Osteoarthritis (OA) affects nearly 27 million Americans, or about 12% of US adults.¹ As the average age of the population increases, the prevalence and burden of this debilitating disorder continue to rise.²

The American College of Rheumatology (ACR)’s guidelines for the medical management of OA of the hip and knee, last updated in 2000,³ focus on controlling pain and improving function and health-related quality of life while minimizing the toxic effects of therapy. The guidelines recommend tramadol—an atypical opioid with 2 distinct mechanisms of action⁴—for moderate-to-severe pain in OA patients who either have contraindications to COX-2 inhibitors and non steroidal anti-inflammatory drugs (NSAIDs) or have failed to respond to previous oral therapy. Patients with severe pain who don’t respond to or are unable to tolerate tramadol may be candidates for more traditional opioid therapy, the guidelines indicate.³

In recent years, however, the use (and abuse) of opioids has skyrocketed. Between 1997 and 2007, US per capita retail purchases of hydrocodone and oxycodone increased 4-fold and 9-fold, respectively.⁵ In a similar time frame (1996-2006), the number of deaths from opioid overdose more than tripled, going from 4000 to 13,800 annually.⁶ Not surprisingly, the use of narcotics for noncancer pain remains controversial.^7,8 But inadequately treated pain continues to be a serious public health problem, as well.⁹

In 2006 and 2009, respectively, the Cochrane Collaboration published systematic reviews of tramadol (for OA in any joint)¹⁰ and other oral and transdermal opioids (for OA of the hip or knee).¹¹ The reviewers’ findings, presented here along with data from more recent trials, can help ensure that you prescribe opioids for patients with OA only when their use is clinically appropriate and evidence-based. We’ve also included a case study (see page 211), so you can assess your knowledge and clinical skills.

Tramadol produces modest results—or none at all

The tramadol review¹⁰ included 11 randomized controlled trials (RCTs) with a total of 1019 participants who took tramadol or tramadol/acetaminophen (paracetamol) and 920 controls. In 6 of the 11 studies, the controls received placebo; the remaining 5 trials used “active controls,” with the control group for each RCT receiving a different analgesic. (To learn more about the methodology, see “How the reviews were conducted”.)

Placebo-controlled trials. Compared with patients on placebo, those receiving tramadol had an average absolute reduction in pain of 8.5 mm on a 0-100 mm visual analog scale (VAS) (95% confidence interval [CI], -12.05 to -4.9). That small benefit, however, did not reach the level defined as the minimal perceptible clinical improvement—a reduction of 9.7 mm on Western Ontario and McMaster Universities (WOMAC)’s OA pain subscale.¹²

Active-controlled trials. In the 5 RCTs comparing tramadol with another active agent, tramadol proved to be no better than the control drug. In fact, in a study of tramadol vs acetaminophen, 500 mg acetaminophen 3 times a day provided more pain relief than 50 mg tramadol 3 times a day.¹³ Although this was a small (N=20), short-term (7-day) study, this finding is notable because participants took less than the usual acetaminophen dose of 1 g up to 4 times a day.

Nor was tramadol superior to the agents it was compared with in the 4 other active-controlled trials—dihydrocodeine,¹⁴ dextropropoxyphene,¹⁵ pentazocine,¹⁶ and diclofenac¹⁷—in reducing pain intensity. It is important to keep in mind, however, that in each of these studies, both the quantity and quality of the evidence was limited. (Two studies did not use numerical scales,^14,16 for example; all had methodological issues; and none lasted longer than 28 days.)

A modest boost in well-being
The reviewers measured function in 2 ways, focusing on both global improvement and improvement in physical function.

Global assessment. For the global assessment, the reviewers defined a treatment response as achieving at least a moderate improvement. By that standard, tramadol may improve overall well-being more than placebo. In the placebo-controlled trials, the number needed to treat (NNT) to elicit one treatment response was 6.

Three of the trials with active controls included global/functional assessments, and the results—bearing in mind the reduced quality and quantity of the evidence—were mixed. In a comparison of tramadol with dextropropoxyphene, tramadol increased the likelihood of moderate improvement by 38% (relative risk, 1.38 (95% CI, 1.15-1.67).¹⁰ In a trial of tramadol vs pentazocine, tramadol was more effective in reducing the duration of morning stiffness (by about 10 minutes), but not its severity. Tramadol was comparable with pentazocine in the 7 other measures of OA and function.¹⁶ In the tramadol-diclofenac study, both drugs were equally effective.¹⁷

Physical function. Four of the 6 placebo-controlled tramadol studies included in the Cochrane review used the WOMAC Index score, which included the physical function subscale. The tramadol group had a larger reduction in the score than the placebo group, by 0.34 mm (95% CI, -0.49 to -0.19). While this was equivalent to an 8.5% relative reduction in mean baseline score, it is still small compared with the minimal perceptible clinical improvement level of 9.3 mm on a 0-100 scale needed for the WOMAC physical function subscale. A similar improvement was reported for those taking tramadol compared with diclofenac—the only one of the active-controlled studies to report on physical function.¹⁷

Other opioids relieve pain, improve function—but how much?

The review of oral and transdermal opioids for OA¹¹ encompassed 10 trials, with a total of 1541 patients receiving opioids and 727 on placebo. The opioids used in the trials were codeine, oxycodone, oxymorphone, morphine, and transdermal fentanyl. (For more details, see “How the reviews were conducted”.)

Pain. The trials included in the review used a variety of scales to measure pain, so the reviewers gauged results by the proportion of patients responding to treatment. Response was defined as a 50% improvement in pain score.

In the overall analysis, 35% of patients taking opioids responded to treatment, vs 31% of those on placebo—or 4 more patients in 100. That represents an NNT of 25. (A subgroup analysis did not demonstrate any significant differences in effect size among the opioids tested. In addition, the effect size was similar regardless of the potency of the opioid or the administration route.)

Function. Seven of the 10 trials (1794 participants, including both the treatment groups and controls) used validated function scores to measure physical function after 4 weeks of treatment. Here, too, the reviewers defined a treatment response as a 50% improvement in score.

Their finding? Opioids had a greater effect on function compared with placebo, equaling 0.7 on a WOMAC disability scale of 1 to 10. This means that about 3 more patients in 100 responded to treatment with opioids vs placebo—an NNT of 30.

But what about safety?

Opioids, including tramadol, are associated with adverse events (AEs), which may be minor or major. To determine when, or whether, the benefits outweigh the risks for treating patients with OA, both reviews reported on AEs and the number of participants who stopped taking the drug because of AEs.

AEs limit tramadol’s usefulness
While tramadol was more effective than placebo at reducing pain intensity, relieving symptoms, and improving function, the benefits were small—with an overall NNT of 6 (TABLE 1). This is similar to acetaminophen (NNT, 4-16),¹⁸ but with a greater downside.

Minor AEs. Four placebo-controlled trials reported on minor AEs.^19-22 Those most commonly reported by patients taking tramadol were nausea, vomiting, dizziness, constipation, somnolence, tiredness, and headache.

Overall, 39% of those who received tramadol experienced minor AEs, compared with 18% of patients receiving placebo—an NNH of 5.¹⁰ Thus, tramadol’s NNH for minor AEs is equivalent to its NNT for pain relief. In active-controlled studies, there was a higher risk of minor AEs in those receiving tramadol compared with diclofenac or dextropropoxyphene, but a lower risk compared with those taking pentazocine.¹⁰

Major AEs. An analysis of the placebo-controlled trials revealed that 21% of those who received tramadol had major AEs—defined as an event that resulted in cessation of treatment—compared with 8% of those taking placebo. By this measure, the NNH was 8: One in 8 patients stopped taking tramadol because of a major AE.¹⁰

Among the active-controlled trials, participants taking tramadol were more likely to report a major AE compared with those receiving either diclofenac or dextropropoxyphene (NNH=5), but less likely compared with patients taking pentazocine. In a trial that compared tramadol alone with paracetamol, 2 out of 10 in the tramadol group discontinued treatment; none in the paracetamol group did.¹³

TABLE 1
Tramadol and other opioids for OA pain: NNT and NNH

Post-review RCTs provide further evidence
We identified 4 double-blind RCTs of tramadol for the treatment of OA that were of at least 6 weeks’ duration,^19-22 published after the 2006 review. The results of these studies (TABLE 2) were broadly consistent with those of the systematic review. Two of the 4 studies had active controls, with one comparing tramadol with diclofenac¹⁹ and the other with celecoxib.²¹ Tramadol and diclofenac were found to be equally effective; celecoxib appeared to be superior in terms of pain relief, global improvement, and physical function, but no statistical comparisons were reported.

TABLE 2
Tramadol for OA: Post-review RCTs are consistent with meta-analysis

Oral and transdermal opioids: Pain relief but high risk
Among the patients with OA of the hip or knee—the study population for the review of oral and transdermal opioids—all the opioids tested were more effective than placebo. The benefits, however, were small to moderate, and were off set by large increases in the risk of AEs and a high dropout rate.

Four of the 10 trials reported the number of patients experiencing any AE: 23% of those taking opioids vs 15% of patients on placebo.¹¹ This represents an NNH of 12 (TABLE 1). All 10 trials reported the number of patients who withdrew due to AEs. Those receiving opioids were 4 times as likely to withdraw due to AEs, compared with those taking placebo. The NNH to cause one additional withdrawal was 19 (95% CI, 13-29).

Bottom line

The data highlight both the limited role of opioids (including tramadol) in OA treatment and—when they are being considered for this patient population—the importance of making patients aware that the risks may outweigh the benefits. Used judiciously and with adequate patient counseling, tramadol may be an option when COX-2-specific inhibitors and NSAIDs fail or cannot be tolerated. Although the small-to-moderate benefits of non-tramadol opioids are generally outweighed by large increases in the risk of AEs, their use may be considered for severe OA pain if tramadol is ineffective or causes intolerable AEs.

CORRESPONDENCE
Faline Howes, BMedSci, MBBS, MPH, FRACGP, Menzies Research Institute Tasmania, Private Bag 23, University of Tasmania, Hobart, Tasmania, Australia 7001; Faline.Howes@ utas.edu.au

Osteoarthritis (OA) affects nearly 27 million Americans, or about 12% of US adults.¹ As the average age of the population increases, the prevalence and burden of this debilitating disorder continue to rise.²

The American College of Rheumatology (ACR)’s guidelines for the medical management of OA of the hip and knee, last updated in 2000,³ focus on controlling pain and improving function and health-related quality of life while minimizing the toxic effects of therapy. The guidelines recommend tramadol—an atypical opioid with 2 distinct mechanisms of action⁴—for moderate-to-severe pain in OA patients who either have contraindications to COX-2 inhibitors and non steroidal anti-inflammatory drugs (NSAIDs) or have failed to respond to previous oral therapy. Patients with severe pain who don’t respond to or are unable to tolerate tramadol may be candidates for more traditional opioid therapy, the guidelines indicate.³

In recent years, however, the use (and abuse) of opioids has skyrocketed. Between 1997 and 2007, US per capita retail purchases of hydrocodone and oxycodone increased 4-fold and 9-fold, respectively.⁵ In a similar time frame (1996-2006), the number of deaths from opioid overdose more than tripled, going from 4000 to 13,800 annually.⁶ Not surprisingly, the use of narcotics for noncancer pain remains controversial.^7,8 But inadequately treated pain continues to be a serious public health problem, as well.⁹

In 2006 and 2009, respectively, the Cochrane Collaboration published systematic reviews of tramadol (for OA in any joint)¹⁰ and other oral and transdermal opioids (for OA of the hip or knee).¹¹ The reviewers’ findings, presented here along with data from more recent trials, can help ensure that you prescribe opioids for patients with OA only when their use is clinically appropriate and evidence-based. We’ve also included a case study (see page 211), so you can assess your knowledge and clinical skills.

Tramadol produces modest results—or none at all

The tramadol review¹⁰ included 11 randomized controlled trials (RCTs) with a total of 1019 participants who took tramadol or tramadol/acetaminophen (paracetamol) and 920 controls. In 6 of the 11 studies, the controls received placebo; the remaining 5 trials used “active controls,” with the control group for each RCT receiving a different analgesic. (To learn more about the methodology, see “How the reviews were conducted”.)

Placebo-controlled trials. Compared with patients on placebo, those receiving tramadol had an average absolute reduction in pain of 8.5 mm on a 0-100 mm visual analog scale (VAS) (95% confidence interval [CI], -12.05 to -4.9). That small benefit, however, did not reach the level defined as the minimal perceptible clinical improvement—a reduction of 9.7 mm on Western Ontario and McMaster Universities (WOMAC)’s OA pain subscale.¹²

Active-controlled trials. In the 5 RCTs comparing tramadol with another active agent, tramadol proved to be no better than the control drug. In fact, in a study of tramadol vs acetaminophen, 500 mg acetaminophen 3 times a day provided more pain relief than 50 mg tramadol 3 times a day.¹³ Although this was a small (N=20), short-term (7-day) study, this finding is notable because participants took less than the usual acetaminophen dose of 1 g up to 4 times a day.

Nor was tramadol superior to the agents it was compared with in the 4 other active-controlled trials—dihydrocodeine,¹⁴ dextropropoxyphene,¹⁵ pentazocine,¹⁶ and diclofenac¹⁷—in reducing pain intensity. It is important to keep in mind, however, that in each of these studies, both the quantity and quality of the evidence was limited. (Two studies did not use numerical scales,^14,16 for example; all had methodological issues; and none lasted longer than 28 days.)

A modest boost in well-being
The reviewers measured function in 2 ways, focusing on both global improvement and improvement in physical function.

Global assessment. For the global assessment, the reviewers defined a treatment response as achieving at least a moderate improvement. By that standard, tramadol may improve overall well-being more than placebo. In the placebo-controlled trials, the number needed to treat (NNT) to elicit one treatment response was 6.

Three of the trials with active controls included global/functional assessments, and the results—bearing in mind the reduced quality and quantity of the evidence—were mixed. In a comparison of tramadol with dextropropoxyphene, tramadol increased the likelihood of moderate improvement by 38% (relative risk, 1.38 (95% CI, 1.15-1.67).¹⁰ In a trial of tramadol vs pentazocine, tramadol was more effective in reducing the duration of morning stiffness (by about 10 minutes), but not its severity. Tramadol was comparable with pentazocine in the 7 other measures of OA and function.¹⁶ In the tramadol-diclofenac study, both drugs were equally effective.¹⁷

Physical function. Four of the 6 placebo-controlled tramadol studies included in the Cochrane review used the WOMAC Index score, which included the physical function subscale. The tramadol group had a larger reduction in the score than the placebo group, by 0.34 mm (95% CI, -0.49 to -0.19). While this was equivalent to an 8.5% relative reduction in mean baseline score, it is still small compared with the minimal perceptible clinical improvement level of 9.3 mm on a 0-100 scale needed for the WOMAC physical function subscale. A similar improvement was reported for those taking tramadol compared with diclofenac—the only one of the active-controlled studies to report on physical function.¹⁷

Other opioids relieve pain, improve function—but how much?

The review of oral and transdermal opioids for OA¹¹ encompassed 10 trials, with a total of 1541 patients receiving opioids and 727 on placebo. The opioids used in the trials were codeine, oxycodone, oxymorphone, morphine, and transdermal fentanyl. (For more details, see “How the reviews were conducted”.)

Pain. The trials included in the review used a variety of scales to measure pain, so the reviewers gauged results by the proportion of patients responding to treatment. Response was defined as a 50% improvement in pain score.

In the overall analysis, 35% of patients taking opioids responded to treatment, vs 31% of those on placebo—or 4 more patients in 100. That represents an NNT of 25. (A subgroup analysis did not demonstrate any significant differences in effect size among the opioids tested. In addition, the effect size was similar regardless of the potency of the opioid or the administration route.)

Function. Seven of the 10 trials (1794 participants, including both the treatment groups and controls) used validated function scores to measure physical function after 4 weeks of treatment. Here, too, the reviewers defined a treatment response as a 50% improvement in score.

Their finding? Opioids had a greater effect on function compared with placebo, equaling 0.7 on a WOMAC disability scale of 1 to 10. This means that about 3 more patients in 100 responded to treatment with opioids vs placebo—an NNT of 30.

But what about safety?

Opioids, including tramadol, are associated with adverse events (AEs), which may be minor or major. To determine when, or whether, the benefits outweigh the risks for treating patients with OA, both reviews reported on AEs and the number of participants who stopped taking the drug because of AEs.

AEs limit tramadol’s usefulness
While tramadol was more effective than placebo at reducing pain intensity, relieving symptoms, and improving function, the benefits were small—with an overall NNT of 6 (TABLE 1). This is similar to acetaminophen (NNT, 4-16),¹⁸ but with a greater downside.

Minor AEs. Four placebo-controlled trials reported on minor AEs.^19-22 Those most commonly reported by patients taking tramadol were nausea, vomiting, dizziness, constipation, somnolence, tiredness, and headache.

Overall, 39% of those who received tramadol experienced minor AEs, compared with 18% of patients receiving placebo—an NNH of 5.¹⁰ Thus, tramadol’s NNH for minor AEs is equivalent to its NNT for pain relief. In active-controlled studies, there was a higher risk of minor AEs in those receiving tramadol compared with diclofenac or dextropropoxyphene, but a lower risk compared with those taking pentazocine.¹⁰

Major AEs. An analysis of the placebo-controlled trials revealed that 21% of those who received tramadol had major AEs—defined as an event that resulted in cessation of treatment—compared with 8% of those taking placebo. By this measure, the NNH was 8: One in 8 patients stopped taking tramadol because of a major AE.¹⁰

Among the active-controlled trials, participants taking tramadol were more likely to report a major AE compared with those receiving either diclofenac or dextropropoxyphene (NNH=5), but less likely compared with patients taking pentazocine. In a trial that compared tramadol alone with paracetamol, 2 out of 10 in the tramadol group discontinued treatment; none in the paracetamol group did.¹³

TABLE 1
Tramadol and other opioids for OA pain: NNT and NNH

Post-review RCTs provide further evidence
We identified 4 double-blind RCTs of tramadol for the treatment of OA that were of at least 6 weeks’ duration,^19-22 published after the 2006 review. The results of these studies (TABLE 2) were broadly consistent with those of the systematic review. Two of the 4 studies had active controls, with one comparing tramadol with diclofenac¹⁹ and the other with celecoxib.²¹ Tramadol and diclofenac were found to be equally effective; celecoxib appeared to be superior in terms of pain relief, global improvement, and physical function, but no statistical comparisons were reported.

TABLE 2
Tramadol for OA: Post-review RCTs are consistent with meta-analysis

Oral and transdermal opioids: Pain relief but high risk
Among the patients with OA of the hip or knee—the study population for the review of oral and transdermal opioids—all the opioids tested were more effective than placebo. The benefits, however, were small to moderate, and were off set by large increases in the risk of AEs and a high dropout rate.

Four of the 10 trials reported the number of patients experiencing any AE: 23% of those taking opioids vs 15% of patients on placebo.¹¹ This represents an NNH of 12 (TABLE 1). All 10 trials reported the number of patients who withdrew due to AEs. Those receiving opioids were 4 times as likely to withdraw due to AEs, compared with those taking placebo. The NNH to cause one additional withdrawal was 19 (95% CI, 13-29).

