Mph

Case

A 25-year-old college student presented to the ED following a near-syncopal episode. The patient stated he had felt lightheaded and had fallen to his knees immediately after taking a shower earlier that morning, but did not experience any loss of consciousness or injury. He denied a history of syncope or any recent trauma or fatigue. A review of the patient’s systems was negative. His medical history was remarkable for irritable bowel syndrome; he had no surgical history. Regarding his social history, he admitted to occasional alcohol use but denied any tobacco or illicit drug use. He was not on any current prescription or over-the-counter medications and denied any allergies.

The patient’s initial vital signs at presentation were: blood pressure, 112/58 mm Hg; heart rate, 86 beats/min; temperature, 97.9°F; and respiratory rate, 18 breaths/min. Oxygen saturation was 100% on room air. The patient reported pain in his left shoulder, epigastric region, and right flank. He rated his pain as a “4” on a 0-to-10 pain scale.

On physical examination, the patient was alert and oriented; he was thin and had mild pallor. His head, eyes, ears, nose, and throat; cardiac; pulmonary; and neurological examinations were normal. The abdominal examination revealed a soft, minimally tender epigastrium but with normal bowel sounds. Initial laboratory studies were remarkable for low hemoglobin (Hgb; 12.0 g/dL) and elevated aspartate transaminase (105 U/L), alanine aminotransferase (168 U/L), total bilirubin (1.6 mg/dL), and glucose (179 mg/dL) levels. The patient’s troponin I and lipase levels were within normal range. An electrocardiogram was unremarkable.

Given the patient’s elevated hepatic enzymes, right upper quadrant ultrasound was obtained, which demonstrated a normal gallbladder, a moderate amount of complicated free fluid (with hyper-echoic densities suggestive of coagulated blood) in all four quadrants, and splenomegaly measuring 13.7 cm (Figure 1a and 1b).

Positive:

• Epstein-Barr virus (EBV)

• Viral capsid antigen (VCA) immuno­globulin G

• VCA immunoglobulin M

Negative:

• Mononuclear spot test
• Human immunodeficiency virus
• Hepatitis B and C
• Antinuclear antibodies
• Venereal disease research laboratory test

The rest of the patient’s recovery was uneventful, and he was discharged home in stable condition on hospital day 3.

Discussion

Although the spleen is the most common intra-abdominal organ that can rupture with blunt abdominal trauma, splenic rupture in the absence of trauma is very rare. Nontraumatic splenic rupture (NSR) has been associated with pathological and nonpathological spleens.^1,2 A systemic review of NSRs showed that 7% of the 845 patients in the review had completely normal spleens; the remaining 93% had some form of splenic pathology.¹

Etiology

The top three causes of splenic enlargement associated with NSR include hematologic malignancies, viral infections, and inflammation.^1,2 Although viruses, such as EBV and cytomegalovirus, represent almost 15% of the pathological causes of NSR, it is not uncommon for a patient to have multiple pathological processes present.¹ Our patient’s enlarged spleen was due to acute infectious mononucleosis.

Signs and Symptoms

Diagnosing NSR can be challenging and it is often missed or discovered incidentally during evaluation (as was initially the case with our patient).³ Several signs and symptoms present in our patient were red herrings that warranted closer analysis. The patient’s complaint of left shoulder pain suggested left hemidiaphragm irritation from the NSR. Furthermore, our patient’s near-syncopal episode was possibly due to acute vagal simulation from the initial contact of blood with the peritoneal cavity.⁴ The maximal vagal stimulus was likely transient, as our patient returned to baseline after a brief near-syncopal episode.

As illustrated in our case, though tachycardia is common in splenic rupture, not all patients present with this sign. The absence of tachycardia in our patient can be explained by the elevation of his baseline enteric vagal tone due to the continued presence of blood in the peritoneum.⁵ There are also other factors associated with the absence of tachycardia. For example, a well-conditioned athlete presenting with states of shock due to splenic rupture may not show signs of tachycardia.⁶

San Francisco Syncope Rule

The San Francisco Syncope Rule (SFSR) is a clinical decision-making risk-stratification tool used to determine outcomes and disposition of ED patients presenting with syncope.⁷ It is important to note that if we had used a straightforward application of the SFSR upon our patient’s initial presentation, the results would have been negative, suggesting he was not at risk for short-term serious outcomes.⁷

Imaging Studies

As demonstrated in our patient, a quick point-of-care (POC) bedside ultrasound scan can reveal the presence of free fluid in the abdomen to help with the diagnosis. On ultrasound, the presence of free fluid in the right upper quadrant is more commonly found in the hepatorenal recess, whereas in the left upper quadrant free fluid is seen sub-diaphragmatic/suprasplenic first before fluid is seen in the splenorenal recess. Bedside ultrasound can accurately detect as little as 100 mL of free fluid in the abdominal cavity, with a 90% sensitivity and 99% specificity.⁸

An ultrasound is highly sensitive as a preliminary screening tool to identify the presence of free intraperitoneal fluid and has some limited utility in identifying any disruption in the splenic echotexture that may suggest a laceration or hematoma. Ultrasound, however, has poor specificity in identifying solid organ injuries.⁹

Computed tomography scanning is the imaging modality of choice for assessing splenic injuries, and should be obtained to confirm the presence of a solid organ injury, as well as to grade the degree of injury and thereby determine the need for surgical intervention.¹⁰ It is worth noting that in a hemodynamically unstable patient, exploratory laparotomy may be embarked upon without a CT scan and positive free fluid on ultrasound.

Splenic Injury Scale

Splenic injury is classified on a scale of 1 (mild injury) to 5 (severe injury) (Table).¹¹

Conclusion

This case illustrates an uncommon presentation of NSR and underscores the importance of considering NSR in the differential diagnoses of patients presenting with abdominal pain—a sign with such a broad differential that NSR could easily be missed during evaluation. Based on its high sensitivity and specificity in detecting the presence of free fluid in the abdominal cavity, POC ultrasound imaging should be used to evaluate patients presenting with abdominal pain and syncopal or near-syncopal symptoms. This case further demonstrates that the absence of tachycardia or signs of shock should not rule out NSR.

Case

A 25-year-old college student presented to the ED following a near-syncopal episode. The patient stated he had felt lightheaded and had fallen to his knees immediately after taking a shower earlier that morning, but did not experience any loss of consciousness or injury. He denied a history of syncope or any recent trauma or fatigue. A review of the patient’s systems was negative. His medical history was remarkable for irritable bowel syndrome; he had no surgical history. Regarding his social history, he admitted to occasional alcohol use but denied any tobacco or illicit drug use. He was not on any current prescription or over-the-counter medications and denied any allergies.

The patient’s initial vital signs at presentation were: blood pressure, 112/58 mm Hg; heart rate, 86 beats/min; temperature, 97.9°F; and respiratory rate, 18 breaths/min. Oxygen saturation was 100% on room air. The patient reported pain in his left shoulder, epigastric region, and right flank. He rated his pain as a “4” on a 0-to-10 pain scale.

On physical examination, the patient was alert and oriented; he was thin and had mild pallor. His head, eyes, ears, nose, and throat; cardiac; pulmonary; and neurological examinations were normal. The abdominal examination revealed a soft, minimally tender epigastrium but with normal bowel sounds. Initial laboratory studies were remarkable for low hemoglobin (Hgb; 12.0 g/dL) and elevated aspartate transaminase (105 U/L), alanine aminotransferase (168 U/L), total bilirubin (1.6 mg/dL), and glucose (179 mg/dL) levels. The patient’s troponin I and lipase levels were within normal range. An electrocardiogram was unremarkable.

Given the patient’s elevated hepatic enzymes, right upper quadrant ultrasound was obtained, which demonstrated a normal gallbladder, a moderate amount of complicated free fluid (with hyper-echoic densities suggestive of coagulated blood) in all four quadrants, and splenomegaly measuring 13.7 cm (Figure 1a and 1b).

Positive:

• Epstein-Barr virus (EBV)

• Viral capsid antigen (VCA) immuno­globulin G

• VCA immunoglobulin M

Negative:

• Mononuclear spot test
• Human immunodeficiency virus
• Hepatitis B and C
• Antinuclear antibodies
• Venereal disease research laboratory test

The rest of the patient’s recovery was uneventful, and he was discharged home in stable condition on hospital day 3.

Discussion

Although the spleen is the most common intra-abdominal organ that can rupture with blunt abdominal trauma, splenic rupture in the absence of trauma is very rare. Nontraumatic splenic rupture (NSR) has been associated with pathological and nonpathological spleens.^1,2 A systemic review of NSRs showed that 7% of the 845 patients in the review had completely normal spleens; the remaining 93% had some form of splenic pathology.¹

Etiology

The top three causes of splenic enlargement associated with NSR include hematologic malignancies, viral infections, and inflammation.^1,2 Although viruses, such as EBV and cytomegalovirus, represent almost 15% of the pathological causes of NSR, it is not uncommon for a patient to have multiple pathological processes present.¹ Our patient’s enlarged spleen was due to acute infectious mononucleosis.

Signs and Symptoms

Diagnosing NSR can be challenging and it is often missed or discovered incidentally during evaluation (as was initially the case with our patient).³ Several signs and symptoms present in our patient were red herrings that warranted closer analysis. The patient’s complaint of left shoulder pain suggested left hemidiaphragm irritation from the NSR. Furthermore, our patient’s near-syncopal episode was possibly due to acute vagal simulation from the initial contact of blood with the peritoneal cavity.⁴ The maximal vagal stimulus was likely transient, as our patient returned to baseline after a brief near-syncopal episode.

As illustrated in our case, though tachycardia is common in splenic rupture, not all patients present with this sign. The absence of tachycardia in our patient can be explained by the elevation of his baseline enteric vagal tone due to the continued presence of blood in the peritoneum.⁵ There are also other factors associated with the absence of tachycardia. For example, a well-conditioned athlete presenting with states of shock due to splenic rupture may not show signs of tachycardia.⁶

San Francisco Syncope Rule

The San Francisco Syncope Rule (SFSR) is a clinical decision-making risk-stratification tool used to determine outcomes and disposition of ED patients presenting with syncope.⁷ It is important to note that if we had used a straightforward application of the SFSR upon our patient’s initial presentation, the results would have been negative, suggesting he was not at risk for short-term serious outcomes.⁷

Imaging Studies

As demonstrated in our patient, a quick point-of-care (POC) bedside ultrasound scan can reveal the presence of free fluid in the abdomen to help with the diagnosis. On ultrasound, the presence of free fluid in the right upper quadrant is more commonly found in the hepatorenal recess, whereas in the left upper quadrant free fluid is seen sub-diaphragmatic/suprasplenic first before fluid is seen in the splenorenal recess. Bedside ultrasound can accurately detect as little as 100 mL of free fluid in the abdominal cavity, with a 90% sensitivity and 99% specificity.⁸

An ultrasound is highly sensitive as a preliminary screening tool to identify the presence of free intraperitoneal fluid and has some limited utility in identifying any disruption in the splenic echotexture that may suggest a laceration or hematoma. Ultrasound, however, has poor specificity in identifying solid organ injuries.⁹

Computed tomography scanning is the imaging modality of choice for assessing splenic injuries, and should be obtained to confirm the presence of a solid organ injury, as well as to grade the degree of injury and thereby determine the need for surgical intervention.¹⁰ It is worth noting that in a hemodynamically unstable patient, exploratory laparotomy may be embarked upon without a CT scan and positive free fluid on ultrasound.

Splenic Injury Scale

Splenic injury is classified on a scale of 1 (mild injury) to 5 (severe injury) (Table).¹¹

Conclusion

This case illustrates an uncommon presentation of NSR and underscores the importance of considering NSR in the differential diagnoses of patients presenting with abdominal pain—a sign with such a broad differential that NSR could easily be missed during evaluation. Based on its high sensitivity and specificity in detecting the presence of free fluid in the abdominal cavity, POC ultrasound imaging should be used to evaluate patients presenting with abdominal pain and syncopal or near-syncopal symptoms. This case further demonstrates that the absence of tachycardia or signs of shock should not rule out NSR.

Case

A 25-year-old college student presented to the ED following a near-syncopal episode. The patient stated he had felt lightheaded and had fallen to his knees immediately after taking a shower earlier that morning, but did not experience any loss of consciousness or injury. He denied a history of syncope or any recent trauma or fatigue. A review of the patient’s systems was negative. His medical history was remarkable for irritable bowel syndrome; he had no surgical history. Regarding his social history, he admitted to occasional alcohol use but denied any tobacco or illicit drug use. He was not on any current prescription or over-the-counter medications and denied any allergies.

The patient’s initial vital signs at presentation were: blood pressure, 112/58 mm Hg; heart rate, 86 beats/min; temperature, 97.9°F; and respiratory rate, 18 breaths/min. Oxygen saturation was 100% on room air. The patient reported pain in his left shoulder, epigastric region, and right flank. He rated his pain as a “4” on a 0-to-10 pain scale.

On physical examination, the patient was alert and oriented; he was thin and had mild pallor. His head, eyes, ears, nose, and throat; cardiac; pulmonary; and neurological examinations were normal. The abdominal examination revealed a soft, minimally tender epigastrium but with normal bowel sounds. Initial laboratory studies were remarkable for low hemoglobin (Hgb; 12.0 g/dL) and elevated aspartate transaminase (105 U/L), alanine aminotransferase (168 U/L), total bilirubin (1.6 mg/dL), and glucose (179 mg/dL) levels. The patient’s troponin I and lipase levels were within normal range. An electrocardiogram was unremarkable.

Given the patient’s elevated hepatic enzymes, right upper quadrant ultrasound was obtained, which demonstrated a normal gallbladder, a moderate amount of complicated free fluid (with hyper-echoic densities suggestive of coagulated blood) in all four quadrants, and splenomegaly measuring 13.7 cm (Figure 1a and 1b).

Positive:

• Epstein-Barr virus (EBV)

• Viral capsid antigen (VCA) immuno­globulin G

• VCA immunoglobulin M

Negative:

• Mononuclear spot test
• Human immunodeficiency virus
• Hepatitis B and C
• Antinuclear antibodies
• Venereal disease research laboratory test

The rest of the patient’s recovery was uneventful, and he was discharged home in stable condition on hospital day 3.

Discussion

Although the spleen is the most common intra-abdominal organ that can rupture with blunt abdominal trauma, splenic rupture in the absence of trauma is very rare. Nontraumatic splenic rupture (NSR) has been associated with pathological and nonpathological spleens.^1,2 A systemic review of NSRs showed that 7% of the 845 patients in the review had completely normal spleens; the remaining 93% had some form of splenic pathology.¹

Etiology

The top three causes of splenic enlargement associated with NSR include hematologic malignancies, viral infections, and inflammation.^1,2 Although viruses, such as EBV and cytomegalovirus, represent almost 15% of the pathological causes of NSR, it is not uncommon for a patient to have multiple pathological processes present.¹ Our patient’s enlarged spleen was due to acute infectious mononucleosis.

Signs and Symptoms

Diagnosing NSR can be challenging and it is often missed or discovered incidentally during evaluation (as was initially the case with our patient).³ Several signs and symptoms present in our patient were red herrings that warranted closer analysis. The patient’s complaint of left shoulder pain suggested left hemidiaphragm irritation from the NSR. Furthermore, our patient’s near-syncopal episode was possibly due to acute vagal simulation from the initial contact of blood with the peritoneal cavity.⁴ The maximal vagal stimulus was likely transient, as our patient returned to baseline after a brief near-syncopal episode.

As illustrated in our case, though tachycardia is common in splenic rupture, not all patients present with this sign. The absence of tachycardia in our patient can be explained by the elevation of his baseline enteric vagal tone due to the continued presence of blood in the peritoneum.⁵ There are also other factors associated with the absence of tachycardia. For example, a well-conditioned athlete presenting with states of shock due to splenic rupture may not show signs of tachycardia.⁶

San Francisco Syncope Rule

The San Francisco Syncope Rule (SFSR) is a clinical decision-making risk-stratification tool used to determine outcomes and disposition of ED patients presenting with syncope.⁷ It is important to note that if we had used a straightforward application of the SFSR upon our patient’s initial presentation, the results would have been negative, suggesting he was not at risk for short-term serious outcomes.⁷

Imaging Studies

As demonstrated in our patient, a quick point-of-care (POC) bedside ultrasound scan can reveal the presence of free fluid in the abdomen to help with the diagnosis. On ultrasound, the presence of free fluid in the right upper quadrant is more commonly found in the hepatorenal recess, whereas in the left upper quadrant free fluid is seen sub-diaphragmatic/suprasplenic first before fluid is seen in the splenorenal recess. Bedside ultrasound can accurately detect as little as 100 mL of free fluid in the abdominal cavity, with a 90% sensitivity and 99% specificity.⁸

An ultrasound is highly sensitive as a preliminary screening tool to identify the presence of free intraperitoneal fluid and has some limited utility in identifying any disruption in the splenic echotexture that may suggest a laceration or hematoma. Ultrasound, however, has poor specificity in identifying solid organ injuries.⁹

Computed tomography scanning is the imaging modality of choice for assessing splenic injuries, and should be obtained to confirm the presence of a solid organ injury, as well as to grade the degree of injury and thereby determine the need for surgical intervention.¹⁰ It is worth noting that in a hemodynamically unstable patient, exploratory laparotomy may be embarked upon without a CT scan and positive free fluid on ultrasound.

Splenic Injury Scale

Splenic injury is classified on a scale of 1 (mild injury) to 5 (severe injury) (Table).¹¹

Conclusion

This case illustrates an uncommon presentation of NSR and underscores the importance of considering NSR in the differential diagnoses of patients presenting with abdominal pain—a sign with such a broad differential that NSR could easily be missed during evaluation. Based on its high sensitivity and specificity in detecting the presence of free fluid in the abdominal cavity, POC ultrasound imaging should be used to evaluate patients presenting with abdominal pain and syncopal or near-syncopal symptoms. This case further demonstrates that the absence of tachycardia or signs of shock should not rule out NSR.

Among National Football League (NFL) and National Collegiate Athletic Association (NCAA) team physicians, there is no consensus on the management of various injuries. At national and regional meetings, the management of football injuries often is debated.

Given the high level of interest in the treatment of elite football players, we wanted to determine treatment patterns by surveying orthopedic team physicians. We conducted a study to determine the demographics of NFL and NCAA team physicians and to identify patterns and variations in the management of common injuries in these groups of elite football players.

Materials and Methods

The study was reviewed by an Institutional Review Board before data collection and was classified as exempt. The study population consisted of head orthopedic team physicians for NFL teams and NCAA Division I universities. The survey (Appendix),

Chi-square tests were used to determine significant differences between groups. P < .05 was considered statistically significant.

