes before she was found.

• A defense verdict was returned
  

Reduced observation blamed for suicide by hanging

Kings County (NY) Supreme Court

A 45-year-old police lieutenant who suffered from alcohol abuse and depression was admitted to a psychiatric care facility. He was classiffied “Q15,” a category assigned to patients who must be visually inspected every 15 minutes, cannot have access to sharp objects or any other material or object they can use to inflict bodily harm, and must request permission to use restrooms. The next day the psychiatrist examined the patient and moved him to a “Q30” status, which halved the frequency of visual inspections, gave him unrestricted access to restrooms, and allowed him to have a bathrobe with a belt. The patient hanged himself the next day, using a restroom door to support a noose he made from the bathrobe belt.

The patient’s family faulted the hospital and psychiatrist for prematurely advancing the patient to “Q30” status. The hospital and psychiatrist claimed the suicide could not have been predicted and argued that given his background as a police lieutenant, the patient would have interpreted more stringent restrictions as incarceration. The psychiatrist argued that such a perception would have impeded the patient’s progress.

• A $71,989 verdict was returned, apportioning fault 65% to the hospital and 35% to the psychiatrist
  

Dr. Grant’s observations

Constant patient observation—such as one-to-one staffing or 15-minute checks—is used to protect patients from harming themselves or others. One study of a psychiatric hospital¹ reported that 13% of psychiatric inpatients required constant observation.

Even 15 minutes is sufficient time to complete a suicide.³ Common methods of inpatient suicide include hanging, overdosing, and jumping from high places.^4,5 One study found that 73% of inpatient suicides in a psychiatric ward occurred after 28 days of admission.⁵

The cost of constant observation may account for as much as 20% of the total nursing budget at a psychiatric hospital and up to 10% at a long-term care facility or general hospital.⁶ The annual cost of constant observation can exceed $500,000, depending on the hospital’s size and monitoring frequency.⁶

Determining responsibility

The outcomes of these 2 cases may appear inconsistent. In the first, the psychiatrist who assessed the patient as a moderate suicide risk was not negligent, even though the family claimed the patient was at high risk. In the second case, the psychiatrist was found partly liable for not maintaining a higher vigilance of suicide risk assessment.

Physicians cannot put every patient on one-to-one monitoring or 15-minute checks because of fear of suicide and malpractice litigation. These 2 cases demonstrate that if a suicide occurs, the courts will look for clinical reasons for the level of observation. The level of suicide precautions—one-to-one vs 15-minute checks—should be based on the patient’s clinical presentation and supported by clinical rationale.⁷

Risk analysis

The courts look to see if the suicide assessment was “clinically reasonable”.⁸ To meet this standard, perform a “suicide risk-benefit analysis” each time you make a significant clinical decision, such as ordering 15-minute checks. The record should include information sources you used (such as family members or previous medical records), factors that entered the clinical decision, and how you balanced these factors in a risk-benefit assessment (Box 1).⁹

Document decisions. Mistakes in clinical judgment do not necessarily constitute negligence,⁸ but deviations in the standard of care cannot be adequately determined in a court of law unless the clinician had documented his or her thought processes at the time of the decision.

Predicting which patients will re-experience or deny suicidal ideation is impossible,⁷ but if the patient is determined to be at high risk for suicide, then implement and document a plan to address this risk. In addition, communicate information regarding the risk-benefit assessment to staff responsible for implementing these precautions.

Box 1

• a patient is admitted for inpatient treatment
  
• observation status changes
  
• a patient’s clinical condition changes substantially
  
• acute psychosocial stressors are discovered during the hospitalization.⁷
  

Patient commits suicide after 15-minute checks are stopped

Honolulu County (HI) Circuit Court

A patient was brought to a hospital and interviewed by a psychiatrist. She was found to be at moderate risk for suicide, was admitted, and ordered to be monitored every 15 minutes. The patient attempted suicide 2 days later by closing a drawer on her neck. She died from the injuries the following day.

The patient’s family claimed that a hospital nurse misread the psychiatrist’s instructions and stopped the 15-minute checks on the morning of the incident, believing that the order was limited to 15-minute checks for the first 24 hours, even though they had been done for almost 2 days. The patient refused medication on the first day of admission, and the psychiatrist had started the procedure to obtain a court order committing the patient and allowing injection of necessary medication. The claims against the hospital were settled for a confidential amount.

The patient’s family claimed the psychiatrist diagnosed the patient with major depression with recurrent suicide ideation but failed to properly assess her for suicide monitoring. The family also said the patient should have been determined to be at least at high risk and required to be within sight of staff.

The psychiatrist claimed to be unaware the 15-minute monitoring had ceased. The psychiatrist saw the patient 30 minutes before she was found collapsed with her head in the drawer. The hospital staff checked the patient approximately 15 to 30 minutes before she was found.

• A defense verdict was returned
  

Reduced observation blamed for suicide by hanging

Kings County (NY) Supreme Court

A 45-year-old police lieutenant who suffered from alcohol abuse and depression was admitted to a psychiatric care facility. He was classiffied “Q15,” a category assigned to patients who must be visually inspected every 15 minutes, cannot have access to sharp objects or any other material or object they can use to inflict bodily harm, and must request permission to use restrooms. The next day the psychiatrist examined the patient and moved him to a “Q30” status, which halved the frequency of visual inspections, gave him unrestricted access to restrooms, and allowed him to have a bathrobe with a belt. The patient hanged himself the next day, using a restroom door to support a noose he made from the bathrobe belt.

The patient’s family faulted the hospital and psychiatrist for prematurely advancing the patient to “Q30” status. The hospital and psychiatrist claimed the suicide could not have been predicted and argued that given his background as a police lieutenant, the patient would have interpreted more stringent restrictions as incarceration. The psychiatrist argued that such a perception would have impeded the patient’s progress.

• A $71,989 verdict was returned, apportioning fault 65% to the hospital and 35% to the psychiatrist
  

Dr. Grant’s observations

Constant patient observation—such as one-to-one staffing or 15-minute checks—is used to protect patients from harming themselves or others. One study of a psychiatric hospital¹ reported that 13% of psychiatric inpatients required constant observation.

Even 15 minutes is sufficient time to complete a suicide.³ Common methods of inpatient suicide include hanging, overdosing, and jumping from high places.^4,5 One study found that 73% of inpatient suicides in a psychiatric ward occurred after 28 days of admission.⁵

The cost of constant observation may account for as much as 20% of the total nursing budget at a psychiatric hospital and up to 10% at a long-term care facility or general hospital.⁶ The annual cost of constant observation can exceed $500,000, depending on the hospital’s size and monitoring frequency.⁶

Determining responsibility

The outcomes of these 2 cases may appear inconsistent. In the first, the psychiatrist who assessed the patient as a moderate suicide risk was not negligent, even though the family claimed the patient was at high risk. In the second case, the psychiatrist was found partly liable for not maintaining a higher vigilance of suicide risk assessment.

Physicians cannot put every patient on one-to-one monitoring or 15-minute checks because of fear of suicide and malpractice litigation. These 2 cases demonstrate that if a suicide occurs, the courts will look for clinical reasons for the level of observation. The level of suicide precautions—one-to-one vs 15-minute checks—should be based on the patient’s clinical presentation and supported by clinical rationale.⁷

Risk analysis

The courts look to see if the suicide assessment was “clinically reasonable”.⁸ To meet this standard, perform a “suicide risk-benefit analysis” each time you make a significant clinical decision, such as ordering 15-minute checks. The record should include information sources you used (such as family members or previous medical records), factors that entered the clinical decision, and how you balanced these factors in a risk-benefit assessment (Box 1).⁹

Document decisions. Mistakes in clinical judgment do not necessarily constitute negligence,⁸ but deviations in the standard of care cannot be adequately determined in a court of law unless the clinician had documented his or her thought processes at the time of the decision.

Predicting which patients will re-experience or deny suicidal ideation is impossible,⁷ but if the patient is determined to be at high risk for suicide, then implement and document a plan to address this risk. In addition, communicate information regarding the risk-benefit assessment to staff responsible for implementing these precautions.

Box 1

• a patient is admitted for inpatient treatment
  
• observation status changes
  
• a patient’s clinical condition changes substantially
  
• acute psychosocial stressors are discovered during the hospitalization.⁷
  

Overlapping symptoms may obscure comorbid bipolar illness

An adult with function-impairing inattention could have attention-deficit/hyperactivity disorder (ADHD), bipolar disorder (BD), or both. Comorbid ADHD and BD often is unrecognized, however, because patients are more likely to report ADHD-related symptoms than manic symptoms.¹

To help you recognize comorbid ADHD/BD—and protect adults who might switch into mania if given stimulants or antidepressants—this article describes a hierarchy to diagnose and treat this comorbidity. Based on the evidence and our experience, we:

• discuss how to differentiate between these disorders with overlapping symptoms
• provide tools and suggestions to screen for BD and adult ADHD
• offer 3 algorithms to guide your diagnosis and choice of medications.