Bottom line

The data highlight both the limited role of opioids (including tramadol) in OA treatment and—when they are being considered for this patient population—the importance of making patients aware that the risks may outweigh the benefits. Used judiciously and with adequate patient counseling, tramadol may be an option when COX-2-specific inhibitors and NSAIDs fail or cannot be tolerated. Although the small-to-moderate benefits of non-tramadol opioids are generally outweighed by large increases in the risk of AEs, their use may be considered for severe OA pain if tramadol is ineffective or causes intolerable AEs.

CORRESPONDENCE
Faline Howes, BMedSci, MBBS, MPH, FRACGP, Menzies Research Institute Tasmania, Private Bag 23, University of Tasmania, Hobart, Tasmania, Australia 7001; Faline.Howes@ utas.edu.au

Osteoarthritis (OA) affects nearly 27 million Americans, or about 12% of US adults.¹ As the average age of the population increases, the prevalence and burden of this debilitating disorder continue to rise.²

The American College of Rheumatology (ACR)’s guidelines for the medical management of OA of the hip and knee, last updated in 2000,³ focus on controlling pain and improving function and health-related quality of life while minimizing the toxic effects of therapy. The guidelines recommend tramadol—an atypical opioid with 2 distinct mechanisms of action⁴—for moderate-to-severe pain in OA patients who either have contraindications to COX-2 inhibitors and non steroidal anti-inflammatory drugs (NSAIDs) or have failed to respond to previous oral therapy. Patients with severe pain who don’t respond to or are unable to tolerate tramadol may be candidates for more traditional opioid therapy, the guidelines indicate.³

In recent years, however, the use (and abuse) of opioids has skyrocketed. Between 1997 and 2007, US per capita retail purchases of hydrocodone and oxycodone increased 4-fold and 9-fold, respectively.⁵ In a similar time frame (1996-2006), the number of deaths from opioid overdose more than tripled, going from 4000 to 13,800 annually.⁶ Not surprisingly, the use of narcotics for noncancer pain remains controversial.^7,8 But inadequately treated pain continues to be a serious public health problem, as well.⁹

In 2006 and 2009, respectively, the Cochrane Collaboration published systematic reviews of tramadol (for OA in any joint)¹⁰ and other oral and transdermal opioids (for OA of the hip or knee).¹¹ The reviewers’ findings, presented here along with data from more recent trials, can help ensure that you prescribe opioids for patients with OA only when their use is clinically appropriate and evidence-based. We’ve also included a case study (see page 211), so you can assess your knowledge and clinical skills.

Tramadol produces modest results—or none at all

The tramadol review¹⁰ included 11 randomized controlled trials (RCTs) with a total of 1019 participants who took tramadol or tramadol/acetaminophen (paracetamol) and 920 controls. In 6 of the 11 studies, the controls received placebo; the remaining 5 trials used “active controls,” with the control group for each RCT receiving a different analgesic. (To learn more about the methodology, see “How the reviews were conducted”.)

Placebo-controlled trials. Compared with patients on placebo, those receiving tramadol had an average absolute reduction in pain of 8.5 mm on a 0-100 mm visual analog scale (VAS) (95% confidence interval [CI], -12.05 to -4.9). That small benefit, however, did not reach the level defined as the minimal perceptible clinical improvement—a reduction of 9.7 mm on Western Ontario and McMaster Universities (WOMAC)’s OA pain subscale.¹²

Active-controlled trials. In the 5 RCTs comparing tramadol with another active agent, tramadol proved to be no better than the control drug. In fact, in a study of tramadol vs acetaminophen, 500 mg acetaminophen 3 times a day provided more pain relief than 50 mg tramadol 3 times a day.¹³ Although this was a small (N=20), short-term (7-day) study, this finding is notable because participants took less than the usual acetaminophen dose of 1 g up to 4 times a day.

Nor was tramadol superior to the agents it was compared with in the 4 other active-controlled trials—dihydrocodeine,¹⁴ dextropropoxyphene,¹⁵ pentazocine,¹⁶ and diclofenac¹⁷—in reducing pain intensity. It is important to keep in mind, however, that in each of these studies, both the quantity and quality of the evidence was limited. (Two studies did not use numerical scales,^14,16 for example; all had methodological issues; and none lasted longer than 28 days.)

A modest boost in well-being
The reviewers measured function in 2 ways, focusing on both global improvement and improvement in physical function.

Global assessment. For the global assessment, the reviewers defined a treatment response as achieving at least a moderate improvement. By that standard, tramadol may improve overall well-being more than placebo. In the placebo-controlled trials, the number needed to treat (NNT) to elicit one treatment response was 6.

Three of the trials with active controls included global/functional assessments, and the results—bearing in mind the reduced quality and quantity of the evidence—were mixed. In a comparison of tramadol with dextropropoxyphene, tramadol increased the likelihood of moderate improvement by 38% (relative risk, 1.38 (95% CI, 1.15-1.67).¹⁰ In a trial of tramadol vs pentazocine, tramadol was more effective in reducing the duration of morning stiffness (by about 10 minutes), but not its severity. Tramadol was comparable with pentazocine in the 7 other measures of OA and function.¹⁶ In the tramadol-diclofenac study, both drugs were equally effective.¹⁷

Physical function. Four of the 6 placebo-controlled tramadol studies included in the Cochrane review used the WOMAC Index score, which included the physical function subscale. The tramadol group had a larger reduction in the score than the placebo group, by 0.34 mm (95% CI, -0.49 to -0.19). While this was equivalent to an 8.5% relative reduction in mean baseline score, it is still small compared with the minimal perceptible clinical improvement level of 9.3 mm on a 0-100 scale needed for the WOMAC physical function subscale. A similar improvement was reported for those taking tramadol compared with diclofenac—the only one of the active-controlled studies to report on physical function.¹⁷

Other opioids relieve pain, improve function—but how much?

The review of oral and transdermal opioids for OA¹¹ encompassed 10 trials, with a total of 1541 patients receiving opioids and 727 on placebo. The opioids used in the trials were codeine, oxycodone, oxymorphone, morphine, and transdermal fentanyl. (For more details, see “How the reviews were conducted”.)

Pain. The trials included in the review used a variety of scales to measure pain, so the reviewers gauged results by the proportion of patients responding to treatment. Response was defined as a 50% improvement in pain score.

In the overall analysis, 35% of patients taking opioids responded to treatment, vs 31% of those on placebo—or 4 more patients in 100. That represents an NNT of 25. (A subgroup analysis did not demonstrate any significant differences in effect size among the opioids tested. In addition, the effect size was similar regardless of the potency of the opioid or the administration route.)

Function. Seven of the 10 trials (1794 participants, including both the treatment groups and controls) used validated function scores to measure physical function after 4 weeks of treatment. Here, too, the reviewers defined a treatment response as a 50% improvement in score.

Their finding? Opioids had a greater effect on function compared with placebo, equaling 0.7 on a WOMAC disability scale of 1 to 10. This means that about 3 more patients in 100 responded to treatment with opioids vs placebo—an NNT of 30.

But what about safety?

Opioids, including tramadol, are associated with adverse events (AEs), which may be minor or major. To determine when, or whether, the benefits outweigh the risks for treating patients with OA, both reviews reported on AEs and the number of participants who stopped taking the drug because of AEs.

AEs limit tramadol’s usefulness
While tramadol was more effective than placebo at reducing pain intensity, relieving symptoms, and improving function, the benefits were small—with an overall NNT of 6 (TABLE 1). This is similar to acetaminophen (NNT, 4-16),¹⁸ but with a greater downside.

Minor AEs. Four placebo-controlled trials reported on minor AEs.^19-22 Those most commonly reported by patients taking tramadol were nausea, vomiting, dizziness, constipation, somnolence, tiredness, and headache.

Overall, 39% of those who received tramadol experienced minor AEs, compared with 18% of patients receiving placebo—an NNH of 5.¹⁰ Thus, tramadol’s NNH for minor AEs is equivalent to its NNT for pain relief. In active-controlled studies, there was a higher risk of minor AEs in those receiving tramadol compared with diclofenac or dextropropoxyphene, but a lower risk compared with those taking pentazocine.¹⁰

Major AEs. An analysis of the placebo-controlled trials revealed that 21% of those who received tramadol had major AEs—defined as an event that resulted in cessation of treatment—compared with 8% of those taking placebo. By this measure, the NNH was 8: One in 8 patients stopped taking tramadol because of a major AE.¹⁰

Among the active-controlled trials, participants taking tramadol were more likely to report a major AE compared with those receiving either diclofenac or dextropropoxyphene (NNH=5), but less likely compared with patients taking pentazocine. In a trial that compared tramadol alone with paracetamol, 2 out of 10 in the tramadol group discontinued treatment; none in the paracetamol group did.¹³

TABLE 1
Tramadol and other opioids for OA pain: NNT and NNH

Post-review RCTs provide further evidence
We identified 4 double-blind RCTs of tramadol for the treatment of OA that were of at least 6 weeks’ duration,^19-22 published after the 2006 review. The results of these studies (TABLE 2) were broadly consistent with those of the systematic review. Two of the 4 studies had active controls, with one comparing tramadol with diclofenac¹⁹ and the other with celecoxib.²¹ Tramadol and diclofenac were found to be equally effective; celecoxib appeared to be superior in terms of pain relief, global improvement, and physical function, but no statistical comparisons were reported.

TABLE 2
Tramadol for OA: Post-review RCTs are consistent with meta-analysis

Oral and transdermal opioids: Pain relief but high risk
Among the patients with OA of the hip or knee—the study population for the review of oral and transdermal opioids—all the opioids tested were more effective than placebo. The benefits, however, were small to moderate, and were off set by large increases in the risk of AEs and a high dropout rate.

Four of the 10 trials reported the number of patients experiencing any AE: 23% of those taking opioids vs 15% of patients on placebo.¹¹ This represents an NNH of 12 (TABLE 1). All 10 trials reported the number of patients who withdrew due to AEs. Those receiving opioids were 4 times as likely to withdraw due to AEs, compared with those taking placebo. The NNH to cause one additional withdrawal was 19 (95% CI, 13-29).

Bottom line

The data highlight both the limited role of opioids (including tramadol) in OA treatment and—when they are being considered for this patient population—the importance of making patients aware that the risks may outweigh the benefits. Used judiciously and with adequate patient counseling, tramadol may be an option when COX-2-specific inhibitors and NSAIDs fail or cannot be tolerated. Although the small-to-moderate benefits of non-tramadol opioids are generally outweighed by large increases in the risk of AEs, their use may be considered for severe OA pain if tramadol is ineffective or causes intolerable AEs.

CORRESPONDENCE
Faline Howes, BMedSci, MBBS, MPH, FRACGP, Menzies Research Institute Tasmania, Private Bag 23, University of Tasmania, Hobart, Tasmania, Australia 7001; Faline.Howes@ utas.edu.au

A mother brings her 4-year-old son to the office because he has been limping. She isn’t aware of a specific trauma. But the boy and his twin brother, while recovering from “colds,” were rough-housing in their room when this son complained of pain. He is afebrile and points to his knee as the area of pain.

Although limping in children is common—the incidence is roughly 2 per 1000¹—it is never normal. It indicates pain, weakness, or structural abnormality.² Most cases result from trauma.¹ Limp usually resolves with little intervention and no sequelae. However, the differential diagnosis is broad and daunting (TABLE 1), and some causes of limp are associated with significant morbidity.

TABLE 1
Possible causes of limp in a child^1-3,17

Helpful tips for your initial assessment

Many textbook authors have described some causes of limp as “painless.” However, truly painless limp is rare, seldom acute, and usually the result of mechanical or neuromuscular disorders.¹ A more likely explanation for acute “painless” limp is that a young child with pain is unable to express pain or accurately identify its location. Further, the child may instinctively avoid painful positions or movements and, thus, may present only with decreased movement of an extremity or refusal to bear weight.³

With a child who has knee pain, remember the pediatrics maxim: “Knee pain equals hip pain,”³ underscoring the diagnostic difficulty with limp.

Also bear in mind that children of different ages tend to have different etiologies of limp (TABLE 2). For example, septic arthritis, osteomyelitis, and transient synovitis occur more commonly in children under 10 years. Legg-Calve-Perthes disease and leukemia are more common in children between the ages of 4 and 10. Slipped capital femoral epiphysis (SCFE) is more common in boys over the age of 11.

TABLE 2
Common causes of limp according to child’s age¹

Fracture
Fracture is a possibility across all age ranges, necessitating radiographs if suspected. Beyond detecting fractures, x-ray films can identify bony changes associated with disease (eg, Legg-Calve-Perthes disease, SCFE). Radiographs can also identify a clinically significant joint effusion at the hip.⁴ However, x-ray results may be falsely negative for some fracture types.

Salter-Harris Type I fractures are transverse fractures through the growth plate with epiphyseal separation from the metaphysis.⁵ Typical findings are a history of trauma and point tenderness over the epiphyseal plate. Type I fractures are radiographically occult, making the injury easy to mistake as a sprain. Nonetheless, growth plate injuries are common in children, requiring immobilization.

Toddler’s fracture was first described as a spiral, oblique undisplaced fracture of the distal tibial shaft in children from 9 months to 3 years of age.⁶ It results from a rotational or twisting force through the tibia while the leg rotates internally on a planted foot.^7,8 This is the most common tibial fracture in infants and young children.⁹ The incidence has been reported as 0.6 to 2.5 per 1000 pediatric visits.¹⁰ Accurate diagnosis is important because current treatment recommendations suggest a long leg cast for 3 to 5 weeks, followed by a short leg cast for a total of 6 weeks.¹¹

Despite being the most common tibial fracture, toddler’s fracture is easily missed. Initial radiographs are only 53% sensitive.^7,10 This implies that nearly 50% of children with tibial fracture will have an initially negative x-ray result. However, nearly 94% of children with a confirmed toddler’s fracture have been unable to bear weight.¹² Evidence suggests that despite negative radiographs, patients with point tenderness over the tibia and an inability to bear weight should be treated for presumed toddler’s fracture.¹²

Another confusing aspect of toddler’s fracture is that the causative injury is often considered insignificant by parents—eg, tripping, falling from a modest height, or a twisting motion.^7,8 These events may occur countless times during the average day of a toddler. Often parents do not witness the injury and are unable to describe the mechanism of injury.⁷

When to suspect child abuse. When a child presents with fracture after an unwitnessed trauma and the story does not match the injury pattern, consider child abuse. With tibial fractures, the location of the fracture can help distinguish a result of abuse from a toddler’s fracture. Toddler’s fracture is classically described as a distal tibial fracture. In contrast, a midshaft tibial fracture often suggests child abuse.^8,13 In a small retrospective study of 37 children diagnosed with toddler’s fracture, 4 midshaft tibial fractures were found.⁸ Child abuse was confirmed in 2 of these cases.⁸ However, other authors, including Dr. Dunbar in his sentinel article,⁶ assert that toddler’s fracture may occasionally extend into the midshaft of the tibia. Consequently, a midshaft tibial fracture is not pathognomonic for child abuse. But the diagnosis should be considered. Perform a careful examination for other signs of abuse or neglect, and do not hesitate to report suspected child abuse to the proper local and state authorities.¹⁴

Transient synovitis vs septic arthritis

A child who limps or refuses to bear weight on a limb often has associated symptoms of acute illness. In these cases, or when radiographs have ruled out apparent abnormalities such as Legg-Calve-Perthes disease, SCFE, and fracture, consider septic arthritis or transient synovitis (FIGURE). Both may present with limp and fever as well as pain, decreased range of motion, bone tenderness, swelling, and warmth.¹⁵

Transient synovitis is the most common cause of hip pain in children up to 10 years of age, with a 3% risk of occurrence through childhood.^16,17 Its cause is unclear, but many experts have proposed a viral agent.¹⁷ Transient synovitis universally resolves without sequelae in 1 to 2 weeks. Therefore, prescribe rest and nonsteroidal anti-inflammatory drugs (NSAIDs) for symptomatic relief, and reassure parents.¹⁶

Septic arthritis, although often similar in presentation to transient synovitis, requires hospitalization, operative drainage, and parenteral antibiotics.¹⁸ A delay in diagnosis is associated with poor outcome, including osteonecrosis, growth arrest, permanent loss of joint function, and sepsis.^3,18

Several studies have shown children with septic arthritis usually appear more acutely ill than those with transient synovitis.^4,18-21 They are described as toxic-appearing, and have leukocytosis, a high erythrocyte sedimentation rate (ESR), and a high fever.¹⁹ However, no single marker or specific laboratory value consistently identifies septic arthritis. Many studies have been performed in an effort to identify a collection of factors, or an algorithm, that can predict the probability of septic arthritis.

Fever, an elevated ESR, and leukocytosis are independent multivariate clinical predictors for septic arthritis. The prediction algorithm published by Jung et al is the only study to have included C-reactive protein (CRP) as a predictive factor,⁴ which happens to be an excellent independent predictor of septic arthritis. Specifically, with a normal CRP <1 mg/dL, the probability of a patientnot having septic arthritis is 87%.²²

While no predictive algorithm has been conclusively validated, the fact that the same clinical and laboratory predictors are consistently identified can be useful. Simply, if a patient presents with joint pain and 2 or more of the 4 predictors, septic arthritis must be fully evaluated. The presence of 2 of 4 predictors suggests a risk of septic arthritis between 10% and 40%.^4,18,20 A single predictor is associated with a risk of 1% to 10%.^4,18,20 Yet, you must interpret these clinical predictors in light of the full clinical picture, as septic arthritis is still possible in patients with only 1 predictor. Such possibilities require cautious management and close follow-up.

With 2 of 4 predictors present, suspect septic arthritis and order an ultrasound of the affected joint. If effusion is present, aspirate the joint. Some authors suggest that all patients with hip pain should undergo ultrasound, and that those with a joint effusion should undergo aspiration.¹⁵ However, joint aspiration, particularly of the hip, can be associated with multiple complications and should be avoided if possible.²² Effusion is also possible with transient synovitis and noninfectious causes of joint pain, but the aspirate will have a negative culture and normal gram stain findings. Ultrasound has been shown to be 100% accurate in predicting the presence of effusion.²³

FIGURE
Diagnostic algorithm for pediatric limp^{3,4,6,8-12,15}

How the opening case resolved
The boy avoided weight-bearing on the affected leg, but had no focal bone tenderness. Moving the hip, but not the knee, reproduced pain. Radiographs were negative for fracture or changes typical of Legg-Calve-Perthes disease. He was afebrile in the office, but the mother described a fever at home. The child appeared ill, but stable. We decided to obtain a blood sample.

Results for CRP, ESR, and white blood cell count were normal. With this information, we reassured the mother that the diagnosis was likely transient synovitis. We advised a weight-appropriate dose of ibuprofen and scheduled a follow-up appointment for 2 days later.