Results

Responses were received from 31 (97%) of the 32 NFL and 111 (93%) of the 119 NCAA team physicians. The 2 groups’ surveys were identical with the exception of question 3, regarding NFL division or NCAA conference.

Team Physician Demographics

All survey respondents were the head orthopedic physicians for their teams. Seventy-one percent were the head team physicians as well; another 25% named a primary care physician as the head team physician. Thirty-nine percent of the NFL team physicians had been a team physician at the NFL level for more than 15 years, and 58% of the NCAA team physicians had been a team physician at the Division I level for more than 15 years. Eighty-one percent of NFL and 66% of NCAA team physicians had fellowship training in sports medicine. For away games, 10% of NFL vs 65% of NCAA teams traveled with 2 physicians; 90% of NFL and 28% of NCAA teams traveled with 3 or more physicians.

Only a small percentage of respondents (NFL, 10%; NCAA, 14%) indicated they had received advertising in exchange for services. Most respondents (NFL, 93%; NCAA, 89%) did not pay to provide team coverage. In contrast, 97% of NFL vs only 31% of NCAA physicians indicated they received a monetary stipend for providing orthopedic coverage.

Anterior Cruciate Ligament Reconstructions

Eighty-seven percent of NFL and 67% of NCAA respondents indicated that patellar tendon autograft was their preferred graft choice (Table 1).

Anterior Shoulder Dislocations (Without Bony Bankart)

Sling use after reduction of anterior shoulder dislocation was varied, with most physicians using a sling 2 weeks or less (Table 2).

Acromioclavicular Joint Injuries

Roughly two-thirds of respondents (NFL, 60%; NCAA, 69%) indicated that, during a game, they managed acute acromioclavicular (AC) joint injuries (type I/II) with injection of a local anesthetic that allowed return to play. In addition, a majority (NFL, 90%; NCAA, 87%) indicated they gave such athletes pregame injections that allowed them to play. About half the physicians (NFL, 57%; NCAA, 52%) injected the AC joint with cortisone during the acute/subacute period (<1 month) to decrease inflammation.

No significant difference was found between the 2 groups in terms of proportion of surgeons electing to treat type III AC joint injuries operatively versus nonoperatively (Table 4).

Medial Collateral Ligament Injuries

There was a significant (P < .0001) difference in use of prophylactic bracing for medial collateral ligament (MCL) injuries (NFL, 28%; NCAA, 89%).

Posterior Cruciate Ligament Injuries

The percentage of physicians who allowed athletes to return to play after a grade I/II posterior cruciate ligament (PCL) injury was significantly (P = .01) higher in NFL physicians (22%) than in NCAA physicians (7%). The amount of time varied up to more than 4 weeks (Figure 4).

Elbow Ulnar Collateral Ligament Tears

A majority of respondents indicated they would treat a complete elbow ulnar collateral ligament (UCL) tear in a quarterback; a much smaller percentage preferred operative repair in athletes playing other positions (Table 6).

Thumb Ulnar Collateral Ligament Tears

For athletes with in-season thumb UCL tears, 63% of NFL and 54% of NCAA physicians indicated they cast the thumb and allowed return to play. Others recommended operative repair and either cast the thumb and allowed return to play (NFL, 30%; NCAA, 41%) or let the thumb heal before allowing return to play (NFL, 7%; NCAA, 5%).

Fifth Metatarsal Fractures

For a large majority of physicians (NFL, 100%; NCAA, 94%), the preferred treatment for fifth metatarsal fractures was screw fixation.

Tibia Fractures

In the 5-year period before the survey, 43% of NFL and 75% of NCAA physicians managed at least one tibia fracture (P < .001) (Figure 7).

Ketorolac Injections

Intramuscular ketorolac injections were frequently given to elite football players, significantly (P < .01) more so in the NFL (93%) than in the NCAA (62%). The average number of injections varied among physicians, though a significantly (P < .0001) higher percentage of NFL (79%) than NCAA (13%) physicians gave 5 or more injections per game.

Discussion

This survey on managing common injuries in elite football players had an overall response rate of 94%. All NFL divisions and NCAA conferences were represented in physicians’ responses. Ninety percent of NFL and 65% of NCAA head team physicians were orthopedists. These findings differ from those of Stockard¹ (1997), who surveyed athletic directors at Division I schools and reported 45% of head team physicians were family medicine-trained and 41% were orthopedists.

Given the high visibility of team coverage and the economics of college football’s highest division, one might expect team physicians to receive financial remuneration. This was not the case, according to our survey: Only 30% of physicians received a monetary stipend for team coverage, and only 14% received advertising in exchange for their services. Twelve NCAA team physicians indicated they pay to be allowed to provide team coverage.

Injury Management

Anterior Cruciate Ligament Injuries. For NFL and NCAA team physicians, the preferred graft choice for ACL reconstruction was patellar tendon autograft. This finding is similar to what Erickson and colleagues² reported from a survey of NFL and NCAA team physicians: 86% of surgeons preferred bone–patellar tendon–bone (BPTB) autograft. However, only 1 surgeon (0.7%) in that study, vs 16% in ours, preferred allograft. Allograft use may be somewhat controversial, as relevant data on competitive athletes are lacking, and it has been shown that the graft rupture rate³ is higher for BPTB allograft than for BPTB autograft in young patients. However, much of the data on higher failure rates with use of allograft in young patients^4,5 has appeared since our data were collected.

Our return-to-play data are similar to data from other studies.^2,6 According to our survey, the most common length of time from ACL reconstruction to return to football was 6 months, and 94% of team physicians allowed return to football by 9 months. In the survey by Erickson and colleagues,² 55% of surgeons waited a minimum of 6 months before returning athletes to play, and only 12% waited at least 9 months. In the study by Bradley and colleagues⁶ (2002), 84% of surgeons waited at least 6 months before returning athletes to play. Of note, we found a significantly higher percentage of NCAA football players than NFL players returning within 6 months after surgery. The difference may be attributable to a more cautious approach being taken with NFL players, whereas most NCAA players are limited in the time remaining in their football careers and want to return to the playing field as soon as possible.

Shoulder Dislocations. Responses to the 5 survey questions on anterior shoulder dislocation showed little consensus with respect to management. The exception pertained to use of a harness for in-season return to play with a dislocation—92% of physicians preferred management with a harness. Of note, 7 of 10 team surgeons performed anterior stabilization through an arthroscopic approach. Despite historical recommendations to perform open anterior stabilization in collision athletes, NFL and NCAA physicians’ practice patterns have evolved.⁷ Although return to contact activity was varied among responses, 94% of physicians allowed return to contact within 6 months.

Acromioclavicular Joint Injuries. For college football players, AC joint injuries are the most common shoulder injuries.⁸ In the NFL Combine, the incidence of AC joint injuries was 15.7 per 100 players.⁸ Several studies have cited favorable results with nonoperative management of type III AC joint injuries.^9-12 Nonoperative management was the preferred treatment in our study as well, yet 26% of surgeons still preferred operative treatment in quarterbacks. Opinions about operative repair of type III injuries in overhead athletes vary,¹³ but nonoperative management clearly is the preferred method for elite football players. A 2013 study by Lynch and colleagues¹⁴ found that only 2 of 40 NFL players with type III AC joint injuries underwent surgery.

For type I and II AC joint injuries that occur during a game, more than two-thirds of the NCAA team physicians in our study favored injecting a local anesthetic to reduce pain and allow return to play in the same game. An even larger majority indicated they gave a pregame injection of an anesthetic to allow play. Similar use of injections for AC joint injuries has been reported in Australian-rules football and rugby.¹⁵Medial Collateral Ligament Injuries. Whether bracing is prophylactic against MCL injuries is controversial.¹⁶ Some studies have found it effective.^17,18 According to our survey, 89% of Division I football teams used prophylactic knee bracing, mainly in offensive linemen but frequently in defensive linemen, too. No schools used bracing in athletes who played skill positions, except quarterbacks. Six schools used bracing on a quarterback’s front leg.

The percentage of teams that used prophylactic MCL bracing was significantly higher in the NCAA than in the NFL. NCAA team physicians generally have more control over players and therefore can implement widespread use of this bracing.

Posterior Cruciate Ligament Injuries. These injuries are infrequent. According to Parolie and Bergfeld,¹⁹ only 2% of college football players at the NFL Combine had a PCL injury. Treatment in athletes remains controversial. Our survey showed physicians’ willingness to return players to competition within 4 weeks after grade I/II PCL injuries. There is no consensus on management or on postinjury bracing. In operative cases, however, the preferred graft is allograft, and the preferred repair method is the arthroscopic single-bundle technique. These findings mirror those of a 2004 survey of the Herodicus Society by Dennis and colleagues.²⁰ Elbow Ulnar Collateral Ligament Tears. In throwing athletes with UCL tears, operative treatment has been recommended.^21,22 A majority of our survey respondents preferred operative treatment for quarterbacks. However, operative treatment is still controversial, and quarterbacks differ from baseball players in their throwing motions and in the stresses acting on the UCLs during throwing. Two systematic reviews of UCL reconstruction have affirmed the positive outcomes of operative treatment in throwing athletes.^21,22 However, most of the studies covered by these reviews focused on baseball players. In athletes playing positions other than quarterback, these injuries were typically treated nonoperatively.

Thumb Ulnar Collateral Ligament Tears. Our survey respondents differed in their opinions on treating thumb UCL tears. About half recommended cast treatment, and the other half recommended operative treatment. Previous data suggest that delaying surgical treatment may be deleterious to the eventual outcome.^23,24Fifth Metatarsal Fractures. For fifth metatarsal fractures, screw fixation was preferred by 90% of our survey respondents—vs 73% of NFL team physicians in a 2004 study by Low and colleagues.²⁵ What remains controversial is the length of time before return to play. Our most frequent response was 4 to 6 weeks, and 46% of our respondents indicated they would wait 7 weeks or longer. These times differ significantly from what Low and colleagues²⁵ reported: 86% of their physicians allowed return to competition after 6 to 12 weeks.

Tibia Fractures. Management of tibia fractures in US football players has not been reported. Chang and colleagues²⁶ described 24 tibial shaft fractures in UK soccer players. Eleven fractures (~50%) were treated with intramedullary nails, 2 with plating, and 11 with conservative management. All players returned to activity, the operative group at 23.3 weeks and the nonoperative group at 27.6 weeks. Our respondents reported treating at least 150 tibial shaft fractures in the 5-year period before our survey, demonstrating the incidence and importance of this type of injury. A vast majority of team surgeons (96%) opted for treatment with intramedullary nailing. This choice may reflect an ability to return to play earlier—the ability to move the knee and maintain strength in the legs. Some have suggested it is important to remove the nail before the player returns to the football field, but this was not common practice among our groups of team surgeons. Other studies have not found any advantage to tibial nail removal.²⁷Ketorolac Injections. Authors have described using ketorolac for the treatment of acute or pregame pain in professional football players.^28-30 According to a 2000 survey, 93% of NFL teams used intramuscular ketorolac, and on average 15 players per team were treated, primarily on game day. Our survey found frequent use of ketorolac, with almost two-thirds of team orthopedists indicating pregame use. Ketorolac use was popular, particularly because of its effect in reducing postoperative pain and its potent effect in reducing pain on game day. However, injections by football team physicians have declined significantly in recent years, ever since an NFL Physician Society task force published recommendations on ketorolac use.³¹

Conclusion

There is a wide variety of patterns in treating athletes who play football at the highest levels of competition. Our findings can initiate further discussion on these topics and assist orthopedists providing game coverage at all levels of play in their decision-making process by helping to define the standard of care for their injured players.

Am J Orthop. 2016;45(6):E319-E327. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.

Among National Football League (NFL) and National Collegiate Athletic Association (NCAA) team physicians, there is no consensus on the management of various injuries. At national and regional meetings, the management of football injuries often is debated.

Given the high level of interest in the treatment of elite football players, we wanted to determine treatment patterns by surveying orthopedic team physicians. We conducted a study to determine the demographics of NFL and NCAA team physicians and to identify patterns and variations in the management of common injuries in these groups of elite football players.

Materials and Methods

The study was reviewed by an Institutional Review Board before data collection and was classified as exempt. The study population consisted of head orthopedic team physicians for NFL teams and NCAA Division I universities. The survey (Appendix),

Chi-square tests were used to determine significant differences between groups. P < .05 was considered statistically significant.

Results

Responses were received from 31 (97%) of the 32 NFL and 111 (93%) of the 119 NCAA team physicians. The 2 groups’ surveys were identical with the exception of question 3, regarding NFL division or NCAA conference.

Team Physician Demographics

All survey respondents were the head orthopedic physicians for their teams. Seventy-one percent were the head team physicians as well; another 25% named a primary care physician as the head team physician. Thirty-nine percent of the NFL team physicians had been a team physician at the NFL level for more than 15 years, and 58% of the NCAA team physicians had been a team physician at the Division I level for more than 15 years. Eighty-one percent of NFL and 66% of NCAA team physicians had fellowship training in sports medicine. For away games, 10% of NFL vs 65% of NCAA teams traveled with 2 physicians; 90% of NFL and 28% of NCAA teams traveled with 3 or more physicians.

Only a small percentage of respondents (NFL, 10%; NCAA, 14%) indicated they had received advertising in exchange for services. Most respondents (NFL, 93%; NCAA, 89%) did not pay to provide team coverage. In contrast, 97% of NFL vs only 31% of NCAA physicians indicated they received a monetary stipend for providing orthopedic coverage.

Anterior Cruciate Ligament Reconstructions

Eighty-seven percent of NFL and 67% of NCAA respondents indicated that patellar tendon autograft was their preferred graft choice (Table 1).

Anterior Shoulder Dislocations (Without Bony Bankart)

Sling use after reduction of anterior shoulder dislocation was varied, with most physicians using a sling 2 weeks or less (Table 2).

Acromioclavicular Joint Injuries

Roughly two-thirds of respondents (NFL, 60%; NCAA, 69%) indicated that, during a game, they managed acute acromioclavicular (AC) joint injuries (type I/II) with injection of a local anesthetic that allowed return to play. In addition, a majority (NFL, 90%; NCAA, 87%) indicated they gave such athletes pregame injections that allowed them to play. About half the physicians (NFL, 57%; NCAA, 52%) injected the AC joint with cortisone during the acute/subacute period (<1 month) to decrease inflammation.

No significant difference was found between the 2 groups in terms of proportion of surgeons electing to treat type III AC joint injuries operatively versus nonoperatively (Table 4).

Medial Collateral Ligament Injuries

There was a significant (P < .0001) difference in use of prophylactic bracing for medial collateral ligament (MCL) injuries (NFL, 28%; NCAA, 89%).

Posterior Cruciate Ligament Injuries

The percentage of physicians who allowed athletes to return to play after a grade I/II posterior cruciate ligament (PCL) injury was significantly (P = .01) higher in NFL physicians (22%) than in NCAA physicians (7%). The amount of time varied up to more than 4 weeks (Figure 4).

Elbow Ulnar Collateral Ligament Tears

A majority of respondents indicated they would treat a complete elbow ulnar collateral ligament (UCL) tear in a quarterback; a much smaller percentage preferred operative repair in athletes playing other positions (Table 6).

Thumb Ulnar Collateral Ligament Tears

For athletes with in-season thumb UCL tears, 63% of NFL and 54% of NCAA physicians indicated they cast the thumb and allowed return to play. Others recommended operative repair and either cast the thumb and allowed return to play (NFL, 30%; NCAA, 41%) or let the thumb heal before allowing return to play (NFL, 7%; NCAA, 5%).

Fifth Metatarsal Fractures

For a large majority of physicians (NFL, 100%; NCAA, 94%), the preferred treatment for fifth metatarsal fractures was screw fixation.

Tibia Fractures

In the 5-year period before the survey, 43% of NFL and 75% of NCAA physicians managed at least one tibia fracture (P < .001) (Figure 7).

Ketorolac Injections

Intramuscular ketorolac injections were frequently given to elite football players, significantly (P < .01) more so in the NFL (93%) than in the NCAA (62%). The average number of injections varied among physicians, though a significantly (P < .0001) higher percentage of NFL (79%) than NCAA (13%) physicians gave 5 or more injections per game.

Discussion

This survey on managing common injuries in elite football players had an overall response rate of 94%. All NFL divisions and NCAA conferences were represented in physicians’ responses. Ninety percent of NFL and 65% of NCAA head team physicians were orthopedists. These findings differ from those of Stockard¹ (1997), who surveyed athletic directors at Division I schools and reported 45% of head team physicians were family medicine-trained and 41% were orthopedists.

Given the high visibility of team coverage and the economics of college football’s highest division, one might expect team physicians to receive financial remuneration. This was not the case, according to our survey: Only 30% of physicians received a monetary stipend for team coverage, and only 14% received advertising in exchange for their services. Twelve NCAA team physicians indicated they pay to be allowed to provide team coverage.

Injury Management

Anterior Cruciate Ligament Injuries. For NFL and NCAA team physicians, the preferred graft choice for ACL reconstruction was patellar tendon autograft. This finding is similar to what Erickson and colleagues² reported from a survey of NFL and NCAA team physicians: 86% of surgeons preferred bone–patellar tendon–bone (BPTB) autograft. However, only 1 surgeon (0.7%) in that study, vs 16% in ours, preferred allograft. Allograft use may be somewhat controversial, as relevant data on competitive athletes are lacking, and it has been shown that the graft rupture rate³ is higher for BPTB allograft than for BPTB autograft in young patients. However, much of the data on higher failure rates with use of allograft in young patients^4,5 has appeared since our data were collected.

Our return-to-play data are similar to data from other studies.^2,6 According to our survey, the most common length of time from ACL reconstruction to return to football was 6 months, and 94% of team physicians allowed return to football by 9 months. In the survey by Erickson and colleagues,² 55% of surgeons waited a minimum of 6 months before returning athletes to play, and only 12% waited at least 9 months. In the study by Bradley and colleagues⁶ (2002), 84% of surgeons waited at least 6 months before returning athletes to play. Of note, we found a significantly higher percentage of NCAA football players than NFL players returning within 6 months after surgery. The difference may be attributable to a more cautious approach being taken with NFL players, whereas most NCAA players are limited in the time remaining in their football careers and want to return to the playing field as soon as possible.

Shoulder Dislocations. Responses to the 5 survey questions on anterior shoulder dislocation showed little consensus with respect to management. The exception pertained to use of a harness for in-season return to play with a dislocation—92% of physicians preferred management with a harness. Of note, 7 of 10 team surgeons performed anterior stabilization through an arthroscopic approach. Despite historical recommendations to perform open anterior stabilization in collision athletes, NFL and NCAA physicians’ practice patterns have evolved.⁷ Although return to contact activity was varied among responses, 94% of physicians allowed return to contact within 6 months.