Clinical challenges

Prevalence is unclear. Adult ADHD—with an estimated prevalence of 4.4%²—is more common than BD. Lifetime prevalences of BD types I and II are 1.6% and 0.5%, respectively.³ Studies of ADHD/BD comorbidity suggest wide-ranging prevalence rates:

• 9% to 21% of BD patients may have adult ADHD^2,4,5
• 5% to 47% of adult ADHD patients may have BD.^2,6-8

Underdiagnosis. Adult ADHD/BD is a more severe illness than ADHD or BD alone and is highly comorbid with agoraphobia, social phobia, posttraumatic stress disorder, and alcohol or drug addiction. Adults with ADHD/BD have more frequent affective episodes, suicide attempts, violence, and legal problems.⁴ Diagnosing this comorbidity remains a challenge, however, because:

• identifying which symptoms are caused by which disorder can be difficult
• BD tends to be underdiagnosed⁹
• patients often misidentify, underreport, or deny manic symptoms^1,10,11
• if a patient presents with active bipolar symptoms, DSM-IV-TR criteria require that ADHD not be diagnosed until mood symptoms are resolved.

Overlapping symptoms. ADHD and bipolar mania share some DSM-IV-TR diagnostic criteria, including talkativeness, distractibility, increased activity or physical restlessness, and loss of social inhibitions (Table 1).¹² Overlapping symptoms also are notable within ADHD diagnostic criteria (Table 2). In the inattention category, for example, “easily distracted by extraneous stimuli,” “difficulty sustaining attention in tasks,” and “fails to give close attention to details” are considered 3 separate symptoms. In the hyperactivity category, “often leaves seat,” “often runs about or climbs excessively,” and “often on the go, or often acts as if driven by a motor” are 3 separate symptoms.

Given ADHD’s relatively loose diagnostic criteria and high comorbidity in adults with mood disorders, the question of whether adult ADHD/BD represents comorbidity or diagnostic overlap remains unresolved. For the clinician, the disorders’ nonoverlapping features (Table 1) can assist with the differential diagnosis. For example:

• ADHD symptoms tend to be chronic and BD symptoms episodic.
• ADHD patients may have high energy but lack increased productivity seen in BD patients.
• ADHD patients do not need less sleep or have inflated self-esteem like symptomatic BD patients.
• Psychotic symptoms such as hallucinations or delusions might be present in severe BD but are absent in ADHD.

Table 1

Overlap between DSM-IV-TR diagnostic criteria for ADHD and bipolar mania

Table 2

DSM-IV-TR diagnostic criteria for attention-deficit/ hyperactivity disorder

Mood symptoms first

A diagnostic hierarchy is implicit in DSM-IV-TR; anxiety disorders are not diagnosed during an active major depressive or manic episode, and schizophrenia is not diagnosed on the basis of psychotic symptoms during an active major depressive or manic episode. Mood disorders sit atop this implied diagnostic hierarchy and must be ruled out before psychotic or anxiety disorders are diagnosed. Similarly, most personality disorders are not diagnosed during an active mood or psychotic episode.

Diagnosing adult ADHD when a patient is actively depressed or manic is inconsistent with this hierarchy and conflicts with extensive nosologic literature.¹³ We suggest that ADHD—a cognitive-behavioral problem—not be diagnosed solely on symptoms observed when a patient is experiencing a mood episode or psychotic illness.

Bipolar disorder. Two useful mnemonics (Table 3) assist in screening for DSM-IV-TR symptoms of BD type I:

• Pure mania consists of euphoric mood and ≥3 of 7 DIGFAST criteria, or irritable mood and ≥4 of 7 DIGFAST criteria
• Mixed mania consists of depressed mood with ≥4 of 7 DIGFAST criteria and ≥4 of 8 SIGECAPS criteria.

To be diagnostic, these symptoms must cause substantial social or occupational dysfunction and be present at least 1 week. Diagnose BD type I if a patient has experienced a single pure or mixed manic episode at any time, unless the episode had a medical cause such as hyperthyroidism or antidepressant use. Because patients with mixed episodes experience depressed mood, assess any patient with clinical depression for manic symptoms. Otherwise, a patient with a mixed episode could be misdiagnosed as having unipolar depression instead of BD type I.¹⁴

BD type II also has been observed in patients with comorbid adult ADHD/BD.^4,6 The main difference between BD types I and II is that manic symptoms in type II are not severe enough to cause functional impairment or psychotic symptoms.¹⁵

Adult ADHD. The clinical interview seeking evidence of inattention and hyperactivity/impulsivity remains the basis of adult ADHD diagnosis (Table 2). Key areas are:

• the patient’s past and current functional impairment
• whether substantial impairment occurs in at least 2 areas of life (such as school, work, or home).

Take medical, educational, social, psychological, and vocational histories, and rule out other conditions before concluding that adult ADHD is the appropriate diagnosis.¹⁶ In adult ADHD, inattentive symptoms become far more prominent, about twice as common as hyperactive symptoms.¹⁷ Inattentive symptoms may manifest as neglect, poor time management, motivational deficits, or poor concentration that results in forgetfulness, distractibility, item misplacement, or excessive mistakes in paperwork.¹⁸ When impulsive symptoms persist in adults, they may manifest as automobile accidents or low tolerance for frustration, which may lead to frequent job changes and unstable, interrupted interpersonal relationships.¹⁸

Neuropsychological testing is not required to make an adult ADHD diagnosis but can help establish the breadth of symptoms or comorbidity.¹⁷ Rating scales can screen, gather data (including presence and severity of symptoms), and measure treatment response.¹⁶ Commonly used rating scales include:

• Conners’ Adult ADHD Rating Scales¹⁹
• Brown Attention Deficit Disorder Rating Scale for Adults²⁰
• Adult ADHD Self-Report Scale.²¹

When using rating scales, remember that adult psychopathology can distort perceptions, and some self-report scales have questionable reliability.¹⁶

Table 3

Mnemonics for diagnostic symptoms of pure and mixed bipolar mania

Treatment recommendations

Limited data. We found only 1 study on adult ADHD/BD treatment. In this open trial,²² 36 adults with comorbid ADHD and BD received bupropion SR, up to 200 mg bid, for ADHD symptoms while maintained on mood stabilizers, antipsychotics, or both. Improvement was defined as ≥30% reduction in ADHD Symptom Checklist Scale scores, without concurrent mania. After 6 weeks, 82% of patients had improved; 1 dropped out at week 2 because of hypomanic activation. Methodologic limitations included trial design (non-randomized, nonblinded, short duration) and patient selection (90% of subjects had BD type II).

In the absence of adequate data on adult ADHD/BD, studies in children suggest:

• stimulants may not be effective for ADHD symptoms in patients with active manic or depressive symptoms
• mood stabilization is a prerequisite for successful pharmacologic treatment of ADHD in patients with both ADHD and manic or depressive symptoms.^23,24

Follow the hierarchy. First treat acute mood symptoms, then reevaluate and possibly treat ADHD symptoms if they persist during euthymia (Algorithm 1). When a patient meets criteria for adult ADHD/BD, first stabilize bipolar manic or depressive symptoms (Algorithm 2). For acute mania, treat with standard mood stabilizers (lithium, valproate, lamotrigine, or carbamazepine) with or without a second-generation antipsychotic.²⁵ Starting stimulants for ADHD when patients have active mood symptoms is sub-optimal and potentially harmful because of the risk of inducing mania. For acute bipolar depression, adjunctive antidepressant treatment has been found to be no more effective than a mood stabilizer alone.²⁶

After bipolar symptoms respond or remit, reassess for adult ADHD. If ADHD symptoms persist during euthymia, additional treatment may be indicated.

Very little evidence exists on treating adult ADHD/BD; as mentioned, bupropion is the only medication studied in this population. For adult ADHD alone, clinical trials have showed varying efficacy with bupropion,^27,28 atomoxetine,²⁹ venlafaxine,^30,31 desipramine,³² methylphenidate,³³ mixed amphetamine salts,³⁴ and guanfacine.³⁵ Whether these treatments can be generalized as safe and efficacious for comorbid adult ADHD/BD is unclear. Nonetheless, we suggest using bupropion first, followed by atomoxetine or guanfacine before you consider amphetamine stimulants (Algorithm 3).

Algorithm 1
Hierarchy for diagnosis and treatment of adult ADHD/BD

ADHD: attention-deficit/hyperactivity disorder; BD: bipolar disorder
*Adler LA, Chua HC. Management of ADHD in adults. J Clin Psychiatry 2002;63(suppl 12):29-35.

Algorithm 2
Treating acute episodes of bipolar disorder

ECT: electroconvulsive therapy; SGA: second-generation antipsychotic; TMS: transcranial magnetic stimulation

Algorithm 3
Suggested approach to adult ADHD with comorbid BD*

* Based on data extrapolated from samples of patients with ADHD alone because of very limited data in ADHD/BD samples.
^† We recommend against combining antidepressants and stimulants because of additive risks of mania in BD. Discontinue stimulant or antidepressant if manic symptoms appear or rapid cycling emerges.

Reducing mania risk

Antidepressants and stimulants may help adults with ADHD alone, but risks of mania and rapid cycling limit their use in adults with ADHD/BD.

Stimulants and mania. One study found a 17% manic switch rate when methylphenidate (≤10 mg bid) was given to 14 bipolar depressed adults (10 BD type I, 2 BD type II, and 2 with secondary mania) taking mood stabilizers.³⁶ A chart review of 82 bipolar children not taking mood stabilizers found an 18% switch rate with methylphenidate or amphetamine.³⁷ Another chart review of 80 children with BD type I found that past amphetamine treatment (but not history of ADHD diagnosis or antidepressant treatment) was associated with more severe bipolar illness.³⁸

No studies have examined predictors of amphetamine-induced mania. In our clinical experience, triggers are similar to those that can cause antidepressant-induced mania, such as:

• recent manic episodes
• current rapid cycling
• past antidepressant-induced mania.