CORRESPONDENCE John Whiteside, MD, St. Mary’s Family Medicine Residency, 1160 Patterson Road, Grand Junction, CO 81506; [email protected]

A mother brings her 4-year-old son to the office because he has been limping. She isn’t aware of a specific trauma. But the boy and his twin brother, while recovering from “colds,” were rough-housing in their room when this son complained of pain. He is afebrile and points to his knee as the area of pain.

Although limping in children is common—the incidence is roughly 2 per 1000¹—it is never normal. It indicates pain, weakness, or structural abnormality.² Most cases result from trauma.¹ Limp usually resolves with little intervention and no sequelae. However, the differential diagnosis is broad and daunting (TABLE 1), and some causes of limp are associated with significant morbidity.

TABLE 1
Possible causes of limp in a child^1-3,17

Helpful tips for your initial assessment

Many textbook authors have described some causes of limp as “painless.” However, truly painless limp is rare, seldom acute, and usually the result of mechanical or neuromuscular disorders.¹ A more likely explanation for acute “painless” limp is that a young child with pain is unable to express pain or accurately identify its location. Further, the child may instinctively avoid painful positions or movements and, thus, may present only with decreased movement of an extremity or refusal to bear weight.³

With a child who has knee pain, remember the pediatrics maxim: “Knee pain equals hip pain,”³ underscoring the diagnostic difficulty with limp.

Also bear in mind that children of different ages tend to have different etiologies of limp (TABLE 2). For example, septic arthritis, osteomyelitis, and transient synovitis occur more commonly in children under 10 years. Legg-Calve-Perthes disease and leukemia are more common in children between the ages of 4 and 10. Slipped capital femoral epiphysis (SCFE) is more common in boys over the age of 11.

TABLE 2
Common causes of limp according to child’s age¹

Fracture
Fracture is a possibility across all age ranges, necessitating radiographs if suspected. Beyond detecting fractures, x-ray films can identify bony changes associated with disease (eg, Legg-Calve-Perthes disease, SCFE). Radiographs can also identify a clinically significant joint effusion at the hip.⁴ However, x-ray results may be falsely negative for some fracture types.

Salter-Harris Type I fractures are transverse fractures through the growth plate with epiphyseal separation from the metaphysis.⁵ Typical findings are a history of trauma and point tenderness over the epiphyseal plate. Type I fractures are radiographically occult, making the injury easy to mistake as a sprain. Nonetheless, growth plate injuries are common in children, requiring immobilization.

Toddler’s fracture was first described as a spiral, oblique undisplaced fracture of the distal tibial shaft in children from 9 months to 3 years of age.⁶ It results from a rotational or twisting force through the tibia while the leg rotates internally on a planted foot.^7,8 This is the most common tibial fracture in infants and young children.⁹ The incidence has been reported as 0.6 to 2.5 per 1000 pediatric visits.¹⁰ Accurate diagnosis is important because current treatment recommendations suggest a long leg cast for 3 to 5 weeks, followed by a short leg cast for a total of 6 weeks.¹¹

Despite being the most common tibial fracture, toddler’s fracture is easily missed. Initial radiographs are only 53% sensitive.^7,10 This implies that nearly 50% of children with tibial fracture will have an initially negative x-ray result. However, nearly 94% of children with a confirmed toddler’s fracture have been unable to bear weight.¹² Evidence suggests that despite negative radiographs, patients with point tenderness over the tibia and an inability to bear weight should be treated for presumed toddler’s fracture.¹²

Another confusing aspect of toddler’s fracture is that the causative injury is often considered insignificant by parents—eg, tripping, falling from a modest height, or a twisting motion.^7,8 These events may occur countless times during the average day of a toddler. Often parents do not witness the injury and are unable to describe the mechanism of injury.⁷

When to suspect child abuse. When a child presents with fracture after an unwitnessed trauma and the story does not match the injury pattern, consider child abuse. With tibial fractures, the location of the fracture can help distinguish a result of abuse from a toddler’s fracture. Toddler’s fracture is classically described as a distal tibial fracture. In contrast, a midshaft tibial fracture often suggests child abuse.^8,13 In a small retrospective study of 37 children diagnosed with toddler’s fracture, 4 midshaft tibial fractures were found.⁸ Child abuse was confirmed in 2 of these cases.⁸ However, other authors, including Dr. Dunbar in his sentinel article,⁶ assert that toddler’s fracture may occasionally extend into the midshaft of the tibia. Consequently, a midshaft tibial fracture is not pathognomonic for child abuse. But the diagnosis should be considered. Perform a careful examination for other signs of abuse or neglect, and do not hesitate to report suspected child abuse to the proper local and state authorities.¹⁴

Transient synovitis vs septic arthritis

A child who limps or refuses to bear weight on a limb often has associated symptoms of acute illness. In these cases, or when radiographs have ruled out apparent abnormalities such as Legg-Calve-Perthes disease, SCFE, and fracture, consider septic arthritis or transient synovitis (FIGURE). Both may present with limp and fever as well as pain, decreased range of motion, bone tenderness, swelling, and warmth.¹⁵

Transient synovitis is the most common cause of hip pain in children up to 10 years of age, with a 3% risk of occurrence through childhood.^16,17 Its cause is unclear, but many experts have proposed a viral agent.¹⁷ Transient synovitis universally resolves without sequelae in 1 to 2 weeks. Therefore, prescribe rest and nonsteroidal anti-inflammatory drugs (NSAIDs) for symptomatic relief, and reassure parents.¹⁶

Septic arthritis, although often similar in presentation to transient synovitis, requires hospitalization, operative drainage, and parenteral antibiotics.¹⁸ A delay in diagnosis is associated with poor outcome, including osteonecrosis, growth arrest, permanent loss of joint function, and sepsis.^3,18

Several studies have shown children with septic arthritis usually appear more acutely ill than those with transient synovitis.^4,18-21 They are described as toxic-appearing, and have leukocytosis, a high erythrocyte sedimentation rate (ESR), and a high fever.¹⁹ However, no single marker or specific laboratory value consistently identifies septic arthritis. Many studies have been performed in an effort to identify a collection of factors, or an algorithm, that can predict the probability of septic arthritis.

Fever, an elevated ESR, and leukocytosis are independent multivariate clinical predictors for septic arthritis. The prediction algorithm published by Jung et al is the only study to have included C-reactive protein (CRP) as a predictive factor,⁴ which happens to be an excellent independent predictor of septic arthritis. Specifically, with a normal CRP <1 mg/dL, the probability of a patientnot having septic arthritis is 87%.²²

While no predictive algorithm has been conclusively validated, the fact that the same clinical and laboratory predictors are consistently identified can be useful. Simply, if a patient presents with joint pain and 2 or more of the 4 predictors, septic arthritis must be fully evaluated. The presence of 2 of 4 predictors suggests a risk of septic arthritis between 10% and 40%.^4,18,20 A single predictor is associated with a risk of 1% to 10%.^4,18,20 Yet, you must interpret these clinical predictors in light of the full clinical picture, as septic arthritis is still possible in patients with only 1 predictor. Such possibilities require cautious management and close follow-up.

With 2 of 4 predictors present, suspect septic arthritis and order an ultrasound of the affected joint. If effusion is present, aspirate the joint. Some authors suggest that all patients with hip pain should undergo ultrasound, and that those with a joint effusion should undergo aspiration.¹⁵ However, joint aspiration, particularly of the hip, can be associated with multiple complications and should be avoided if possible.²² Effusion is also possible with transient synovitis and noninfectious causes of joint pain, but the aspirate will have a negative culture and normal gram stain findings. Ultrasound has been shown to be 100% accurate in predicting the presence of effusion.²³

FIGURE
Diagnostic algorithm for pediatric limp^{3,4,6,8-12,15}

How the opening case resolved
The boy avoided weight-bearing on the affected leg, but had no focal bone tenderness. Moving the hip, but not the knee, reproduced pain. Radiographs were negative for fracture or changes typical of Legg-Calve-Perthes disease. He was afebrile in the office, but the mother described a fever at home. The child appeared ill, but stable. We decided to obtain a blood sample.

Results for CRP, ESR, and white blood cell count were normal. With this information, we reassured the mother that the diagnosis was likely transient synovitis. We advised a weight-appropriate dose of ibuprofen and scheduled a follow-up appointment for 2 days later.

CORRESPONDENCE John Whiteside, MD, St. Mary’s Family Medicine Residency, 1160 Patterson Road, Grand Junction, CO 81506; [email protected]

A mother brings her 4-year-old son to the office because he has been limping. She isn’t aware of a specific trauma. But the boy and his twin brother, while recovering from “colds,” were rough-housing in their room when this son complained of pain. He is afebrile and points to his knee as the area of pain.

Although limping in children is common—the incidence is roughly 2 per 1000¹—it is never normal. It indicates pain, weakness, or structural abnormality.² Most cases result from trauma.¹ Limp usually resolves with little intervention and no sequelae. However, the differential diagnosis is broad and daunting (TABLE 1), and some causes of limp are associated with significant morbidity.

TABLE 1
Possible causes of limp in a child^1-3,17

Helpful tips for your initial assessment

Many textbook authors have described some causes of limp as “painless.” However, truly painless limp is rare, seldom acute, and usually the result of mechanical or neuromuscular disorders.¹ A more likely explanation for acute “painless” limp is that a young child with pain is unable to express pain or accurately identify its location. Further, the child may instinctively avoid painful positions or movements and, thus, may present only with decreased movement of an extremity or refusal to bear weight.³

With a child who has knee pain, remember the pediatrics maxim: “Knee pain equals hip pain,”³ underscoring the diagnostic difficulty with limp.

Also bear in mind that children of different ages tend to have different etiologies of limp (TABLE 2). For example, septic arthritis, osteomyelitis, and transient synovitis occur more commonly in children under 10 years. Legg-Calve-Perthes disease and leukemia are more common in children between the ages of 4 and 10. Slipped capital femoral epiphysis (SCFE) is more common in boys over the age of 11.

TABLE 2
Common causes of limp according to child’s age¹

Fracture
Fracture is a possibility across all age ranges, necessitating radiographs if suspected. Beyond detecting fractures, x-ray films can identify bony changes associated with disease (eg, Legg-Calve-Perthes disease, SCFE). Radiographs can also identify a clinically significant joint effusion at the hip.⁴ However, x-ray results may be falsely negative for some fracture types.

Salter-Harris Type I fractures are transverse fractures through the growth plate with epiphyseal separation from the metaphysis.⁵ Typical findings are a history of trauma and point tenderness over the epiphyseal plate. Type I fractures are radiographically occult, making the injury easy to mistake as a sprain. Nonetheless, growth plate injuries are common in children, requiring immobilization.

Toddler’s fracture was first described as a spiral, oblique undisplaced fracture of the distal tibial shaft in children from 9 months to 3 years of age.⁶ It results from a rotational or twisting force through the tibia while the leg rotates internally on a planted foot.^7,8 This is the most common tibial fracture in infants and young children.⁹ The incidence has been reported as 0.6 to 2.5 per 1000 pediatric visits.¹⁰ Accurate diagnosis is important because current treatment recommendations suggest a long leg cast for 3 to 5 weeks, followed by a short leg cast for a total of 6 weeks.¹¹

Despite being the most common tibial fracture, toddler’s fracture is easily missed. Initial radiographs are only 53% sensitive.^7,10 This implies that nearly 50% of children with tibial fracture will have an initially negative x-ray result. However, nearly 94% of children with a confirmed toddler’s fracture have been unable to bear weight.¹² Evidence suggests that despite negative radiographs, patients with point tenderness over the tibia and an inability to bear weight should be treated for presumed toddler’s fracture.¹²

Another confusing aspect of toddler’s fracture is that the causative injury is often considered insignificant by parents—eg, tripping, falling from a modest height, or a twisting motion.^7,8 These events may occur countless times during the average day of a toddler. Often parents do not witness the injury and are unable to describe the mechanism of injury.⁷

When to suspect child abuse. When a child presents with fracture after an unwitnessed trauma and the story does not match the injury pattern, consider child abuse. With tibial fractures, the location of the fracture can help distinguish a result of abuse from a toddler’s fracture. Toddler’s fracture is classically described as a distal tibial fracture. In contrast, a midshaft tibial fracture often suggests child abuse.^8,13 In a small retrospective study of 37 children diagnosed with toddler’s fracture, 4 midshaft tibial fractures were found.⁸ Child abuse was confirmed in 2 of these cases.⁸ However, other authors, including Dr. Dunbar in his sentinel article,⁶ assert that toddler’s fracture may occasionally extend into the midshaft of the tibia. Consequently, a midshaft tibial fracture is not pathognomonic for child abuse. But the diagnosis should be considered. Perform a careful examination for other signs of abuse or neglect, and do not hesitate to report suspected child abuse to the proper local and state authorities.¹⁴

Transient synovitis vs septic arthritis

A child who limps or refuses to bear weight on a limb often has associated symptoms of acute illness. In these cases, or when radiographs have ruled out apparent abnormalities such as Legg-Calve-Perthes disease, SCFE, and fracture, consider septic arthritis or transient synovitis (FIGURE). Both may present with limp and fever as well as pain, decreased range of motion, bone tenderness, swelling, and warmth.¹⁵

Transient synovitis is the most common cause of hip pain in children up to 10 years of age, with a 3% risk of occurrence through childhood.^16,17 Its cause is unclear, but many experts have proposed a viral agent.¹⁷ Transient synovitis universally resolves without sequelae in 1 to 2 weeks. Therefore, prescribe rest and nonsteroidal anti-inflammatory drugs (NSAIDs) for symptomatic relief, and reassure parents.¹⁶

Septic arthritis, although often similar in presentation to transient synovitis, requires hospitalization, operative drainage, and parenteral antibiotics.¹⁸ A delay in diagnosis is associated with poor outcome, including osteonecrosis, growth arrest, permanent loss of joint function, and sepsis.^3,18

Several studies have shown children with septic arthritis usually appear more acutely ill than those with transient synovitis.^4,18-21 They are described as toxic-appearing, and have leukocytosis, a high erythrocyte sedimentation rate (ESR), and a high fever.¹⁹ However, no single marker or specific laboratory value consistently identifies septic arthritis. Many studies have been performed in an effort to identify a collection of factors, or an algorithm, that can predict the probability of septic arthritis.

Fever, an elevated ESR, and leukocytosis are independent multivariate clinical predictors for septic arthritis. The prediction algorithm published by Jung et al is the only study to have included C-reactive protein (CRP) as a predictive factor,⁴ which happens to be an excellent independent predictor of septic arthritis. Specifically, with a normal CRP <1 mg/dL, the probability of a patientnot having septic arthritis is 87%.²²

While no predictive algorithm has been conclusively validated, the fact that the same clinical and laboratory predictors are consistently identified can be useful. Simply, if a patient presents with joint pain and 2 or more of the 4 predictors, septic arthritis must be fully evaluated. The presence of 2 of 4 predictors suggests a risk of septic arthritis between 10% and 40%.^4,18,20 A single predictor is associated with a risk of 1% to 10%.^4,18,20 Yet, you must interpret these clinical predictors in light of the full clinical picture, as septic arthritis is still possible in patients with only 1 predictor. Such possibilities require cautious management and close follow-up.

With 2 of 4 predictors present, suspect septic arthritis and order an ultrasound of the affected joint. If effusion is present, aspirate the joint. Some authors suggest that all patients with hip pain should undergo ultrasound, and that those with a joint effusion should undergo aspiration.¹⁵ However, joint aspiration, particularly of the hip, can be associated with multiple complications and should be avoided if possible.²² Effusion is also possible with transient synovitis and noninfectious causes of joint pain, but the aspirate will have a negative culture and normal gram stain findings. Ultrasound has been shown to be 100% accurate in predicting the presence of effusion.²³

FIGURE
Diagnostic algorithm for pediatric limp^{3,4,6,8-12,15}

How the opening case resolved
The boy avoided weight-bearing on the affected leg, but had no focal bone tenderness. Moving the hip, but not the knee, reproduced pain. Radiographs were negative for fracture or changes typical of Legg-Calve-Perthes disease. He was afebrile in the office, but the mother described a fever at home. The child appeared ill, but stable. We decided to obtain a blood sample.

Results for CRP, ESR, and white blood cell count were normal. With this information, we reassured the mother that the diagnosis was likely transient synovitis. We advised a weight-appropriate dose of ibuprofen and scheduled a follow-up appointment for 2 days later.

CORRESPONDENCE John Whiteside, MD, St. Mary’s Family Medicine Residency, 1160 Patterson Road, Grand Junction, CO 81506; [email protected]

It took 13 years before an 82-year-old patient learned what had caused the pain and tingling in his feet that he’d been living with all those years.

In 1996 he had a coronary stent insertion, and after the procedure, began taking a beta-blocker and atorvastatin. He subsequently noticed a sensory change in his toes bilaterally. This slowly progressed to paresthesia in the anterior segments of both feet on the plantar and dorsal surfaces.

A nerve conduction study (TABLE) confirmed the presence of a sensorimotor polyneuropathy, despite the fact that he did not have diabetes, or any other condition known to predispose him to polyneuropathy. The patient’s left sural peak latency and amplitude, a measure of sensory nerve action potential (SNAP), was absent. The right sural SNAP demonstrated a mild decrease of the amplitude with a normal distal latency. The left peroneal F wave response (a measure of nerve conduction velocity) was within the upper limits of normal. The left tibial F wave response was normal. The left peroneal and left tibial CMAPs (compound muscle action potentials) were normal.

A nerve biopsy was not considered for this patient because its main use is in the identification of specific lesions that are generally lacking in acquired, distal, symmetrical sensory neuropathy. (Plus, biopsy gives no more information than electrophysiological tests.)¹

TABLE
A look at the patient’s nerve conduction results

Connecting the dots years later

Neither the patient’s cardiologist, nor his general physician, was aware of any connection between statins and neuropathy, but the patient stopped taking the drug in 2003. And while the neuropathy never went away, it did subside slightly to a fairly constant level.

In August 2009, because of suboptimal levels of low-density lipoprotein (LDL), high-density lipoprotein (HDL), and C-reactive protein, his cardiologist prescribed simvastatin 5 mg daily.

On the third day, the patient experienced a marked increase of the neuropathy, which extended above his ankles. Cutaneous sensory loss became more extensive and pronounced. He stopped the statin that day, but the paresthesia did not lessen. In addition, he developed intermittent pins and needles in both hands and some instability in his gait. To date, there has been no improvement in his symptoms. Nerve conduction studies were not repeated.

Discussion: The various causes of neuropathy

In 2003, this journal published a question, “Do statins cause myopathy?”² The item concluded that if they did, the risk was very low, although isolated case reports suggested a myopathy risk for all statins, ranging from benign myalgia to fatal rhabdomyolysis.

It is now widely acknowledged that statins can cause myopathy in as many as 10% of patients taking these drugs.³

The involvement of peripheral nerves bilaterally, usually affecting distal axons of the feet and legs, is the most common form of polyneuropathy and its presentation generally excludes consideration of other forms of neuropathy, such as the mononeuropathies and neuritis. Affected nerves may be sensory, motor, or autonomic.

Symptoms include all varieties of paresthesia, sensory loss, muscle weakness, and pain. The most common cause is diabetes mellitus, which must be the first condition to be excluded. Other conditions, such as vitamin deficiencies, have also been linked with this complication.

