The Philadelphia Eagles faced off against NFC rival Los Angeles Rams in a contest that many think could be a potential NFC Championship preview. The Eagles came out with a victory, winning 43-35 but suffered a more important loss. In the third quarter, the Eagles star quarterback Carson Wentz dived forward for what was initially thought was a touchdown but took a big hit to both of his legs. The touchdown was called back on a holding penalty but Wentz went on to complete the drive with several hand offs and a great throw in the pocket to receiver Alshon Jeffery for a touchdown. Wentz left the field on his own volition after the drive and walked back to the locker room amid the long faces of the Eagles support staff. It was reported later that Wentz had torn his left ACL which will end his potential MVP season. This is devastating for the Philadelphia Eagles who were super bowl favorites and currently own a 11-2 record, best in the NFC.
Anterior Cruciate Ligament injuries are a very common orthopedic injury in all sports but most notably in sports played on grass/turf due to the high level of cutting required. ACL injuries are frequently non-contact such as when pushing off or pivoting during which the distal aspect of the lower extremity is pushed laterally causing the knee to buckle inwards (known as a Valgus Stress) which places a large amount of stress on the ligaments of the knee most notably the ACL and the Medial Collateral Ligament. ACL injuries can also be from contact or blunt force trauma as in the case of Wentz. A blow to the lateral side of the knee can cause a large valgus force that can lead to an ACL tear.
The ACL is one of the key stabilizing ligaments of the knee along with the posterior cruciate ligament, medial collateral ligament and the lateral collateral ligament. The ACL’s primary function is to control anterior translation of the lower leg(Tibia) on the upper leg(Femur). When one or more of the knee ligaments are not intact, the knee becomes inherently unstable and can cause the knee to buckle or suffer additional soft tissue injuries. For athletes, this is especially problematic as they will not be able to confidently cut or pivot on their affected knee. When a high level professional athlete suffers a complete rupture of the ACL, reconstruction of the ligament is necessary if the athlete wishes to return to sport.
Rehabilitation for an athlete undergoing ACL reconstruction generally takes about 6-8 months to return to sport but can sometimes take over a year. It is important to make sure that the graft that is used to replace the deficient ACL is as strong as it needs to be to tolerate the extreme stresses at the knee of high level sports. It is also important for the athlete to regain as much knee/hip strength (most notably the hamstring which assists the ACL in preventing anterior translation of the tibias) as possible to regain stability at the knee. The athlete must also gain the confidence to compete at a high level on their affected knee which can often be the limiting factor in returning to sport. Early ACL rehab focuses on the athlete regaining full knee range of motion as well as volitional quadriceps strength to allow them to fully straighten the knee. Focus in the first few months is placed on strengthening all of the muscles of the knee/hip/ankle as well as working on balance and proprioception to help return the knee to its pre-injured state. Once the new graft has been given ample time to set (10-12 weeks) more high level strengthening and some sports specific training can begin.
Bears Tight End Zach Miller has Emergency Vascular Surgery Following Knee Dislocation by Sean Sullivan, PT DPT
While orthopedic injuries tend to dominate the headlines in professional sports leagues such as the NFL, neurological or vascular injuries can occur in conjunction and often can be limb/life threatening. Chicago Bears tight end Zach Miller caught a pass in the end zone during their game against the New Orleans Saints when he landed awkwardly on his left leg and came up lame in obvious pain/distress.
His injury was initially diagnosed as a fracture of his leg but was later diagnosed as a knee dislocation. A dislocation the bones that make up that joint are separated often times due to trauma. In Miller’s case, his Femur(thigh bone) and Tibia(shin bone) were separated. It is not known at this time whether Miller suffered any fractures along with this dislocation but it is likely that he will require surgery to repair any soft tissue(ligament) damage that occurred.
What happened in conjunction with Miller’s dislocation turned out to be the more pressing concern for the NFL veteran. Miller also suffered a rupture of his popliteal artery. Miller’s leg was stabilized by on field medical personnel and was rushed to the University Medical Center of New Orleans where he underwent emergency vascular surgery to repair the damaged blood vessel. He is currently being monitored to ensure proper healing/blood flow following his surgery.