Antidepressants and mania. When 64 patients with acute bipolar depression received both antidepressants and mood stabilizers in a randomized, double-blind trial, switch rates into mania or hypomania were 10% for bupropion, 9% for sertraline, and 29% for venlafaxine.³⁹ In a meta analysis of clinical trials using selective serotonin reuptake inhibitors (SSRIs) or tricyclic antidepressants (TCAs), the manic switch rate was threefold higher with TCAs than SSRIs.⁴⁰ Antidepressant use in bipolar patients was associated with rapid cycling in the only randomized study of this topic.⁴¹

Insufficient data exist to clarify whether mania induction with antidepressants is dose-dependent.⁴² Factors associated with antidepressant-induced mania include:

• previous antidepressant-induced mania
• family history of BD
• exposure to multiple antidepressant trials⁴²
• history of substance abuse and/or dependence.⁴³

Related resources

• Bipolar disorder information and resources. www.psycheducation.org.
• ADHD Information and resources. www.adhdnews.com.
• Phelps J. Why am I still depressed? Recognizing and managing the ups and downs of bipolar II and soft bipolar disorder. New York: McGraw-Hill; 2006.

Drug brand names

• Amphetamine/Dextroamphetamine • Adderall
• Aripiprazole • Abilify
• Atomoxetine • Strattera
• Bupropion • Wellbutrin
• Carbamazepine • Tegretol
• Desipramine • Norpramin
• Dextroamphetamine • Dexedrine
• Guanfacine • Tenex
• Lamotrigine • Lamictal
• Lithium • Eskalith, Lithobid
• Methylphenidate • Ritalin
• Quetiapine • Seroquel
• Sertraline • Zoloft
• Valproate • Depakote
• Venlafaxine • Effexor
• Ziprasidone • Geodon

Disclosures

Dr. Wingo reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Dr. Ghaemi receives research grants from GlaxoSmithKline and Pfizer and is a speaker for GlaxoSmithKline, AstraZeneca, Pfizer, and Abbott Laboratories. Neither he nor his family hold equity positions in pharmaceutical companies.

Overlapping symptoms may obscure comorbid bipolar illness

An adult with function-impairing inattention could have attention-deficit/hyperactivity disorder (ADHD), bipolar disorder (BD), or both. Comorbid ADHD and BD often is unrecognized, however, because patients are more likely to report ADHD-related symptoms than manic symptoms.¹

To help you recognize comorbid ADHD/BD—and protect adults who might switch into mania if given stimulants or antidepressants—this article describes a hierarchy to diagnose and treat this comorbidity. Based on the evidence and our experience, we:

• discuss how to differentiate between these disorders with overlapping symptoms
• provide tools and suggestions to screen for BD and adult ADHD
• offer 3 algorithms to guide your diagnosis and choice of medications.

Clinical challenges

Prevalence is unclear. Adult ADHD—with an estimated prevalence of 4.4%²—is more common than BD. Lifetime prevalences of BD types I and II are 1.6% and 0.5%, respectively.³ Studies of ADHD/BD comorbidity suggest wide-ranging prevalence rates:

• 9% to 21% of BD patients may have adult ADHD^2,4,5
• 5% to 47% of adult ADHD patients may have BD.^2,6-8

Underdiagnosis. Adult ADHD/BD is a more severe illness than ADHD or BD alone and is highly comorbid with agoraphobia, social phobia, posttraumatic stress disorder, and alcohol or drug addiction. Adults with ADHD/BD have more frequent affective episodes, suicide attempts, violence, and legal problems.⁴ Diagnosing this comorbidity remains a challenge, however, because:

• identifying which symptoms are caused by which disorder can be difficult
• BD tends to be underdiagnosed⁹
• patients often misidentify, underreport, or deny manic symptoms^1,10,11
• if a patient presents with active bipolar symptoms, DSM-IV-TR criteria require that ADHD not be diagnosed until mood symptoms are resolved.

Overlapping symptoms. ADHD and bipolar mania share some DSM-IV-TR diagnostic criteria, including talkativeness, distractibility, increased activity or physical restlessness, and loss of social inhibitions (Table 1).¹² Overlapping symptoms also are notable within ADHD diagnostic criteria (Table 2). In the inattention category, for example, “easily distracted by extraneous stimuli,” “difficulty sustaining attention in tasks,” and “fails to give close attention to details” are considered 3 separate symptoms. In the hyperactivity category, “often leaves seat,” “often runs about or climbs excessively,” and “often on the go, or often acts as if driven by a motor” are 3 separate symptoms.

Given ADHD’s relatively loose diagnostic criteria and high comorbidity in adults with mood disorders, the question of whether adult ADHD/BD represents comorbidity or diagnostic overlap remains unresolved. For the clinician, the disorders’ nonoverlapping features (Table 1) can assist with the differential diagnosis. For example:

• ADHD symptoms tend to be chronic and BD symptoms episodic.
• ADHD patients may have high energy but lack increased productivity seen in BD patients.
• ADHD patients do not need less sleep or have inflated self-esteem like symptomatic BD patients.
• Psychotic symptoms such as hallucinations or delusions might be present in severe BD but are absent in ADHD.

Table 1

Overlap between DSM-IV-TR diagnostic criteria for ADHD and bipolar mania

Table 2

DSM-IV-TR diagnostic criteria for attention-deficit/ hyperactivity disorder

Mood symptoms first

A diagnostic hierarchy is implicit in DSM-IV-TR; anxiety disorders are not diagnosed during an active major depressive or manic episode, and schizophrenia is not diagnosed on the basis of psychotic symptoms during an active major depressive or manic episode. Mood disorders sit atop this implied diagnostic hierarchy and must be ruled out before psychotic or anxiety disorders are diagnosed. Similarly, most personality disorders are not diagnosed during an active mood or psychotic episode.

Diagnosing adult ADHD when a patient is actively depressed or manic is inconsistent with this hierarchy and conflicts with extensive nosologic literature.¹³ We suggest that ADHD—a cognitive-behavioral problem—not be diagnosed solely on symptoms observed when a patient is experiencing a mood episode or psychotic illness.

Bipolar disorder. Two useful mnemonics (Table 3) assist in screening for DSM-IV-TR symptoms of BD type I:

• Pure mania consists of euphoric mood and ≥3 of 7 DIGFAST criteria, or irritable mood and ≥4 of 7 DIGFAST criteria
• Mixed mania consists of depressed mood with ≥4 of 7 DIGFAST criteria and ≥4 of 8 SIGECAPS criteria.

To be diagnostic, these symptoms must cause substantial social or occupational dysfunction and be present at least 1 week. Diagnose BD type I if a patient has experienced a single pure or mixed manic episode at any time, unless the episode had a medical cause such as hyperthyroidism or antidepressant use. Because patients with mixed episodes experience depressed mood, assess any patient with clinical depression for manic symptoms. Otherwise, a patient with a mixed episode could be misdiagnosed as having unipolar depression instead of BD type I.¹⁴

BD type II also has been observed in patients with comorbid adult ADHD/BD.^4,6 The main difference between BD types I and II is that manic symptoms in type II are not severe enough to cause functional impairment or psychotic symptoms.¹⁵

Adult ADHD. The clinical interview seeking evidence of inattention and hyperactivity/impulsivity remains the basis of adult ADHD diagnosis (Table 2). Key areas are:

• the patient’s past and current functional impairment
• whether substantial impairment occurs in at least 2 areas of life (such as school, work, or home).

Take medical, educational, social, psychological, and vocational histories, and rule out other conditions before concluding that adult ADHD is the appropriate diagnosis.¹⁶ In adult ADHD, inattentive symptoms become far more prominent, about twice as common as hyperactive symptoms.¹⁷ Inattentive symptoms may manifest as neglect, poor time management, motivational deficits, or poor concentration that results in forgetfulness, distractibility, item misplacement, or excessive mistakes in paperwork.¹⁸ When impulsive symptoms persist in adults, they may manifest as automobile accidents or low tolerance for frustration, which may lead to frequent job changes and unstable, interrupted interpersonal relationships.¹⁸

Neuropsychological testing is not required to make an adult ADHD diagnosis but can help establish the breadth of symptoms or comorbidity.¹⁷ Rating scales can screen, gather data (including presence and severity of symptoms), and measure treatment response.¹⁶ Commonly used rating scales include:

• Conners’ Adult ADHD Rating Scales¹⁹
• Brown Attention Deficit Disorder Rating Scale for Adults²⁰
• Adult ADHD Self-Report Scale.²¹

When using rating scales, remember that adult psychopathology can distort perceptions, and some self-report scales have questionable reliability.¹⁶

Table 3

Mnemonics for diagnostic symptoms of pure and mixed bipolar mania

Treatment recommendations

Limited data. We found only 1 study on adult ADHD/BD treatment. In this open trial,²² 36 adults with comorbid ADHD and BD received bupropion SR, up to 200 mg bid, for ADHD symptoms while maintained on mood stabilizers, antipsychotics, or both. Improvement was defined as ≥30% reduction in ADHD Symptom Checklist Scale scores, without concurrent mania. After 6 weeks, 82% of patients had improved; 1 dropped out at week 2 because of hypomanic activation. Methodologic limitations included trial design (non-randomized, nonblinded, short duration) and patient selection (90% of subjects had BD type II).