Laboratory work-up, aside from blood glucose testing for diabetes, should include routine complete blood count and SMA-12, as well as thyroid profile and vitamin deficiency status (particularly vitamins B12 and B1).

Is a medication—perhaps a statin— to blame?
Numerous drugs are known to be associated with neuropathy.⁴ These include chemotherapy agents (cisplatin, taxoids), certain antibiotics, nucleoside analogs, dapsone, metronidazole, and certain cardiovascular drugs (amiodarone, hydralazine, statins).⁴ Recent work has indicated that simvastatin inhibits central nervous system remyelination by blocking progenitor cell differentiation.⁵ By extension, it probably inhibits progenitor cells in the peripheral nervous system.

The possibility of an association between statins and peripheral neuropathy has expanded from several case reports to a population-based study involving 465,000 subjects.⁶ More recently, a review of the literature⁷ concluded that exposure to statins may increase the risk of polyneuropathy and that statins should be considered the cause when other etiologies have been excluded. The authors suggested that the incidence of peripheral neuropathy due to statins is approximately 1 person/14,000 person-years of treatment.

An exposure, a “break,” and another exposure
The reappearance or aggravation of symptoms after cessation of statin therapy and subsequent second exposure has been described in the literature.⁸ In the case described here, the time between re-exposure and symptoms was suggestive of a T-cell-mediated hypersensitivity reaction. It has been proposed that tumor necrosis factor (TNF)-alpha released by T cells may contribute to the pathogenesis of demyelinating neuropathy.⁹

Managing this patient’s lipid levels going forward
The patient described in this report is now receiving ezetimibe 10 mg daily, which reduces the absorption of cholesterol from the diet, and niacin 2 g daily, which he can tolerate. His most recent fasting lipid panel showed the following results: cholesterol, 171 mg/dL; LDL cholesterol, calculated, 113 mg/dL; HDL cholesterol, 37 mg/dL; triglycerides, 106 mg/dL; and non-HDL cholesterol, 134 mg/dL.

Controlling the patient’s pain was another matter. Drugs commonly used for paresthesia and pain (including opiates) did not provide relief. Pregabalin (Lyrica) also had little effect. Transcutaneous electrical nerve stimulation did not perceptibly lessen his symptoms, and was also discontinued.

At the present time, this patient is not on any specific treatment for his neuropathy.

CORRESPONDENCE
Walter F. Coulson, MD, Department of Pathology, UCLA, CHS, Los Angeles, CA 90095-1732; [email protected]

It took 13 years before an 82-year-old patient learned what had caused the pain and tingling in his feet that he’d been living with all those years.

In 1996 he had a coronary stent insertion, and after the procedure, began taking a beta-blocker and atorvastatin. He subsequently noticed a sensory change in his toes bilaterally. This slowly progressed to paresthesia in the anterior segments of both feet on the plantar and dorsal surfaces.

A nerve conduction study (TABLE) confirmed the presence of a sensorimotor polyneuropathy, despite the fact that he did not have diabetes, or any other condition known to predispose him to polyneuropathy. The patient’s left sural peak latency and amplitude, a measure of sensory nerve action potential (SNAP), was absent. The right sural SNAP demonstrated a mild decrease of the amplitude with a normal distal latency. The left peroneal F wave response (a measure of nerve conduction velocity) was within the upper limits of normal. The left tibial F wave response was normal. The left peroneal and left tibial CMAPs (compound muscle action potentials) were normal.

A nerve biopsy was not considered for this patient because its main use is in the identification of specific lesions that are generally lacking in acquired, distal, symmetrical sensory neuropathy. (Plus, biopsy gives no more information than electrophysiological tests.)¹

TABLE
A look at the patient’s nerve conduction results

Connecting the dots years later

Neither the patient’s cardiologist, nor his general physician, was aware of any connection between statins and neuropathy, but the patient stopped taking the drug in 2003. And while the neuropathy never went away, it did subside slightly to a fairly constant level.

In August 2009, because of suboptimal levels of low-density lipoprotein (LDL), high-density lipoprotein (HDL), and C-reactive protein, his cardiologist prescribed simvastatin 5 mg daily.

On the third day, the patient experienced a marked increase of the neuropathy, which extended above his ankles. Cutaneous sensory loss became more extensive and pronounced. He stopped the statin that day, but the paresthesia did not lessen. In addition, he developed intermittent pins and needles in both hands and some instability in his gait. To date, there has been no improvement in his symptoms. Nerve conduction studies were not repeated.

Discussion: The various causes of neuropathy

In 2003, this journal published a question, “Do statins cause myopathy?”² The item concluded that if they did, the risk was very low, although isolated case reports suggested a myopathy risk for all statins, ranging from benign myalgia to fatal rhabdomyolysis.

It is now widely acknowledged that statins can cause myopathy in as many as 10% of patients taking these drugs.³

The involvement of peripheral nerves bilaterally, usually affecting distal axons of the feet and legs, is the most common form of polyneuropathy and its presentation generally excludes consideration of other forms of neuropathy, such as the mononeuropathies and neuritis. Affected nerves may be sensory, motor, or autonomic.

Symptoms include all varieties of paresthesia, sensory loss, muscle weakness, and pain. The most common cause is diabetes mellitus, which must be the first condition to be excluded. Other conditions, such as vitamin deficiencies, have also been linked with this complication.

Laboratory work-up, aside from blood glucose testing for diabetes, should include routine complete blood count and SMA-12, as well as thyroid profile and vitamin deficiency status (particularly vitamins B12 and B1).

Is a medication—perhaps a statin— to blame?
Numerous drugs are known to be associated with neuropathy.⁴ These include chemotherapy agents (cisplatin, taxoids), certain antibiotics, nucleoside analogs, dapsone, metronidazole, and certain cardiovascular drugs (amiodarone, hydralazine, statins).⁴ Recent work has indicated that simvastatin inhibits central nervous system remyelination by blocking progenitor cell differentiation.⁵ By extension, it probably inhibits progenitor cells in the peripheral nervous system.

The possibility of an association between statins and peripheral neuropathy has expanded from several case reports to a population-based study involving 465,000 subjects.⁶ More recently, a review of the literature⁷ concluded that exposure to statins may increase the risk of polyneuropathy and that statins should be considered the cause when other etiologies have been excluded. The authors suggested that the incidence of peripheral neuropathy due to statins is approximately 1 person/14,000 person-years of treatment.

An exposure, a “break,” and another exposure
The reappearance or aggravation of symptoms after cessation of statin therapy and subsequent second exposure has been described in the literature.⁸ In the case described here, the time between re-exposure and symptoms was suggestive of a T-cell-mediated hypersensitivity reaction. It has been proposed that tumor necrosis factor (TNF)-alpha released by T cells may contribute to the pathogenesis of demyelinating neuropathy.⁹

Managing this patient’s lipid levels going forward
The patient described in this report is now receiving ezetimibe 10 mg daily, which reduces the absorption of cholesterol from the diet, and niacin 2 g daily, which he can tolerate. His most recent fasting lipid panel showed the following results: cholesterol, 171 mg/dL; LDL cholesterol, calculated, 113 mg/dL; HDL cholesterol, 37 mg/dL; triglycerides, 106 mg/dL; and non-HDL cholesterol, 134 mg/dL.

Controlling the patient’s pain was another matter. Drugs commonly used for paresthesia and pain (including opiates) did not provide relief. Pregabalin (Lyrica) also had little effect. Transcutaneous electrical nerve stimulation did not perceptibly lessen his symptoms, and was also discontinued.

At the present time, this patient is not on any specific treatment for his neuropathy.

CORRESPONDENCE
Walter F. Coulson, MD, Department of Pathology, UCLA, CHS, Los Angeles, CA 90095-1732; [email protected]

It took 13 years before an 82-year-old patient learned what had caused the pain and tingling in his feet that he’d been living with all those years.

In 1996 he had a coronary stent insertion, and after the procedure, began taking a beta-blocker and atorvastatin. He subsequently noticed a sensory change in his toes bilaterally. This slowly progressed to paresthesia in the anterior segments of both feet on the plantar and dorsal surfaces.

A nerve conduction study (TABLE) confirmed the presence of a sensorimotor polyneuropathy, despite the fact that he did not have diabetes, or any other condition known to predispose him to polyneuropathy. The patient’s left sural peak latency and amplitude, a measure of sensory nerve action potential (SNAP), was absent. The right sural SNAP demonstrated a mild decrease of the amplitude with a normal distal latency. The left peroneal F wave response (a measure of nerve conduction velocity) was within the upper limits of normal. The left tibial F wave response was normal. The left peroneal and left tibial CMAPs (compound muscle action potentials) were normal.

A nerve biopsy was not considered for this patient because its main use is in the identification of specific lesions that are generally lacking in acquired, distal, symmetrical sensory neuropathy. (Plus, biopsy gives no more information than electrophysiological tests.)¹

TABLE
A look at the patient’s nerve conduction results

Connecting the dots years later

Neither the patient’s cardiologist, nor his general physician, was aware of any connection between statins and neuropathy, but the patient stopped taking the drug in 2003. And while the neuropathy never went away, it did subside slightly to a fairly constant level.

In August 2009, because of suboptimal levels of low-density lipoprotein (LDL), high-density lipoprotein (HDL), and C-reactive protein, his cardiologist prescribed simvastatin 5 mg daily.

On the third day, the patient experienced a marked increase of the neuropathy, which extended above his ankles. Cutaneous sensory loss became more extensive and pronounced. He stopped the statin that day, but the paresthesia did not lessen. In addition, he developed intermittent pins and needles in both hands and some instability in his gait. To date, there has been no improvement in his symptoms. Nerve conduction studies were not repeated.

Discussion: The various causes of neuropathy

In 2003, this journal published a question, “Do statins cause myopathy?”² The item concluded that if they did, the risk was very low, although isolated case reports suggested a myopathy risk for all statins, ranging from benign myalgia to fatal rhabdomyolysis.

It is now widely acknowledged that statins can cause myopathy in as many as 10% of patients taking these drugs.³

The involvement of peripheral nerves bilaterally, usually affecting distal axons of the feet and legs, is the most common form of polyneuropathy and its presentation generally excludes consideration of other forms of neuropathy, such as the mononeuropathies and neuritis. Affected nerves may be sensory, motor, or autonomic.

Symptoms include all varieties of paresthesia, sensory loss, muscle weakness, and pain. The most common cause is diabetes mellitus, which must be the first condition to be excluded. Other conditions, such as vitamin deficiencies, have also been linked with this complication.

Laboratory work-up, aside from blood glucose testing for diabetes, should include routine complete blood count and SMA-12, as well as thyroid profile and vitamin deficiency status (particularly vitamins B12 and B1).

Is a medication—perhaps a statin— to blame?
Numerous drugs are known to be associated with neuropathy.⁴ These include chemotherapy agents (cisplatin, taxoids), certain antibiotics, nucleoside analogs, dapsone, metronidazole, and certain cardiovascular drugs (amiodarone, hydralazine, statins).⁴ Recent work has indicated that simvastatin inhibits central nervous system remyelination by blocking progenitor cell differentiation.⁵ By extension, it probably inhibits progenitor cells in the peripheral nervous system.

The possibility of an association between statins and peripheral neuropathy has expanded from several case reports to a population-based study involving 465,000 subjects.⁶ More recently, a review of the literature⁷ concluded that exposure to statins may increase the risk of polyneuropathy and that statins should be considered the cause when other etiologies have been excluded. The authors suggested that the incidence of peripheral neuropathy due to statins is approximately 1 person/14,000 person-years of treatment.

An exposure, a “break,” and another exposure
The reappearance or aggravation of symptoms after cessation of statin therapy and subsequent second exposure has been described in the literature.⁸ In the case described here, the time between re-exposure and symptoms was suggestive of a T-cell-mediated hypersensitivity reaction. It has been proposed that tumor necrosis factor (TNF)-alpha released by T cells may contribute to the pathogenesis of demyelinating neuropathy.⁹

Managing this patient’s lipid levels going forward
The patient described in this report is now receiving ezetimibe 10 mg daily, which reduces the absorption of cholesterol from the diet, and niacin 2 g daily, which he can tolerate. His most recent fasting lipid panel showed the following results: cholesterol, 171 mg/dL; LDL cholesterol, calculated, 113 mg/dL; HDL cholesterol, 37 mg/dL; triglycerides, 106 mg/dL; and non-HDL cholesterol, 134 mg/dL.

Controlling the patient’s pain was another matter. Drugs commonly used for paresthesia and pain (including opiates) did not provide relief. Pregabalin (Lyrica) also had little effect. Transcutaneous electrical nerve stimulation did not perceptibly lessen his symptoms, and was also discontinued.

At the present time, this patient is not on any specific treatment for his neuropathy.

CORRESPONDENCE
Walter F. Coulson, MD, Department of Pathology, UCLA, CHS, Los Angeles, CA 90095-1732; [email protected]

www.aagl.org/obgynnews

A successful laparoscopic myomectomy begins with the correct assessment of the size, number, and location of the myomata inside the uterus. In the past, I have recommended multiple techniques for evaluation, including hysteroscopy, two-dimensional (2-D) ultrasound (transvaginal, transabdominal), 3-D ultrasound (transvaginal, transabdominal), the 2-D saline infusion sonohysterogram (2-D SIS), the 3-D SIS, and magnetic resonance imaging (MRI).

At this juncture, because of improved diagnostic acumen, I now recommend MRI or saline infusion sonography. MRI (

In my estimation, the 3-D saline infusion sonogram is superior to 2-D evaluation. The ability to render a three-dimensional image – and thus manipulate the ability to visualize the saline infusion sonogram image further – enhances fibroid mapping.

Although the saline infusion sonohysterogram is far better for evaluating uterine leiomyomata than is the hysterosalpingogram, the technique does not allow evaluation of the fallopian tubes. Recently, I helped launch Femasys Inc.'s Femvue System (

This testing does not, however, diminish the importance of physician examination prior to surgery. Through the physical exam, the minimally invasive gynecologic surgeon is able to determine how large the uterus/leiomyomata complex is, relative to the patient's size, and therefore where ports should be placed, as well as the potential difficulty of surgery. If the surgeon considers the uterus/leiomyomata complex too large, or if anemia is noted, a gonadotropin-releasing hormone (GnRH) agonist can be given for 3 months to attempt shrinkage of the leiomyomata or to enable hemoglobin to rise (through the resultant amenorrhea) prior to surgery.

Laparoscopic Myomectomy

The laparoscopic surgery is scheduled in the proliferative phase of the cycle to avoid thickened endometrium. This is especially important in the case of removal of a type II submucosal leiomyomata or one that is impinging on the endometrial cavity.

On the day of surgery, prior to the laparoscopic myomectomy and after the patient has been placed into the dorsal lithotomy position and a Foley catheter has been placed in the bladder, hysteroscopy is performed to treat any abnormalities that are seen within the endometrial cavity. This may include hysteroscopic myomectomy on a leiomyomata previously believed to be located away from the endometrial cavity.

Once hysteroscopy has been completed, a uterine manipulator must be placed inside the uterine cavity. It is imperative to utilize a manipulator that can be placed deep enough into the cavity to enable anterior/posterior and lateral uterus flexion. I consider this function to be so important for the success of laparoscopic myomectomy that a surgical assistant, standing between the patient's legs, continues to manipulate the uterus throughout the duration of the procedure.

Generally, the 5-mm laparoscope is placed initially through the umbilicus, unless periumbilical adhesions are anticipated. In this latter case, I proceed to make a left-upper-quadrant incision. Lateral ports are then placed under direct visualization. These ports must be placed above and lateral to the uterus fibroid complex (See

To minimize blood loss, a dilute solution of vasopressin (30 U of vasopressin in 100 cc of normal saline) is placed in the myoma bed via an 18-gauge spinal needle placed percutaneously through a small skin nick. (See

If the myoma is pedunculated, on a broad base, the vasopressin should not be placed into the pedicle itself, as bleeding can be excessive; rather, the vasopressin is placed in the uterus around the pedicle. It is imperative to aspirate prior to injection of vasopressin in order to prevent inadvertent intravascular injection of the vasopressin.

If possible, to reduce the risk of adhesions, make an anterior incision in the uterus and try to remove as many fibroids through the single incision as possible. For years, my instrument of choice has been the curved blade of Ethicon Endo-Surgery Inc.'s Harmonic Scalpel. Harmonic energy allows excellent cutting with minimal tissue desiccation. Moreover, the curve of the blade allows easier dissection between the myoma and myometrium. When a posterior incision is required, I use a vertical incision to decrease risk of adhesion formation near the adnexa.

If multiple fibroids are removed, I place a #1 nylon suture with a Keith needle transcutaneously into the pelvis. The numerous leiomyomata are then strung on this suture to avoid losing a myoma in the abdomen or pelvis. (See

Although suturing in the “vertical zone” (with two ports placed on the same side of the pelvis) has become a popular technique, I continue to profess cross-table suturing. When the surgeon stands cephalad to the incisions, the repair is quite comfortable to perform. Furthermore, the ports can be placed higher on the abdomen to accommodate the very large uterus, and can be positioned more widely apart to improve triangulation.

I have always recommended multiple-layer closure of the uterus to minimize hematoma formation, and have advised skimming the myometrium rather than taking deep bites of tissue in order to minimize tissue destruction. When I began to perform laparoscopic myomectomy in earnest more than 20 years ago, closure of the uterine cavity was performed with Ethicon Inc.'s nonbraided PDS II 3-0 suture placed in an interrupted or mattress style using a “knot pusher.”

Even now, when the endometrial cavity is entered at the time of myomectomy, this is the technique I currently recommend, with the interrupted or mattress sutures placed immediately above the endometrium. During the past 15 years, I have advised repairing the uterus via a running-suture technique. After multiple layers are placed, the two suture ends are tied together via an intracorporeal suture technique. This has not only proved to be more efficient, but also allows the various layers to collapse upon themselves. Ultimately, the serosa is repaired via a baseball closure (suture placed in to out, in to out, and so on). (See

In my opinion, the recent introduction of barbed sutures has served as a monumental advance in our ability to repair the uterus in multiple layers. Both Covidien's V-Loc and Angiotech Pharmaceuticals Inc.'s Quill sutures do not have to be tied. Moreover, the barbs enable consistent tension on the suture line. In order to secure the suture from slipping, the Quill uses a bidirectional barb (See

My current barbed suture of choice is the 3-0 V-Loc, which is created from 2-0 suture. When a barbed suture is used, it is imperative that the physician “hide” the suture as much as possible and thus use a baseball closure; theoretically, the barbs could catch bowel or omentum, leading to adhesion formation.

To allow for a better cosmetic repair and to minimize the risk of postoperative hernia, I recommend utilizing a larger umbilical incision for tissue extraction – I use a 12-mm umbilical port – while maintaining other ports at 5 mm. At the conclusion of the uterine repair and after placement of an antiadhesive barrier (Ethicon Inc.'s Interceed), the umbilical port is removed. Large cervical dilators are then used to stretch the umbilical incision to allow direct placement of the 15-mm morcellator. Currently, I use Karl Storz Endoscopy America Inc.'s Storz Rotocut Morcellation System. This morcellator is reusable to decrease costs, and it has a beveled tip to enhance the “apple peel” shaving of the fibroid, a very durable blade to maximize cutting ability, and variable speed to enhance the morcellation procedure.