Acromioclavicular Joint Injuries. For college football players, AC joint injuries are the most common shoulder injuries.⁸ In the NFL Combine, the incidence of AC joint injuries was 15.7 per 100 players.⁸ Several studies have cited favorable results with nonoperative management of type III AC joint injuries.^9-12 Nonoperative management was the preferred treatment in our study as well, yet 26% of surgeons still preferred operative treatment in quarterbacks. Opinions about operative repair of type III injuries in overhead athletes vary,¹³ but nonoperative management clearly is the preferred method for elite football players. A 2013 study by Lynch and colleagues¹⁴ found that only 2 of 40 NFL players with type III AC joint injuries underwent surgery.

For type I and II AC joint injuries that occur during a game, more than two-thirds of the NCAA team physicians in our study favored injecting a local anesthetic to reduce pain and allow return to play in the same game. An even larger majority indicated they gave a pregame injection of an anesthetic to allow play. Similar use of injections for AC joint injuries has been reported in Australian-rules football and rugby.¹⁵Medial Collateral Ligament Injuries. Whether bracing is prophylactic against MCL injuries is controversial.¹⁶ Some studies have found it effective.^17,18 According to our survey, 89% of Division I football teams used prophylactic knee bracing, mainly in offensive linemen but frequently in defensive linemen, too. No schools used bracing in athletes who played skill positions, except quarterbacks. Six schools used bracing on a quarterback’s front leg.

The percentage of teams that used prophylactic MCL bracing was significantly higher in the NCAA than in the NFL. NCAA team physicians generally have more control over players and therefore can implement widespread use of this bracing.

Posterior Cruciate Ligament Injuries. These injuries are infrequent. According to Parolie and Bergfeld,¹⁹ only 2% of college football players at the NFL Combine had a PCL injury. Treatment in athletes remains controversial. Our survey showed physicians’ willingness to return players to competition within 4 weeks after grade I/II PCL injuries. There is no consensus on management or on postinjury bracing. In operative cases, however, the preferred graft is allograft, and the preferred repair method is the arthroscopic single-bundle technique. These findings mirror those of a 2004 survey of the Herodicus Society by Dennis and colleagues.²⁰ Elbow Ulnar Collateral Ligament Tears. In throwing athletes with UCL tears, operative treatment has been recommended.^21,22 A majority of our survey respondents preferred operative treatment for quarterbacks. However, operative treatment is still controversial, and quarterbacks differ from baseball players in their throwing motions and in the stresses acting on the UCLs during throwing. Two systematic reviews of UCL reconstruction have affirmed the positive outcomes of operative treatment in throwing athletes.^21,22 However, most of the studies covered by these reviews focused on baseball players. In athletes playing positions other than quarterback, these injuries were typically treated nonoperatively.

Thumb Ulnar Collateral Ligament Tears. Our survey respondents differed in their opinions on treating thumb UCL tears. About half recommended cast treatment, and the other half recommended operative treatment. Previous data suggest that delaying surgical treatment may be deleterious to the eventual outcome.^23,24Fifth Metatarsal Fractures. For fifth metatarsal fractures, screw fixation was preferred by 90% of our survey respondents—vs 73% of NFL team physicians in a 2004 study by Low and colleagues.²⁵ What remains controversial is the length of time before return to play. Our most frequent response was 4 to 6 weeks, and 46% of our respondents indicated they would wait 7 weeks or longer. These times differ significantly from what Low and colleagues²⁵ reported: 86% of their physicians allowed return to competition after 6 to 12 weeks.

Tibia Fractures. Management of tibia fractures in US football players has not been reported. Chang and colleagues²⁶ described 24 tibial shaft fractures in UK soccer players. Eleven fractures (~50%) were treated with intramedullary nails, 2 with plating, and 11 with conservative management. All players returned to activity, the operative group at 23.3 weeks and the nonoperative group at 27.6 weeks. Our respondents reported treating at least 150 tibial shaft fractures in the 5-year period before our survey, demonstrating the incidence and importance of this type of injury. A vast majority of team surgeons (96%) opted for treatment with intramedullary nailing. This choice may reflect an ability to return to play earlier—the ability to move the knee and maintain strength in the legs. Some have suggested it is important to remove the nail before the player returns to the football field, but this was not common practice among our groups of team surgeons. Other studies have not found any advantage to tibial nail removal.²⁷Ketorolac Injections. Authors have described using ketorolac for the treatment of acute or pregame pain in professional football players.^28-30 According to a 2000 survey, 93% of NFL teams used intramuscular ketorolac, and on average 15 players per team were treated, primarily on game day. Our survey found frequent use of ketorolac, with almost two-thirds of team orthopedists indicating pregame use. Ketorolac use was popular, particularly because of its effect in reducing postoperative pain and its potent effect in reducing pain on game day. However, injections by football team physicians have declined significantly in recent years, ever since an NFL Physician Society task force published recommendations on ketorolac use.³¹

Conclusion

There is a wide variety of patterns in treating athletes who play football at the highest levels of competition. Our findings can initiate further discussion on these topics and assist orthopedists providing game coverage at all levels of play in their decision-making process by helping to define the standard of care for their injured players.

Am J Orthop. 2016;45(6):E319-E327. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.

Among National Football League (NFL) and National Collegiate Athletic Association (NCAA) team physicians, there is no consensus on the management of various injuries. At national and regional meetings, the management of football injuries often is debated.

Given the high level of interest in the treatment of elite football players, we wanted to determine treatment patterns by surveying orthopedic team physicians. We conducted a study to determine the demographics of NFL and NCAA team physicians and to identify patterns and variations in the management of common injuries in these groups of elite football players.

Materials and Methods

The study was reviewed by an Institutional Review Board before data collection and was classified as exempt. The study population consisted of head orthopedic team physicians for NFL teams and NCAA Division I universities. The survey (Appendix),

Chi-square tests were used to determine significant differences between groups. P < .05 was considered statistically significant.

Results

Responses were received from 31 (97%) of the 32 NFL and 111 (93%) of the 119 NCAA team physicians. The 2 groups’ surveys were identical with the exception of question 3, regarding NFL division or NCAA conference.

Team Physician Demographics

All survey respondents were the head orthopedic physicians for their teams. Seventy-one percent were the head team physicians as well; another 25% named a primary care physician as the head team physician. Thirty-nine percent of the NFL team physicians had been a team physician at the NFL level for more than 15 years, and 58% of the NCAA team physicians had been a team physician at the Division I level for more than 15 years. Eighty-one percent of NFL and 66% of NCAA team physicians had fellowship training in sports medicine. For away games, 10% of NFL vs 65% of NCAA teams traveled with 2 physicians; 90% of NFL and 28% of NCAA teams traveled with 3 or more physicians.

Only a small percentage of respondents (NFL, 10%; NCAA, 14%) indicated they had received advertising in exchange for services. Most respondents (NFL, 93%; NCAA, 89%) did not pay to provide team coverage. In contrast, 97% of NFL vs only 31% of NCAA physicians indicated they received a monetary stipend for providing orthopedic coverage.

Anterior Cruciate Ligament Reconstructions

Eighty-seven percent of NFL and 67% of NCAA respondents indicated that patellar tendon autograft was their preferred graft choice (Table 1).

Anterior Shoulder Dislocations (Without Bony Bankart)

Sling use after reduction of anterior shoulder dislocation was varied, with most physicians using a sling 2 weeks or less (Table 2).

Acromioclavicular Joint Injuries

Roughly two-thirds of respondents (NFL, 60%; NCAA, 69%) indicated that, during a game, they managed acute acromioclavicular (AC) joint injuries (type I/II) with injection of a local anesthetic that allowed return to play. In addition, a majority (NFL, 90%; NCAA, 87%) indicated they gave such athletes pregame injections that allowed them to play. About half the physicians (NFL, 57%; NCAA, 52%) injected the AC joint with cortisone during the acute/subacute period (<1 month) to decrease inflammation.

No significant difference was found between the 2 groups in terms of proportion of surgeons electing to treat type III AC joint injuries operatively versus nonoperatively (Table 4).

Medial Collateral Ligament Injuries

There was a significant (P < .0001) difference in use of prophylactic bracing for medial collateral ligament (MCL) injuries (NFL, 28%; NCAA, 89%).

Posterior Cruciate Ligament Injuries

The percentage of physicians who allowed athletes to return to play after a grade I/II posterior cruciate ligament (PCL) injury was significantly (P = .01) higher in NFL physicians (22%) than in NCAA physicians (7%). The amount of time varied up to more than 4 weeks (Figure 4).

Elbow Ulnar Collateral Ligament Tears

A majority of respondents indicated they would treat a complete elbow ulnar collateral ligament (UCL) tear in a quarterback; a much smaller percentage preferred operative repair in athletes playing other positions (Table 6).

Thumb Ulnar Collateral Ligament Tears

For athletes with in-season thumb UCL tears, 63% of NFL and 54% of NCAA physicians indicated they cast the thumb and allowed return to play. Others recommended operative repair and either cast the thumb and allowed return to play (NFL, 30%; NCAA, 41%) or let the thumb heal before allowing return to play (NFL, 7%; NCAA, 5%).

Fifth Metatarsal Fractures

For a large majority of physicians (NFL, 100%; NCAA, 94%), the preferred treatment for fifth metatarsal fractures was screw fixation.

Tibia Fractures

In the 5-year period before the survey, 43% of NFL and 75% of NCAA physicians managed at least one tibia fracture (P < .001) (Figure 7).

Ketorolac Injections

Intramuscular ketorolac injections were frequently given to elite football players, significantly (P < .01) more so in the NFL (93%) than in the NCAA (62%). The average number of injections varied among physicians, though a significantly (P < .0001) higher percentage of NFL (79%) than NCAA (13%) physicians gave 5 or more injections per game.

Discussion

This survey on managing common injuries in elite football players had an overall response rate of 94%. All NFL divisions and NCAA conferences were represented in physicians’ responses. Ninety percent of NFL and 65% of NCAA head team physicians were orthopedists. These findings differ from those of Stockard¹ (1997), who surveyed athletic directors at Division I schools and reported 45% of head team physicians were family medicine-trained and 41% were orthopedists.

Given the high visibility of team coverage and the economics of college football’s highest division, one might expect team physicians to receive financial remuneration. This was not the case, according to our survey: Only 30% of physicians received a monetary stipend for team coverage, and only 14% received advertising in exchange for their services. Twelve NCAA team physicians indicated they pay to be allowed to provide team coverage.

Injury Management

Anterior Cruciate Ligament Injuries. For NFL and NCAA team physicians, the preferred graft choice for ACL reconstruction was patellar tendon autograft. This finding is similar to what Erickson and colleagues² reported from a survey of NFL and NCAA team physicians: 86% of surgeons preferred bone–patellar tendon–bone (BPTB) autograft. However, only 1 surgeon (0.7%) in that study, vs 16% in ours, preferred allograft. Allograft use may be somewhat controversial, as relevant data on competitive athletes are lacking, and it has been shown that the graft rupture rate³ is higher for BPTB allograft than for BPTB autograft in young patients. However, much of the data on higher failure rates with use of allograft in young patients^4,5 has appeared since our data were collected.

Our return-to-play data are similar to data from other studies.^2,6 According to our survey, the most common length of time from ACL reconstruction to return to football was 6 months, and 94% of team physicians allowed return to football by 9 months. In the survey by Erickson and colleagues,² 55% of surgeons waited a minimum of 6 months before returning athletes to play, and only 12% waited at least 9 months. In the study by Bradley and colleagues⁶ (2002), 84% of surgeons waited at least 6 months before returning athletes to play. Of note, we found a significantly higher percentage of NCAA football players than NFL players returning within 6 months after surgery. The difference may be attributable to a more cautious approach being taken with NFL players, whereas most NCAA players are limited in the time remaining in their football careers and want to return to the playing field as soon as possible.

Shoulder Dislocations. Responses to the 5 survey questions on anterior shoulder dislocation showed little consensus with respect to management. The exception pertained to use of a harness for in-season return to play with a dislocation—92% of physicians preferred management with a harness. Of note, 7 of 10 team surgeons performed anterior stabilization through an arthroscopic approach. Despite historical recommendations to perform open anterior stabilization in collision athletes, NFL and NCAA physicians’ practice patterns have evolved.⁷ Although return to contact activity was varied among responses, 94% of physicians allowed return to contact within 6 months.

Acromioclavicular Joint Injuries. For college football players, AC joint injuries are the most common shoulder injuries.⁸ In the NFL Combine, the incidence of AC joint injuries was 15.7 per 100 players.⁸ Several studies have cited favorable results with nonoperative management of type III AC joint injuries.^9-12 Nonoperative management was the preferred treatment in our study as well, yet 26% of surgeons still preferred operative treatment in quarterbacks. Opinions about operative repair of type III injuries in overhead athletes vary,¹³ but nonoperative management clearly is the preferred method for elite football players. A 2013 study by Lynch and colleagues¹⁴ found that only 2 of 40 NFL players with type III AC joint injuries underwent surgery.

For type I and II AC joint injuries that occur during a game, more than two-thirds of the NCAA team physicians in our study favored injecting a local anesthetic to reduce pain and allow return to play in the same game. An even larger majority indicated they gave a pregame injection of an anesthetic to allow play. Similar use of injections for AC joint injuries has been reported in Australian-rules football and rugby.¹⁵Medial Collateral Ligament Injuries. Whether bracing is prophylactic against MCL injuries is controversial.¹⁶ Some studies have found it effective.^17,18 According to our survey, 89% of Division I football teams used prophylactic knee bracing, mainly in offensive linemen but frequently in defensive linemen, too. No schools used bracing in athletes who played skill positions, except quarterbacks. Six schools used bracing on a quarterback’s front leg.

The percentage of teams that used prophylactic MCL bracing was significantly higher in the NCAA than in the NFL. NCAA team physicians generally have more control over players and therefore can implement widespread use of this bracing.

Posterior Cruciate Ligament Injuries. These injuries are infrequent. According to Parolie and Bergfeld,¹⁹ only 2% of college football players at the NFL Combine had a PCL injury. Treatment in athletes remains controversial. Our survey showed physicians’ willingness to return players to competition within 4 weeks after grade I/II PCL injuries. There is no consensus on management or on postinjury bracing. In operative cases, however, the preferred graft is allograft, and the preferred repair method is the arthroscopic single-bundle technique. These findings mirror those of a 2004 survey of the Herodicus Society by Dennis and colleagues.²⁰ Elbow Ulnar Collateral Ligament Tears. In throwing athletes with UCL tears, operative treatment has been recommended.^21,22 A majority of our survey respondents preferred operative treatment for quarterbacks. However, operative treatment is still controversial, and quarterbacks differ from baseball players in their throwing motions and in the stresses acting on the UCLs during throwing. Two systematic reviews of UCL reconstruction have affirmed the positive outcomes of operative treatment in throwing athletes.^21,22 However, most of the studies covered by these reviews focused on baseball players. In athletes playing positions other than quarterback, these injuries were typically treated nonoperatively.

Thumb Ulnar Collateral Ligament Tears. Our survey respondents differed in their opinions on treating thumb UCL tears. About half recommended cast treatment, and the other half recommended operative treatment. Previous data suggest that delaying surgical treatment may be deleterious to the eventual outcome.^23,24Fifth Metatarsal Fractures. For fifth metatarsal fractures, screw fixation was preferred by 90% of our survey respondents—vs 73% of NFL team physicians in a 2004 study by Low and colleagues.²⁵ What remains controversial is the length of time before return to play. Our most frequent response was 4 to 6 weeks, and 46% of our respondents indicated they would wait 7 weeks or longer. These times differ significantly from what Low and colleagues²⁵ reported: 86% of their physicians allowed return to competition after 6 to 12 weeks.

Tibia Fractures. Management of tibia fractures in US football players has not been reported. Chang and colleagues²⁶ described 24 tibial shaft fractures in UK soccer players. Eleven fractures (~50%) were treated with intramedullary nails, 2 with plating, and 11 with conservative management. All players returned to activity, the operative group at 23.3 weeks and the nonoperative group at 27.6 weeks. Our respondents reported treating at least 150 tibial shaft fractures in the 5-year period before our survey, demonstrating the incidence and importance of this type of injury. A vast majority of team surgeons (96%) opted for treatment with intramedullary nailing. This choice may reflect an ability to return to play earlier—the ability to move the knee and maintain strength in the legs. Some have suggested it is important to remove the nail before the player returns to the football field, but this was not common practice among our groups of team surgeons. Other studies have not found any advantage to tibial nail removal.²⁷Ketorolac Injections. Authors have described using ketorolac for the treatment of acute or pregame pain in professional football players.^28-30 According to a 2000 survey, 93% of NFL teams used intramuscular ketorolac, and on average 15 players per team were treated, primarily on game day. Our survey found frequent use of ketorolac, with almost two-thirds of team orthopedists indicating pregame use. Ketorolac use was popular, particularly because of its effect in reducing postoperative pain and its potent effect in reducing pain on game day. However, injections by football team physicians have declined significantly in recent years, ever since an NFL Physician Society task force published recommendations on ketorolac use.³¹

Conclusion

There is a wide variety of patterns in treating athletes who play football at the highest levels of competition. Our findings can initiate further discussion on these topics and assist orthopedists providing game coverage at all levels of play in their decision-making process by helping to define the standard of care for their injured players.

Am J Orthop. 2016;45(6):E319-E327. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.

Football, one of the most popular sports in the United States, is additionally recognized as a leading contributor to sports injury secondary to the contact collision nature of the endeavor. There are an estimated 1.1 million high school football players with another 100,000 participants combined in the National Football League (NFL), college, junior college, Arena Football League, and semipro levels of play.¹ USA Football estimates that an additional 3 million youth participate in community football leagues.¹ The National Center for Catastrophic Sports Injury Research recently calculated a fatality rate of 0.14 per 100,000 participants in 2014 for the 4.2 million who play football at all levels—and 0.45 per 100,000 in high school.¹ While direct deaths from head and spine injury remain a significant contributor to the number of catastrophic injuries, indirect deaths (systemic failure) predominate. Exertional heat stroke (EHS) has emerged as one of the leading indirect causes of death in high school and collegiate football. Boden and colleagues² reported that high school and college football players sustain approximately 12 fatalities annually, with indirect systemic causes being twice as common as direct blunt trauma.²The most common indirect causes identified included cardiac failure, heat illness, and complications of sickle cell trait (SCT). It was also noted that the risk of SCT, heat-related, and cardiac deaths increased during the second decade of the study, indicating these conditions may require a greater emphasis on diagnosis, treatment, and prevention. This review details for the team physician the unique challenge of exercising in the heat to the football player, and the prevention, diagnosis, management and return-to-play issues pertinent to exertional heat illness (EHI).