The popliteal artery originates from the femoral artery which runs from our groin down the front/inside of our thigh. The Popliteal artery can be found on the posterior aspect of our knee and branches into its various divisions below the knee where it supplies blood flow to our entire lower leg. It is not difficult to see why a rupture of this artery( or any for that matter) is an emergency medical condition. When an artery is damaged, the blood flow to the areas of the body that are supplied by that vessel is impaired which leads to tissue ischemia. Prolonged ischemia of 6-8 hours can lead to irreversible tissue death and can result in amputation being the only means of preserving a limb.
While Miller’s injury is a very rare case, it is important for all medical personnel (on or off the field) to properly evaluate neurovascular integrity of a patient’s limbs following trauma. This means checking all pulses distal to the injury sight and assessing sensation to rule out any nerve or blood vessel damage. Making sure to not forget this crucial step can ensure that patients do not endure long term health ramifications due to late detection of neurovascular damage.
The 2017-18 NBA season tipped off last night with a rematch of last years Eastern Conference Finals pitting the Cleveland Cavaliers against the Boston Celtics. Just minutes into the first quarter Celtic small Forward Gordon Hayward went up for an alley-oop dunk from guard Kyrie Irving when came down awkwardly on his left ankle. The photo below shows Hayward in the air before landing on his left leg. The next photo shows Hayward sitting on the court in visible pain and gives a great view of how his ankle looked after the fall. Those who are squeamish, scroll down with caution.
While further details are still to come on the specifics of Hayward’s injury, what we do know is that he sustained a fracture of his left Tibia(Shin Bone) and a dislocation of his ankle joint. He is set to have surgery on that ankle Wednesday back in Boston. He will likely require a plate/screw/nail fixation(Open reduction with internal fixation) to keep his ankle joint stable and possibly a repair of the ligaments that work to stabilize his ankle. Luckily the Celtics medical staff were able to reduce/relocate his ankle on the court before placing it in an air cast which helped to reduce his pain. He also likely avoided any nerve/blood vessel damage that can occur with this type of injury as this would require immediate surgery.
Rehab for this type of surgery is likely to be at least 3-4 months but possibly longer depending on the degree of soft tissue damage that Hayward sustained. This is important because when a joint is dislocated, often times the surrounding ligaments become compromised, as they work passively to stabilize the joint. As discussed in my post on high ankle sprains, soft tissue such as ligaments do not heal as quickly as bone due to their poor blood supply. If the damage to the surrounding ligaments of Hayward’s ankle is severe, this will likely add months to his recovery and will make his return this season very unlikely.
The NFL suffered another painful blow to their star power when Aaron Rodgers left during the 1st quarter of the Green Bay Packers game against the Minnesota Vikings after suffering a fracture of his right clavicle. Rodgers was tackled by Vikings linebacker Anthony Barr and was drilled into the ground. Barr was not penalized for the hit and while deemed legal by NFL rules many felt the roughness of the tackle was unnecessary. Rodgers will have surgery to repair the fracture which will likely end his regular season.
The mechanism of injury for Rodgers is typically how a clavicle fracture occurs which is a direct blow or fall onto the lateral shoulder. The most common area of the clavicle to be fractured is the middle third of the clavicle and these types of fractures typically heal well without surgery if the fracture is not complex or displaced. These type of fractures can heal with a period of immobilization in a sling. If the fracture is at the distal end of the clavicle or is a complex fracture, this will almost always require surgical treatment.
It has not come out what type of fracture Aaron Rodgers suffered but what we do know is that he will require surgical treatment which likely will involve an open reduction internal fixation. This means that the surgeon will need to perform an open surgery to allow them to put the fracture back in place and then use some type of fixation(Screw, nail, plate) to hold the fracture in place while it heals. Since the clavicle does move slightly with shoulder elevation, it is important to limit overhead activity for the first few weeks. Rodgers will likely be in a sling for the first 4-6 weeks and will not be able to start throwing until at least 3 months.