With this laparoscopic technique, I utilize laparotomy in fewer than 1% percent of more than 200 myomectomy cases per year, of which more than 30% involve fibroids greater than 8 cm and of which nearly 20% involve five or more fibroids.

Major complication rates continue to be fewer than 1% percent, and heterologous transfusions occur in fewer than 0.5% of cases.

More than 20 years after its inception, laparoscopic myomectomy continues to be an evolving procedure – one that, especially with current advancements, should become a more common technique in the armamentarium of the minimally invasive gynecologic surgeon.

Dr. Miller disclosed that he is a consultant for Covidien and Femasys Inc., and a consultant and speaker for Ethicon Endo-Surgery Inc.

Laparoscopic Myomectomy

In this month's installment of the Master Class in Gynecologic Surgery, we are taking an interesting twist and featuring the expertise of our own medical editor, Dr. Charles E. Miller, an internationally renowned expert in minimally invasive gynecologic surgery.

When Dr. Miller inaugurated this column more than 7 years ago with a feature on “Maximizing Myomectomy” (

In his opening Master Class feature, Dr. Miller detailed the advantages of laparoscopic myomectomy and shared some pearls he acquired from a retrospective study of almost 300 laparoscopic myomectomy patients whom he had managed. He advised us on patient selection, presurgery planning, port placement, equipment, and key components of surgical technique.

At this point, laparoscopic myomectomy is a procedure that Dr. Miller has been performing for more than 20 years. And as he tells us here, it is a procedure that is still evolving and one that – even more so than in the past – should become a more common technique in the armamentarium of the minimally invasive gynecologic surgeon.

Laparoscopic myomectomy is one of Dr. Miller's key research and practice concerns. In this Master Class, he gives us a valuable update. He explains how he has honed his selection of diagnostic tools for preoperative evaluation, and details how to minimize blood loss and the risk of adhesions and hematoma formation. He also provides some suturing pearls and weighs in on the role and use of recently introduced barbed sutures.

www.aagl.org/obgynnews

A successful laparoscopic myomectomy begins with the correct assessment of the size, number, and location of the myomata inside the uterus. In the past, I have recommended multiple techniques for evaluation, including hysteroscopy, two-dimensional (2-D) ultrasound (transvaginal, transabdominal), 3-D ultrasound (transvaginal, transabdominal), the 2-D saline infusion sonohysterogram (2-D SIS), the 3-D SIS, and magnetic resonance imaging (MRI).

At this juncture, because of improved diagnostic acumen, I now recommend MRI or saline infusion sonography. MRI (

In my estimation, the 3-D saline infusion sonogram is superior to 2-D evaluation. The ability to render a three-dimensional image – and thus manipulate the ability to visualize the saline infusion sonogram image further – enhances fibroid mapping.

Although the saline infusion sonohysterogram is far better for evaluating uterine leiomyomata than is the hysterosalpingogram, the technique does not allow evaluation of the fallopian tubes. Recently, I helped launch Femasys Inc.'s Femvue System (

This testing does not, however, diminish the importance of physician examination prior to surgery. Through the physical exam, the minimally invasive gynecologic surgeon is able to determine how large the uterus/leiomyomata complex is, relative to the patient's size, and therefore where ports should be placed, as well as the potential difficulty of surgery. If the surgeon considers the uterus/leiomyomata complex too large, or if anemia is noted, a gonadotropin-releasing hormone (GnRH) agonist can be given for 3 months to attempt shrinkage of the leiomyomata or to enable hemoglobin to rise (through the resultant amenorrhea) prior to surgery.

Laparoscopic Myomectomy

The laparoscopic surgery is scheduled in the proliferative phase of the cycle to avoid thickened endometrium. This is especially important in the case of removal of a type II submucosal leiomyomata or one that is impinging on the endometrial cavity.

On the day of surgery, prior to the laparoscopic myomectomy and after the patient has been placed into the dorsal lithotomy position and a Foley catheter has been placed in the bladder, hysteroscopy is performed to treat any abnormalities that are seen within the endometrial cavity. This may include hysteroscopic myomectomy on a leiomyomata previously believed to be located away from the endometrial cavity.

Once hysteroscopy has been completed, a uterine manipulator must be placed inside the uterine cavity. It is imperative to utilize a manipulator that can be placed deep enough into the cavity to enable anterior/posterior and lateral uterus flexion. I consider this function to be so important for the success of laparoscopic myomectomy that a surgical assistant, standing between the patient's legs, continues to manipulate the uterus throughout the duration of the procedure.

Generally, the 5-mm laparoscope is placed initially through the umbilicus, unless periumbilical adhesions are anticipated. In this latter case, I proceed to make a left-upper-quadrant incision. Lateral ports are then placed under direct visualization. These ports must be placed above and lateral to the uterus fibroid complex (See

To minimize blood loss, a dilute solution of vasopressin (30 U of vasopressin in 100 cc of normal saline) is placed in the myoma bed via an 18-gauge spinal needle placed percutaneously through a small skin nick. (See

If the myoma is pedunculated, on a broad base, the vasopressin should not be placed into the pedicle itself, as bleeding can be excessive; rather, the vasopressin is placed in the uterus around the pedicle. It is imperative to aspirate prior to injection of vasopressin in order to prevent inadvertent intravascular injection of the vasopressin.

If possible, to reduce the risk of adhesions, make an anterior incision in the uterus and try to remove as many fibroids through the single incision as possible. For years, my instrument of choice has been the curved blade of Ethicon Endo-Surgery Inc.'s Harmonic Scalpel. Harmonic energy allows excellent cutting with minimal tissue desiccation. Moreover, the curve of the blade allows easier dissection between the myoma and myometrium. When a posterior incision is required, I use a vertical incision to decrease risk of adhesion formation near the adnexa.

If multiple fibroids are removed, I place a #1 nylon suture with a Keith needle transcutaneously into the pelvis. The numerous leiomyomata are then strung on this suture to avoid losing a myoma in the abdomen or pelvis. (See

Although suturing in the “vertical zone” (with two ports placed on the same side of the pelvis) has become a popular technique, I continue to profess cross-table suturing. When the surgeon stands cephalad to the incisions, the repair is quite comfortable to perform. Furthermore, the ports can be placed higher on the abdomen to accommodate the very large uterus, and can be positioned more widely apart to improve triangulation.

I have always recommended multiple-layer closure of the uterus to minimize hematoma formation, and have advised skimming the myometrium rather than taking deep bites of tissue in order to minimize tissue destruction. When I began to perform laparoscopic myomectomy in earnest more than 20 years ago, closure of the uterine cavity was performed with Ethicon Inc.'s nonbraided PDS II 3-0 suture placed in an interrupted or mattress style using a “knot pusher.”

Even now, when the endometrial cavity is entered at the time of myomectomy, this is the technique I currently recommend, with the interrupted or mattress sutures placed immediately above the endometrium. During the past 15 years, I have advised repairing the uterus via a running-suture technique. After multiple layers are placed, the two suture ends are tied together via an intracorporeal suture technique. This has not only proved to be more efficient, but also allows the various layers to collapse upon themselves. Ultimately, the serosa is repaired via a baseball closure (suture placed in to out, in to out, and so on). (See

In my opinion, the recent introduction of barbed sutures has served as a monumental advance in our ability to repair the uterus in multiple layers. Both Covidien's V-Loc and Angiotech Pharmaceuticals Inc.'s Quill sutures do not have to be tied. Moreover, the barbs enable consistent tension on the suture line. In order to secure the suture from slipping, the Quill uses a bidirectional barb (See

My current barbed suture of choice is the 3-0 V-Loc, which is created from 2-0 suture. When a barbed suture is used, it is imperative that the physician “hide” the suture as much as possible and thus use a baseball closure; theoretically, the barbs could catch bowel or omentum, leading to adhesion formation.

To allow for a better cosmetic repair and to minimize the risk of postoperative hernia, I recommend utilizing a larger umbilical incision for tissue extraction – I use a 12-mm umbilical port – while maintaining other ports at 5 mm. At the conclusion of the uterine repair and after placement of an antiadhesive barrier (Ethicon Inc.'s Interceed), the umbilical port is removed. Large cervical dilators are then used to stretch the umbilical incision to allow direct placement of the 15-mm morcellator. Currently, I use Karl Storz Endoscopy America Inc.'s Storz Rotocut Morcellation System. This morcellator is reusable to decrease costs, and it has a beveled tip to enhance the “apple peel” shaving of the fibroid, a very durable blade to maximize cutting ability, and variable speed to enhance the morcellation procedure.

With this laparoscopic technique, I utilize laparotomy in fewer than 1% percent of more than 200 myomectomy cases per year, of which more than 30% involve fibroids greater than 8 cm and of which nearly 20% involve five or more fibroids.

Major complication rates continue to be fewer than 1% percent, and heterologous transfusions occur in fewer than 0.5% of cases.

More than 20 years after its inception, laparoscopic myomectomy continues to be an evolving procedure – one that, especially with current advancements, should become a more common technique in the armamentarium of the minimally invasive gynecologic surgeon.

Dr. Miller disclosed that he is a consultant for Covidien and Femasys Inc., and a consultant and speaker for Ethicon Endo-Surgery Inc.

Laparoscopic Myomectomy

In this month's installment of the Master Class in Gynecologic Surgery, we are taking an interesting twist and featuring the expertise of our own medical editor, Dr. Charles E. Miller, an internationally renowned expert in minimally invasive gynecologic surgery.

When Dr. Miller inaugurated this column more than 7 years ago with a feature on “Maximizing Myomectomy” (

In his opening Master Class feature, Dr. Miller detailed the advantages of laparoscopic myomectomy and shared some pearls he acquired from a retrospective study of almost 300 laparoscopic myomectomy patients whom he had managed. He advised us on patient selection, presurgery planning, port placement, equipment, and key components of surgical technique.

At this point, laparoscopic myomectomy is a procedure that Dr. Miller has been performing for more than 20 years. And as he tells us here, it is a procedure that is still evolving and one that – even more so than in the past – should become a more common technique in the armamentarium of the minimally invasive gynecologic surgeon.

Laparoscopic myomectomy is one of Dr. Miller's key research and practice concerns. In this Master Class, he gives us a valuable update. He explains how he has honed his selection of diagnostic tools for preoperative evaluation, and details how to minimize blood loss and the risk of adhesions and hematoma formation. He also provides some suturing pearls and weighs in on the role and use of recently introduced barbed sutures.

www.aagl.org/obgynnews

A successful laparoscopic myomectomy begins with the correct assessment of the size, number, and location of the myomata inside the uterus. In the past, I have recommended multiple techniques for evaluation, including hysteroscopy, two-dimensional (2-D) ultrasound (transvaginal, transabdominal), 3-D ultrasound (transvaginal, transabdominal), the 2-D saline infusion sonohysterogram (2-D SIS), the 3-D SIS, and magnetic resonance imaging (MRI).

At this juncture, because of improved diagnostic acumen, I now recommend MRI or saline infusion sonography. MRI (

In my estimation, the 3-D saline infusion sonogram is superior to 2-D evaluation. The ability to render a three-dimensional image – and thus manipulate the ability to visualize the saline infusion sonogram image further – enhances fibroid mapping.

Although the saline infusion sonohysterogram is far better for evaluating uterine leiomyomata than is the hysterosalpingogram, the technique does not allow evaluation of the fallopian tubes. Recently, I helped launch Femasys Inc.'s Femvue System (

This testing does not, however, diminish the importance of physician examination prior to surgery. Through the physical exam, the minimally invasive gynecologic surgeon is able to determine how large the uterus/leiomyomata complex is, relative to the patient's size, and therefore where ports should be placed, as well as the potential difficulty of surgery. If the surgeon considers the uterus/leiomyomata complex too large, or if anemia is noted, a gonadotropin-releasing hormone (GnRH) agonist can be given for 3 months to attempt shrinkage of the leiomyomata or to enable hemoglobin to rise (through the resultant amenorrhea) prior to surgery.

Laparoscopic Myomectomy

The laparoscopic surgery is scheduled in the proliferative phase of the cycle to avoid thickened endometrium. This is especially important in the case of removal of a type II submucosal leiomyomata or one that is impinging on the endometrial cavity.

On the day of surgery, prior to the laparoscopic myomectomy and after the patient has been placed into the dorsal lithotomy position and a Foley catheter has been placed in the bladder, hysteroscopy is performed to treat any abnormalities that are seen within the endometrial cavity. This may include hysteroscopic myomectomy on a leiomyomata previously believed to be located away from the endometrial cavity.

Once hysteroscopy has been completed, a uterine manipulator must be placed inside the uterine cavity. It is imperative to utilize a manipulator that can be placed deep enough into the cavity to enable anterior/posterior and lateral uterus flexion. I consider this function to be so important for the success of laparoscopic myomectomy that a surgical assistant, standing between the patient's legs, continues to manipulate the uterus throughout the duration of the procedure.

Generally, the 5-mm laparoscope is placed initially through the umbilicus, unless periumbilical adhesions are anticipated. In this latter case, I proceed to make a left-upper-quadrant incision. Lateral ports are then placed under direct visualization. These ports must be placed above and lateral to the uterus fibroid complex (See

To minimize blood loss, a dilute solution of vasopressin (30 U of vasopressin in 100 cc of normal saline) is placed in the myoma bed via an 18-gauge spinal needle placed percutaneously through a small skin nick. (See

If the myoma is pedunculated, on a broad base, the vasopressin should not be placed into the pedicle itself, as bleeding can be excessive; rather, the vasopressin is placed in the uterus around the pedicle. It is imperative to aspirate prior to injection of vasopressin in order to prevent inadvertent intravascular injection of the vasopressin.

If possible, to reduce the risk of adhesions, make an anterior incision in the uterus and try to remove as many fibroids through the single incision as possible. For years, my instrument of choice has been the curved blade of Ethicon Endo-Surgery Inc.'s Harmonic Scalpel. Harmonic energy allows excellent cutting with minimal tissue desiccation. Moreover, the curve of the blade allows easier dissection between the myoma and myometrium. When a posterior incision is required, I use a vertical incision to decrease risk of adhesion formation near the adnexa.

If multiple fibroids are removed, I place a #1 nylon suture with a Keith needle transcutaneously into the pelvis. The numerous leiomyomata are then strung on this suture to avoid losing a myoma in the abdomen or pelvis. (See

Although suturing in the “vertical zone” (with two ports placed on the same side of the pelvis) has become a popular technique, I continue to profess cross-table suturing. When the surgeon stands cephalad to the incisions, the repair is quite comfortable to perform. Furthermore, the ports can be placed higher on the abdomen to accommodate the very large uterus, and can be positioned more widely apart to improve triangulation.

I have always recommended multiple-layer closure of the uterus to minimize hematoma formation, and have advised skimming the myometrium rather than taking deep bites of tissue in order to minimize tissue destruction. When I began to perform laparoscopic myomectomy in earnest more than 20 years ago, closure of the uterine cavity was performed with Ethicon Inc.'s nonbraided PDS II 3-0 suture placed in an interrupted or mattress style using a “knot pusher.”

Even now, when the endometrial cavity is entered at the time of myomectomy, this is the technique I currently recommend, with the interrupted or mattress sutures placed immediately above the endometrium. During the past 15 years, I have advised repairing the uterus via a running-suture technique. After multiple layers are placed, the two suture ends are tied together via an intracorporeal suture technique. This has not only proved to be more efficient, but also allows the various layers to collapse upon themselves. Ultimately, the serosa is repaired via a baseball closure (suture placed in to out, in to out, and so on). (See

In my opinion, the recent introduction of barbed sutures has served as a monumental advance in our ability to repair the uterus in multiple layers. Both Covidien's V-Loc and Angiotech Pharmaceuticals Inc.'s Quill sutures do not have to be tied. Moreover, the barbs enable consistent tension on the suture line. In order to secure the suture from slipping, the Quill uses a bidirectional barb (See

My current barbed suture of choice is the 3-0 V-Loc, which is created from 2-0 suture. When a barbed suture is used, it is imperative that the physician “hide” the suture as much as possible and thus use a baseball closure; theoretically, the barbs could catch bowel or omentum, leading to adhesion formation.

To allow for a better cosmetic repair and to minimize the risk of postoperative hernia, I recommend utilizing a larger umbilical incision for tissue extraction – I use a 12-mm umbilical port – while maintaining other ports at 5 mm. At the conclusion of the uterine repair and after placement of an antiadhesive barrier (Ethicon Inc.'s Interceed), the umbilical port is removed. Large cervical dilators are then used to stretch the umbilical incision to allow direct placement of the 15-mm morcellator. Currently, I use Karl Storz Endoscopy America Inc.'s Storz Rotocut Morcellation System. This morcellator is reusable to decrease costs, and it has a beveled tip to enhance the “apple peel” shaving of the fibroid, a very durable blade to maximize cutting ability, and variable speed to enhance the morcellation procedure.

With this laparoscopic technique, I utilize laparotomy in fewer than 1% percent of more than 200 myomectomy cases per year, of which more than 30% involve fibroids greater than 8 cm and of which nearly 20% involve five or more fibroids.

Major complication rates continue to be fewer than 1% percent, and heterologous transfusions occur in fewer than 0.5% of cases.

More than 20 years after its inception, laparoscopic myomectomy continues to be an evolving procedure – one that, especially with current advancements, should become a more common technique in the armamentarium of the minimally invasive gynecologic surgeon.

Dr. Miller disclosed that he is a consultant for Covidien and Femasys Inc., and a consultant and speaker for Ethicon Endo-Surgery Inc.

Laparoscopic Myomectomy

In this month's installment of the Master Class in Gynecologic Surgery, we are taking an interesting twist and featuring the expertise of our own medical editor, Dr. Charles E. Miller, an internationally renowned expert in minimally invasive gynecologic surgery.

When Dr. Miller inaugurated this column more than 7 years ago with a feature on “Maximizing Myomectomy” (

In his opening Master Class feature, Dr. Miller detailed the advantages of laparoscopic myomectomy and shared some pearls he acquired from a retrospective study of almost 300 laparoscopic myomectomy patients whom he had managed. He advised us on patient selection, presurgery planning, port placement, equipment, and key components of surgical technique.

At this point, laparoscopic myomectomy is a procedure that Dr. Miller has been performing for more than 20 years. And as he tells us here, it is a procedure that is still evolving and one that – even more so than in the past – should become a more common technique in the armamentarium of the minimally invasive gynecologic surgeon.

Laparoscopic myomectomy is one of Dr. Miller's key research and practice concerns. In this Master Class, he gives us a valuable update. He explains how he has honed his selection of diagnostic tools for preoperative evaluation, and details how to minimize blood loss and the risk of adhesions and hematoma formation. He also provides some suturing pearls and weighs in on the role and use of recently introduced barbed sutures.

Thirty years ago, the Graduate Medical Education National Advisory Committee predicted a surplus of 145,000 physicians, including cardiologists, by the year 2000, and recommended a limitation of the number of entering positions in U.S. medical schools and the number of international graduates coming to the United States.