The Challenge

EHS represents the most severe manifestation of EHI—a gamut of diseases commonly encountered during the hot summer months when American football season begins. The breadth of EHI includes several important clinical diagnoses: exercise-associated muscle cramps (heat cramps); heat exhaustion with and without syncope; heat injury with evidence of end organ injury (eg, rhabdomyolysis); and EHS. EHS is defined as “a form of hyperthermia associated with a systemic inflammatory response leading to a syndrome of multi-organ dysfunction in which encephalopathy predominates.”³ EHS, if left untreated, or even if clinical treatment is delayed, may result in significant end organ morbidity and/or mortality.

During exercise, the human thermoregulatory system mitigates heat gain by increasing skin blood flow and sweating, causing an increased dissipation of heat to the surrounding environment by leveraging conduction, convection, and evaporation.^4,5 Elevated environmental temperatures, increased humidity, and dehydration can impede the body’s ability to dissipate heat at a rate needed to maintain thermoregulation. This imbalance can result in hyperthermia secondary to uncompensated heat stress,⁵ which in turn can lead to EHI. Football players have unique challenges that make them particularly vulnerable to EHI. The summer heat during early-season participation and the requirement for equipment that covers nearly 60% of body surfaces pose increased risk of volume losses and hyperthermia that trigger the onset of EHI.⁶ Football athletes’ body compositions and physical size are additional contributing risk factors; the relatively high muscle and fat content increase thermogenicity, which require their bodies to dissipate more heat.⁷

An estimated 9000 cases of EHI occur annually across all high school sports,⁸ with an incidence of 1.6:100,000 athlete-exposures.^8,9 Studies have demonstrated, however, that EHI occurs in football 11.4 times more often than in all other high school sports combined.¹⁰ The incidence of nonfatal EHI in all levels of football is 4.42-5:100,000.^8,9 Between 2000 and 2014, 41 football players died from EHS.¹ In football, approximately 75% of all EHI events occurred during practices, while only 25% of incidents occurred during games.⁸

Given these potentially deadly consequences, it is important that football team physicians are not only alert to the early symptoms of heat illness and prepared to intervene to prevent the progression to EHS, but are critical leaders in educating coaches and players in evidence-based EHI prevention practices and policies.

Prevention

EHS is a preventable condition, arguably the most common cause of preventable nontraumatic exertional death in young athletes in the United States. Close attention to mitigating risk factors should begin prior to the onset of preseason practice and continue through the early season, where athletes are at the highest risk of developing heat illness.

Primary Prevention

Primary prevention is fundamental to minimizing the occurrences of EHI. It focuses on the following methods: recognition of inherent risk factors, acclimatization, hydration, and avoidance of inciting substances (including supplements).

Pre-Participation Examination. The purpose of the pre-participation examination (PPE) is to maximize an athlete’s safety by identifying medical conditions that place the athlete at risk.^11,12 The Preparticipation Physical Evaluation, 4th edition, the most widely used consensus publication, specifically queries if an athlete has a previous history of heat injury. However, it only indirectly addresses intrinsic risk factors that may predispose an athlete to EHI who has never had an EHI before. Therefore, providers should take the opportunity of the PPE to inquire about additional risk factors that may make an athlete high risk for sustaining a heat injury. Common risk factors for EHI are listed in Table 1.

Secondary Prevention

Despite physicians’ best efforts to prevent all cases of EHI, athletes will still experience the effects of exercise-induced hyperthermia. The goal of secondary prevention is to slow the progression of this hyperthermia so that it does not progress to more dangerous EHI.

Hydration. Dehydration is an important risk factor for EHI. Sweat maintains thermoregulation by dissipating heat generated during exercise; however, it also contributes to body water losses. Furthermore, intravascular depletion decreases stroke volume, thereby increasing cardiovascular strain. It is estimated that for every 1% loss in body mass from dehydration, body temperature rises 0.22°C in comparison to a euhydrated state.⁶ Dehydration occurs more rapidly in hot environments, as fluid is lost through increased sweat production.⁷ After approximately 6% to 10% body weight volume loss, cardiac output cannot be maintained, diminishing sweat production and blood flow to both skin and muscle and causing diminished performance and a significant risk of heat exhaustion.⁷ If left unchecked, these physiologic changes result in further elevations in body temperature and increased cardiovascular strain, ultimately placing the athlete at significant risk for development of EHS.

Adequate hydration to maintain euvolemia is an important step in avoiding possible EHI. Multiple studies have shown that football players experience a baseline hypovolemia during their competition season,⁶ a deficit that is most marked during the first week of practices.¹⁷ This deficit is multifactorial, as football players expend a significant amount of fluid through sweat, are not able to adequately replace these losses during practice, and do not appropriately hydrate off the field.^6,18 Some players, especially linemen, sweat at a higher rate than their teammates, posing a possible risk of significant dehydration.⁶ Coaches and players alike should be educated on the importance of adequate hydration to meet their fluid needs.

The goal of hydration during exercise is to prevent large fluid losses that can adversely affect performance and increase risk of EHI;⁶ it may be unrealistic to replace all fluid losses during the practice period. Instead, athletes should target complete volume replacement over the post-exercise period.⁶ Some recommend hydrating based upon thirst drive; however, thirst is activated following a volume loss of approximately 2% body mass, the same degree of losses that place athletes at an increased risk for performance impairment and EHI.^4,6,11,12 Individuals should have access to fluids throughout practice and competition and be encouraged to hydrate as needed.^6,12,15 Furthermore, staff should modify their practices based upon WBGT and acclimatization status to provide more frequent hydration breaks.

Hyperhydration and Salt Intake. Of note, there are inherent risks to hyperhydration. Athletes with low sweat rates have an increased risk of overhydration and the development of exercise-associated hyponatremia (EAH),⁶ a condition whose presentation is very similar to EHS. In addition, inadequate sodium intake and excessive sweating can also contribute to the development of EAH. EAH has been implicated in the deaths of 2 football players in 2014.^1,6 Establishing team hydration guidelines and educating players and staff on appropriate hydration and dietary salt intake is essential to reduce the risk of both dehydration and hyperhydration and their complications.⁶Intra-Event Cooling. During exercise, team physicians can employ strategies for cooling athletes during exertion to mitigate their risk of EHI by decreasing thermal and cardiovascular strain.^4,19 Cooling during exercise is hypothesized to allow for accelerated heat dissipation, where heat is lost from the body more effectively. This accelerated loss enables athletes to maintain a higher heat storage capacity over the duration of exercise, avoiding uncompensated heat stresses that ultimately cause EHI.¹⁹

Some intra-event cooling strategies include the use of cooling garments, cooling packs, and cold water/slurry ingestion. Cooling garments lower skin temperature, which in turn can decrease thermoregulatory strains;⁴ a recent meta-analysis of intra-event cooling modalities revealed that wearing an ice vest during exercise resulted in the greatest decrease in thermal heat strain.¹⁹ Internal cooling strategies—namely ingestion of cold fluids/ice slurry—have shown some mild benefit in decreasing internal temperatures; however, some studies have demonstrated some decrease in sweat production associated with cold oral intake used in isolation.¹⁹ Overall, studies have shown that combining external (cooling clothing, ice packs, fanning) and internal (cold water, ice slurry) cooling methods result in a greater cooling effect than a use of a single method.⁴

Tertiary Prevention

The goal of tertiary prevention is to mitigate the risk of long-term adverse outcomes following an EHS event. The most effective means of reducing risk for morbidity and mortality is rapid identification and treatment of EHS as well as close evaluation of an athlete’s return to activity in heat. This process is spearheaded by an effective and well-rehearsed emergency action plan.

Diagnosis and Management

Rapid identification and treatment of EHS is crucial to minimizing the risk of poor outcomes.⁷ Any delay in the treatment of EHS can dramatically increase the likelihood of associated morbidity and mortality.²⁰

EHS is diagnosed by an elevated rectal temperature ≥40°C (104°F) and associated central nervous system (CNS) dysfunction.²¹ EHS should be strongly suspected in any athlete exercising in heat who exhibits signs of CNS dysfunction, including disorientation, confusion, dizziness, erratic behavior, irritability, headache, loss of coordination, delirium, collapse, or seizures.^7,12,15 EHS may also present with symptoms of heat exhaustion, including fatigue, hyperventilation, tachycardia, vomiting, diarrhea, and hypotension.^7,12,15

Rectal temperature should be taken for any athlete with suspected EHS, as other modalities—oral, skin, axillary, and aural—can be inaccurate and easily modified by ambient confounders such as ambient and skin temperature, athlete hyperventilation, and consumption of liquids.^7,11,12 Athletes exhibiting CNS symptoms with moderately elevated rectal temperatures that do not exceed 40°C should also be assumed to be suffering from EHS and treated with rapid cooling.¹¹ On the other hand, athletes with CNS symptoms who are normothermic should be assumed to have EAH until ruled out by electrolyte assessment; IV fluids should be at no more than keep vein open (KVO) pending this determination.¹¹ In some cases, an athlete may initially present with altered mental status but return to “normal.” However, this improvement may represent a “lucid period”; evaluation should continue with rectal temperature and treatment, as EHS in these cases may progress quickly.¹⁵

Treatment is centered on rapid, whole body cooling initiated at the first sign of heat illness.^7,22 The goal of treatment is to achieve a rectal temperature <38.9°C within 30 minutes of the onset of EHS.¹⁵ Upon diagnosis, the athlete should be quickly placed in a tub of ice water to facilitate cold water immersion (CWI) therapy. Some guidelines suggest the athlete’s clothing be removed to potentiate evaporative cooling during CWI;¹² however, cooling should not be delayed due to difficulties in removing equipment. CWI, where a heat stroke victim is submerged in ice water up to their neck while water is continuously circulated, is generally considered to be the gold standard treatment as it is the modality with the highest recorded cooling rates and the lowest rate of morbidity and mortality.^7,20,21 Multiple studies of CWI have shown that survival nears 100% when aggressive cooling starts within 5 minutes of collapse or identification of EHS.^20,21,22

If whole body CWI is unavailable, alternative methods of rapid cooling should be employed. Partial CWI, with torso immersion being preferable to the extremities, has been shown to achieve an acceptable rate of cooling to achieve sufficient drops in internal body temperature.^20,23 However, one popular treatment—applying ice packs to the whole body, in particular to the groin and axillae—has not been shown to be sufficient to achieve standard cooling goals.²⁰ None of these methods have been shown to be as effective as CWI.²³

Intravenous access should be initiated with fluid resuscitation dictated by the provider’s assessment. Normal saline is recommended as the resuscitative fluid of choice, with the rate dictated by clinical judgment and adjusted as guided by electrolyte determination and clinical response. It cannot be overstated that in normothermic patients with confusion, EAH is the diagnosis of exclusion and aggressive fluid resuscitation should be withheld until electrolyte determination.

Once rectal temperature descends appropriately (~38.9°C), the cooling process should stop and the individual should be transported to a hospital for further observation²⁰ and evaluation of possible sequelae, including rhabdomyolysis and renal injury, cardiac dysfunction and arrhythmia, severe electrolyte abnormalities, acute respiratory distress syndrome, lactic acidosis, and other forms of end-organ failure (Figure).

Emergency Action Plan

Team physicians should be proactive in developing an emergency action plan to address possible EHS events. These plans should be site-specific, addressing procedures for all practice and home competition locations.¹² All competition venues should have a CWI tub on-site in events where there is an increased risk of EHS.^12,15,20 This tub should be set up and functional for all high-risk activities, including practices.¹²

Following recognition of a potential case of EHS, treatment teams should have procedures in place to transport athletes to the treatment area, obtain rectal temperature, initiate rapid cooling, and stabilize the athlete for transport to an emergency department (ED) for further evaluation.^12,15 A written record of treatments and medications provided during athlete stabilization should be maintained and transported with the athlete to the ED.¹⁵ A list of helpful equipment and supplies for treatment of EHS can be found in Table 5.

Return to Play

Perhaps the most challenging and important role the team physician has is determining an athlete’s return to play following EHI, as there currently are no evidence-based guidelines for return to activity for these athletes.⁷ The decisions surrounding return to play are highly individualized, as recovery from EHS and heat injury is associated with the duration of internal body temperature elevation above the critical level (40°C).^7,20 Guidelines for return to activity following recovery from EHI differ among experts and institutions.^7,25 The general consensus from these guidelines is that, at minimum, athletes should not participate in any physical activity until they are asymptomatic and all blood tests have normalized.¹¹ Following this asymptomatic period, most guidelines advocate for a slow, deliberate return to activity.¹¹ The American College of Sports Medicine (ACSM) offers one reasonable approach to the returning athlete following EHS:⁷

• No exercise for at least 7 days following release from medical care.
• Follow-up with a physician 1 week after release from medical care for physical examination and any warranted lab or radiologic studies (based upon organ systems affected during EHS).
• Once cleared to return to activity, the athlete begins exercise in a cool environment, gradually increasing the duration, intensity, and heat exposure over 2 weeks to demonstrate heat tolerance and acclimatization.
• Athletes who cannot resume vigorous activity due to recurrent symptoms (eg, excessive fatigue) should be reevaluated after 4 weeks. Laboratory exercise-heat tolerance testing may be useful in this setting.
• The athlete may resume full competition once they are able to participate in full training in the heat for 2 to 4 weeks without adverse effects.

Heat tolerance testing (HTT) in these athletes remains controversial.^{5 26} The ACSM recommends that HTT be considered only for those unable to return to vigorous activity after a suitable period (approximately 4 weeks). In contrast, the Israeli Defense Force (IDF) uses HTT to evaluate soldiers following EHS to guide decision-making about return to duty.²⁷ The IDF HTT assumes that individuals will respond differently to heat stresses. They identify individuals who are “heat intolerant” as being unable to tolerate specific heat challenges, indicated by increases in body temperature occurring more rapidly than normal responders under identical environmental and exercise conditions. However, despite being used for more than 30 years, there is no clear evidence that HTT adequately predicts who will experience subsequent episodes of EHS.

Conclusion

While the recognized cornerstone of being a team physician is the provision of medical care, the ACSM Team Physician Consensus Statement²⁸ further delineates the medical and administrative responsibilities as both (1) understanding medical management and prevention of injury and illness in athletes; and (2) awareness of or involvement in the development and rehearsal of an emergency action plan. These tenets are critical for the team physician who accepts the responsibility to cover sports at the high school level or higher. Football team physicians play an essential role in mitigating risk of EHI in their athletes. Through development and execution of both comprehensive prevention strategies and emergency action plans, physicians can work to minimize athletes’ risk of both developing and experiencing significant adverse outcomes from an EHI.

Am J Orthop. 2016;45(6):340-348. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.

Football, one of the most popular sports in the United States, is additionally recognized as a leading contributor to sports injury secondary to the contact collision nature of the endeavor. There are an estimated 1.1 million high school football players with another 100,000 participants combined in the National Football League (NFL), college, junior college, Arena Football League, and semipro levels of play.¹ USA Football estimates that an additional 3 million youth participate in community football leagues.¹ The National Center for Catastrophic Sports Injury Research recently calculated a fatality rate of 0.14 per 100,000 participants in 2014 for the 4.2 million who play football at all levels—and 0.45 per 100,000 in high school.¹ While direct deaths from head and spine injury remain a significant contributor to the number of catastrophic injuries, indirect deaths (systemic failure) predominate. Exertional heat stroke (EHS) has emerged as one of the leading indirect causes of death in high school and collegiate football. Boden and colleagues² reported that high school and college football players sustain approximately 12 fatalities annually, with indirect systemic causes being twice as common as direct blunt trauma.²The most common indirect causes identified included cardiac failure, heat illness, and complications of sickle cell trait (SCT). It was also noted that the risk of SCT, heat-related, and cardiac deaths increased during the second decade of the study, indicating these conditions may require a greater emphasis on diagnosis, treatment, and prevention. This review details for the team physician the unique challenge of exercising in the heat to the football player, and the prevention, diagnosis, management and return-to-play issues pertinent to exertional heat illness (EHI).

The Challenge

EHS represents the most severe manifestation of EHI—a gamut of diseases commonly encountered during the hot summer months when American football season begins. The breadth of EHI includes several important clinical diagnoses: exercise-associated muscle cramps (heat cramps); heat exhaustion with and without syncope; heat injury with evidence of end organ injury (eg, rhabdomyolysis); and EHS. EHS is defined as “a form of hyperthermia associated with a systemic inflammatory response leading to a syndrome of multi-organ dysfunction in which encephalopathy predominates.”³ EHS, if left untreated, or even if clinical treatment is delayed, may result in significant end organ morbidity and/or mortality.

During exercise, the human thermoregulatory system mitigates heat gain by increasing skin blood flow and sweating, causing an increased dissipation of heat to the surrounding environment by leveraging conduction, convection, and evaporation.^4,5 Elevated environmental temperatures, increased humidity, and dehydration can impede the body’s ability to dissipate heat at a rate needed to maintain thermoregulation. This imbalance can result in hyperthermia secondary to uncompensated heat stress,⁵ which in turn can lead to EHI. Football players have unique challenges that make them particularly vulnerable to EHI. The summer heat during early-season participation and the requirement for equipment that covers nearly 60% of body surfaces pose increased risk of volume losses and hyperthermia that trigger the onset of EHI.⁶ Football athletes’ body compositions and physical size are additional contributing risk factors; the relatively high muscle and fat content increase thermogenicity, which require their bodies to dissipate more heat.⁷

An estimated 9000 cases of EHI occur annually across all high school sports,⁸ with an incidence of 1.6:100,000 athlete-exposures.^8,9 Studies have demonstrated, however, that EHI occurs in football 11.4 times more often than in all other high school sports combined.¹⁰ The incidence of nonfatal EHI in all levels of football is 4.42-5:100,000.^8,9 Between 2000 and 2014, 41 football players died from EHS.¹ In football, approximately 75% of all EHI events occurred during practices, while only 25% of incidents occurred during games.⁸

Given these potentially deadly consequences, it is important that football team physicians are not only alert to the early symptoms of heat illness and prepared to intervene to prevent the progression to EHS, but are critical leaders in educating coaches and players in evidence-based EHI prevention practices and policies.

Prevention

EHS is a preventable condition, arguably the most common cause of preventable nontraumatic exertional death in young athletes in the United States. Close attention to mitigating risk factors should begin prior to the onset of preseason practice and continue through the early season, where athletes are at the highest risk of developing heat illness.

Primary Prevention

Primary prevention is fundamental to minimizing the occurrences of EHI. It focuses on the following methods: recognition of inherent risk factors, acclimatization, hydration, and avoidance of inciting substances (including supplements).