In the absence of adequate data on adult ADHD/BD, studies in children suggest:

• stimulants may not be effective for ADHD symptoms in patients with active manic or depressive symptoms
• mood stabilization is a prerequisite for successful pharmacologic treatment of ADHD in patients with both ADHD and manic or depressive symptoms.^23,24

Follow the hierarchy. First treat acute mood symptoms, then reevaluate and possibly treat ADHD symptoms if they persist during euthymia (Algorithm 1). When a patient meets criteria for adult ADHD/BD, first stabilize bipolar manic or depressive symptoms (Algorithm 2). For acute mania, treat with standard mood stabilizers (lithium, valproate, lamotrigine, or carbamazepine) with or without a second-generation antipsychotic.²⁵ Starting stimulants for ADHD when patients have active mood symptoms is sub-optimal and potentially harmful because of the risk of inducing mania. For acute bipolar depression, adjunctive antidepressant treatment has been found to be no more effective than a mood stabilizer alone.²⁶

After bipolar symptoms respond or remit, reassess for adult ADHD. If ADHD symptoms persist during euthymia, additional treatment may be indicated.

Very little evidence exists on treating adult ADHD/BD; as mentioned, bupropion is the only medication studied in this population. For adult ADHD alone, clinical trials have showed varying efficacy with bupropion,^27,28 atomoxetine,²⁹ venlafaxine,^30,31 desipramine,³² methylphenidate,³³ mixed amphetamine salts,³⁴ and guanfacine.³⁵ Whether these treatments can be generalized as safe and efficacious for comorbid adult ADHD/BD is unclear. Nonetheless, we suggest using bupropion first, followed by atomoxetine or guanfacine before you consider amphetamine stimulants (Algorithm 3).

Algorithm 1
Hierarchy for diagnosis and treatment of adult ADHD/BD

ADHD: attention-deficit/hyperactivity disorder; BD: bipolar disorder
*Adler LA, Chua HC. Management of ADHD in adults. J Clin Psychiatry 2002;63(suppl 12):29-35.

Algorithm 2
Treating acute episodes of bipolar disorder

ECT: electroconvulsive therapy; SGA: second-generation antipsychotic; TMS: transcranial magnetic stimulation

Algorithm 3
Suggested approach to adult ADHD with comorbid BD*

* Based on data extrapolated from samples of patients with ADHD alone because of very limited data in ADHD/BD samples.
^† We recommend against combining antidepressants and stimulants because of additive risks of mania in BD. Discontinue stimulant or antidepressant if manic symptoms appear or rapid cycling emerges.

Reducing mania risk

Antidepressants and stimulants may help adults with ADHD alone, but risks of mania and rapid cycling limit their use in adults with ADHD/BD.

Stimulants and mania. One study found a 17% manic switch rate when methylphenidate (≤10 mg bid) was given to 14 bipolar depressed adults (10 BD type I, 2 BD type II, and 2 with secondary mania) taking mood stabilizers.³⁶ A chart review of 82 bipolar children not taking mood stabilizers found an 18% switch rate with methylphenidate or amphetamine.³⁷ Another chart review of 80 children with BD type I found that past amphetamine treatment (but not history of ADHD diagnosis or antidepressant treatment) was associated with more severe bipolar illness.³⁸

No studies have examined predictors of amphetamine-induced mania. In our clinical experience, triggers are similar to those that can cause antidepressant-induced mania, such as:

• recent manic episodes
• current rapid cycling
• past antidepressant-induced mania.

Antidepressants and mania. When 64 patients with acute bipolar depression received both antidepressants and mood stabilizers in a randomized, double-blind trial, switch rates into mania or hypomania were 10% for bupropion, 9% for sertraline, and 29% for venlafaxine.³⁹ In a meta analysis of clinical trials using selective serotonin reuptake inhibitors (SSRIs) or tricyclic antidepressants (TCAs), the manic switch rate was threefold higher with TCAs than SSRIs.⁴⁰ Antidepressant use in bipolar patients was associated with rapid cycling in the only randomized study of this topic.⁴¹

Insufficient data exist to clarify whether mania induction with antidepressants is dose-dependent.⁴² Factors associated with antidepressant-induced mania include:

• previous antidepressant-induced mania
• family history of BD
• exposure to multiple antidepressant trials⁴²
• history of substance abuse and/or dependence.⁴³

Related resources

• Bipolar disorder information and resources. www.psycheducation.org.
• ADHD Information and resources. www.adhdnews.com.
• Phelps J. Why am I still depressed? Recognizing and managing the ups and downs of bipolar II and soft bipolar disorder. New York: McGraw-Hill; 2006.

Drug brand names

• Amphetamine/Dextroamphetamine • Adderall
• Aripiprazole • Abilify
• Atomoxetine • Strattera
• Bupropion • Wellbutrin
• Carbamazepine • Tegretol
• Desipramine • Norpramin
• Dextroamphetamine • Dexedrine
• Guanfacine • Tenex
• Lamotrigine • Lamictal
• Lithium • Eskalith, Lithobid
• Methylphenidate • Ritalin
• Quetiapine • Seroquel
• Sertraline • Zoloft
• Valproate • Depakote
• Venlafaxine • Effexor
• Ziprasidone • Geodon

Disclosures

Dr. Wingo reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Dr. Ghaemi receives research grants from GlaxoSmithKline and Pfizer and is a speaker for GlaxoSmithKline, AstraZeneca, Pfizer, and Abbott Laboratories. Neither he nor his family hold equity positions in pharmaceutical companies.

Overlapping symptoms may obscure comorbid bipolar illness

An adult with function-impairing inattention could have attention-deficit/hyperactivity disorder (ADHD), bipolar disorder (BD), or both. Comorbid ADHD and BD often is unrecognized, however, because patients are more likely to report ADHD-related symptoms than manic symptoms.¹

To help you recognize comorbid ADHD/BD—and protect adults who might switch into mania if given stimulants or antidepressants—this article describes a hierarchy to diagnose and treat this comorbidity. Based on the evidence and our experience, we:

• discuss how to differentiate between these disorders with overlapping symptoms
• provide tools and suggestions to screen for BD and adult ADHD
• offer 3 algorithms to guide your diagnosis and choice of medications.

Clinical challenges

Prevalence is unclear. Adult ADHD—with an estimated prevalence of 4.4%²—is more common than BD. Lifetime prevalences of BD types I and II are 1.6% and 0.5%, respectively.³ Studies of ADHD/BD comorbidity suggest wide-ranging prevalence rates:

• 9% to 21% of BD patients may have adult ADHD^2,4,5
• 5% to 47% of adult ADHD patients may have BD.^2,6-8

Underdiagnosis. Adult ADHD/BD is a more severe illness than ADHD or BD alone and is highly comorbid with agoraphobia, social phobia, posttraumatic stress disorder, and alcohol or drug addiction. Adults with ADHD/BD have more frequent affective episodes, suicide attempts, violence, and legal problems.⁴ Diagnosing this comorbidity remains a challenge, however, because:

• identifying which symptoms are caused by which disorder can be difficult
• BD tends to be underdiagnosed⁹
• patients often misidentify, underreport, or deny manic symptoms^1,10,11
• if a patient presents with active bipolar symptoms, DSM-IV-TR criteria require that ADHD not be diagnosed until mood symptoms are resolved.

Overlapping symptoms. ADHD and bipolar mania share some DSM-IV-TR diagnostic criteria, including talkativeness, distractibility, increased activity or physical restlessness, and loss of social inhibitions (Table 1).¹² Overlapping symptoms also are notable within ADHD diagnostic criteria (Table 2). In the inattention category, for example, “easily distracted by extraneous stimuli,” “difficulty sustaining attention in tasks,” and “fails to give close attention to details” are considered 3 separate symptoms. In the hyperactivity category, “often leaves seat,” “often runs about or climbs excessively,” and “often on the go, or often acts as if driven by a motor” are 3 separate symptoms.

Given ADHD’s relatively loose diagnostic criteria and high comorbidity in adults with mood disorders, the question of whether adult ADHD/BD represents comorbidity or diagnostic overlap remains unresolved. For the clinician, the disorders’ nonoverlapping features (Table 1) can assist with the differential diagnosis. For example:

• ADHD symptoms tend to be chronic and BD symptoms episodic.
• ADHD patients may have high energy but lack increased productivity seen in BD patients.
• ADHD patients do not need less sleep or have inflated self-esteem like symptomatic BD patients.
• Psychotic symptoms such as hallucinations or delusions might be present in severe BD but are absent in ADHD.

Table 1

Overlap between DSM-IV-TR diagnostic criteria for ADHD and bipolar mania

Table 2

DSM-IV-TR diagnostic criteria for attention-deficit/ hyperactivity disorder

Mood symptoms first

A diagnostic hierarchy is implicit in DSM-IV-TR; anxiety disorders are not diagnosed during an active major depressive or manic episode, and schizophrenia is not diagnosed on the basis of psychotic symptoms during an active major depressive or manic episode. Mood disorders sit atop this implied diagnostic hierarchy and must be ruled out before psychotic or anxiety disorders are diagnosed. Similarly, most personality disorders are not diagnosed during an active mood or psychotic episode.