Although there was no restriction placed on international graduates coming to the United States, the number of positions available for students to enter U.S. medical schools has remained static until the last 2 years. This obstruction to medical school entry led many students to seek education at offshore medical schools (OMS), particularly in the Caribbean.

The flawed predictions of a surplus of doctors were made in anticipation of an expanded role of health maintenance organizations as gatekeepers for access to both family and specialty doctors. GMENAC also failed to foresee the expansion of the elderly population as a result of the baby boomer generation and the increased availability of new diagnostic and therapeutic technologies.

It is now estimated that by 2020 or 2025 there will be a shortage of almost 200,000 doctors in the United States (J. Gen. Intern. Med. 2007;22:264–8). U.S. medical schools are now projected to graduate 16,000 doctors annually, and that number is expected to increase by 30% in 2015, unless the proposed restrictions to education budgets by Congress come into place. However, this increase will continue to fall short of national requirements if physician retirement is factored into the estimates.

I recently had an opportunity to visit one of the Caribbean medical schools and to observe the students in the classroom. I also learned a great deal about the role that the OMS play in mitigating the doctor shortage in the United States. The students in these schools are clearly different from those who attend American medical schools. They are distinguished, not exclusively by their MCAT scores, as though that really matters, but also by being very motivated to become doctors. Many had been out of undergraduate programs for sometime – some as long 15 years – and had tested other careers and come to the realization that medicine is what they really wanted.

Most of these students will spend 2 years in the Caribbean and then move to clinical training in hospitals throughout the United States, ultimately entering residency programs and practice in mainland America.

One of the first hurdles that the OMS students will face is passing the United States Medical Licensing Examination taken by both U.S. and International Medical Graduates (IMGs). Measured against U.S. medical school graduates, who have a first-time passing rate of about 95%, they unfortunately fall short: The rate for non-U.S. IMGs is 73%, and that for American IMGs is lower still, at 60% (Health Aff. 2009;28:1226–33).

Upon the completion of their training, although they may go into subspecialties as do U.S. students, more of the Caribbean students enter family practice, a fact that has not been lost on health planners.

There have been some recent attempts to limit the number of training slots available for OMS students in New York City hospitals because of the presumed lack of total residency positions.

However, the state legislators, aware of current needs, have been reluctant to erect any barriers for physicians interested in family practice.

Currently there are 40 OMS in the Caribbean basin including Mexico, 24 of which were started in the last 10 years, which graduate more than 4,000 students annually in three classes, which vary in size between 60 and 600 students. Tuition is similar to that of U.S. schools and ranges from &dollar;47,500 to &dollar;186,085 for the 4 years. U.S. medical schools must be accredited by the Liaison Committee on Medical Education, but there is no accreditation process for OMS.

The LCME is now partnering with the Caribbean Accreditation Authority for Education in Medicine and Other Health Professions to establish similar accreditation processes. Federally supported scholarships are available to U.S. citizens in the OMS just as they are for students enrolled in U.S. schools. As a result of the high tuition and relatively low overhead, some of these schools have been targets for venture capitalists.

Of the 800,000 actively practicing doctors in the United States, 23.7% are IMGs, a percentage that is sure to increase. Approximately 60% of the IMGs are from the offshore medical schools.

It is clear that the United States has become increasingly dependent on OMS to meet our doctor supply. It is also clear that a vigorous attempt to improve the certification process for OMS would go a long way to ensure the quality of our future doctors.

Thirty years ago, the Graduate Medical Education National Advisory Committee predicted a surplus of 145,000 physicians, including cardiologists, by the year 2000, and recommended a limitation of the number of entering positions in U.S. medical schools and the number of international graduates coming to the United States.

Although there was no restriction placed on international graduates coming to the United States, the number of positions available for students to enter U.S. medical schools has remained static until the last 2 years. This obstruction to medical school entry led many students to seek education at offshore medical schools (OMS), particularly in the Caribbean.

The flawed predictions of a surplus of doctors were made in anticipation of an expanded role of health maintenance organizations as gatekeepers for access to both family and specialty doctors. GMENAC also failed to foresee the expansion of the elderly population as a result of the baby boomer generation and the increased availability of new diagnostic and therapeutic technologies.

It is now estimated that by 2020 or 2025 there will be a shortage of almost 200,000 doctors in the United States (J. Gen. Intern. Med. 2007;22:264–8). U.S. medical schools are now projected to graduate 16,000 doctors annually, and that number is expected to increase by 30% in 2015, unless the proposed restrictions to education budgets by Congress come into place. However, this increase will continue to fall short of national requirements if physician retirement is factored into the estimates.

I recently had an opportunity to visit one of the Caribbean medical schools and to observe the students in the classroom. I also learned a great deal about the role that the OMS play in mitigating the doctor shortage in the United States. The students in these schools are clearly different from those who attend American medical schools. They are distinguished, not exclusively by their MCAT scores, as though that really matters, but also by being very motivated to become doctors. Many had been out of undergraduate programs for sometime – some as long 15 years – and had tested other careers and come to the realization that medicine is what they really wanted.

Most of these students will spend 2 years in the Caribbean and then move to clinical training in hospitals throughout the United States, ultimately entering residency programs and practice in mainland America.

One of the first hurdles that the OMS students will face is passing the United States Medical Licensing Examination taken by both U.S. and International Medical Graduates (IMGs). Measured against U.S. medical school graduates, who have a first-time passing rate of about 95%, they unfortunately fall short: The rate for non-U.S. IMGs is 73%, and that for American IMGs is lower still, at 60% (Health Aff. 2009;28:1226–33).

Upon the completion of their training, although they may go into subspecialties as do U.S. students, more of the Caribbean students enter family practice, a fact that has not been lost on health planners.

There have been some recent attempts to limit the number of training slots available for OMS students in New York City hospitals because of the presumed lack of total residency positions.

However, the state legislators, aware of current needs, have been reluctant to erect any barriers for physicians interested in family practice.

Currently there are 40 OMS in the Caribbean basin including Mexico, 24 of which were started in the last 10 years, which graduate more than 4,000 students annually in three classes, which vary in size between 60 and 600 students. Tuition is similar to that of U.S. schools and ranges from &dollar;47,500 to &dollar;186,085 for the 4 years. U.S. medical schools must be accredited by the Liaison Committee on Medical Education, but there is no accreditation process for OMS.

The LCME is now partnering with the Caribbean Accreditation Authority for Education in Medicine and Other Health Professions to establish similar accreditation processes. Federally supported scholarships are available to U.S. citizens in the OMS just as they are for students enrolled in U.S. schools. As a result of the high tuition and relatively low overhead, some of these schools have been targets for venture capitalists.

Of the 800,000 actively practicing doctors in the United States, 23.7% are IMGs, a percentage that is sure to increase. Approximately 60% of the IMGs are from the offshore medical schools.

It is clear that the United States has become increasingly dependent on OMS to meet our doctor supply. It is also clear that a vigorous attempt to improve the certification process for OMS would go a long way to ensure the quality of our future doctors.

Thirty years ago, the Graduate Medical Education National Advisory Committee predicted a surplus of 145,000 physicians, including cardiologists, by the year 2000, and recommended a limitation of the number of entering positions in U.S. medical schools and the number of international graduates coming to the United States.

Although there was no restriction placed on international graduates coming to the United States, the number of positions available for students to enter U.S. medical schools has remained static until the last 2 years. This obstruction to medical school entry led many students to seek education at offshore medical schools (OMS), particularly in the Caribbean.

The flawed predictions of a surplus of doctors were made in anticipation of an expanded role of health maintenance organizations as gatekeepers for access to both family and specialty doctors. GMENAC also failed to foresee the expansion of the elderly population as a result of the baby boomer generation and the increased availability of new diagnostic and therapeutic technologies.

It is now estimated that by 2020 or 2025 there will be a shortage of almost 200,000 doctors in the United States (J. Gen. Intern. Med. 2007;22:264–8). U.S. medical schools are now projected to graduate 16,000 doctors annually, and that number is expected to increase by 30% in 2015, unless the proposed restrictions to education budgets by Congress come into place. However, this increase will continue to fall short of national requirements if physician retirement is factored into the estimates.

I recently had an opportunity to visit one of the Caribbean medical schools and to observe the students in the classroom. I also learned a great deal about the role that the OMS play in mitigating the doctor shortage in the United States. The students in these schools are clearly different from those who attend American medical schools. They are distinguished, not exclusively by their MCAT scores, as though that really matters, but also by being very motivated to become doctors. Many had been out of undergraduate programs for sometime – some as long 15 years – and had tested other careers and come to the realization that medicine is what they really wanted.

Most of these students will spend 2 years in the Caribbean and then move to clinical training in hospitals throughout the United States, ultimately entering residency programs and practice in mainland America.

One of the first hurdles that the OMS students will face is passing the United States Medical Licensing Examination taken by both U.S. and International Medical Graduates (IMGs). Measured against U.S. medical school graduates, who have a first-time passing rate of about 95%, they unfortunately fall short: The rate for non-U.S. IMGs is 73%, and that for American IMGs is lower still, at 60% (Health Aff. 2009;28:1226–33).

Upon the completion of their training, although they may go into subspecialties as do U.S. students, more of the Caribbean students enter family practice, a fact that has not been lost on health planners.

There have been some recent attempts to limit the number of training slots available for OMS students in New York City hospitals because of the presumed lack of total residency positions.

However, the state legislators, aware of current needs, have been reluctant to erect any barriers for physicians interested in family practice.

Currently there are 40 OMS in the Caribbean basin including Mexico, 24 of which were started in the last 10 years, which graduate more than 4,000 students annually in three classes, which vary in size between 60 and 600 students. Tuition is similar to that of U.S. schools and ranges from &dollar;47,500 to &dollar;186,085 for the 4 years. U.S. medical schools must be accredited by the Liaison Committee on Medical Education, but there is no accreditation process for OMS.

The LCME is now partnering with the Caribbean Accreditation Authority for Education in Medicine and Other Health Professions to establish similar accreditation processes. Federally supported scholarships are available to U.S. citizens in the OMS just as they are for students enrolled in U.S. schools. As a result of the high tuition and relatively low overhead, some of these schools have been targets for venture capitalists.

Of the 800,000 actively practicing doctors in the United States, 23.7% are IMGs, a percentage that is sure to increase. Approximately 60% of the IMGs are from the offshore medical schools.

It is clear that the United States has become increasingly dependent on OMS to meet our doctor supply. It is also clear that a vigorous attempt to improve the certification process for OMS would go a long way to ensure the quality of our future doctors.

Overuse injuries are very common in children and teenagers, especially among kids who play sports throughout the year.

A high volume of sports puts your patients at higher risk for an overuse injury. Ask which sports they play, how often they play them, and how many teams they play for when taking the patient history. It is more and more common now that kids play on multiple teams at the same time or that sports seasons overlap. Here in the South, for example, baseball can start in January or February, while basketball – a winter sport – is still going on.

Year-round participation in multiple sports has an advantage as well – it becomes a form of built-in cross training. Your patients will be using the same muscles but developing them in different ways.

Encourage your athletic patients to play different sports and discourage “early specialization.” You can counsel patients regularly about sports diversification – during well-child visits and school or sports physical examinations. Patients who play football or soccer in the fall; basketball or wrestling in the winter; and then softball or lacrosse in the spring generally are at a lower risk for overuse injuries.

In contrast, specialization in the same sport throughout the year increases the risk for overuse injuries as well as “burnout.” For example, a child who starts at age 7 or 8 years and plays the same sport for years might find participation becomes less fun by age 13 or 14 years. In some cases, parents get enthusiastic, pay for private lessons to extend the “season” to 12 months, and the kids just never have a time to rest.

For some families, it seems like success of the team or success on the playing field becomes more important than the health of the child. You can face a dilemma if you recommend rest for a child about to play a big game or tournament. The best way I found around that is to spend sufficient time to explain why you are making your recommendations. If you just say, “His knee hurts, and he shouldn't play,” the patient and parents are less likely to be compliant.

We give advice. We rarely forbid a kid from playing. But you can explain what could happen if they don't follow recommendations. You might say something like, “Here is what I think you have, here is what I think you should do, and here's why. If you don't, the risk of making this a stress fracture is higher.” You can also explain that a nonsurgical elbow injury could become surgical if you continue to throw, play, or tumble.

Pediatricians can manage most overuse injuries. Watch for signs that can warrant referral, however, such as a swollen joint, limitation of joint movement, or symptoms of trauma/acute injury. Consider consulting a subspecialist when the child cannot completely bend or extend the elbow, for example. These findings suggest something worse than just overuse.

In general, the best way to treat an overuse injury is to underuse the affected area. Apply the PRICEMM techniques (protection, rest, ice, compression, elevation, medication, and [physical therapy] modalities) for 2 or 3 days. If there is no improvement, expand your differential diagnosis. Overuse injuries should improve quickly if patients start underusing the affected area in addition to modifying their workouts and using ice and anti-inflammatory medications.

Recommend the patient back off after you identify the likely source of pain. If a baseball player presents with elbow pain, for example, he might improve by pitching less or switching from shortstop to first base. Rarely do children need to stop playing altogether. Modification of the workout a little bit might be all it takes to give the body a chance to adapt. You could recommend a child play only part of the soccer game or avoid particular conditioning drills during practice, for example.

An overuse injury is defined as repetitive, submaximal stress applied to a tissue that occurs when the adaptive capability of the tissue is exceeded and injury results. A blister is a perfect example. If you put on a new shoe that starts rubbing your foot too much, eventually the skin breaks down. But if you wear the new shoes for a little bit, then switch to sandals, then boots, and finally put your new shoes back on, you slowly introduce those stresses. This way, the body has a chance to adapt, the skin will become callused, and you won't develop a blister.

Acute trauma is another reason to consider referring the child to a sports medicine specialist. If a child comes to you with instant pain from a jump off the monkey bars or a slide into home, she should be referred to rule out something more serious, such as a fracture or a cartilage or a ligament tear.

Another time to refer is anytime you feel uncomfortable. If you sense something isn't right, you will never be faulted for referring the patient to a specialist. So, when in doubt, go ahead and refer.

Typically, a good history and physical examination will be sufficient, with or without x-rays, for a pediatrician to determine the best recommendations for the patient.

Although x-rays are a necessity for evaluation of most orthopedic or sports injuries, it is preferable to refer the child and have the subspecialist order imaging tests. This avoids duplication of radiation exposure for the child and the unnecessary time and expense of repeated x-rays. In addition, laboratory assays typically do not help in the evaluation of a suspected overuse injury, unless you suspect a comorbid condition such as arthritis or joint infection.

Overuse injuries are very common in children and teenagers, especially among kids who play sports throughout the year.

A high volume of sports puts your patients at higher risk for an overuse injury. Ask which sports they play, how often they play them, and how many teams they play for when taking the patient history. It is more and more common now that kids play on multiple teams at the same time or that sports seasons overlap. Here in the South, for example, baseball can start in January or February, while basketball – a winter sport – is still going on.

Year-round participation in multiple sports has an advantage as well – it becomes a form of built-in cross training. Your patients will be using the same muscles but developing them in different ways.

Encourage your athletic patients to play different sports and discourage “early specialization.” You can counsel patients regularly about sports diversification – during well-child visits and school or sports physical examinations. Patients who play football or soccer in the fall; basketball or wrestling in the winter; and then softball or lacrosse in the spring generally are at a lower risk for overuse injuries.

In contrast, specialization in the same sport throughout the year increases the risk for overuse injuries as well as “burnout.” For example, a child who starts at age 7 or 8 years and plays the same sport for years might find participation becomes less fun by age 13 or 14 years. In some cases, parents get enthusiastic, pay for private lessons to extend the “season” to 12 months, and the kids just never have a time to rest.

For some families, it seems like success of the team or success on the playing field becomes more important than the health of the child. You can face a dilemma if you recommend rest for a child about to play a big game or tournament. The best way I found around that is to spend sufficient time to explain why you are making your recommendations. If you just say, “His knee hurts, and he shouldn't play,” the patient and parents are less likely to be compliant.

We give advice. We rarely forbid a kid from playing. But you can explain what could happen if they don't follow recommendations. You might say something like, “Here is what I think you have, here is what I think you should do, and here's why. If you don't, the risk of making this a stress fracture is higher.” You can also explain that a nonsurgical elbow injury could become surgical if you continue to throw, play, or tumble.

Pediatricians can manage most overuse injuries. Watch for signs that can warrant referral, however, such as a swollen joint, limitation of joint movement, or symptoms of trauma/acute injury. Consider consulting a subspecialist when the child cannot completely bend or extend the elbow, for example. These findings suggest something worse than just overuse.

In general, the best way to treat an overuse injury is to underuse the affected area. Apply the PRICEMM techniques (protection, rest, ice, compression, elevation, medication, and [physical therapy] modalities) for 2 or 3 days. If there is no improvement, expand your differential diagnosis. Overuse injuries should improve quickly if patients start underusing the affected area in addition to modifying their workouts and using ice and anti-inflammatory medications.

Recommend the patient back off after you identify the likely source of pain. If a baseball player presents with elbow pain, for example, he might improve by pitching less or switching from shortstop to first base. Rarely do children need to stop playing altogether. Modification of the workout a little bit might be all it takes to give the body a chance to adapt. You could recommend a child play only part of the soccer game or avoid particular conditioning drills during practice, for example.

An overuse injury is defined as repetitive, submaximal stress applied to a tissue that occurs when the adaptive capability of the tissue is exceeded and injury results. A blister is a perfect example. If you put on a new shoe that starts rubbing your foot too much, eventually the skin breaks down. But if you wear the new shoes for a little bit, then switch to sandals, then boots, and finally put your new shoes back on, you slowly introduce those stresses. This way, the body has a chance to adapt, the skin will become callused, and you won't develop a blister.

Acute trauma is another reason to consider referring the child to a sports medicine specialist. If a child comes to you with instant pain from a jump off the monkey bars or a slide into home, she should be referred to rule out something more serious, such as a fracture or a cartilage or a ligament tear.

Another time to refer is anytime you feel uncomfortable. If you sense something isn't right, you will never be faulted for referring the patient to a specialist. So, when in doubt, go ahead and refer.

Typically, a good history and physical examination will be sufficient, with or without x-rays, for a pediatrician to determine the best recommendations for the patient.

Although x-rays are a necessity for evaluation of most orthopedic or sports injuries, it is preferable to refer the child and have the subspecialist order imaging tests. This avoids duplication of radiation exposure for the child and the unnecessary time and expense of repeated x-rays. In addition, laboratory assays typically do not help in the evaluation of a suspected overuse injury, unless you suspect a comorbid condition such as arthritis or joint infection.

Overuse injuries are very common in children and teenagers, especially among kids who play sports throughout the year.

A high volume of sports puts your patients at higher risk for an overuse injury. Ask which sports they play, how often they play them, and how many teams they play for when taking the patient history. It is more and more common now that kids play on multiple teams at the same time or that sports seasons overlap. Here in the South, for example, baseball can start in January or February, while basketball – a winter sport – is still going on.