Pre-Participation Examination. The purpose of the pre-participation examination (PPE) is to maximize an athlete’s safety by identifying medical conditions that place the athlete at risk.^11,12 The Preparticipation Physical Evaluation, 4th edition, the most widely used consensus publication, specifically queries if an athlete has a previous history of heat injury. However, it only indirectly addresses intrinsic risk factors that may predispose an athlete to EHI who has never had an EHI before. Therefore, providers should take the opportunity of the PPE to inquire about additional risk factors that may make an athlete high risk for sustaining a heat injury. Common risk factors for EHI are listed in Table 1.

Secondary Prevention

Despite physicians’ best efforts to prevent all cases of EHI, athletes will still experience the effects of exercise-induced hyperthermia. The goal of secondary prevention is to slow the progression of this hyperthermia so that it does not progress to more dangerous EHI.

Hydration. Dehydration is an important risk factor for EHI. Sweat maintains thermoregulation by dissipating heat generated during exercise; however, it also contributes to body water losses. Furthermore, intravascular depletion decreases stroke volume, thereby increasing cardiovascular strain. It is estimated that for every 1% loss in body mass from dehydration, body temperature rises 0.22°C in comparison to a euhydrated state.⁶ Dehydration occurs more rapidly in hot environments, as fluid is lost through increased sweat production.⁷ After approximately 6% to 10% body weight volume loss, cardiac output cannot be maintained, diminishing sweat production and blood flow to both skin and muscle and causing diminished performance and a significant risk of heat exhaustion.⁷ If left unchecked, these physiologic changes result in further elevations in body temperature and increased cardiovascular strain, ultimately placing the athlete at significant risk for development of EHS.

Adequate hydration to maintain euvolemia is an important step in avoiding possible EHI. Multiple studies have shown that football players experience a baseline hypovolemia during their competition season,⁶ a deficit that is most marked during the first week of practices.¹⁷ This deficit is multifactorial, as football players expend a significant amount of fluid through sweat, are not able to adequately replace these losses during practice, and do not appropriately hydrate off the field.^6,18 Some players, especially linemen, sweat at a higher rate than their teammates, posing a possible risk of significant dehydration.⁶ Coaches and players alike should be educated on the importance of adequate hydration to meet their fluid needs.

The goal of hydration during exercise is to prevent large fluid losses that can adversely affect performance and increase risk of EHI;⁶ it may be unrealistic to replace all fluid losses during the practice period. Instead, athletes should target complete volume replacement over the post-exercise period.⁶ Some recommend hydrating based upon thirst drive; however, thirst is activated following a volume loss of approximately 2% body mass, the same degree of losses that place athletes at an increased risk for performance impairment and EHI.^4,6,11,12 Individuals should have access to fluids throughout practice and competition and be encouraged to hydrate as needed.^6,12,15 Furthermore, staff should modify their practices based upon WBGT and acclimatization status to provide more frequent hydration breaks.

Hyperhydration and Salt Intake. Of note, there are inherent risks to hyperhydration. Athletes with low sweat rates have an increased risk of overhydration and the development of exercise-associated hyponatremia (EAH),⁶ a condition whose presentation is very similar to EHS. In addition, inadequate sodium intake and excessive sweating can also contribute to the development of EAH. EAH has been implicated in the deaths of 2 football players in 2014.^1,6 Establishing team hydration guidelines and educating players and staff on appropriate hydration and dietary salt intake is essential to reduce the risk of both dehydration and hyperhydration and their complications.⁶Intra-Event Cooling. During exercise, team physicians can employ strategies for cooling athletes during exertion to mitigate their risk of EHI by decreasing thermal and cardiovascular strain.^4,19 Cooling during exercise is hypothesized to allow for accelerated heat dissipation, where heat is lost from the body more effectively. This accelerated loss enables athletes to maintain a higher heat storage capacity over the duration of exercise, avoiding uncompensated heat stresses that ultimately cause EHI.¹⁹

Some intra-event cooling strategies include the use of cooling garments, cooling packs, and cold water/slurry ingestion. Cooling garments lower skin temperature, which in turn can decrease thermoregulatory strains;⁴ a recent meta-analysis of intra-event cooling modalities revealed that wearing an ice vest during exercise resulted in the greatest decrease in thermal heat strain.¹⁹ Internal cooling strategies—namely ingestion of cold fluids/ice slurry—have shown some mild benefit in decreasing internal temperatures; however, some studies have demonstrated some decrease in sweat production associated with cold oral intake used in isolation.¹⁹ Overall, studies have shown that combining external (cooling clothing, ice packs, fanning) and internal (cold water, ice slurry) cooling methods result in a greater cooling effect than a use of a single method.⁴

Tertiary Prevention

The goal of tertiary prevention is to mitigate the risk of long-term adverse outcomes following an EHS event. The most effective means of reducing risk for morbidity and mortality is rapid identification and treatment of EHS as well as close evaluation of an athlete’s return to activity in heat. This process is spearheaded by an effective and well-rehearsed emergency action plan.

Diagnosis and Management

Rapid identification and treatment of EHS is crucial to minimizing the risk of poor outcomes.⁷ Any delay in the treatment of EHS can dramatically increase the likelihood of associated morbidity and mortality.²⁰

EHS is diagnosed by an elevated rectal temperature ≥40°C (104°F) and associated central nervous system (CNS) dysfunction.²¹ EHS should be strongly suspected in any athlete exercising in heat who exhibits signs of CNS dysfunction, including disorientation, confusion, dizziness, erratic behavior, irritability, headache, loss of coordination, delirium, collapse, or seizures.^7,12,15 EHS may also present with symptoms of heat exhaustion, including fatigue, hyperventilation, tachycardia, vomiting, diarrhea, and hypotension.^7,12,15

Rectal temperature should be taken for any athlete with suspected EHS, as other modalities—oral, skin, axillary, and aural—can be inaccurate and easily modified by ambient confounders such as ambient and skin temperature, athlete hyperventilation, and consumption of liquids.^7,11,12 Athletes exhibiting CNS symptoms with moderately elevated rectal temperatures that do not exceed 40°C should also be assumed to be suffering from EHS and treated with rapid cooling.¹¹ On the other hand, athletes with CNS symptoms who are normothermic should be assumed to have EAH until ruled out by electrolyte assessment; IV fluids should be at no more than keep vein open (KVO) pending this determination.¹¹ In some cases, an athlete may initially present with altered mental status but return to “normal.” However, this improvement may represent a “lucid period”; evaluation should continue with rectal temperature and treatment, as EHS in these cases may progress quickly.¹⁵

Treatment is centered on rapid, whole body cooling initiated at the first sign of heat illness.^7,22 The goal of treatment is to achieve a rectal temperature <38.9°C within 30 minutes of the onset of EHS.¹⁵ Upon diagnosis, the athlete should be quickly placed in a tub of ice water to facilitate cold water immersion (CWI) therapy. Some guidelines suggest the athlete’s clothing be removed to potentiate evaporative cooling during CWI;¹² however, cooling should not be delayed due to difficulties in removing equipment. CWI, where a heat stroke victim is submerged in ice water up to their neck while water is continuously circulated, is generally considered to be the gold standard treatment as it is the modality with the highest recorded cooling rates and the lowest rate of morbidity and mortality.^7,20,21 Multiple studies of CWI have shown that survival nears 100% when aggressive cooling starts within 5 minutes of collapse or identification of EHS.^20,21,22

If whole body CWI is unavailable, alternative methods of rapid cooling should be employed. Partial CWI, with torso immersion being preferable to the extremities, has been shown to achieve an acceptable rate of cooling to achieve sufficient drops in internal body temperature.^20,23 However, one popular treatment—applying ice packs to the whole body, in particular to the groin and axillae—has not been shown to be sufficient to achieve standard cooling goals.²⁰ None of these methods have been shown to be as effective as CWI.²³

Intravenous access should be initiated with fluid resuscitation dictated by the provider’s assessment. Normal saline is recommended as the resuscitative fluid of choice, with the rate dictated by clinical judgment and adjusted as guided by electrolyte determination and clinical response. It cannot be overstated that in normothermic patients with confusion, EAH is the diagnosis of exclusion and aggressive fluid resuscitation should be withheld until electrolyte determination.

Once rectal temperature descends appropriately (~38.9°C), the cooling process should stop and the individual should be transported to a hospital for further observation²⁰ and evaluation of possible sequelae, including rhabdomyolysis and renal injury, cardiac dysfunction and arrhythmia, severe electrolyte abnormalities, acute respiratory distress syndrome, lactic acidosis, and other forms of end-organ failure (Figure).

Emergency Action Plan

Team physicians should be proactive in developing an emergency action plan to address possible EHS events. These plans should be site-specific, addressing procedures for all practice and home competition locations.¹² All competition venues should have a CWI tub on-site in events where there is an increased risk of EHS.^12,15,20 This tub should be set up and functional for all high-risk activities, including practices.¹²

Following recognition of a potential case of EHS, treatment teams should have procedures in place to transport athletes to the treatment area, obtain rectal temperature, initiate rapid cooling, and stabilize the athlete for transport to an emergency department (ED) for further evaluation.^12,15 A written record of treatments and medications provided during athlete stabilization should be maintained and transported with the athlete to the ED.¹⁵ A list of helpful equipment and supplies for treatment of EHS can be found in Table 5.

Return to Play

Perhaps the most challenging and important role the team physician has is determining an athlete’s return to play following EHI, as there currently are no evidence-based guidelines for return to activity for these athletes.⁷ The decisions surrounding return to play are highly individualized, as recovery from EHS and heat injury is associated with the duration of internal body temperature elevation above the critical level (40°C).^7,20 Guidelines for return to activity following recovery from EHI differ among experts and institutions.^7,25 The general consensus from these guidelines is that, at minimum, athletes should not participate in any physical activity until they are asymptomatic and all blood tests have normalized.¹¹ Following this asymptomatic period, most guidelines advocate for a slow, deliberate return to activity.¹¹ The American College of Sports Medicine (ACSM) offers one reasonable approach to the returning athlete following EHS:⁷

• No exercise for at least 7 days following release from medical care.
• Follow-up with a physician 1 week after release from medical care for physical examination and any warranted lab or radiologic studies (based upon organ systems affected during EHS).
• Once cleared to return to activity, the athlete begins exercise in a cool environment, gradually increasing the duration, intensity, and heat exposure over 2 weeks to demonstrate heat tolerance and acclimatization.
• Athletes who cannot resume vigorous activity due to recurrent symptoms (eg, excessive fatigue) should be reevaluated after 4 weeks. Laboratory exercise-heat tolerance testing may be useful in this setting.
• The athlete may resume full competition once they are able to participate in full training in the heat for 2 to 4 weeks without adverse effects.

Heat tolerance testing (HTT) in these athletes remains controversial.^{5 26} The ACSM recommends that HTT be considered only for those unable to return to vigorous activity after a suitable period (approximately 4 weeks). In contrast, the Israeli Defense Force (IDF) uses HTT to evaluate soldiers following EHS to guide decision-making about return to duty.²⁷ The IDF HTT assumes that individuals will respond differently to heat stresses. They identify individuals who are “heat intolerant” as being unable to tolerate specific heat challenges, indicated by increases in body temperature occurring more rapidly than normal responders under identical environmental and exercise conditions. However, despite being used for more than 30 years, there is no clear evidence that HTT adequately predicts who will experience subsequent episodes of EHS.

Conclusion

While the recognized cornerstone of being a team physician is the provision of medical care, the ACSM Team Physician Consensus Statement²⁸ further delineates the medical and administrative responsibilities as both (1) understanding medical management and prevention of injury and illness in athletes; and (2) awareness of or involvement in the development and rehearsal of an emergency action plan. These tenets are critical for the team physician who accepts the responsibility to cover sports at the high school level or higher. Football team physicians play an essential role in mitigating risk of EHI in their athletes. Through development and execution of both comprehensive prevention strategies and emergency action plans, physicians can work to minimize athletes’ risk of both developing and experiencing significant adverse outcomes from an EHI.

Am J Orthop. 2016;45(6):340-348. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.

Football, one of the most popular sports in the United States, is additionally recognized as a leading contributor to sports injury secondary to the contact collision nature of the endeavor. There are an estimated 1.1 million high school football players with another 100,000 participants combined in the National Football League (NFL), college, junior college, Arena Football League, and semipro levels of play.¹ USA Football estimates that an additional 3 million youth participate in community football leagues.¹ The National Center for Catastrophic Sports Injury Research recently calculated a fatality rate of 0.14 per 100,000 participants in 2014 for the 4.2 million who play football at all levels—and 0.45 per 100,000 in high school.¹ While direct deaths from head and spine injury remain a significant contributor to the number of catastrophic injuries, indirect deaths (systemic failure) predominate. Exertional heat stroke (EHS) has emerged as one of the leading indirect causes of death in high school and collegiate football. Boden and colleagues² reported that high school and college football players sustain approximately 12 fatalities annually, with indirect systemic causes being twice as common as direct blunt trauma.²The most common indirect causes identified included cardiac failure, heat illness, and complications of sickle cell trait (SCT). It was also noted that the risk of SCT, heat-related, and cardiac deaths increased during the second decade of the study, indicating these conditions may require a greater emphasis on diagnosis, treatment, and prevention. This review details for the team physician the unique challenge of exercising in the heat to the football player, and the prevention, diagnosis, management and return-to-play issues pertinent to exertional heat illness (EHI).

The Challenge

EHS represents the most severe manifestation of EHI—a gamut of diseases commonly encountered during the hot summer months when American football season begins. The breadth of EHI includes several important clinical diagnoses: exercise-associated muscle cramps (heat cramps); heat exhaustion with and without syncope; heat injury with evidence of end organ injury (eg, rhabdomyolysis); and EHS. EHS is defined as “a form of hyperthermia associated with a systemic inflammatory response leading to a syndrome of multi-organ dysfunction in which encephalopathy predominates.”³ EHS, if left untreated, or even if clinical treatment is delayed, may result in significant end organ morbidity and/or mortality.

During exercise, the human thermoregulatory system mitigates heat gain by increasing skin blood flow and sweating, causing an increased dissipation of heat to the surrounding environment by leveraging conduction, convection, and evaporation.^4,5 Elevated environmental temperatures, increased humidity, and dehydration can impede the body’s ability to dissipate heat at a rate needed to maintain thermoregulation. This imbalance can result in hyperthermia secondary to uncompensated heat stress,⁵ which in turn can lead to EHI. Football players have unique challenges that make them particularly vulnerable to EHI. The summer heat during early-season participation and the requirement for equipment that covers nearly 60% of body surfaces pose increased risk of volume losses and hyperthermia that trigger the onset of EHI.⁶ Football athletes’ body compositions and physical size are additional contributing risk factors; the relatively high muscle and fat content increase thermogenicity, which require their bodies to dissipate more heat.⁷

An estimated 9000 cases of EHI occur annually across all high school sports,⁸ with an incidence of 1.6:100,000 athlete-exposures.^8,9 Studies have demonstrated, however, that EHI occurs in football 11.4 times more often than in all other high school sports combined.¹⁰ The incidence of nonfatal EHI in all levels of football is 4.42-5:100,000.^8,9 Between 2000 and 2014, 41 football players died from EHS.¹ In football, approximately 75% of all EHI events occurred during practices, while only 25% of incidents occurred during games.⁸

Given these potentially deadly consequences, it is important that football team physicians are not only alert to the early symptoms of heat illness and prepared to intervene to prevent the progression to EHS, but are critical leaders in educating coaches and players in evidence-based EHI prevention practices and policies.

Prevention

EHS is a preventable condition, arguably the most common cause of preventable nontraumatic exertional death in young athletes in the United States. Close attention to mitigating risk factors should begin prior to the onset of preseason practice and continue through the early season, where athletes are at the highest risk of developing heat illness.

Primary Prevention

Primary prevention is fundamental to minimizing the occurrences of EHI. It focuses on the following methods: recognition of inherent risk factors, acclimatization, hydration, and avoidance of inciting substances (including supplements).

Pre-Participation Examination. The purpose of the pre-participation examination (PPE) is to maximize an athlete’s safety by identifying medical conditions that place the athlete at risk.^11,12 The Preparticipation Physical Evaluation, 4th edition, the most widely used consensus publication, specifically queries if an athlete has a previous history of heat injury. However, it only indirectly addresses intrinsic risk factors that may predispose an athlete to EHI who has never had an EHI before. Therefore, providers should take the opportunity of the PPE to inquire about additional risk factors that may make an athlete high risk for sustaining a heat injury. Common risk factors for EHI are listed in Table 1.

Secondary Prevention

Despite physicians’ best efforts to prevent all cases of EHI, athletes will still experience the effects of exercise-induced hyperthermia. The goal of secondary prevention is to slow the progression of this hyperthermia so that it does not progress to more dangerous EHI.

Hydration. Dehydration is an important risk factor for EHI. Sweat maintains thermoregulation by dissipating heat generated during exercise; however, it also contributes to body water losses. Furthermore, intravascular depletion decreases stroke volume, thereby increasing cardiovascular strain. It is estimated that for every 1% loss in body mass from dehydration, body temperature rises 0.22°C in comparison to a euhydrated state.⁶ Dehydration occurs more rapidly in hot environments, as fluid is lost through increased sweat production.⁷ After approximately 6% to 10% body weight volume loss, cardiac output cannot be maintained, diminishing sweat production and blood flow to both skin and muscle and causing diminished performance and a significant risk of heat exhaustion.⁷ If left unchecked, these physiologic changes result in further elevations in body temperature and increased cardiovascular strain, ultimately placing the athlete at significant risk for development of EHS.

Adequate hydration to maintain euvolemia is an important step in avoiding possible EHI. Multiple studies have shown that football players experience a baseline hypovolemia during their competition season,⁶ a deficit that is most marked during the first week of practices.¹⁷ This deficit is multifactorial, as football players expend a significant amount of fluid through sweat, are not able to adequately replace these losses during practice, and do not appropriately hydrate off the field.^6,18 Some players, especially linemen, sweat at a higher rate than their teammates, posing a possible risk of significant dehydration.⁶ Coaches and players alike should be educated on the importance of adequate hydration to meet their fluid needs.

The goal of hydration during exercise is to prevent large fluid losses that can adversely affect performance and increase risk of EHI;⁶ it may be unrealistic to replace all fluid losses during the practice period. Instead, athletes should target complete volume replacement over the post-exercise period.⁶ Some recommend hydrating based upon thirst drive; however, thirst is activated following a volume loss of approximately 2% body mass, the same degree of losses that place athletes at an increased risk for performance impairment and EHI.^4,6,11,12 Individuals should have access to fluids throughout practice and competition and be encouraged to hydrate as needed.^6,12,15 Furthermore, staff should modify their practices based upon WBGT and acclimatization status to provide more frequent hydration breaks.