Diagnosing adult ADHD when a patient is actively depressed or manic is inconsistent with this hierarchy and conflicts with extensive nosologic literature.¹³ We suggest that ADHD—a cognitive-behavioral problem—not be diagnosed solely on symptoms observed when a patient is experiencing a mood episode or psychotic illness.

Bipolar disorder. Two useful mnemonics (Table 3) assist in screening for DSM-IV-TR symptoms of BD type I:

• Pure mania consists of euphoric mood and ≥3 of 7 DIGFAST criteria, or irritable mood and ≥4 of 7 DIGFAST criteria
• Mixed mania consists of depressed mood with ≥4 of 7 DIGFAST criteria and ≥4 of 8 SIGECAPS criteria.

To be diagnostic, these symptoms must cause substantial social or occupational dysfunction and be present at least 1 week. Diagnose BD type I if a patient has experienced a single pure or mixed manic episode at any time, unless the episode had a medical cause such as hyperthyroidism or antidepressant use. Because patients with mixed episodes experience depressed mood, assess any patient with clinical depression for manic symptoms. Otherwise, a patient with a mixed episode could be misdiagnosed as having unipolar depression instead of BD type I.¹⁴

BD type II also has been observed in patients with comorbid adult ADHD/BD.^4,6 The main difference between BD types I and II is that manic symptoms in type II are not severe enough to cause functional impairment or psychotic symptoms.¹⁵

Adult ADHD. The clinical interview seeking evidence of inattention and hyperactivity/impulsivity remains the basis of adult ADHD diagnosis (Table 2). Key areas are:

• the patient’s past and current functional impairment
• whether substantial impairment occurs in at least 2 areas of life (such as school, work, or home).

Take medical, educational, social, psychological, and vocational histories, and rule out other conditions before concluding that adult ADHD is the appropriate diagnosis.¹⁶ In adult ADHD, inattentive symptoms become far more prominent, about twice as common as hyperactive symptoms.¹⁷ Inattentive symptoms may manifest as neglect, poor time management, motivational deficits, or poor concentration that results in forgetfulness, distractibility, item misplacement, or excessive mistakes in paperwork.¹⁸ When impulsive symptoms persist in adults, they may manifest as automobile accidents or low tolerance for frustration, which may lead to frequent job changes and unstable, interrupted interpersonal relationships.¹⁸

Neuropsychological testing is not required to make an adult ADHD diagnosis but can help establish the breadth of symptoms or comorbidity.¹⁷ Rating scales can screen, gather data (including presence and severity of symptoms), and measure treatment response.¹⁶ Commonly used rating scales include:

• Conners’ Adult ADHD Rating Scales¹⁹
• Brown Attention Deficit Disorder Rating Scale for Adults²⁰
• Adult ADHD Self-Report Scale.²¹

When using rating scales, remember that adult psychopathology can distort perceptions, and some self-report scales have questionable reliability.¹⁶

Table 3

Mnemonics for diagnostic symptoms of pure and mixed bipolar mania

Treatment recommendations

Limited data. We found only 1 study on adult ADHD/BD treatment. In this open trial,²² 36 adults with comorbid ADHD and BD received bupropion SR, up to 200 mg bid, for ADHD symptoms while maintained on mood stabilizers, antipsychotics, or both. Improvement was defined as ≥30% reduction in ADHD Symptom Checklist Scale scores, without concurrent mania. After 6 weeks, 82% of patients had improved; 1 dropped out at week 2 because of hypomanic activation. Methodologic limitations included trial design (non-randomized, nonblinded, short duration) and patient selection (90% of subjects had BD type II).

In the absence of adequate data on adult ADHD/BD, studies in children suggest:

• stimulants may not be effective for ADHD symptoms in patients with active manic or depressive symptoms
• mood stabilization is a prerequisite for successful pharmacologic treatment of ADHD in patients with both ADHD and manic or depressive symptoms.^23,24

Follow the hierarchy. First treat acute mood symptoms, then reevaluate and possibly treat ADHD symptoms if they persist during euthymia (Algorithm 1). When a patient meets criteria for adult ADHD/BD, first stabilize bipolar manic or depressive symptoms (Algorithm 2). For acute mania, treat with standard mood stabilizers (lithium, valproate, lamotrigine, or carbamazepine) with or without a second-generation antipsychotic.²⁵ Starting stimulants for ADHD when patients have active mood symptoms is sub-optimal and potentially harmful because of the risk of inducing mania. For acute bipolar depression, adjunctive antidepressant treatment has been found to be no more effective than a mood stabilizer alone.²⁶

After bipolar symptoms respond or remit, reassess for adult ADHD. If ADHD symptoms persist during euthymia, additional treatment may be indicated.

Very little evidence exists on treating adult ADHD/BD; as mentioned, bupropion is the only medication studied in this population. For adult ADHD alone, clinical trials have showed varying efficacy with bupropion,^27,28 atomoxetine,²⁹ venlafaxine,^30,31 desipramine,³² methylphenidate,³³ mixed amphetamine salts,³⁴ and guanfacine.³⁵ Whether these treatments can be generalized as safe and efficacious for comorbid adult ADHD/BD is unclear. Nonetheless, we suggest using bupropion first, followed by atomoxetine or guanfacine before you consider amphetamine stimulants (Algorithm 3).

Algorithm 1
Hierarchy for diagnosis and treatment of adult ADHD/BD

ADHD: attention-deficit/hyperactivity disorder; BD: bipolar disorder
*Adler LA, Chua HC. Management of ADHD in adults. J Clin Psychiatry 2002;63(suppl 12):29-35.

Algorithm 2
Treating acute episodes of bipolar disorder

ECT: electroconvulsive therapy; SGA: second-generation antipsychotic; TMS: transcranial magnetic stimulation

Algorithm 3
Suggested approach to adult ADHD with comorbid BD*

* Based on data extrapolated from samples of patients with ADHD alone because of very limited data in ADHD/BD samples.
^† We recommend against combining antidepressants and stimulants because of additive risks of mania in BD. Discontinue stimulant or antidepressant if manic symptoms appear or rapid cycling emerges.

Reducing mania risk

Antidepressants and stimulants may help adults with ADHD alone, but risks of mania and rapid cycling limit their use in adults with ADHD/BD.

Stimulants and mania. One study found a 17% manic switch rate when methylphenidate (≤10 mg bid) was given to 14 bipolar depressed adults (10 BD type I, 2 BD type II, and 2 with secondary mania) taking mood stabilizers.³⁶ A chart review of 82 bipolar children not taking mood stabilizers found an 18% switch rate with methylphenidate or amphetamine.³⁷ Another chart review of 80 children with BD type I found that past amphetamine treatment (but not history of ADHD diagnosis or antidepressant treatment) was associated with more severe bipolar illness.³⁸

No studies have examined predictors of amphetamine-induced mania. In our clinical experience, triggers are similar to those that can cause antidepressant-induced mania, such as:

• recent manic episodes
• current rapid cycling
• past antidepressant-induced mania.

Antidepressants and mania. When 64 patients with acute bipolar depression received both antidepressants and mood stabilizers in a randomized, double-blind trial, switch rates into mania or hypomania were 10% for bupropion, 9% for sertraline, and 29% for venlafaxine.³⁹ In a meta analysis of clinical trials using selective serotonin reuptake inhibitors (SSRIs) or tricyclic antidepressants (TCAs), the manic switch rate was threefold higher with TCAs than SSRIs.⁴⁰ Antidepressant use in bipolar patients was associated with rapid cycling in the only randomized study of this topic.⁴¹

Insufficient data exist to clarify whether mania induction with antidepressants is dose-dependent.⁴² Factors associated with antidepressant-induced mania include:

• previous antidepressant-induced mania
• family history of BD
• exposure to multiple antidepressant trials⁴²
• history of substance abuse and/or dependence.⁴³

Related resources

• Bipolar disorder information and resources. www.psycheducation.org.
• ADHD Information and resources. www.adhdnews.com.
• Phelps J. Why am I still depressed? Recognizing and managing the ups and downs of bipolar II and soft bipolar disorder. New York: McGraw-Hill; 2006.

Drug brand names

• Amphetamine/Dextroamphetamine • Adderall
• Aripiprazole • Abilify
• Atomoxetine • Strattera
• Bupropion • Wellbutrin
• Carbamazepine • Tegretol
• Desipramine • Norpramin
• Dextroamphetamine • Dexedrine
• Guanfacine • Tenex
• Lamotrigine • Lamictal
• Lithium • Eskalith, Lithobid
• Methylphenidate • Ritalin
• Quetiapine • Seroquel
• Sertraline • Zoloft
• Valproate • Depakote
• Venlafaxine • Effexor
• Ziprasidone • Geodon

Disclosures

Dr. Wingo reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Dr. Ghaemi receives research grants from GlaxoSmithKline and Pfizer and is a speaker for GlaxoSmithKline, AstraZeneca, Pfizer, and Abbott Laboratories. Neither he nor his family hold equity positions in pharmaceutical companies.