Year-round participation in multiple sports has an advantage as well – it becomes a form of built-in cross training. Your patients will be using the same muscles but developing them in different ways.

Encourage your athletic patients to play different sports and discourage “early specialization.” You can counsel patients regularly about sports diversification – during well-child visits and school or sports physical examinations. Patients who play football or soccer in the fall; basketball or wrestling in the winter; and then softball or lacrosse in the spring generally are at a lower risk for overuse injuries.

In contrast, specialization in the same sport throughout the year increases the risk for overuse injuries as well as “burnout.” For example, a child who starts at age 7 or 8 years and plays the same sport for years might find participation becomes less fun by age 13 or 14 years. In some cases, parents get enthusiastic, pay for private lessons to extend the “season” to 12 months, and the kids just never have a time to rest.

For some families, it seems like success of the team or success on the playing field becomes more important than the health of the child. You can face a dilemma if you recommend rest for a child about to play a big game or tournament. The best way I found around that is to spend sufficient time to explain why you are making your recommendations. If you just say, “His knee hurts, and he shouldn't play,” the patient and parents are less likely to be compliant.

We give advice. We rarely forbid a kid from playing. But you can explain what could happen if they don't follow recommendations. You might say something like, “Here is what I think you have, here is what I think you should do, and here's why. If you don't, the risk of making this a stress fracture is higher.” You can also explain that a nonsurgical elbow injury could become surgical if you continue to throw, play, or tumble.

Pediatricians can manage most overuse injuries. Watch for signs that can warrant referral, however, such as a swollen joint, limitation of joint movement, or symptoms of trauma/acute injury. Consider consulting a subspecialist when the child cannot completely bend or extend the elbow, for example. These findings suggest something worse than just overuse.

In general, the best way to treat an overuse injury is to underuse the affected area. Apply the PRICEMM techniques (protection, rest, ice, compression, elevation, medication, and [physical therapy] modalities) for 2 or 3 days. If there is no improvement, expand your differential diagnosis. Overuse injuries should improve quickly if patients start underusing the affected area in addition to modifying their workouts and using ice and anti-inflammatory medications.

Recommend the patient back off after you identify the likely source of pain. If a baseball player presents with elbow pain, for example, he might improve by pitching less or switching from shortstop to first base. Rarely do children need to stop playing altogether. Modification of the workout a little bit might be all it takes to give the body a chance to adapt. You could recommend a child play only part of the soccer game or avoid particular conditioning drills during practice, for example.

An overuse injury is defined as repetitive, submaximal stress applied to a tissue that occurs when the adaptive capability of the tissue is exceeded and injury results. A blister is a perfect example. If you put on a new shoe that starts rubbing your foot too much, eventually the skin breaks down. But if you wear the new shoes for a little bit, then switch to sandals, then boots, and finally put your new shoes back on, you slowly introduce those stresses. This way, the body has a chance to adapt, the skin will become callused, and you won't develop a blister.

Acute trauma is another reason to consider referring the child to a sports medicine specialist. If a child comes to you with instant pain from a jump off the monkey bars or a slide into home, she should be referred to rule out something more serious, such as a fracture or a cartilage or a ligament tear.

Another time to refer is anytime you feel uncomfortable. If you sense something isn't right, you will never be faulted for referring the patient to a specialist. So, when in doubt, go ahead and refer.

Typically, a good history and physical examination will be sufficient, with or without x-rays, for a pediatrician to determine the best recommendations for the patient.

Although x-rays are a necessity for evaluation of most orthopedic or sports injuries, it is preferable to refer the child and have the subspecialist order imaging tests. This avoids duplication of radiation exposure for the child and the unnecessary time and expense of repeated x-rays. In addition, laboratory assays typically do not help in the evaluation of a suspected overuse injury, unless you suspect a comorbid condition such as arthritis or joint infection.

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Some parents of very young children – those 6 years old and younger – will come to you exhausted, feeling inadequate as parents, and even angry at their children.

Parents will report that their children with attention-deficit/hyperactivity disorder are very difficult at home and in preschool. Probably when their children were around age 2, 3, or 4 years old, their parents began wondering if the youngsters were immature, were more impulsive, and had a shorter attention span, compared with peers.

Pediatricians will recognize this pattern as likely ADHD and, in addition to making an accurate diagnosis, know that much is at stake in guiding and supporting parents. A critical relationship is at risk as the child's behavior evokes criticism and a negative tone from parents. Pediatricians should help parents set reasonable expectations and focus on behaviors and activities that build self-esteem. For some families, this work can be difficult and time consuming, requiring counseling and behavioral reward training – probably better delegated to a mental health specialist.

Attention span, impulsivity, and motoric hyperactivity are active concerns every waking hour of the child's day. Certain demands in preschool, at a longer dinner, or in church may exacerbate the symptoms, whereas playing in the park or playing a fun-filled computer game may ease the symptoms. The pediatrician can sort through a typical day and recommend approaches that are consistent with developmentally reasonable expectations, and modified for the child's ADHD symptoms.

Family history is another consideration. About 30% of children with ADHD come from fathers who had or have the disorder. Reminding a father of his difficulties growing up or any ongoing ADHD symptoms can be helpful in eliciting some empathy from him for his child's suffering.

Beyond family life, ADHD will affect the choice of school and activities. Based on what works for the child, consider how many hours a child should spend in preschool and how much structure is helpful. How will the culture of the school fit the child's style? Remember that the last thing a child with ADHD needs is an early school experience characterized by criticism and a sense of not being able to please teachers. A school with more recess and activity opportunities, as well as after-school programs, might be a good choice, and might offer some respite for parents.

As part of building self-esteem, ask parents if there is anything the child is really good at. For example, I treated a 6-year-old with ADHD who was gifted with computers. He was able to teach his peers and play games with friends, and he felt genuine pride working with a machine that was tolerant and nonjudgmental, and could be reset as needed. Might this not lead to a path of an after-school computer club or computer summer camp (that of course would include other activities)? Other young children may show strength in music, art, or a sport, and these activities are at least as important as remediating weaknesses.

Awareness of the different ADHD subtypes is important in general, but also can guide you in when to refer these children. Some kids with ADHD are more moody or depressed, some are more anxious, and others are more physically aggressive. Consider referral to a child and adolescent psychiatrist if one of these subtypes becomes more difficult to manage. A mental health consultation can help these higher-risk children.

Some children with ADHD also have learning disabilities, and diagnosis at a young age, before school failure, is invaluable. If you suspect this in a particular patient, you might want to recommend some early testing through the schools to avoid creation of unrealistic expectations in the classroom.

Parents may tell you their children are impulsive. While other kids are more predictable when playing in the sandbox, their children with ADHD may do something unpredictable. They might jump out of the sandbox or grab a toy from another child, for example. A mother of a 3-year-old with ADHD will stay closer to the sandbox because she doesn't know what that child is going to do next.

Typically, the child also will have a shorter attention span. The parents cannot relax because they know the sandbox, or a particular project in the sandbox, won't hold their child as long. Other children may be occupied for 15, 20, or even 30 minutes, but their young child with ADHD might last only 3 or 4 minutes and then need to move on. That, as you can imagine, is going to make the parenting demands much higher. Remember this doesn't happen for just 1 or 2 hours per day; children with true ADHD are going to be like this from the time they get up until the time they go to sleep.

All these behaviors associated with ADHD set these children up for a fair amount of criticism. The parents are tempted, especially if they don't understand the disorder, to say: “Don't do that!”; “Put that down!”; “I just bought you this – why don't you want to play with it?”; “Why can't you play like your friend Johnny does?”; “Why can't you sit still for a minute while Mommy fixes dinner?”

These children are subject to a lot of negative feedback from their environment. The world is not very tolerant of a young child, or even an older child, with ADHD. My guess is if these children are in preschool, the teacher is having the same issues with their behaviors. They may get criticized during circle time or while doing a certain project. Except for recess and lunch, they are going to be under a lot of scrutiny and most of the feedback is going to be negative.

We can see how children with ADHD, in a typical day, can hear 10, if not 25, negative comments. That is about two to three per hour. That degree of criticism begins to become part of how they see themselves, and they become fairly self-critical.

One of the key risks from ADHD at this young age is that it's hard for these children to differentiate if what they are doing is bad or if they are bad. Their self-esteem is very vulnerable. One principle that guides a lot of my management of these youngsters with ADHD is figuring out how to protect or enhance their self-esteem. Therefore, one of the initial things I ask parents to do is to think about how much negative criticism their child is hearing. Next, I ask them to think about what are reasonable expectations for that particular child.

Any opportunity to build self-esteem and build a sense of success based on reasonable expectations is worthwhile. A lot of parents will start sports for their children when they are 4 or 5. Kids with ADHD don't do very well in the outfield of T-ball because they are distracted. They don't stand out there waiting for the hit, and then they get yelled at for missing the ball. Help parents choose a sport that fits their children. I've seen some ADHD kids be goalies because they have to pay attention for a few seconds when the ball is coming, and then when the ball is somewhere else they can daydream with impunity. A lot of children with ADHD do well with swimming, for example, because there are fewer rules and they have a little more freedom. Others thrive with the structure and sense of accomplishment that comes from the “belt” system of karate.

Clearly one of the most effective treatments for the symptoms of ADHD is medication. Medication will increase attention span in school, church, or at dinner. Of course, every parent has concerns about how young to start children on medication, or whether to use medication at all. For those families, the first set of efforts may be directed to setting reasonable expectations and reviewing daily activities.

This focus will help, but will not be enough, and medication will be a critical part of treatment. Medication adds some risk, but the benefits to the child's functioning and self-esteem often outweigh these risks.

One of the things that medication probably does best is reduce the amount of negative feedback because the child will not be as impulsive and will appear to have a longer attention span. Again, you can ask too much of a child, but you will see higher expectations if the child is taking medication that is working correctly. Once ADHD is diagnosed in a young child, the pediatrician has a key role in trying to protect and enhance the child's self-esteem, advising on the child's day-to-day functioning, and supporting the overall care with appropriate use of medications.

[email protected]

Some parents of very young children – those 6 years old and younger – will come to you exhausted, feeling inadequate as parents, and even angry at their children.

Parents will report that their children with attention-deficit/hyperactivity disorder are very difficult at home and in preschool. Probably when their children were around age 2, 3, or 4 years old, their parents began wondering if the youngsters were immature, were more impulsive, and had a shorter attention span, compared with peers.

Pediatricians will recognize this pattern as likely ADHD and, in addition to making an accurate diagnosis, know that much is at stake in guiding and supporting parents. A critical relationship is at risk as the child's behavior evokes criticism and a negative tone from parents. Pediatricians should help parents set reasonable expectations and focus on behaviors and activities that build self-esteem. For some families, this work can be difficult and time consuming, requiring counseling and behavioral reward training – probably better delegated to a mental health specialist.

Attention span, impulsivity, and motoric hyperactivity are active concerns every waking hour of the child's day. Certain demands in preschool, at a longer dinner, or in church may exacerbate the symptoms, whereas playing in the park or playing a fun-filled computer game may ease the symptoms. The pediatrician can sort through a typical day and recommend approaches that are consistent with developmentally reasonable expectations, and modified for the child's ADHD symptoms.

Family history is another consideration. About 30% of children with ADHD come from fathers who had or have the disorder. Reminding a father of his difficulties growing up or any ongoing ADHD symptoms can be helpful in eliciting some empathy from him for his child's suffering.

Beyond family life, ADHD will affect the choice of school and activities. Based on what works for the child, consider how many hours a child should spend in preschool and how much structure is helpful. How will the culture of the school fit the child's style? Remember that the last thing a child with ADHD needs is an early school experience characterized by criticism and a sense of not being able to please teachers. A school with more recess and activity opportunities, as well as after-school programs, might be a good choice, and might offer some respite for parents.

As part of building self-esteem, ask parents if there is anything the child is really good at. For example, I treated a 6-year-old with ADHD who was gifted with computers. He was able to teach his peers and play games with friends, and he felt genuine pride working with a machine that was tolerant and nonjudgmental, and could be reset as needed. Might this not lead to a path of an after-school computer club or computer summer camp (that of course would include other activities)? Other young children may show strength in music, art, or a sport, and these activities are at least as important as remediating weaknesses.

Awareness of the different ADHD subtypes is important in general, but also can guide you in when to refer these children. Some kids with ADHD are more moody or depressed, some are more anxious, and others are more physically aggressive. Consider referral to a child and adolescent psychiatrist if one of these subtypes becomes more difficult to manage. A mental health consultation can help these higher-risk children.

Some children with ADHD also have learning disabilities, and diagnosis at a young age, before school failure, is invaluable. If you suspect this in a particular patient, you might want to recommend some early testing through the schools to avoid creation of unrealistic expectations in the classroom.

Parents may tell you their children are impulsive. While other kids are more predictable when playing in the sandbox, their children with ADHD may do something unpredictable. They might jump out of the sandbox or grab a toy from another child, for example. A mother of a 3-year-old with ADHD will stay closer to the sandbox because she doesn't know what that child is going to do next.

Typically, the child also will have a shorter attention span. The parents cannot relax because they know the sandbox, or a particular project in the sandbox, won't hold their child as long. Other children may be occupied for 15, 20, or even 30 minutes, but their young child with ADHD might last only 3 or 4 minutes and then need to move on. That, as you can imagine, is going to make the parenting demands much higher. Remember this doesn't happen for just 1 or 2 hours per day; children with true ADHD are going to be like this from the time they get up until the time they go to sleep.

All these behaviors associated with ADHD set these children up for a fair amount of criticism. The parents are tempted, especially if they don't understand the disorder, to say: “Don't do that!”; “Put that down!”; “I just bought you this – why don't you want to play with it?”; “Why can't you play like your friend Johnny does?”; “Why can't you sit still for a minute while Mommy fixes dinner?”

These children are subject to a lot of negative feedback from their environment. The world is not very tolerant of a young child, or even an older child, with ADHD. My guess is if these children are in preschool, the teacher is having the same issues with their behaviors. They may get criticized during circle time or while doing a certain project. Except for recess and lunch, they are going to be under a lot of scrutiny and most of the feedback is going to be negative.

We can see how children with ADHD, in a typical day, can hear 10, if not 25, negative comments. That is about two to three per hour. That degree of criticism begins to become part of how they see themselves, and they become fairly self-critical.

One of the key risks from ADHD at this young age is that it's hard for these children to differentiate if what they are doing is bad or if they are bad. Their self-esteem is very vulnerable. One principle that guides a lot of my management of these youngsters with ADHD is figuring out how to protect or enhance their self-esteem. Therefore, one of the initial things I ask parents to do is to think about how much negative criticism their child is hearing. Next, I ask them to think about what are reasonable expectations for that particular child.

Any opportunity to build self-esteem and build a sense of success based on reasonable expectations is worthwhile. A lot of parents will start sports for their children when they are 4 or 5. Kids with ADHD don't do very well in the outfield of T-ball because they are distracted. They don't stand out there waiting for the hit, and then they get yelled at for missing the ball. Help parents choose a sport that fits their children. I've seen some ADHD kids be goalies because they have to pay attention for a few seconds when the ball is coming, and then when the ball is somewhere else they can daydream with impunity. A lot of children with ADHD do well with swimming, for example, because there are fewer rules and they have a little more freedom. Others thrive with the structure and sense of accomplishment that comes from the “belt” system of karate.

Clearly one of the most effective treatments for the symptoms of ADHD is medication. Medication will increase attention span in school, church, or at dinner. Of course, every parent has concerns about how young to start children on medication, or whether to use medication at all. For those families, the first set of efforts may be directed to setting reasonable expectations and reviewing daily activities.

This focus will help, but will not be enough, and medication will be a critical part of treatment. Medication adds some risk, but the benefits to the child's functioning and self-esteem often outweigh these risks.

One of the things that medication probably does best is reduce the amount of negative feedback because the child will not be as impulsive and will appear to have a longer attention span. Again, you can ask too much of a child, but you will see higher expectations if the child is taking medication that is working correctly. Once ADHD is diagnosed in a young child, the pediatrician has a key role in trying to protect and enhance the child's self-esteem, advising on the child's day-to-day functioning, and supporting the overall care with appropriate use of medications.

[email protected]

Some parents of very young children – those 6 years old and younger – will come to you exhausted, feeling inadequate as parents, and even angry at their children.

Parents will report that their children with attention-deficit/hyperactivity disorder are very difficult at home and in preschool. Probably when their children were around age 2, 3, or 4 years old, their parents began wondering if the youngsters were immature, were more impulsive, and had a shorter attention span, compared with peers.

Pediatricians will recognize this pattern as likely ADHD and, in addition to making an accurate diagnosis, know that much is at stake in guiding and supporting parents. A critical relationship is at risk as the child's behavior evokes criticism and a negative tone from parents. Pediatricians should help parents set reasonable expectations and focus on behaviors and activities that build self-esteem. For some families, this work can be difficult and time consuming, requiring counseling and behavioral reward training – probably better delegated to a mental health specialist.

Attention span, impulsivity, and motoric hyperactivity are active concerns every waking hour of the child's day. Certain demands in preschool, at a longer dinner, or in church may exacerbate the symptoms, whereas playing in the park or playing a fun-filled computer game may ease the symptoms. The pediatrician can sort through a typical day and recommend approaches that are consistent with developmentally reasonable expectations, and modified for the child's ADHD symptoms.

Family history is another consideration. About 30% of children with ADHD come from fathers who had or have the disorder. Reminding a father of his difficulties growing up or any ongoing ADHD symptoms can be helpful in eliciting some empathy from him for his child's suffering.

Beyond family life, ADHD will affect the choice of school and activities. Based on what works for the child, consider how many hours a child should spend in preschool and how much structure is helpful. How will the culture of the school fit the child's style? Remember that the last thing a child with ADHD needs is an early school experience characterized by criticism and a sense of not being able to please teachers. A school with more recess and activity opportunities, as well as after-school programs, might be a good choice, and might offer some respite for parents.

As part of building self-esteem, ask parents if there is anything the child is really good at. For example, I treated a 6-year-old with ADHD who was gifted with computers. He was able to teach his peers and play games with friends, and he felt genuine pride working with a machine that was tolerant and nonjudgmental, and could be reset as needed. Might this not lead to a path of an after-school computer club or computer summer camp (that of course would include other activities)? Other young children may show strength in music, art, or a sport, and these activities are at least as important as remediating weaknesses.

Awareness of the different ADHD subtypes is important in general, but also can guide you in when to refer these children. Some kids with ADHD are more moody or depressed, some are more anxious, and others are more physically aggressive. Consider referral to a child and adolescent psychiatrist if one of these subtypes becomes more difficult to manage. A mental health consultation can help these higher-risk children.

Some children with ADHD also have learning disabilities, and diagnosis at a young age, before school failure, is invaluable. If you suspect this in a particular patient, you might want to recommend some early testing through the schools to avoid creation of unrealistic expectations in the classroom.

Parents may tell you their children are impulsive. While other kids are more predictable when playing in the sandbox, their children with ADHD may do something unpredictable. They might jump out of the sandbox or grab a toy from another child, for example. A mother of a 3-year-old with ADHD will stay closer to the sandbox because she doesn't know what that child is going to do next.