Hyperhydration and Salt Intake. Of note, there are inherent risks to hyperhydration. Athletes with low sweat rates have an increased risk of overhydration and the development of exercise-associated hyponatremia (EAH),⁶ a condition whose presentation is very similar to EHS. In addition, inadequate sodium intake and excessive sweating can also contribute to the development of EAH. EAH has been implicated in the deaths of 2 football players in 2014.^1,6 Establishing team hydration guidelines and educating players and staff on appropriate hydration and dietary salt intake is essential to reduce the risk of both dehydration and hyperhydration and their complications.⁶Intra-Event Cooling. During exercise, team physicians can employ strategies for cooling athletes during exertion to mitigate their risk of EHI by decreasing thermal and cardiovascular strain.^4,19 Cooling during exercise is hypothesized to allow for accelerated heat dissipation, where heat is lost from the body more effectively. This accelerated loss enables athletes to maintain a higher heat storage capacity over the duration of exercise, avoiding uncompensated heat stresses that ultimately cause EHI.¹⁹

Some intra-event cooling strategies include the use of cooling garments, cooling packs, and cold water/slurry ingestion. Cooling garments lower skin temperature, which in turn can decrease thermoregulatory strains;⁴ a recent meta-analysis of intra-event cooling modalities revealed that wearing an ice vest during exercise resulted in the greatest decrease in thermal heat strain.¹⁹ Internal cooling strategies—namely ingestion of cold fluids/ice slurry—have shown some mild benefit in decreasing internal temperatures; however, some studies have demonstrated some decrease in sweat production associated with cold oral intake used in isolation.¹⁹ Overall, studies have shown that combining external (cooling clothing, ice packs, fanning) and internal (cold water, ice slurry) cooling methods result in a greater cooling effect than a use of a single method.⁴

Tertiary Prevention

The goal of tertiary prevention is to mitigate the risk of long-term adverse outcomes following an EHS event. The most effective means of reducing risk for morbidity and mortality is rapid identification and treatment of EHS as well as close evaluation of an athlete’s return to activity in heat. This process is spearheaded by an effective and well-rehearsed emergency action plan.

Diagnosis and Management

Rapid identification and treatment of EHS is crucial to minimizing the risk of poor outcomes.⁷ Any delay in the treatment of EHS can dramatically increase the likelihood of associated morbidity and mortality.²⁰

EHS is diagnosed by an elevated rectal temperature ≥40°C (104°F) and associated central nervous system (CNS) dysfunction.²¹ EHS should be strongly suspected in any athlete exercising in heat who exhibits signs of CNS dysfunction, including disorientation, confusion, dizziness, erratic behavior, irritability, headache, loss of coordination, delirium, collapse, or seizures.^7,12,15 EHS may also present with symptoms of heat exhaustion, including fatigue, hyperventilation, tachycardia, vomiting, diarrhea, and hypotension.^7,12,15

Rectal temperature should be taken for any athlete with suspected EHS, as other modalities—oral, skin, axillary, and aural—can be inaccurate and easily modified by ambient confounders such as ambient and skin temperature, athlete hyperventilation, and consumption of liquids.^7,11,12 Athletes exhibiting CNS symptoms with moderately elevated rectal temperatures that do not exceed 40°C should also be assumed to be suffering from EHS and treated with rapid cooling.¹¹ On the other hand, athletes with CNS symptoms who are normothermic should be assumed to have EAH until ruled out by electrolyte assessment; IV fluids should be at no more than keep vein open (KVO) pending this determination.¹¹ In some cases, an athlete may initially present with altered mental status but return to “normal.” However, this improvement may represent a “lucid period”; evaluation should continue with rectal temperature and treatment, as EHS in these cases may progress quickly.¹⁵

Treatment is centered on rapid, whole body cooling initiated at the first sign of heat illness.^7,22 The goal of treatment is to achieve a rectal temperature <38.9°C within 30 minutes of the onset of EHS.¹⁵ Upon diagnosis, the athlete should be quickly placed in a tub of ice water to facilitate cold water immersion (CWI) therapy. Some guidelines suggest the athlete’s clothing be removed to potentiate evaporative cooling during CWI;¹² however, cooling should not be delayed due to difficulties in removing equipment. CWI, where a heat stroke victim is submerged in ice water up to their neck while water is continuously circulated, is generally considered to be the gold standard treatment as it is the modality with the highest recorded cooling rates and the lowest rate of morbidity and mortality.^7,20,21 Multiple studies of CWI have shown that survival nears 100% when aggressive cooling starts within 5 minutes of collapse or identification of EHS.^20,21,22

If whole body CWI is unavailable, alternative methods of rapid cooling should be employed. Partial CWI, with torso immersion being preferable to the extremities, has been shown to achieve an acceptable rate of cooling to achieve sufficient drops in internal body temperature.^20,23 However, one popular treatment—applying ice packs to the whole body, in particular to the groin and axillae—has not been shown to be sufficient to achieve standard cooling goals.²⁰ None of these methods have been shown to be as effective as CWI.²³

Intravenous access should be initiated with fluid resuscitation dictated by the provider’s assessment. Normal saline is recommended as the resuscitative fluid of choice, with the rate dictated by clinical judgment and adjusted as guided by electrolyte determination and clinical response. It cannot be overstated that in normothermic patients with confusion, EAH is the diagnosis of exclusion and aggressive fluid resuscitation should be withheld until electrolyte determination.

Once rectal temperature descends appropriately (~38.9°C), the cooling process should stop and the individual should be transported to a hospital for further observation²⁰ and evaluation of possible sequelae, including rhabdomyolysis and renal injury, cardiac dysfunction and arrhythmia, severe electrolyte abnormalities, acute respiratory distress syndrome, lactic acidosis, and other forms of end-organ failure (Figure).

Emergency Action Plan

Team physicians should be proactive in developing an emergency action plan to address possible EHS events. These plans should be site-specific, addressing procedures for all practice and home competition locations.¹² All competition venues should have a CWI tub on-site in events where there is an increased risk of EHS.^12,15,20 This tub should be set up and functional for all high-risk activities, including practices.¹²

Following recognition of a potential case of EHS, treatment teams should have procedures in place to transport athletes to the treatment area, obtain rectal temperature, initiate rapid cooling, and stabilize the athlete for transport to an emergency department (ED) for further evaluation.^12,15 A written record of treatments and medications provided during athlete stabilization should be maintained and transported with the athlete to the ED.¹⁵ A list of helpful equipment and supplies for treatment of EHS can be found in Table 5.

Return to Play

Perhaps the most challenging and important role the team physician has is determining an athlete’s return to play following EHI, as there currently are no evidence-based guidelines for return to activity for these athletes.⁷ The decisions surrounding return to play are highly individualized, as recovery from EHS and heat injury is associated with the duration of internal body temperature elevation above the critical level (40°C).^7,20 Guidelines for return to activity following recovery from EHI differ among experts and institutions.^7,25 The general consensus from these guidelines is that, at minimum, athletes should not participate in any physical activity until they are asymptomatic and all blood tests have normalized.¹¹ Following this asymptomatic period, most guidelines advocate for a slow, deliberate return to activity.¹¹ The American College of Sports Medicine (ACSM) offers one reasonable approach to the returning athlete following EHS:⁷

• No exercise for at least 7 days following release from medical care.
• Follow-up with a physician 1 week after release from medical care for physical examination and any warranted lab or radiologic studies (based upon organ systems affected during EHS).
• Once cleared to return to activity, the athlete begins exercise in a cool environment, gradually increasing the duration, intensity, and heat exposure over 2 weeks to demonstrate heat tolerance and acclimatization.
• Athletes who cannot resume vigorous activity due to recurrent symptoms (eg, excessive fatigue) should be reevaluated after 4 weeks. Laboratory exercise-heat tolerance testing may be useful in this setting.
• The athlete may resume full competition once they are able to participate in full training in the heat for 2 to 4 weeks without adverse effects.

Heat tolerance testing (HTT) in these athletes remains controversial.^{5 26} The ACSM recommends that HTT be considered only for those unable to return to vigorous activity after a suitable period (approximately 4 weeks). In contrast, the Israeli Defense Force (IDF) uses HTT to evaluate soldiers following EHS to guide decision-making about return to duty.²⁷ The IDF HTT assumes that individuals will respond differently to heat stresses. They identify individuals who are “heat intolerant” as being unable to tolerate specific heat challenges, indicated by increases in body temperature occurring more rapidly than normal responders under identical environmental and exercise conditions. However, despite being used for more than 30 years, there is no clear evidence that HTT adequately predicts who will experience subsequent episodes of EHS.

Conclusion

While the recognized cornerstone of being a team physician is the provision of medical care, the ACSM Team Physician Consensus Statement²⁸ further delineates the medical and administrative responsibilities as both (1) understanding medical management and prevention of injury and illness in athletes; and (2) awareness of or involvement in the development and rehearsal of an emergency action plan. These tenets are critical for the team physician who accepts the responsibility to cover sports at the high school level or higher. Football team physicians play an essential role in mitigating risk of EHI in their athletes. Through development and execution of both comprehensive prevention strategies and emergency action plans, physicians can work to minimize athletes’ risk of both developing and experiencing significant adverse outcomes from an EHI.

Am J Orthop. 2016;45(6):340-348. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.

From the VA Eastern Colorado Health Care System, University of Colorado School of Medicine, and the Colorado Cardiovascular Outcomes Research Group, Denver and Aurora, CO.

Abstract

• Objective: To review the use of elective percutaneous coronary intervention (PCI), evaluate what is currently known about elective PCI in the context of appropriate use criteria, and offer insight into next steps to optimize the use of elective PCI to achieve high-quality care.
• Methods: Review of the scientific literature, appropriate use criteria, and professional society guidelines relevant to elective PCI.
• Results: Recent studies have demonstrated as many as 1 in 6 elective PCIs are inappropriate as determined by appropriate use criteria. These inappropriate PCIs are not anticipated to benefit patients and result in unnecessary patient risk and cost. While these studies are consistent with regard to overuse of elective PCI, less is known about potential underuse of PCI for elective indications. We lack health status data on populations of ischemic heart disease patients to inform PCI underuse that may contribute to patient symptom burden, functional status, and quality of life. Optimal use of PCI will be attained with longitudinal capture of patient-reported health status, study of factors contributing to overuse and underuse, refinement of the appropriate use criteria with particular focus on patient-centered measures, and incorporation of patient preference and shared decision making into appropriateness evaluation tools.
• Conclusion: The use of elective PCI is less than optimal in current clinical practice. Continued effort is needed to ensure elective PCI is targeted to patients with anticipated benefit and use of the procedure is aligned with patient preferences.

Providing the right care to the right patient at the right time is essential to the practice of high-quality care. Reducing overuse of health care services is part of this equation, and initiatives to reduce inappropriate use and to encourage physicians and patients to “choose wisely” have been introduced [1]. One procedure that is being examined with a focus on appropriateness is percutaneous coronary intervention (PCI). This procedure is common (nearly 1 million inpatient PCI procedures performed in 2010), presents risks to the patient, and is expensive (attributable cost approximately $10 billion in 2010) [2,3]. While the clinical benefit of PCI in acute settings such as ST-segment elevation myocardial infarction is well established [4], the benefit of PCI in nonacute (elective) settings is less robust [5–7]. Prior studies have demonstrated PCI for stable ischemic heart disease does not result in mortality benefit [6]. Furthermore, PCI as an initial strategy for symptom relief of stable angina may offer little benefit relative to medications alone [5]. Given that PCI is common, costly, and associated with both short- and long-term risks [8,9], ensuring this therapy is provided to the right patient at the right time is important.

In 2009, appropriate use criteria (AUC) were developed by 6 professional organizations to support the rational and judicious use of PCI [10]; a focused update was published in 2012 [11]. In this review, we discuss the recommendations for appropriate use and their application and offer thoughts on next steps to optimize the use of elective PCI as part of high-quality care.

Variation in the Use of PCI

Additionally, significant public attention has been focused on the issue of overuse after lay press investigations into community practice patterns. In particular, a case study presented in the New York Times highlighted the community of Elyria, Ohio, which was found to have a PCI rate that was 4 times the national average [16]. This investigation sparked public debate and further focused attention on the issue of overuse of elective PCI. Conversely, others have pointed to data that suggest underuse of coronary procedural care, particularly among women and racial and ethnic minorities [17–22].

Appropriate Use Criteria

Development Methodology

AUC for PCI, which were developed through the collaborative efforts of 6 major cardiovascular professional organizations, are intended to support the effective, efficient, and equitable use of PCI [10,11]. They were developed in response to a growing need to support rational use of cardiovascular procedures as part of high-quality care. The methods of development for the AUC have been described in detail in the criteria publications [10,11]. We briefly review these methods here.

Panel members first individually assigned ratings to each clinical scenario that ranged from 1 (least appropriate) to 9 (most appropriate). This was followed by an in-person meeting in which technical panel members discussed scenarios for which there was wide variation in appropriateness assessment. After this meeting, technical panel members again assigned ratings for each scenario from 1 to 9. After this second round, the median values for the pooled ratings were used as the appropriateness classification for each scenario. Scenarios with median values of 1–3 were classified as “inappropriate,” 4–6 as “uncertain,” and 7–9 as “appropriate.” A rating of “appropriate” represented clinical scenarios in which the indication is considered generally acceptable and likely to improve health outcomes or survival. A rating of “uncertain” represented clinical scenarios where the indication may be reasonable but more research is necessary to further understand the relative benefits and risks of PCI in this setting. Finally, a rating of “inappropriate” represented clinical scenarios in which the indication is not generally acceptable as it is unlikely to improve health outcomes or survival.

The approach used for AUC development appears to be valid, as Class III indications for PCI in the ACC/AHA clinical guideline [24] (Class III = PCI should NOT be performed since it is not helpful and may be harmful) and AUC scenarios rated as inappropriate are in 100% agreement (personal communication, Ralph Brindis, past president of the American College of Cardiology).

Application

It is important to remember that the AUC are intended to aid in patient selection and are not absolute. Unique clinical factors and patient preference cannot feasibly be captured by the AUC scenarios. It should also be noted that the intent of the AUC is not to be punitive but rather to identify and assess variation in practice patterns. To reflect this intent, the terminology applied to appropriateness ratings has recently changed. Clinical scenarios previously classified as “inappropriate” are now termed “rarely appropriate” and clinical scenarios classified as “uncertain” are now termed “may be appropriate.”

Although the AUC were developed to help evaluate practice patterns of care delivery and serve as guides for clinical decision making, they were not intended to serve as mandates for or against treatment in individual patients or to be tied to reimbursement for individual patients. Despite this, health care organizations and payors have used other AUC documents for incentive pay and prior authorization programs, specifically for cardiovascular imaging [25]. Use of the AUC in this manner may still be reasonable if application and measurement is at the level of the practice, rather than the individual patient, but much remains to be understood about the implications of applying AUC in reimbursement
decisions.

Refinement

The AUC for PCI are designed to be dynamic and continually updated. As additional evidence becomes available regarding the efficacy of PCI in specific clinical scenarios, there will be ongoing efforts to update the AUC to reflect this new evidence. This is highlighted by the first update to the AUC occurring less than 3 years after the original publication date [11].

In addition to perpetual review of the data used to inform scenario ratings, there are opportunities to improve measurement of the clinical variables that are considered in rating PCI appropriateness (eg, clinical presentation, symptom severity, ischemia severity, extent of medical therapy, extent of anatomic disease). For example, in the current AUC, symptom severity is dependent on clinician assessment using the Canadian Cardiovascular Society Classification [25]. Moving toward a patient-centered assessment of symptom severity would ensure that the AUC more closely reflect the patient-perceived symptom burden. Further, the use of a patient-centered instrument would reduce the possibility of physician manipulation of symptom severity to influence the apparent appropriateness of PCI. There are similar opportunities to improve reporting of noninvasive stress test data, such as through standardized reporting of ischemic risk. Finally, the use of physiologic assessments of stenosis severity (eg, fractional flow reserve) and quantitative coronary angiography to standardize interpretations of diagnostic angiography may further optimize the assessment of PCI appropriateness.

Application of the Appropriate Use Criteria in Clinical Practice—Study Results

Application of the AUC to clinical practice has highlighted potential overuse of PCI (Table). The first report came from applying the AUC to the National Cardiovascular Data Registry (NCDR) CathPCI Registry [26]. In this study of more than 500,000 PCIs from over 1000 facilities across the country, the authors found that PCIs performed in the acute setting (STEMI, NSTEMI, and high-risk unstable angina) were almost uniformly classified as appropriate. However, for nonacute (elective) PCI, application of the AUC resulted in the classification of 50% as appropriate, 38% as uncertain, and 12% as inappropriate. The majority of patients who received inappropriate PCI had a low-risk stress test (72%) or were asymptomatic (54%). Additionally, 96% of patients who received PCI classified as inappropriate had not been given a trial of adequate anti-anginal therapy. This analysis was supported by subsequent analyses of 2 other state-specific registries (New York and Washington), which found similar rates of PCI for nonacute indications rated as inappropriate [27,28]. Additionally, all 3 studies showed wide facility-level variation in the percentage of appropriate and inappropriate PCI for elective indications.

These studies also highlight a gap in preprocedural care. The anticipated benefit of elective PCI is related to patient symptom burden, adequacy of anti-anginal therapy, and ischemic risk as determined by noninvasive stress testing. However, 30% to 50% of patients undergo elective PCI without evidence of preprocedural stress testing. Attempts are being made to address this gap with the recent release of PCI performance measures [29]. These performance measures, intended for cardiac catheterization labs, include comprehensive documentation of the indication for PCI, which is central to determination of appropriateness. This integration of procedural indication into a performance measure marks the first such occurrence in cardiology.

As documentation of procedural indication and appropriateness have become part and parcel of assessing quality of care, concerns about “gaming” have become more pertinent. Providers who perform PCI could potentially enhance the appearance of appropriateness by overstating the clinical symptom burden or stress test findings. The incorporation of validated, patient-centered health status questionnaires along with data audit programs have been proposed as measures to prevent this type of abuse. Addressing quality gaps in preprocedural assessment and documentation is critical to optimizing use of elective PCI [28].