The hospital is the only proper college in which to rear a true disciple of Aesculapius.—John Abernethy (1764-1831), surgeon and teacher

With this quote Sir William Osler began his address, “The Hospital as a College?” to the Academy of Medicine in New York in 1903. His second quote for this report was from the famed physician Oliver Wendell Holmes Sr. in 1867:

“The most essential part of a student’s instruction is obtained, as I believe, not in the lecture room, but at the bedside. Nothing seen there is lost: the rhythms of disease are learned by frequent repetition: its unforeseen occurrence stamp themselves indelibly on the memory. Before the student is aware of what he had acquired he has learned the aspects and causes and probable issue of the disease he has seen with his teacher and the proper mode of dealing with them, as far as his master knows.”

In his report Osler was celebrating a quarter century’s success in education. He demanded a better general education for students, a lengthened period for professional study, and the substitution of theoretical by practical learning. He wanted the student not to learn only from dissecting the sympathetic nervous system but to learn to “take a blood pressure observation” with a kymograph (an instrument used to record the temporal variations of any physiological or muscular process; it consists essentially of a revolving drum, bearing a record sheet on which a stylus travels).

Osler observed that there should be no teaching without a patient for a text: “The whole of medicine is in observation” that the teacher’s art is educating the student’s finger to feel and eyes to see. Give the student good methods and a proper point of view, and experience will do the rest.

Osler expressed confidence that students would keep the hospital physician from slovenliness and improve the care of patients. He was also concerned that “we ask too much of the resident physicians, whose number has not increased in proportion to the enormous amount of work thrust upon them.” Students were the answer, the proto-scut-monkey.

The practicality of working out of a teaching hospital was outlined at length in Osler’s report. The student’s third year should begin with a systematic physical diagnosis course, first in history taking, then in writing reports. Concurrently, a physical examination course should be given several days a week with individual cases assigned to students to follow, and instruction is accessing the literature. Next comes clinical microscopy—an essential in an era where there was often no lab to call upon. In general, medical clinic occurs one day a week when interesting cases are brought from the wards. Of note, committees were appointed to report on every case of pneumonia.

In revamping medical education Osler brought the third-year students to the outpatient clinic and the fourth-year students to the wards. What implication does this have for us as hospitalists?

I have no pretensions about being another Osler (I am barely a Newman on my best days), but still my colleagues and I trudge along in our teaching duties. What education do we really do? I sat down after reading Osler’s paper, stimulated by a tangential question from the esteemed Tom Baudenistel, MD, and decided to see exactly whom we were teaching.

First there are medical students. We are faculty on their first-year selectives, offering a shadow experience. We staff the introduction to physical exam courses in second year. Third-year students rotate on our services, and seniors take our elective as well as taking acting internships on our teaching services. We act as mentors and interest group leaders. There is certainly more to this list. We also spend time teaching NP and PA students.

The internal medicine residents rotate on our hospitalist services, and we staff the general medical services. We interact with them daily when they are on consult services, trying to set a role model. General medicine, geriatric, and hospital medicine fellows rotate through as well.

We also teach the nurses on services and through in-services and daily rounds to cement the working relationship and improve communication. We teach each other. A day rarely goes by without a colleague passing on a tasty medical tidbit. (Of course, for me, a tabla blanca, no shortage of space for pearls). And finally we teach our patients and their families. Every day we do this, and if we don’t then we are missing the point of our profession entirely.

Each party—patient or student—has something to learn from us, but more importantly we have something to learn from them. Osler wrote that “The stimulus of their presence (the student) neutralizes the clinical apathy certain, sooner or later, to beset the man who makes lonely “rounds” with his house physician.”

One hundred years plus later, much of what was written is still true: Whether in a teaching institution or making “lonely rounds” we must strive to continue to educate ourselves, our colleagues, and our patients. And what better place to do it than the hospital? TH

Dr. Newman is the physician editor of The Hospitalist. He’s also consultant, Hospital Internal Medicine, and assistant professor of internal medicine and medical history, Mayo Clinic College of Medicine, Rochester, Minn.

Bibliography

Osler W (Sir) Aequanimitas. 1945. The Blakiston Company, Philadelphia. p. 311-327.

The hospital is the only proper college in which to rear a true disciple of Aesculapius.—John Abernethy (1764-1831), surgeon and teacher

With this quote Sir William Osler began his address, “The Hospital as a College?” to the Academy of Medicine in New York in 1903. His second quote for this report was from the famed physician Oliver Wendell Holmes Sr. in 1867:

“The most essential part of a student’s instruction is obtained, as I believe, not in the lecture room, but at the bedside. Nothing seen there is lost: the rhythms of disease are learned by frequent repetition: its unforeseen occurrence stamp themselves indelibly on the memory. Before the student is aware of what he had acquired he has learned the aspects and causes and probable issue of the disease he has seen with his teacher and the proper mode of dealing with them, as far as his master knows.”

In his report Osler was celebrating a quarter century’s success in education. He demanded a better general education for students, a lengthened period for professional study, and the substitution of theoretical by practical learning. He wanted the student not to learn only from dissecting the sympathetic nervous system but to learn to “take a blood pressure observation” with a kymograph (an instrument used to record the temporal variations of any physiological or muscular process; it consists essentially of a revolving drum, bearing a record sheet on which a stylus travels).

Osler observed that there should be no teaching without a patient for a text: “The whole of medicine is in observation” that the teacher’s art is educating the student’s finger to feel and eyes to see. Give the student good methods and a proper point of view, and experience will do the rest.

Osler expressed confidence that students would keep the hospital physician from slovenliness and improve the care of patients. He was also concerned that “we ask too much of the resident physicians, whose number has not increased in proportion to the enormous amount of work thrust upon them.” Students were the answer, the proto-scut-monkey.

The practicality of working out of a teaching hospital was outlined at length in Osler’s report. The student’s third year should begin with a systematic physical diagnosis course, first in history taking, then in writing reports. Concurrently, a physical examination course should be given several days a week with individual cases assigned to students to follow, and instruction is accessing the literature. Next comes clinical microscopy—an essential in an era where there was often no lab to call upon. In general, medical clinic occurs one day a week when interesting cases are brought from the wards. Of note, committees were appointed to report on every case of pneumonia.

In revamping medical education Osler brought the third-year students to the outpatient clinic and the fourth-year students to the wards. What implication does this have for us as hospitalists?

I have no pretensions about being another Osler (I am barely a Newman on my best days), but still my colleagues and I trudge along in our teaching duties. What education do we really do? I sat down after reading Osler’s paper, stimulated by a tangential question from the esteemed Tom Baudenistel, MD, and decided to see exactly whom we were teaching.

First there are medical students. We are faculty on their first-year selectives, offering a shadow experience. We staff the introduction to physical exam courses in second year. Third-year students rotate on our services, and seniors take our elective as well as taking acting internships on our teaching services. We act as mentors and interest group leaders. There is certainly more to this list. We also spend time teaching NP and PA students.

The internal medicine residents rotate on our hospitalist services, and we staff the general medical services. We interact with them daily when they are on consult services, trying to set a role model. General medicine, geriatric, and hospital medicine fellows rotate through as well.

We also teach the nurses on services and through in-services and daily rounds to cement the working relationship and improve communication. We teach each other. A day rarely goes by without a colleague passing on a tasty medical tidbit. (Of course, for me, a tabla blanca, no shortage of space for pearls). And finally we teach our patients and their families. Every day we do this, and if we don’t then we are missing the point of our profession entirely.

Each party—patient or student—has something to learn from us, but more importantly we have something to learn from them. Osler wrote that “The stimulus of their presence (the student) neutralizes the clinical apathy certain, sooner or later, to beset the man who makes lonely “rounds” with his house physician.”

One hundred years plus later, much of what was written is still true: Whether in a teaching institution or making “lonely rounds” we must strive to continue to educate ourselves, our colleagues, and our patients. And what better place to do it than the hospital? TH

Dr. Newman is the physician editor of The Hospitalist. He’s also consultant, Hospital Internal Medicine, and assistant professor of internal medicine and medical history, Mayo Clinic College of Medicine, Rochester, Minn.

Bibliography

Osler W (Sir) Aequanimitas. 1945. The Blakiston Company, Philadelphia. p. 311-327.

The hospital is the only proper college in which to rear a true disciple of Aesculapius.—John Abernethy (1764-1831), surgeon and teacher

With this quote Sir William Osler began his address, “The Hospital as a College?” to the Academy of Medicine in New York in 1903. His second quote for this report was from the famed physician Oliver Wendell Holmes Sr. in 1867:

“The most essential part of a student’s instruction is obtained, as I believe, not in the lecture room, but at the bedside. Nothing seen there is lost: the rhythms of disease are learned by frequent repetition: its unforeseen occurrence stamp themselves indelibly on the memory. Before the student is aware of what he had acquired he has learned the aspects and causes and probable issue of the disease he has seen with his teacher and the proper mode of dealing with them, as far as his master knows.”

In his report Osler was celebrating a quarter century’s success in education. He demanded a better general education for students, a lengthened period for professional study, and the substitution of theoretical by practical learning. He wanted the student not to learn only from dissecting the sympathetic nervous system but to learn to “take a blood pressure observation” with a kymograph (an instrument used to record the temporal variations of any physiological or muscular process; it consists essentially of a revolving drum, bearing a record sheet on which a stylus travels).

Osler observed that there should be no teaching without a patient for a text: “The whole of medicine is in observation” that the teacher’s art is educating the student’s finger to feel and eyes to see. Give the student good methods and a proper point of view, and experience will do the rest.