Typically, the child also will have a shorter attention span. The parents cannot relax because they know the sandbox, or a particular project in the sandbox, won't hold their child as long. Other children may be occupied for 15, 20, or even 30 minutes, but their young child with ADHD might last only 3 or 4 minutes and then need to move on. That, as you can imagine, is going to make the parenting demands much higher. Remember this doesn't happen for just 1 or 2 hours per day; children with true ADHD are going to be like this from the time they get up until the time they go to sleep.

All these behaviors associated with ADHD set these children up for a fair amount of criticism. The parents are tempted, especially if they don't understand the disorder, to say: “Don't do that!”; “Put that down!”; “I just bought you this – why don't you want to play with it?”; “Why can't you play like your friend Johnny does?”; “Why can't you sit still for a minute while Mommy fixes dinner?”

These children are subject to a lot of negative feedback from their environment. The world is not very tolerant of a young child, or even an older child, with ADHD. My guess is if these children are in preschool, the teacher is having the same issues with their behaviors. They may get criticized during circle time or while doing a certain project. Except for recess and lunch, they are going to be under a lot of scrutiny and most of the feedback is going to be negative.

We can see how children with ADHD, in a typical day, can hear 10, if not 25, negative comments. That is about two to three per hour. That degree of criticism begins to become part of how they see themselves, and they become fairly self-critical.

One of the key risks from ADHD at this young age is that it's hard for these children to differentiate if what they are doing is bad or if they are bad. Their self-esteem is very vulnerable. One principle that guides a lot of my management of these youngsters with ADHD is figuring out how to protect or enhance their self-esteem. Therefore, one of the initial things I ask parents to do is to think about how much negative criticism their child is hearing. Next, I ask them to think about what are reasonable expectations for that particular child.

Any opportunity to build self-esteem and build a sense of success based on reasonable expectations is worthwhile. A lot of parents will start sports for their children when they are 4 or 5. Kids with ADHD don't do very well in the outfield of T-ball because they are distracted. They don't stand out there waiting for the hit, and then they get yelled at for missing the ball. Help parents choose a sport that fits their children. I've seen some ADHD kids be goalies because they have to pay attention for a few seconds when the ball is coming, and then when the ball is somewhere else they can daydream with impunity. A lot of children with ADHD do well with swimming, for example, because there are fewer rules and they have a little more freedom. Others thrive with the structure and sense of accomplishment that comes from the “belt” system of karate.

Clearly one of the most effective treatments for the symptoms of ADHD is medication. Medication will increase attention span in school, church, or at dinner. Of course, every parent has concerns about how young to start children on medication, or whether to use medication at all. For those families, the first set of efforts may be directed to setting reasonable expectations and reviewing daily activities.

This focus will help, but will not be enough, and medication will be a critical part of treatment. Medication adds some risk, but the benefits to the child's functioning and self-esteem often outweigh these risks.

One of the things that medication probably does best is reduce the amount of negative feedback because the child will not be as impulsive and will appear to have a longer attention span. Again, you can ask too much of a child, but you will see higher expectations if the child is taking medication that is working correctly. Once ADHD is diagnosed in a young child, the pediatrician has a key role in trying to protect and enhance the child's self-esteem, advising on the child's day-to-day functioning, and supporting the overall care with appropriate use of medications.

The American Academy of Pediatrics, citing a substantial increase in scientific evidence backing best practices for child passenger safety, is recommending changes in child car seat use that include keeping most infants and toddlers in rear-facing safety seats until they reach age 2 years, according to a new policy statement.

The new guidelines also recommend forward-facing car safety seats for most children until they outgrow the weight or height limits on those seats; belt-positioning booster seats for most children through age 8 years or well beyond; and lap-and-shoulder belts for all those children who have outgrown booster seats. In addition, the policy statement recommends that all children ride in the back seat of vehicles through age 12 years (Pediatrics 2011;127:788–93).

Although the AAP policy recommendations are not binding, states use them in crafting and revising child safety seat laws, said Dr. Benjamin Hoffman, an expert in child passenger safety and associate professor of pediatrics at the University of New Mexico, Albuquerque. Previous academy recommendations regarding the use of booster seats prompted many states to enact laws requiring booster seats for older children, which has improved safety dramatically, he said.

“The best way to get people to use child safety seats appropriately is to have state laws requiring their use,” Dr. Hoffman said in an interview. “Our job is to help consumer organizations and states understand what the best practice is.”

The new AAP guidelines represent big changes in the way car safety seat use has been viewed, said Dr. Hoffman, a new member of the AAP's committee on injury, violence, and poison prevention, which crafted the recommendations. Now, there's much more emphasis on the transitions between different types of seats – rear-facing seats to forward-facing seats, forward-facing seats to booster seats, and booster seats to seat belts.

“In these transitions, you lose protection every step of the way,” he noted. “Therefore, you need to delay these transitions for as long as possible.”

However, many parents and even older children themselves view the transitions as milestones, which encourages them to make the transition as quickly as they legally can, he said. “Parents are really viewing these transitions as graduations. There's a perception that this graduation is a positive thing. It's not.”

Instead of making the switch to a lower level of protection as soon as they're legally able, parents should keep their children in safety seats until they outgrow the weight and height limits, Dr. Hoffman said. For example, many rear-facing seats can handle children up to 35 pounds, and parents should use these seats in their rear-facing configuration until their children no longer can fit in them.

Likewise, parents should keep their children in forward-facing car seats until they have outgrown the weight or height limits on those seats, and should use a belt-positioning booster seat until the vehicle lap-and-shoulder belt fits properly, typically when children have reached 4 feet, 9 inches in height and are between 8 and 12 years of age.

According to the technical report by committee member Dr. Dennis R. Durbin, professor of pediatrics and epidemiology at The Children's Hospital of Philadelphia, research in Sweden shows that rear-facing child safety seats reduce the risk of significant injuries by 90% relative to unrestrained children. Many infants and children in Sweden remain in rear-facing seats until age 4 years, when they transition directly to booster seats, according to the report (Pediatrics 2011;127:e1050–66). h

“There's a 500% increased risk of injury” for toddlers between the ages of 1 and 2 years when seated in a forward-facing seat, compared with a rear-facing seat, Dr. Hoffman said.

Analysis of the data also indicates substantial benefits for children aged 2 years and older seated in forward-facing car seats, compared with just booster seats or seat belts, and for children seated in booster seats who have outgrown car seats but who have not yet reached 4 feet, 9 inches, according to the report.

Some forward-facing seats can accommodate children up to 65 or 80 pounds, and should be used until that weight limit, according to the report.

Pediatricians should counsel their patients on these new recommendations at every well-child visit, the guidelines say.

“Pediatricians don't have to know how to install car seats, but they have to know what the best recommendations are,” said Dr. Hoffman. “They should know what the resources are in their communities [for car seat installation help], and it would be even better for them to make contact with those resources” in order to facilitate assistance for patients who might need it.

In addition, pediatricians should counsel parents to follow the AAP recommendations for the utmost car seat safety rather than simply follow state laws, which may allow “graduation” to the next level before the child is large enough, Dr. Hoffman said.

“The laws of physics will always trump the laws of the state,” he concluded.

All authors filed conflict of interest statements with the AAP, and any conflicts have been resolved through a process approved by the AAP Board of Directors, according to a statement in the journal.

A list of formal car seat inspection stations is available at www.seatcheck.orghttp://cert.safekids.org

The American Academy of Pediatrics, citing a substantial increase in scientific evidence backing best practices for child passenger safety, is recommending changes in child car seat use that include keeping most infants and toddlers in rear-facing safety seats until they reach age 2 years, according to a new policy statement.

The new guidelines also recommend forward-facing car safety seats for most children until they outgrow the weight or height limits on those seats; belt-positioning booster seats for most children through age 8 years or well beyond; and lap-and-shoulder belts for all those children who have outgrown booster seats. In addition, the policy statement recommends that all children ride in the back seat of vehicles through age 12 years (Pediatrics 2011;127:788–93).

Although the AAP policy recommendations are not binding, states use them in crafting and revising child safety seat laws, said Dr. Benjamin Hoffman, an expert in child passenger safety and associate professor of pediatrics at the University of New Mexico, Albuquerque. Previous academy recommendations regarding the use of booster seats prompted many states to enact laws requiring booster seats for older children, which has improved safety dramatically, he said.

“The best way to get people to use child safety seats appropriately is to have state laws requiring their use,” Dr. Hoffman said in an interview. “Our job is to help consumer organizations and states understand what the best practice is.”

The new AAP guidelines represent big changes in the way car safety seat use has been viewed, said Dr. Hoffman, a new member of the AAP's committee on injury, violence, and poison prevention, which crafted the recommendations. Now, there's much more emphasis on the transitions between different types of seats – rear-facing seats to forward-facing seats, forward-facing seats to booster seats, and booster seats to seat belts.

“In these transitions, you lose protection every step of the way,” he noted. “Therefore, you need to delay these transitions for as long as possible.”

However, many parents and even older children themselves view the transitions as milestones, which encourages them to make the transition as quickly as they legally can, he said. “Parents are really viewing these transitions as graduations. There's a perception that this graduation is a positive thing. It's not.”

Instead of making the switch to a lower level of protection as soon as they're legally able, parents should keep their children in safety seats until they outgrow the weight and height limits, Dr. Hoffman said. For example, many rear-facing seats can handle children up to 35 pounds, and parents should use these seats in their rear-facing configuration until their children no longer can fit in them.

Likewise, parents should keep their children in forward-facing car seats until they have outgrown the weight or height limits on those seats, and should use a belt-positioning booster seat until the vehicle lap-and-shoulder belt fits properly, typically when children have reached 4 feet, 9 inches in height and are between 8 and 12 years of age.

According to the technical report by committee member Dr. Dennis R. Durbin, professor of pediatrics and epidemiology at The Children's Hospital of Philadelphia, research in Sweden shows that rear-facing child safety seats reduce the risk of significant injuries by 90% relative to unrestrained children. Many infants and children in Sweden remain in rear-facing seats until age 4 years, when they transition directly to booster seats, according to the report (Pediatrics 2011;127:e1050–66). h

“There's a 500% increased risk of injury” for toddlers between the ages of 1 and 2 years when seated in a forward-facing seat, compared with a rear-facing seat, Dr. Hoffman said.

Analysis of the data also indicates substantial benefits for children aged 2 years and older seated in forward-facing car seats, compared with just booster seats or seat belts, and for children seated in booster seats who have outgrown car seats but who have not yet reached 4 feet, 9 inches, according to the report.

Some forward-facing seats can accommodate children up to 65 or 80 pounds, and should be used until that weight limit, according to the report.

Pediatricians should counsel their patients on these new recommendations at every well-child visit, the guidelines say.

“Pediatricians don't have to know how to install car seats, but they have to know what the best recommendations are,” said Dr. Hoffman. “They should know what the resources are in their communities [for car seat installation help], and it would be even better for them to make contact with those resources” in order to facilitate assistance for patients who might need it.

In addition, pediatricians should counsel parents to follow the AAP recommendations for the utmost car seat safety rather than simply follow state laws, which may allow “graduation” to the next level before the child is large enough, Dr. Hoffman said.

“The laws of physics will always trump the laws of the state,” he concluded.

All authors filed conflict of interest statements with the AAP, and any conflicts have been resolved through a process approved by the AAP Board of Directors, according to a statement in the journal.

A list of formal car seat inspection stations is available at www.seatcheck.orghttp://cert.safekids.org

The American Academy of Pediatrics, citing a substantial increase in scientific evidence backing best practices for child passenger safety, is recommending changes in child car seat use that include keeping most infants and toddlers in rear-facing safety seats until they reach age 2 years, according to a new policy statement.

The new guidelines also recommend forward-facing car safety seats for most children until they outgrow the weight or height limits on those seats; belt-positioning booster seats for most children through age 8 years or well beyond; and lap-and-shoulder belts for all those children who have outgrown booster seats. In addition, the policy statement recommends that all children ride in the back seat of vehicles through age 12 years (Pediatrics 2011;127:788–93).

Although the AAP policy recommendations are not binding, states use them in crafting and revising child safety seat laws, said Dr. Benjamin Hoffman, an expert in child passenger safety and associate professor of pediatrics at the University of New Mexico, Albuquerque. Previous academy recommendations regarding the use of booster seats prompted many states to enact laws requiring booster seats for older children, which has improved safety dramatically, he said.

“The best way to get people to use child safety seats appropriately is to have state laws requiring their use,” Dr. Hoffman said in an interview. “Our job is to help consumer organizations and states understand what the best practice is.”

The new AAP guidelines represent big changes in the way car safety seat use has been viewed, said Dr. Hoffman, a new member of the AAP's committee on injury, violence, and poison prevention, which crafted the recommendations. Now, there's much more emphasis on the transitions between different types of seats – rear-facing seats to forward-facing seats, forward-facing seats to booster seats, and booster seats to seat belts.

“In these transitions, you lose protection every step of the way,” he noted. “Therefore, you need to delay these transitions for as long as possible.”

However, many parents and even older children themselves view the transitions as milestones, which encourages them to make the transition as quickly as they legally can, he said. “Parents are really viewing these transitions as graduations. There's a perception that this graduation is a positive thing. It's not.”

Instead of making the switch to a lower level of protection as soon as they're legally able, parents should keep their children in safety seats until they outgrow the weight and height limits, Dr. Hoffman said. For example, many rear-facing seats can handle children up to 35 pounds, and parents should use these seats in their rear-facing configuration until their children no longer can fit in them.

Likewise, parents should keep their children in forward-facing car seats until they have outgrown the weight or height limits on those seats, and should use a belt-positioning booster seat until the vehicle lap-and-shoulder belt fits properly, typically when children have reached 4 feet, 9 inches in height and are between 8 and 12 years of age.

According to the technical report by committee member Dr. Dennis R. Durbin, professor of pediatrics and epidemiology at The Children's Hospital of Philadelphia, research in Sweden shows that rear-facing child safety seats reduce the risk of significant injuries by 90% relative to unrestrained children. Many infants and children in Sweden remain in rear-facing seats until age 4 years, when they transition directly to booster seats, according to the report (Pediatrics 2011;127:e1050–66). h

“There's a 500% increased risk of injury” for toddlers between the ages of 1 and 2 years when seated in a forward-facing seat, compared with a rear-facing seat, Dr. Hoffman said.

Analysis of the data also indicates substantial benefits for children aged 2 years and older seated in forward-facing car seats, compared with just booster seats or seat belts, and for children seated in booster seats who have outgrown car seats but who have not yet reached 4 feet, 9 inches, according to the report.

Some forward-facing seats can accommodate children up to 65 or 80 pounds, and should be used until that weight limit, according to the report.

Pediatricians should counsel their patients on these new recommendations at every well-child visit, the guidelines say.

“Pediatricians don't have to know how to install car seats, but they have to know what the best recommendations are,” said Dr. Hoffman. “They should know what the resources are in their communities [for car seat installation help], and it would be even better for them to make contact with those resources” in order to facilitate assistance for patients who might need it.

In addition, pediatricians should counsel parents to follow the AAP recommendations for the utmost car seat safety rather than simply follow state laws, which may allow “graduation” to the next level before the child is large enough, Dr. Hoffman said.

“The laws of physics will always trump the laws of the state,” he concluded.

All authors filed conflict of interest statements with the AAP, and any conflicts have been resolved through a process approved by the AAP Board of Directors, according to a statement in the journal.

A list of formal car seat inspection stations is available at www.seatcheck.orghttp://cert.safekids.org

A supplement to Internal Medicine News®. This supplement was sponsored by Boehringer Ingelheim Pharmaceuticals, Inc. and Eli Lilly and Company.

• Topics
• Faculty

Topics

• Epidemiology of CKD/RI With DM
• Risk Factors for CKD/RI in Patients With T2DM
• Early Identification and Screening
• CKD Strongly Effects CV Outcomes in Patients With DM
• Awareness of the Importance of CKD/RI Is Lacking
• CKD/RI Increases the Risk for Hypoglycemia in DM Treatment
• Multifactorial Therapy May Benefit Outcomes in Patients With T2DM and CKD

Faculty/Faculty Disclosure Mark Stolar, MD
Associate Professor of Clinical Medicine
Northwestern University Medical School
Chicago, IL

Michael Kodack, PharmD
Vice President, Medical
BlueSpark Healthcare Communications LLC
Basking Ridge, NJ

Mark Stolar, MD, has served on the Speakers Bureau of Takeda Pharmaceutical Company Limited and has developed educational programs for the TCL Institute and NACE. Michael Kodack, PharmD, is an employee of BlueSpark Healthcare Communications LLC.

Copyright © 2011 Elsevier Inc.

A supplement to Internal Medicine News®. This supplement was sponsored by Boehringer Ingelheim Pharmaceuticals, Inc. and Eli Lilly and Company.

• Topics
• Faculty

Topics

• Epidemiology of CKD/RI With DM
• Risk Factors for CKD/RI in Patients With T2DM
• Early Identification and Screening
• CKD Strongly Effects CV Outcomes in Patients With DM
• Awareness of the Importance of CKD/RI Is Lacking
• CKD/RI Increases the Risk for Hypoglycemia in DM Treatment
• Multifactorial Therapy May Benefit Outcomes in Patients With T2DM and CKD

Faculty/Faculty Disclosure Mark Stolar, MD
Associate Professor of Clinical Medicine
Northwestern University Medical School
Chicago, IL

Michael Kodack, PharmD
Vice President, Medical
BlueSpark Healthcare Communications LLC
Basking Ridge, NJ

Mark Stolar, MD, has served on the Speakers Bureau of Takeda Pharmaceutical Company Limited and has developed educational programs for the TCL Institute and NACE. Michael Kodack, PharmD, is an employee of BlueSpark Healthcare Communications LLC.

Copyright © 2011 Elsevier Inc.

A supplement to Internal Medicine News®. This supplement was sponsored by Boehringer Ingelheim Pharmaceuticals, Inc. and Eli Lilly and Company.

• Topics
• Faculty

Topics

• Epidemiology of CKD/RI With DM
• Risk Factors for CKD/RI in Patients With T2DM
• Early Identification and Screening
• CKD Strongly Effects CV Outcomes in Patients With DM
• Awareness of the Importance of CKD/RI Is Lacking
• CKD/RI Increases the Risk for Hypoglycemia in DM Treatment
• Multifactorial Therapy May Benefit Outcomes in Patients With T2DM and CKD

Faculty/Faculty Disclosure Mark Stolar, MD
Associate Professor of Clinical Medicine
Northwestern University Medical School
Chicago, IL

Michael Kodack, PharmD
Vice President, Medical
BlueSpark Healthcare Communications LLC
Basking Ridge, NJ

Mark Stolar, MD, has served on the Speakers Bureau of Takeda Pharmaceutical Company Limited and has developed educational programs for the TCL Institute and NACE. Michael Kodack, PharmD, is an employee of BlueSpark Healthcare Communications LLC.

Copyright © 2011 Elsevier Inc.

--Jame Abraham, MD, Editor

--Jame Abraham, MD, Editor

--Jame Abraham, MD, Editor