The apparent overuse of PCI for elective indications may be a reflection of our fragmented, fee-for-service health care delivery system. However, recent studies challenge these assumptions. In a Canadian study, Ko et al found that 18% of elective PCIs were classified as inappropriate, a proportion similar to what had been found previously in the United States [30]. In a US study of Medicare beneficiaries, Matlock and colleagues observed a fourfold regional variation in use of elective coronary angiography and PCI in both Medicare fee-for-service and capitated Medicare Advantage beneficiaries [31]. Collectively, these studies suggest barriers to optimal patient selection for invasive coronary procedures in both capitated and fee-for-service health care systems. Without addressing factors that contribute to variation in the absence of fee-for-service incentives, efforts to improve integration and reduce fee-for-service reimbursement may be inadequate to optimize PCI use.

Evaluating Underuse

While potential underuse of PCI has been described for acute indications [17–22], study of underuse of PCI for elective indications is more challenging. Population data on the effect of underuse of elective PCI on patient symptom burden, functional status, and quality of life is lacking.

A population-based study from Australia highlights the potential importance of underuse in the care of patients with stable coronary disease. This study assessed symptom burden among patients with chronic stable angina using the Seattle Angina Questionnaire and included patients cared for by 207 primary care practitioners [32]. The authors noted that there was considerable variation in patient symptom burden between practices, with 14% of practices having no patients with more than 1 episode of angina per week and 18% of clinics having more than half of enrolled patients with at least 1 episode of angina per week. The authors postulate that this variability may be due to differences among providers in the identification and management of angina, including using PCI to minimize symptom burden.

In the Ko study mentioned earlier, the AUC was used to examine potential underuse of coronary revascularization procedures. In this study, they analyzed the association between AUC ratings and outcomes in patients undergoing diagnostic coronary angiography [30]. Of patients considered “appropriate” for revascularization following completion of diagnostic angiography, only 69% underwent revascularization. However, the clinical aspects that influence the decision to proceed with revascularization may not be fully captured in this study. Thus, the true degree of underuse of PCI remains elusive.

In summary, the relative lack of data that would allow for the assessment of underuse of elective PCI is an important quality concern. Health systems should work to systematically capture patient-reported health status, including symptom burden data, to identify inadequate symptom control and potential underuse of procedural care for CAD.

Facilitating Optimal Use

In current practice, the AUC hold promise to minimize the overuse of elective PCI. This likely involves addressing processes occurring upstream of the cardiac catheterization lab, including employing systems to ensure that procedures are avoided in patients who are unlikely to benefit (eg, asymptomatic, low ischemic burden) (Figure 3) [33]. Studying hospitals that already have low rates of inappropriate PCI may inform the design and dissemination of strategies that will help improve patient selection at hospitals with higher rates. Although professional organizations have developed tools intended to facilitate appropriateness evaluation at the point-of-care [34], the use of these tools are likely to be sporadic without greater integration into the health care delivery system. Further, these applications are currently limited to determination of appropriateness of PCI after completion of the diagnostic coronary angiogram. Identifying processes prior to catheterization that contribute to PCI appropriateness may also streamline appropriate ad hoc PCI, as the need to reassess appropriateness after the diagnostic angiogram may be mitigated.

Significant barriers exist to the application of the AUC for determination of procedural underuse. As described above, we lack adequate data to ascertain gaps in symptom management that could be mitigated by proper use of PCI. Further study of symptom burden in populations of patients with coronary artery disease is needed. This may help in the identification of patient populations whose symptom burden may warrant consideration of invasive coronary procedures, including coronary angiography and PCI.

Finally, it is important to note that the AUC are based on technical considerations, ie, practice guidelines and trial evidence. They do not take into consideration patient preferences. For example, PCI can be technically appropriate for the scenario but inappropriate for the individual if the procedure is not desired by the patient. Similarly, a procedure may be of uncertain benefit but appropriate if the patient desires more aggressive procedural care and has a full understanding of the risks and benefits. Currently, we fail to convey this information to patients, as evidenced by patients’ overestimation of the benefits of PCI [34]. As we continue to work toward optimal use of PCI, we must not only address the technical appropriateness of care, but move toward incorporating patient preferences through a robust process of shared decision-making.

Corresponding author: Preston M. Schneider, MD, VA Eastern Colorado Health Care System, Cardiology Section (111B), 1055 Clermont St., Denver, CO 80220, Preston.Schneider@ucdenver.edu.

Funding/support: Dr. Schneider is supported by a T32 training grant from the National Institutes of Health (5T32HL00
7822-15). Dr. Bradley is supported by a Career Development Award (HSR&D-CDA2 10-199) from VA Health Services Research & Development.

Financial disclosures: None.

From the VA Eastern Colorado Health Care System, University of Colorado School of Medicine, and the Colorado Cardiovascular Outcomes Research Group, Denver and Aurora, CO.

Abstract

• Objective: To review the use of elective percutaneous coronary intervention (PCI), evaluate what is currently known about elective PCI in the context of appropriate use criteria, and offer insight into next steps to optimize the use of elective PCI to achieve high-quality care.
• Methods: Review of the scientific literature, appropriate use criteria, and professional society guidelines relevant to elective PCI.
• Results: Recent studies have demonstrated as many as 1 in 6 elective PCIs are inappropriate as determined by appropriate use criteria. These inappropriate PCIs are not anticipated to benefit patients and result in unnecessary patient risk and cost. While these studies are consistent with regard to overuse of elective PCI, less is known about potential underuse of PCI for elective indications. We lack health status data on populations of ischemic heart disease patients to inform PCI underuse that may contribute to patient symptom burden, functional status, and quality of life. Optimal use of PCI will be attained with longitudinal capture of patient-reported health status, study of factors contributing to overuse and underuse, refinement of the appropriate use criteria with particular focus on patient-centered measures, and incorporation of patient preference and shared decision making into appropriateness evaluation tools.
• Conclusion: The use of elective PCI is less than optimal in current clinical practice. Continued effort is needed to ensure elective PCI is targeted to patients with anticipated benefit and use of the procedure is aligned with patient preferences.

Providing the right care to the right patient at the right time is essential to the practice of high-quality care. Reducing overuse of health care services is part of this equation, and initiatives to reduce inappropriate use and to encourage physicians and patients to “choose wisely” have been introduced [1]. One procedure that is being examined with a focus on appropriateness is percutaneous coronary intervention (PCI). This procedure is common (nearly 1 million inpatient PCI procedures performed in 2010), presents risks to the patient, and is expensive (attributable cost approximately $10 billion in 2010) [2,3]. While the clinical benefit of PCI in acute settings such as ST-segment elevation myocardial infarction is well established [4], the benefit of PCI in nonacute (elective) settings is less robust [5–7]. Prior studies have demonstrated PCI for stable ischemic heart disease does not result in mortality benefit [6]. Furthermore, PCI as an initial strategy for symptom relief of stable angina may offer little benefit relative to medications alone [5]. Given that PCI is common, costly, and associated with both short- and long-term risks [8,9], ensuring this therapy is provided to the right patient at the right time is important.

In 2009, appropriate use criteria (AUC) were developed by 6 professional organizations to support the rational and judicious use of PCI [10]; a focused update was published in 2012 [11]. In this review, we discuss the recommendations for appropriate use and their application and offer thoughts on next steps to optimize the use of elective PCI as part of high-quality care.

Variation in the Use of PCI

Additionally, significant public attention has been focused on the issue of overuse after lay press investigations into community practice patterns. In particular, a case study presented in the New York Times highlighted the community of Elyria, Ohio, which was found to have a PCI rate that was 4 times the national average [16]. This investigation sparked public debate and further focused attention on the issue of overuse of elective PCI. Conversely, others have pointed to data that suggest underuse of coronary procedural care, particularly among women and racial and ethnic minorities [17–22].

Appropriate Use Criteria

Development Methodology

AUC for PCI, which were developed through the collaborative efforts of 6 major cardiovascular professional organizations, are intended to support the effective, efficient, and equitable use of PCI [10,11]. They were developed in response to a growing need to support rational use of cardiovascular procedures as part of high-quality care. The methods of development for the AUC have been described in detail in the criteria publications [10,11]. We briefly review these methods here.

Panel members first individually assigned ratings to each clinical scenario that ranged from 1 (least appropriate) to 9 (most appropriate). This was followed by an in-person meeting in which technical panel members discussed scenarios for which there was wide variation in appropriateness assessment. After this meeting, technical panel members again assigned ratings for each scenario from 1 to 9. After this second round, the median values for the pooled ratings were used as the appropriateness classification for each scenario. Scenarios with median values of 1–3 were classified as “inappropriate,” 4–6 as “uncertain,” and 7–9 as “appropriate.” A rating of “appropriate” represented clinical scenarios in which the indication is considered generally acceptable and likely to improve health outcomes or survival. A rating of “uncertain” represented clinical scenarios where the indication may be reasonable but more research is necessary to further understand the relative benefits and risks of PCI in this setting. Finally, a rating of “inappropriate” represented clinical scenarios in which the indication is not generally acceptable as it is unlikely to improve health outcomes or survival.

The approach used for AUC development appears to be valid, as Class III indications for PCI in the ACC/AHA clinical guideline [24] (Class III = PCI should NOT be performed since it is not helpful and may be harmful) and AUC scenarios rated as inappropriate are in 100% agreement (personal communication, Ralph Brindis, past president of the American College of Cardiology).

Application

It is important to remember that the AUC are intended to aid in patient selection and are not absolute. Unique clinical factors and patient preference cannot feasibly be captured by the AUC scenarios. It should also be noted that the intent of the AUC is not to be punitive but rather to identify and assess variation in practice patterns. To reflect this intent, the terminology applied to appropriateness ratings has recently changed. Clinical scenarios previously classified as “inappropriate” are now termed “rarely appropriate” and clinical scenarios classified as “uncertain” are now termed “may be appropriate.”

Although the AUC were developed to help evaluate practice patterns of care delivery and serve as guides for clinical decision making, they were not intended to serve as mandates for or against treatment in individual patients or to be tied to reimbursement for individual patients. Despite this, health care organizations and payors have used other AUC documents for incentive pay and prior authorization programs, specifically for cardiovascular imaging [25]. Use of the AUC in this manner may still be reasonable if application and measurement is at the level of the practice, rather than the individual patient, but much remains to be understood about the implications of applying AUC in reimbursement
decisions.

Refinement

The AUC for PCI are designed to be dynamic and continually updated. As additional evidence becomes available regarding the efficacy of PCI in specific clinical scenarios, there will be ongoing efforts to update the AUC to reflect this new evidence. This is highlighted by the first update to the AUC occurring less than 3 years after the original publication date [11].

In addition to perpetual review of the data used to inform scenario ratings, there are opportunities to improve measurement of the clinical variables that are considered in rating PCI appropriateness (eg, clinical presentation, symptom severity, ischemia severity, extent of medical therapy, extent of anatomic disease). For example, in the current AUC, symptom severity is dependent on clinician assessment using the Canadian Cardiovascular Society Classification [25]. Moving toward a patient-centered assessment of symptom severity would ensure that the AUC more closely reflect the patient-perceived symptom burden. Further, the use of a patient-centered instrument would reduce the possibility of physician manipulation of symptom severity to influence the apparent appropriateness of PCI. There are similar opportunities to improve reporting of noninvasive stress test data, such as through standardized reporting of ischemic risk. Finally, the use of physiologic assessments of stenosis severity (eg, fractional flow reserve) and quantitative coronary angiography to standardize interpretations of diagnostic angiography may further optimize the assessment of PCI appropriateness.

Application of the Appropriate Use Criteria in Clinical Practice—Study Results

Application of the AUC to clinical practice has highlighted potential overuse of PCI (Table). The first report came from applying the AUC to the National Cardiovascular Data Registry (NCDR) CathPCI Registry [26]. In this study of more than 500,000 PCIs from over 1000 facilities across the country, the authors found that PCIs performed in the acute setting (STEMI, NSTEMI, and high-risk unstable angina) were almost uniformly classified as appropriate. However, for nonacute (elective) PCI, application of the AUC resulted in the classification of 50% as appropriate, 38% as uncertain, and 12% as inappropriate. The majority of patients who received inappropriate PCI had a low-risk stress test (72%) or were asymptomatic (54%). Additionally, 96% of patients who received PCI classified as inappropriate had not been given a trial of adequate anti-anginal therapy. This analysis was supported by subsequent analyses of 2 other state-specific registries (New York and Washington), which found similar rates of PCI for nonacute indications rated as inappropriate [27,28]. Additionally, all 3 studies showed wide facility-level variation in the percentage of appropriate and inappropriate PCI for elective indications.

These studies also highlight a gap in preprocedural care. The anticipated benefit of elective PCI is related to patient symptom burden, adequacy of anti-anginal therapy, and ischemic risk as determined by noninvasive stress testing. However, 30% to 50% of patients undergo elective PCI without evidence of preprocedural stress testing. Attempts are being made to address this gap with the recent release of PCI performance measures [29]. These performance measures, intended for cardiac catheterization labs, include comprehensive documentation of the indication for PCI, which is central to determination of appropriateness. This integration of procedural indication into a performance measure marks the first such occurrence in cardiology.

As documentation of procedural indication and appropriateness have become part and parcel of assessing quality of care, concerns about “gaming” have become more pertinent. Providers who perform PCI could potentially enhance the appearance of appropriateness by overstating the clinical symptom burden or stress test findings. The incorporation of validated, patient-centered health status questionnaires along with data audit programs have been proposed as measures to prevent this type of abuse. Addressing quality gaps in preprocedural assessment and documentation is critical to optimizing use of elective PCI [28].

The apparent overuse of PCI for elective indications may be a reflection of our fragmented, fee-for-service health care delivery system. However, recent studies challenge these assumptions. In a Canadian study, Ko et al found that 18% of elective PCIs were classified as inappropriate, a proportion similar to what had been found previously in the United States [30]. In a US study of Medicare beneficiaries, Matlock and colleagues observed a fourfold regional variation in use of elective coronary angiography and PCI in both Medicare fee-for-service and capitated Medicare Advantage beneficiaries [31]. Collectively, these studies suggest barriers to optimal patient selection for invasive coronary procedures in both capitated and fee-for-service health care systems. Without addressing factors that contribute to variation in the absence of fee-for-service incentives, efforts to improve integration and reduce fee-for-service reimbursement may be inadequate to optimize PCI use.

Evaluating Underuse

While potential underuse of PCI has been described for acute indications [17–22], study of underuse of PCI for elective indications is more challenging. Population data on the effect of underuse of elective PCI on patient symptom burden, functional status, and quality of life is lacking.

A population-based study from Australia highlights the potential importance of underuse in the care of patients with stable coronary disease. This study assessed symptom burden among patients with chronic stable angina using the Seattle Angina Questionnaire and included patients cared for by 207 primary care practitioners [32]. The authors noted that there was considerable variation in patient symptom burden between practices, with 14% of practices having no patients with more than 1 episode of angina per week and 18% of clinics having more than half of enrolled patients with at least 1 episode of angina per week. The authors postulate that this variability may be due to differences among providers in the identification and management of angina, including using PCI to minimize symptom burden.

In the Ko study mentioned earlier, the AUC was used to examine potential underuse of coronary revascularization procedures. In this study, they analyzed the association between AUC ratings and outcomes in patients undergoing diagnostic coronary angiography [30]. Of patients considered “appropriate” for revascularization following completion of diagnostic angiography, only 69% underwent revascularization. However, the clinical aspects that influence the decision to proceed with revascularization may not be fully captured in this study. Thus, the true degree of underuse of PCI remains elusive.

In summary, the relative lack of data that would allow for the assessment of underuse of elective PCI is an important quality concern. Health systems should work to systematically capture patient-reported health status, including symptom burden data, to identify inadequate symptom control and potential underuse of procedural care for CAD.

Facilitating Optimal Use

In current practice, the AUC hold promise to minimize the overuse of elective PCI. This likely involves addressing processes occurring upstream of the cardiac catheterization lab, including employing systems to ensure that procedures are avoided in patients who are unlikely to benefit (eg, asymptomatic, low ischemic burden) (Figure 3) [33]. Studying hospitals that already have low rates of inappropriate PCI may inform the design and dissemination of strategies that will help improve patient selection at hospitals with higher rates. Although professional organizations have developed tools intended to facilitate appropriateness evaluation at the point-of-care [34], the use of these tools are likely to be sporadic without greater integration into the health care delivery system. Further, these applications are currently limited to determination of appropriateness of PCI after completion of the diagnostic coronary angiogram. Identifying processes prior to catheterization that contribute to PCI appropriateness may also streamline appropriate ad hoc PCI, as the need to reassess appropriateness after the diagnostic angiogram may be mitigated.

Significant barriers exist to the application of the AUC for determination of procedural underuse. As described above, we lack adequate data to ascertain gaps in symptom management that could be mitigated by proper use of PCI. Further study of symptom burden in populations of patients with coronary artery disease is needed. This may help in the identification of patient populations whose symptom burden may warrant consideration of invasive coronary procedures, including coronary angiography and PCI.

Finally, it is important to note that the AUC are based on technical considerations, ie, practice guidelines and trial evidence. They do not take into consideration patient preferences. For example, PCI can be technically appropriate for the scenario but inappropriate for the individual if the procedure is not desired by the patient. Similarly, a procedure may be of uncertain benefit but appropriate if the patient desires more aggressive procedural care and has a full understanding of the risks and benefits. Currently, we fail to convey this information to patients, as evidenced by patients’ overestimation of the benefits of PCI [34]. As we continue to work toward optimal use of PCI, we must not only address the technical appropriateness of care, but move toward incorporating patient preferences through a robust process of shared decision-making.

Corresponding author: Preston M. Schneider, MD, VA Eastern Colorado Health Care System, Cardiology Section (111B), 1055 Clermont St., Denver, CO 80220, Preston.Schneider@ucdenver.edu.

Funding/support: Dr. Schneider is supported by a T32 training grant from the National Institutes of Health (5T32HL00
7822-15). Dr. Bradley is supported by a Career Development Award (HSR&D-CDA2 10-199) from VA Health Services Research & Development.

Financial disclosures: None.

From the VA Eastern Colorado Health Care System, University of Colorado School of Medicine, and the Colorado Cardiovascular Outcomes Research Group, Denver and Aurora, CO.

Abstract

• Objective: To review the use of elective percutaneous coronary intervention (PCI), evaluate what is currently known about elective PCI in the context of appropriate use criteria, and offer insight into next steps to optimize the use of elective PCI to achieve high-quality care.
• Methods: Review of the scientific literature, appropriate use criteria, and professional society guidelines relevant to elective PCI.
• Results: Recent studies have demonstrated as many as 1 in 6 elective PCIs are inappropriate as determined by appropriate use criteria. These inappropriate PCIs are not anticipated to benefit patients and result in unnecessary patient risk and cost. While these studies are consistent with regard to overuse of elective PCI, less is known about potential underuse of PCI for elective indications. We lack health status data on populations of ischemic heart disease patients to inform PCI underuse that may contribute to patient symptom burden, functional status, and quality of life. Optimal use of PCI will be attained with longitudinal capture of patient-reported health status, study of factors contributing to overuse and underuse, refinement of the appropriate use criteria with particular focus on patient-centered measures, and incorporation of patient preference and shared decision making into appropriateness evaluation tools.
• Conclusion: The use of elective PCI is less than optimal in current clinical practice. Continued effort is needed to ensure elective PCI is targeted to patients with anticipated benefit and use of the procedure is aligned with patient preferences.