Osler expressed confidence that students would keep the hospital physician from slovenliness and improve the care of patients. He was also concerned that “we ask too much of the resident physicians, whose number has not increased in proportion to the enormous amount of work thrust upon them.” Students were the answer, the proto-scut-monkey.

The practicality of working out of a teaching hospital was outlined at length in Osler’s report. The student’s third year should begin with a systematic physical diagnosis course, first in history taking, then in writing reports. Concurrently, a physical examination course should be given several days a week with individual cases assigned to students to follow, and instruction is accessing the literature. Next comes clinical microscopy—an essential in an era where there was often no lab to call upon. In general, medical clinic occurs one day a week when interesting cases are brought from the wards. Of note, committees were appointed to report on every case of pneumonia.

In revamping medical education Osler brought the third-year students to the outpatient clinic and the fourth-year students to the wards. What implication does this have for us as hospitalists?

I have no pretensions about being another Osler (I am barely a Newman on my best days), but still my colleagues and I trudge along in our teaching duties. What education do we really do? I sat down after reading Osler’s paper, stimulated by a tangential question from the esteemed Tom Baudenistel, MD, and decided to see exactly whom we were teaching.

First there are medical students. We are faculty on their first-year selectives, offering a shadow experience. We staff the introduction to physical exam courses in second year. Third-year students rotate on our services, and seniors take our elective as well as taking acting internships on our teaching services. We act as mentors and interest group leaders. There is certainly more to this list. We also spend time teaching NP and PA students.

The internal medicine residents rotate on our hospitalist services, and we staff the general medical services. We interact with them daily when they are on consult services, trying to set a role model. General medicine, geriatric, and hospital medicine fellows rotate through as well.

We also teach the nurses on services and through in-services and daily rounds to cement the working relationship and improve communication. We teach each other. A day rarely goes by without a colleague passing on a tasty medical tidbit. (Of course, for me, a tabla blanca, no shortage of space for pearls). And finally we teach our patients and their families. Every day we do this, and if we don’t then we are missing the point of our profession entirely.

Each party—patient or student—has something to learn from us, but more importantly we have something to learn from them. Osler wrote that “The stimulus of their presence (the student) neutralizes the clinical apathy certain, sooner or later, to beset the man who makes lonely “rounds” with his house physician.”

One hundred years plus later, much of what was written is still true: Whether in a teaching institution or making “lonely rounds” we must strive to continue to educate ourselves, our colleagues, and our patients. And what better place to do it than the hospital? TH

Dr. Newman is the physician editor of The Hospitalist. He’s also consultant, Hospital Internal Medicine, and assistant professor of internal medicine and medical history, Mayo Clinic College of Medicine, Rochester, Minn.

Bibliography

Osler W (Sir) Aequanimitas. 1945. The Blakiston Company, Philadelphia. p. 311-327.

SHM has presented the 2008 Awards of Excellence to four hospitalists and one quality improvement team. Their work and research have contributed significantly to hospital medicine and the betterment of patient care and quality improvement. The winners were recognized at Hospital Medicine 2008.

Award for Clinical Excellence: Kevin O’Leary, MD, associate professor of medicine and the associate chief of the Division of Hospital Medicine at Northwestern University’s Feinberg School of Medicine in Chicago.

Dr. O’Leary leads strategic initiatives for the division in his job as associate chief of the Division of Hospital Medicine, especially in patient safety and quality. He also chairs the department’s Quality Management Committee.

An active member of SHM since 2002, Dr. O’Leary has served on the Core Competencies Task Force, the Annual Meeting Planning Committee, and the Annual Meeting Precourse Planning Committee. He also is active in SHM’s Chicago chapter, where he serves as vice president. He serves as an assistant editor for the Journal of Hospital Medicine.

Dr. O’Leary received his bachelor’s inbiology and medical degree from the University of Illinois. He completed his residency at Northwestern University.

Award for Excellence in Research: Peter Lindenauer, MD, MSc, medical director of clinical and quality informatics at Baystate Health in Springfield, Mass., and associate professor of medicine at Tufts University School of Medicine in Boston.

Dr. Lindenauer is responsible for lending the development of an electronic medical record at a large integrated delivery network in western Massachusetts in his job as medical director of clinical and quality informatics.

He has served on technical expert panels for Medicare, patient safety, monitoring systems, and surgical care improvement projects. He also has been a part of the National Quality Forum’s Hospital Quality Measures Development Group and has served on the inpatient functionality work group of the Certifying Committee for Healthcare Information Technology.

As a founding member of SHM, Dr. Lindenauer has served on the society’s board of directors and is a member of the Hospital Quality and Patient Safety Standards Committee.

A graduate of the University of Chicago, Dr. Lindenauer received his bachelor’s in history and received his graduate degree from the Herndon School of Economics and Political Science in Health Planning and Financing. He received his medical degree from the University of Pennsylvania and completed residency training at the University of California, San Francisco.

Award for Excellence in Teaching: Anjala Tess, MD, associate program director for the Internal Medicine Residency Program and director of education for the hospital medicine program, as well as a medical unit director and practicing hospitalist at Beth Israel Deaconess Medical Center in Boston.

Dr. Tess is in charge of the quality improvement teaching program and curriculum for the entire residency program at Beth Israel Deaconess. She also helps oversee the resident elective in hospital medicine and directs educational activities for the group. Her goal is to involve residents in process improvement in the hospital by giving them a hands-on role in quality improvement and peer review.

She has received numerous awards, including the Hermann Blumgart Teaching Award at Beth Israel Deaconess and first prize in SHM’s Innovations Poster Competition.

As an undergraduate, Dr. Tess earned her degree from Brown University, in Rhode Island, and received her medical degree at Washington University’s St. Louis School of Medicine. She completed her residency at Beth Israel Deaconess. She also completed fellowships at Harvard Medical School, the Carl J. Shapiro Institute for Education Research and Beth Israel Deaconess Medical Center.

Award for Outstanding Service in Hospital Medicine: David Zipes, MD, director of pediatric hospitalist service at the Peyton Manning Children’s Hospital in Indianapolis, Ind.

Dr. Zipes oversees all hospitalists and staff, leads strategic planning for the group and the hospital, oversees the business and financial issues of the group and provides general medical direction and leadership of the pediatric units at both the Peyton Manning’s Children’s Hospital and its suburban campus.

As a founding member of SHM, Dr. Zipes is active on its Annual Meeting Planning Committee, Pediatrics Committee, and Pediatrics Core Competencies Task Force. He is also a contributing author for Pediatric Hospital Medicine and the Textbook of Pediatric Hospital Medicine, and a founding member of the annual pediatric hospital medicine meeting.

He also has been the recipient of several awards, including the Family Medicine Teacher of the Year Annual Award (2002, 2005, and 2006) and the St. Vincent Spirit of Caring Award for Service and Dedication to the Hospital (2006 and 2007.)

Dr. Zipes earned his bachelor’s and medical degrees from Indiana University. He completed his residency at Children’s Hospital Medicine Center in Cincinnati, Ohio.

Award for Team Approaches in Quality Improvement: Team Leader, Greg Maynard, MD, MSc, professor of clinical medicine and chief of the division of hospital medicine at the University of California, San Diego.

Dr. Maynard and his team (Ian Jenkins, MD, Sarah Stone, MD, Josh Lee, MD, Ed Fink, Tim Morris, MD, Peter Fedullo, MD, Robert Schoenhaus, PharmD, Doug Humber, PharmD, Marian Renvall, Pat Cal, and Isabella London) are the recipients of the first Team Approaches in Quality Improvement Award for their project “Optimizing Prevention of Hospital-Acquired Venous Thromboembolism.”

Dr. Maynard led the three-year project, which has been implemented at more than 25 sites. Using proven performance-improvement methods and a multidisciplinary team structure, Maynard and his team designed a VTE-prevention protocol for all adult inpatients at their academic center. The protocol integrated a simple VTE risk assessment with a menu of prophylaxis options preferred at each level of risk.

During three years of study, the percentage of patients with adequate VTE prophylaxis regimens increased from 55% to 98%, and the number of patients suffering from hospital-acquired VTE decreased dramatically.

SHM has presented the 2008 Awards of Excellence to four hospitalists and one quality improvement team. Their work and research have contributed significantly to hospital medicine and the betterment of patient care and quality improvement. The winners were recognized at Hospital Medicine 2008.

Award for Clinical Excellence: Kevin O’Leary, MD, associate professor of medicine and the associate chief of the Division of Hospital Medicine at Northwestern University’s Feinberg School of Medicine in Chicago.

Dr. O’Leary leads strategic initiatives for the division in his job as associate chief of the Division of Hospital Medicine, especially in patient safety and quality. He also chairs the department’s Quality Management Committee.

An active member of SHM since 2002, Dr. O’Leary has served on the Core Competencies Task Force, the Annual Meeting Planning Committee, and the Annual Meeting Precourse Planning Committee. He also is active in SHM’s Chicago chapter, where he serves as vice president. He serves as an assistant editor for the Journal of Hospital Medicine.

Dr. O’Leary received his bachelor’s inbiology and medical degree from the University of Illinois. He completed his residency at Northwestern University.

Award for Excellence in Research: Peter Lindenauer, MD, MSc, medical director of clinical and quality informatics at Baystate Health in Springfield, Mass., and associate professor of medicine at Tufts University School of Medicine in Boston.

Dr. Lindenauer is responsible for lending the development of an electronic medical record at a large integrated delivery network in western Massachusetts in his job as medical director of clinical and quality informatics.