Providing the right care to the right patient at the right time is essential to the practice of high-quality care. Reducing overuse of health care services is part of this equation, and initiatives to reduce inappropriate use and to encourage physicians and patients to “choose wisely” have been introduced [1]. One procedure that is being examined with a focus on appropriateness is percutaneous coronary intervention (PCI). This procedure is common (nearly 1 million inpatient PCI procedures performed in 2010), presents risks to the patient, and is expensive (attributable cost approximately $10 billion in 2010) [2,3]. While the clinical benefit of PCI in acute settings such as ST-segment elevation myocardial infarction is well established [4], the benefit of PCI in nonacute (elective) settings is less robust [5–7]. Prior studies have demonstrated PCI for stable ischemic heart disease does not result in mortality benefit [6]. Furthermore, PCI as an initial strategy for symptom relief of stable angina may offer little benefit relative to medications alone [5]. Given that PCI is common, costly, and associated with both short- and long-term risks [8,9], ensuring this therapy is provided to the right patient at the right time is important.

In 2009, appropriate use criteria (AUC) were developed by 6 professional organizations to support the rational and judicious use of PCI [10]; a focused update was published in 2012 [11]. In this review, we discuss the recommendations for appropriate use and their application and offer thoughts on next steps to optimize the use of elective PCI as part of high-quality care.

Variation in the Use of PCI

Additionally, significant public attention has been focused on the issue of overuse after lay press investigations into community practice patterns. In particular, a case study presented in the New York Times highlighted the community of Elyria, Ohio, which was found to have a PCI rate that was 4 times the national average [16]. This investigation sparked public debate and further focused attention on the issue of overuse of elective PCI. Conversely, others have pointed to data that suggest underuse of coronary procedural care, particularly among women and racial and ethnic minorities [17–22].

Appropriate Use Criteria

Development Methodology

AUC for PCI, which were developed through the collaborative efforts of 6 major cardiovascular professional organizations, are intended to support the effective, efficient, and equitable use of PCI [10,11]. They were developed in response to a growing need to support rational use of cardiovascular procedures as part of high-quality care. The methods of development for the AUC have been described in detail in the criteria publications [10,11]. We briefly review these methods here.

Panel members first individually assigned ratings to each clinical scenario that ranged from 1 (least appropriate) to 9 (most appropriate). This was followed by an in-person meeting in which technical panel members discussed scenarios for which there was wide variation in appropriateness assessment. After this meeting, technical panel members again assigned ratings for each scenario from 1 to 9. After this second round, the median values for the pooled ratings were used as the appropriateness classification for each scenario. Scenarios with median values of 1–3 were classified as “inappropriate,” 4–6 as “uncertain,” and 7–9 as “appropriate.” A rating of “appropriate” represented clinical scenarios in which the indication is considered generally acceptable and likely to improve health outcomes or survival. A rating of “uncertain” represented clinical scenarios where the indication may be reasonable but more research is necessary to further understand the relative benefits and risks of PCI in this setting. Finally, a rating of “inappropriate” represented clinical scenarios in which the indication is not generally acceptable as it is unlikely to improve health outcomes or survival.

The approach used for AUC development appears to be valid, as Class III indications for PCI in the ACC/AHA clinical guideline [24] (Class III = PCI should NOT be performed since it is not helpful and may be harmful) and AUC scenarios rated as inappropriate are in 100% agreement (personal communication, Ralph Brindis, past president of the American College of Cardiology).

Application

It is important to remember that the AUC are intended to aid in patient selection and are not absolute. Unique clinical factors and patient preference cannot feasibly be captured by the AUC scenarios. It should also be noted that the intent of the AUC is not to be punitive but rather to identify and assess variation in practice patterns. To reflect this intent, the terminology applied to appropriateness ratings has recently changed. Clinical scenarios previously classified as “inappropriate” are now termed “rarely appropriate” and clinical scenarios classified as “uncertain” are now termed “may be appropriate.”

Although the AUC were developed to help evaluate practice patterns of care delivery and serve as guides for clinical decision making, they were not intended to serve as mandates for or against treatment in individual patients or to be tied to reimbursement for individual patients. Despite this, health care organizations and payors have used other AUC documents for incentive pay and prior authorization programs, specifically for cardiovascular imaging [25]. Use of the AUC in this manner may still be reasonable if application and measurement is at the level of the practice, rather than the individual patient, but much remains to be understood about the implications of applying AUC in reimbursement
decisions.

Refinement

The AUC for PCI are designed to be dynamic and continually updated. As additional evidence becomes available regarding the efficacy of PCI in specific clinical scenarios, there will be ongoing efforts to update the AUC to reflect this new evidence. This is highlighted by the first update to the AUC occurring less than 3 years after the original publication date [11].

In addition to perpetual review of the data used to inform scenario ratings, there are opportunities to improve measurement of the clinical variables that are considered in rating PCI appropriateness (eg, clinical presentation, symptom severity, ischemia severity, extent of medical therapy, extent of anatomic disease). For example, in the current AUC, symptom severity is dependent on clinician assessment using the Canadian Cardiovascular Society Classification [25]. Moving toward a patient-centered assessment of symptom severity would ensure that the AUC more closely reflect the patient-perceived symptom burden. Further, the use of a patient-centered instrument would reduce the possibility of physician manipulation of symptom severity to influence the apparent appropriateness of PCI. There are similar opportunities to improve reporting of noninvasive stress test data, such as through standardized reporting of ischemic risk. Finally, the use of physiologic assessments of stenosis severity (eg, fractional flow reserve) and quantitative coronary angiography to standardize interpretations of diagnostic angiography may further optimize the assessment of PCI appropriateness.

Application of the Appropriate Use Criteria in Clinical Practice—Study Results

Application of the AUC to clinical practice has highlighted potential overuse of PCI (Table). The first report came from applying the AUC to the National Cardiovascular Data Registry (NCDR) CathPCI Registry [26]. In this study of more than 500,000 PCIs from over 1000 facilities across the country, the authors found that PCIs performed in the acute setting (STEMI, NSTEMI, and high-risk unstable angina) were almost uniformly classified as appropriate. However, for nonacute (elective) PCI, application of the AUC resulted in the classification of 50% as appropriate, 38% as uncertain, and 12% as inappropriate. The majority of patients who received inappropriate PCI had a low-risk stress test (72%) or were asymptomatic (54%). Additionally, 96% of patients who received PCI classified as inappropriate had not been given a trial of adequate anti-anginal therapy. This analysis was supported by subsequent analyses of 2 other state-specific registries (New York and Washington), which found similar rates of PCI for nonacute indications rated as inappropriate [27,28]. Additionally, all 3 studies showed wide facility-level variation in the percentage of appropriate and inappropriate PCI for elective indications.

These studies also highlight a gap in preprocedural care. The anticipated benefit of elective PCI is related to patient symptom burden, adequacy of anti-anginal therapy, and ischemic risk as determined by noninvasive stress testing. However, 30% to 50% of patients undergo elective PCI without evidence of preprocedural stress testing. Attempts are being made to address this gap with the recent release of PCI performance measures [29]. These performance measures, intended for cardiac catheterization labs, include comprehensive documentation of the indication for PCI, which is central to determination of appropriateness. This integration of procedural indication into a performance measure marks the first such occurrence in cardiology.

As documentation of procedural indication and appropriateness have become part and parcel of assessing quality of care, concerns about “gaming” have become more pertinent. Providers who perform PCI could potentially enhance the appearance of appropriateness by overstating the clinical symptom burden or stress test findings. The incorporation of validated, patient-centered health status questionnaires along with data audit programs have been proposed as measures to prevent this type of abuse. Addressing quality gaps in preprocedural assessment and documentation is critical to optimizing use of elective PCI [28].

The apparent overuse of PCI for elective indications may be a reflection of our fragmented, fee-for-service health care delivery system. However, recent studies challenge these assumptions. In a Canadian study, Ko et al found that 18% of elective PCIs were classified as inappropriate, a proportion similar to what had been found previously in the United States [30]. In a US study of Medicare beneficiaries, Matlock and colleagues observed a fourfold regional variation in use of elective coronary angiography and PCI in both Medicare fee-for-service and capitated Medicare Advantage beneficiaries [31]. Collectively, these studies suggest barriers to optimal patient selection for invasive coronary procedures in both capitated and fee-for-service health care systems. Without addressing factors that contribute to variation in the absence of fee-for-service incentives, efforts to improve integration and reduce fee-for-service reimbursement may be inadequate to optimize PCI use.

Evaluating Underuse

While potential underuse of PCI has been described for acute indications [17–22], study of underuse of PCI for elective indications is more challenging. Population data on the effect of underuse of elective PCI on patient symptom burden, functional status, and quality of life is lacking.

A population-based study from Australia highlights the potential importance of underuse in the care of patients with stable coronary disease. This study assessed symptom burden among patients with chronic stable angina using the Seattle Angina Questionnaire and included patients cared for by 207 primary care practitioners [32]. The authors noted that there was considerable variation in patient symptom burden between practices, with 14% of practices having no patients with more than 1 episode of angina per week and 18% of clinics having more than half of enrolled patients with at least 1 episode of angina per week. The authors postulate that this variability may be due to differences among providers in the identification and management of angina, including using PCI to minimize symptom burden.

In the Ko study mentioned earlier, the AUC was used to examine potential underuse of coronary revascularization procedures. In this study, they analyzed the association between AUC ratings and outcomes in patients undergoing diagnostic coronary angiography [30]. Of patients considered “appropriate” for revascularization following completion of diagnostic angiography, only 69% underwent revascularization. However, the clinical aspects that influence the decision to proceed with revascularization may not be fully captured in this study. Thus, the true degree of underuse of PCI remains elusive.

In summary, the relative lack of data that would allow for the assessment of underuse of elective PCI is an important quality concern. Health systems should work to systematically capture patient-reported health status, including symptom burden data, to identify inadequate symptom control and potential underuse of procedural care for CAD.

Facilitating Optimal Use

In current practice, the AUC hold promise to minimize the overuse of elective PCI. This likely involves addressing processes occurring upstream of the cardiac catheterization lab, including employing systems to ensure that procedures are avoided in patients who are unlikely to benefit (eg, asymptomatic, low ischemic burden) (Figure 3) [33]. Studying hospitals that already have low rates of inappropriate PCI may inform the design and dissemination of strategies that will help improve patient selection at hospitals with higher rates. Although professional organizations have developed tools intended to facilitate appropriateness evaluation at the point-of-care [34], the use of these tools are likely to be sporadic without greater integration into the health care delivery system. Further, these applications are currently limited to determination of appropriateness of PCI after completion of the diagnostic coronary angiogram. Identifying processes prior to catheterization that contribute to PCI appropriateness may also streamline appropriate ad hoc PCI, as the need to reassess appropriateness after the diagnostic angiogram may be mitigated.

Significant barriers exist to the application of the AUC for determination of procedural underuse. As described above, we lack adequate data to ascertain gaps in symptom management that could be mitigated by proper use of PCI. Further study of symptom burden in populations of patients with coronary artery disease is needed. This may help in the identification of patient populations whose symptom burden may warrant consideration of invasive coronary procedures, including coronary angiography and PCI.

Finally, it is important to note that the AUC are based on technical considerations, ie, practice guidelines and trial evidence. They do not take into consideration patient preferences. For example, PCI can be technically appropriate for the scenario but inappropriate for the individual if the procedure is not desired by the patient. Similarly, a procedure may be of uncertain benefit but appropriate if the patient desires more aggressive procedural care and has a full understanding of the risks and benefits. Currently, we fail to convey this information to patients, as evidenced by patients’ overestimation of the benefits of PCI [34]. As we continue to work toward optimal use of PCI, we must not only address the technical appropriateness of care, but move toward incorporating patient preferences through a robust process of shared decision-making.

Corresponding author: Preston M. Schneider, MD, VA Eastern Colorado Health Care System, Cardiology Section (111B), 1055 Clermont St., Denver, CO 80220, Preston.Schneider@ucdenver.edu.

Funding/support: Dr. Schneider is supported by a T32 training grant from the National Institutes of Health (5T32HL00
7822-15). Dr. Bradley is supported by a Career Development Award (HSR&D-CDA2 10-199) from VA Health Services Research & Development.

Financial disclosures: None.

Background

Levamisole is a pharmaceutical with anthelminthic and immunomodulatory properties that received approval from the Food and Drug Administration in 1991 as part of adjuvant chemotherapy regimens for colorectal cancer. The addition of levamisole to 5-flouroruacil (5-FU) was first evaluated by the North Central Cancer Treatment Group in a 3-arm clinical trial that found that 5-FUlevamisole for 12 months was superior to either surgery alone or surgery followed by levamisole alone (recurrence rate was reduced by 40% and the death rate by 33% in Dukes’ C colon cancer).1 A subsequent trial intergroup trial randomized patients with Dukes’ B2 and C colon cancer to surgery alone or 1 year of adjuvant levamisole or 5FUlevamisole and confirmed the efficacy of 5FUlevamisole with respect to disease free survival and overall survival.2 As a result, adjuvant chemotherapy became the standard for stage III colon cancer as reported by an National Cancer Institute consensus development panel.3 Subsequently, primarily because of toxicity reasons, leucovorin replaced levamisole in most adjuvant chemotheraoy regimens for stage III colorectal cancer. Clinical toxicity of levamisole was noted as early as 1976 when several cases of leukopenia and agranulocytosis were reported. Recurrence with re-exposure was well described and agranulocytosis spontaneously reversed upon discontinuation of therapy. Vasculitis secondary to levamisole treatment was first reported in 1978, presenting primarily as leukocytoclastic vasculitis, cutaneous necrotising vasculitis and thrombotic vasculopathy without vasculitis. These findings typically, but not invariably, involve the ear lobes. In the early 1990s, levamisole became unavailable for human use in the United States due to toxicity concerns. Various neurological side effects were described with levamisole therapy, the most concerning complication being multifocal inflammatory leukoencephalopathy. Recently, several persons have developed a novel syndrome characterized by necrotic noses and ears, leg ulcers, agranulocytosis, thrombovasculopathy, and positive antineutrophil cytoplasmic antibodies (ANCAs) as a result of the drug cocaine being adulterated with levamisole. We describe the drug below.

Background

Levamisole is a pharmaceutical with anthelminthic and immunomodulatory properties that received approval from the Food and Drug Administration in 1991 as part of adjuvant chemotherapy regimens for colorectal cancer. The addition of levamisole to 5-flouroruacil (5-FU) was first evaluated by the North Central Cancer Treatment Group in a 3-arm clinical trial that found that 5-FUlevamisole for 12 months was superior to either surgery alone or surgery followed by levamisole alone (recurrence rate was reduced by 40% and the death rate by 33% in Dukes’ C colon cancer).1 A subsequent trial intergroup trial randomized patients with Dukes’ B2 and C colon cancer to surgery alone or 1 year of adjuvant levamisole or 5FUlevamisole and confirmed the efficacy of 5FUlevamisole with respect to disease free survival and overall survival.2 As a result, adjuvant chemotherapy became the standard for stage III colon cancer as reported by an National Cancer Institute consensus development panel.3 Subsequently, primarily because of toxicity reasons, leucovorin replaced levamisole in most adjuvant chemotheraoy regimens for stage III colorectal cancer. Clinical toxicity of levamisole was noted as early as 1976 when several cases of leukopenia and agranulocytosis were reported. Recurrence with re-exposure was well described and agranulocytosis spontaneously reversed upon discontinuation of therapy. Vasculitis secondary to levamisole treatment was first reported in 1978, presenting primarily as leukocytoclastic vasculitis, cutaneous necrotising vasculitis and thrombotic vasculopathy without vasculitis. These findings typically, but not invariably, involve the ear lobes. In the early 1990s, levamisole became unavailable for human use in the United States due to toxicity concerns. Various neurological side effects were described with levamisole therapy, the most concerning complication being multifocal inflammatory leukoencephalopathy. Recently, several persons have developed a novel syndrome characterized by necrotic noses and ears, leg ulcers, agranulocytosis, thrombovasculopathy, and positive antineutrophil cytoplasmic antibodies (ANCAs) as a result of the drug cocaine being adulterated with levamisole. We describe the drug below.

Background

Levamisole is a pharmaceutical with anthelminthic and immunomodulatory properties that received approval from the Food and Drug Administration in 1991 as part of adjuvant chemotherapy regimens for colorectal cancer. The addition of levamisole to 5-flouroruacil (5-FU) was first evaluated by the North Central Cancer Treatment Group in a 3-arm clinical trial that found that 5-FUlevamisole for 12 months was superior to either surgery alone or surgery followed by levamisole alone (recurrence rate was reduced by 40% and the death rate by 33% in Dukes’ C colon cancer).1 A subsequent trial intergroup trial randomized patients with Dukes’ B2 and C colon cancer to surgery alone or 1 year of adjuvant levamisole or 5FUlevamisole and confirmed the efficacy of 5FUlevamisole with respect to disease free survival and overall survival.2 As a result, adjuvant chemotherapy became the standard for stage III colon cancer as reported by an National Cancer Institute consensus development panel.3 Subsequently, primarily because of toxicity reasons, leucovorin replaced levamisole in most adjuvant chemotheraoy regimens for stage III colorectal cancer. Clinical toxicity of levamisole was noted as early as 1976 when several cases of leukopenia and agranulocytosis were reported. Recurrence with re-exposure was well described and agranulocytosis spontaneously reversed upon discontinuation of therapy. Vasculitis secondary to levamisole treatment was first reported in 1978, presenting primarily as leukocytoclastic vasculitis, cutaneous necrotising vasculitis and thrombotic vasculopathy without vasculitis. These findings typically, but not invariably, involve the ear lobes. In the early 1990s, levamisole became unavailable for human use in the United States due to toxicity concerns. Various neurological side effects were described with levamisole therapy, the most concerning complication being multifocal inflammatory leukoencephalopathy. Recently, several persons have developed a novel syndrome characterized by necrotic noses and ears, leg ulcers, agranulocytosis, thrombovasculopathy, and positive antineutrophil cytoplasmic antibodies (ANCAs) as a result of the drug cocaine being adulterated with levamisole. We describe the drug below.