He has served on technical expert panels for Medicare, patient safety, monitoring systems, and surgical care improvement projects. He also has been a part of the National Quality Forum’s Hospital Quality Measures Development Group and has served on the inpatient functionality work group of the Certifying Committee for Healthcare Information Technology.

As a founding member of SHM, Dr. Lindenauer has served on the society’s board of directors and is a member of the Hospital Quality and Patient Safety Standards Committee.

A graduate of the University of Chicago, Dr. Lindenauer received his bachelor’s in history and received his graduate degree from the Herndon School of Economics and Political Science in Health Planning and Financing. He received his medical degree from the University of Pennsylvania and completed residency training at the University of California, San Francisco.

Award for Excellence in Teaching: Anjala Tess, MD, associate program director for the Internal Medicine Residency Program and director of education for the hospital medicine program, as well as a medical unit director and practicing hospitalist at Beth Israel Deaconess Medical Center in Boston.

Dr. Tess is in charge of the quality improvement teaching program and curriculum for the entire residency program at Beth Israel Deaconess. She also helps oversee the resident elective in hospital medicine and directs educational activities for the group. Her goal is to involve residents in process improvement in the hospital by giving them a hands-on role in quality improvement and peer review.

She has received numerous awards, including the Hermann Blumgart Teaching Award at Beth Israel Deaconess and first prize in SHM’s Innovations Poster Competition.

As an undergraduate, Dr. Tess earned her degree from Brown University, in Rhode Island, and received her medical degree at Washington University’s St. Louis School of Medicine. She completed her residency at Beth Israel Deaconess. She also completed fellowships at Harvard Medical School, the Carl J. Shapiro Institute for Education Research and Beth Israel Deaconess Medical Center.

Award for Outstanding Service in Hospital Medicine: David Zipes, MD, director of pediatric hospitalist service at the Peyton Manning Children’s Hospital in Indianapolis, Ind.

Dr. Zipes oversees all hospitalists and staff, leads strategic planning for the group and the hospital, oversees the business and financial issues of the group and provides general medical direction and leadership of the pediatric units at both the Peyton Manning’s Children’s Hospital and its suburban campus.

As a founding member of SHM, Dr. Zipes is active on its Annual Meeting Planning Committee, Pediatrics Committee, and Pediatrics Core Competencies Task Force. He is also a contributing author for Pediatric Hospital Medicine and the Textbook of Pediatric Hospital Medicine, and a founding member of the annual pediatric hospital medicine meeting.

He also has been the recipient of several awards, including the Family Medicine Teacher of the Year Annual Award (2002, 2005, and 2006) and the St. Vincent Spirit of Caring Award for Service and Dedication to the Hospital (2006 and 2007.)

Dr. Zipes earned his bachelor’s and medical degrees from Indiana University. He completed his residency at Children’s Hospital Medicine Center in Cincinnati, Ohio.

Award for Team Approaches in Quality Improvement: Team Leader, Greg Maynard, MD, MSc, professor of clinical medicine and chief of the division of hospital medicine at the University of California, San Diego.

Dr. Maynard and his team (Ian Jenkins, MD, Sarah Stone, MD, Josh Lee, MD, Ed Fink, Tim Morris, MD, Peter Fedullo, MD, Robert Schoenhaus, PharmD, Doug Humber, PharmD, Marian Renvall, Pat Cal, and Isabella London) are the recipients of the first Team Approaches in Quality Improvement Award for their project “Optimizing Prevention of Hospital-Acquired Venous Thromboembolism.”

Dr. Maynard led the three-year project, which has been implemented at more than 25 sites. Using proven performance-improvement methods and a multidisciplinary team structure, Maynard and his team designed a VTE-prevention protocol for all adult inpatients at their academic center. The protocol integrated a simple VTE risk assessment with a menu of prophylaxis options preferred at each level of risk.

During three years of study, the percentage of patients with adequate VTE prophylaxis regimens increased from 55% to 98%, and the number of patients suffering from hospital-acquired VTE decreased dramatically.

SHM has presented the 2008 Awards of Excellence to four hospitalists and one quality improvement team. Their work and research have contributed significantly to hospital medicine and the betterment of patient care and quality improvement. The winners were recognized at Hospital Medicine 2008.

Award for Clinical Excellence: Kevin O’Leary, MD, associate professor of medicine and the associate chief of the Division of Hospital Medicine at Northwestern University’s Feinberg School of Medicine in Chicago.

Dr. O’Leary leads strategic initiatives for the division in his job as associate chief of the Division of Hospital Medicine, especially in patient safety and quality. He also chairs the department’s Quality Management Committee.

An active member of SHM since 2002, Dr. O’Leary has served on the Core Competencies Task Force, the Annual Meeting Planning Committee, and the Annual Meeting Precourse Planning Committee. He also is active in SHM’s Chicago chapter, where he serves as vice president. He serves as an assistant editor for the Journal of Hospital Medicine.

Dr. O’Leary received his bachelor’s inbiology and medical degree from the University of Illinois. He completed his residency at Northwestern University.

Award for Excellence in Research: Peter Lindenauer, MD, MSc, medical director of clinical and quality informatics at Baystate Health in Springfield, Mass., and associate professor of medicine at Tufts University School of Medicine in Boston.

Dr. Lindenauer is responsible for lending the development of an electronic medical record at a large integrated delivery network in western Massachusetts in his job as medical director of clinical and quality informatics.

He has served on technical expert panels for Medicare, patient safety, monitoring systems, and surgical care improvement projects. He also has been a part of the National Quality Forum’s Hospital Quality Measures Development Group and has served on the inpatient functionality work group of the Certifying Committee for Healthcare Information Technology.

As a founding member of SHM, Dr. Lindenauer has served on the society’s board of directors and is a member of the Hospital Quality and Patient Safety Standards Committee.

A graduate of the University of Chicago, Dr. Lindenauer received his bachelor’s in history and received his graduate degree from the Herndon School of Economics and Political Science in Health Planning and Financing. He received his medical degree from the University of Pennsylvania and completed residency training at the University of California, San Francisco.

Award for Excellence in Teaching: Anjala Tess, MD, associate program director for the Internal Medicine Residency Program and director of education for the hospital medicine program, as well as a medical unit director and practicing hospitalist at Beth Israel Deaconess Medical Center in Boston.

Dr. Tess is in charge of the quality improvement teaching program and curriculum for the entire residency program at Beth Israel Deaconess. She also helps oversee the resident elective in hospital medicine and directs educational activities for the group. Her goal is to involve residents in process improvement in the hospital by giving them a hands-on role in quality improvement and peer review.

She has received numerous awards, including the Hermann Blumgart Teaching Award at Beth Israel Deaconess and first prize in SHM’s Innovations Poster Competition.

As an undergraduate, Dr. Tess earned her degree from Brown University, in Rhode Island, and received her medical degree at Washington University’s St. Louis School of Medicine. She completed her residency at Beth Israel Deaconess. She also completed fellowships at Harvard Medical School, the Carl J. Shapiro Institute for Education Research and Beth Israel Deaconess Medical Center.

Award for Outstanding Service in Hospital Medicine: David Zipes, MD, director of pediatric hospitalist service at the Peyton Manning Children’s Hospital in Indianapolis, Ind.

Dr. Zipes oversees all hospitalists and staff, leads strategic planning for the group and the hospital, oversees the business and financial issues of the group and provides general medical direction and leadership of the pediatric units at both the Peyton Manning’s Children’s Hospital and its suburban campus.

As a founding member of SHM, Dr. Zipes is active on its Annual Meeting Planning Committee, Pediatrics Committee, and Pediatrics Core Competencies Task Force. He is also a contributing author for Pediatric Hospital Medicine and the Textbook of Pediatric Hospital Medicine, and a founding member of the annual pediatric hospital medicine meeting.

He also has been the recipient of several awards, including the Family Medicine Teacher of the Year Annual Award (2002, 2005, and 2006) and the St. Vincent Spirit of Caring Award for Service and Dedication to the Hospital (2006 and 2007.)

Dr. Zipes earned his bachelor’s and medical degrees from Indiana University. He completed his residency at Children’s Hospital Medicine Center in Cincinnati, Ohio.

Award for Team Approaches in Quality Improvement: Team Leader, Greg Maynard, MD, MSc, professor of clinical medicine and chief of the division of hospital medicine at the University of California, San Diego.

Dr. Maynard and his team (Ian Jenkins, MD, Sarah Stone, MD, Josh Lee, MD, Ed Fink, Tim Morris, MD, Peter Fedullo, MD, Robert Schoenhaus, PharmD, Doug Humber, PharmD, Marian Renvall, Pat Cal, and Isabella London) are the recipients of the first Team Approaches in Quality Improvement Award for their project “Optimizing Prevention of Hospital-Acquired Venous Thromboembolism.”

Dr. Maynard led the three-year project, which has been implemented at more than 25 sites. Using proven performance-improvement methods and a multidisciplinary team structure, Maynard and his team designed a VTE-prevention protocol for all adult inpatients at their academic center. The protocol integrated a simple VTE risk assessment with a menu of prophylaxis options preferred at each level of risk.

During three years of study, the percentage of patients with adequate VTE prophylaxis regimens increased from 55% to 98%, and the number of patients suffering from hospital-acquired VTE decreased dramatically.