Week 4 of the NFL season just concluded on Monday night following the Kansas City Chiefs last second win over the Washington Redskins. As with just about every week of NFL games comes a host of injuries to key players on contending teams, often times of the season ending variety.
Rookie running back Chris Carson of the Seattle Seahawks suffered a season ending left leg injury during the Seahawks win over the Colts on Sunday night. What was originally diagnosed as a fracture of his left lower leg turned out to be more severe. In addition to the fracture that he suffered in his fibula, Carson suffered a severe syndesmosis tear otherwise known as a “High Ankle Sprain”.
The syndesmosis is a series of ligaments that connect the ends of the two lower leg bones, the tibia and the fibula. A tear of one of these ligaments is a common injury in American football and is generally caused when the athlete’s foot/ankle is pushed into extreme external rotation. It can also be caused by a blow to the lateral aspect of the knee/lower leg with the foot planted which causes the syndesmosis to be over stretched which is what happened in Carson’s case as seen in the picture below.
The words “High ankle sprain” are words an athlete never wants to hear. Unlike a typical lateral ankle sprain which is a tear of one of the lateral ankle ligaments, a syndesmosis tear takes more time to heal. If there is a disruption of the any of the syndesmosis ligaments, these ligaments are stressed any time the athlete tries to bear weight on that limb as the athlete’s body weight and gravity put stress through the lower leg and tries to separate the tibia and fibula. This is the primary reason why recovery from a high ankle sprain can take longer to heal and are prone to reoccurrence.
MRIs are the gold standard for diagnosing a high ankle sprain. Depending on the grade of the tear, a patient may or may not be instructed to bear weight following the injury. Upon imaging, if there is no widening of the space between the tibia/fibula, the fracture is considered stable and are treated conservatively with rest/rehab and can weight bear as tolerated. If there is mild widening of less than 4cm, then the athlete is generally immobilized in a walking boot. If there is significant widening of the mortise of greater than 4cm, this will require surgical treatment which unfortunately is what will end Carson’s season. Following surgery, Carson will likely be immobilized in a plaster cast for 2 weeks and transferred to a cast boot for another 4-6 weeks during which he will be non weight bearing to avoid stress to the healing fracture/ligaments.
On Monday night, the San Antonio Spurs bowed to the Golden State Warriors in Game 4 of the Western Conference Finals. It wasn’t much of a contest. After another stellar regular season, early playoff injuries robbed the Spurs of veteran point guard, Tony Parker (quad tendon rupture), and the electric small forward, Kawhi Leonard (ankle sprain). On Saturday, when Spurs’ center/power forward, David Lee partially tore his patellar tendon, it was all but over. This wasn’t the first time that the 34 year-old Lee underwent significant post season surgery. He’d had a torn hip flexor repaired in May of 2013 having seen very limited playoff action once sustaining the injury the month prior. Read More ›
The Boston Celtics announced on Saturday that Isaiah Thomas, their 28-year-old star point guard, re-aggravated a “right femoral-acetabular impingement with labral tear” in game two of the Eastern Conference Finals against Cleveland. The injury will keep him out for the remainder of the playoffs and may require surgery. The initial insult to the hip occurred on March 15th and it was evidently exacerbated in a semifinal round contest on May 12th. Read More ›
Mets first baseman Wilmer Flores was placed on the DL on Friday and spent the weekend in the hospital to receive IV treatment for a knee infection. Evidently, Flores had played with discomfort for a couple of days before seeking medical attention.
Though this diagnosis may not sound like much, it is one that can be quite serious. It is considered an emergent condition with high risk of morbidity or mortality if not quickly and aggressively addressed. The outcome of treatment hinges on it. Read More ›
Mets’ first baseman Lucas Duda suffered a hyperextended left elbow in the fifth inning on Wednesday when Cesar Hernandez, the Phillies’ second baseman, tried to run out an infield hit up the first base line and ran into Duda’s glove with his left shoulder as he fielded the throw from the pitcher. Though he remained in the game through the half inning, Duda was removed for a pinch hitter in the bottom of the fifth. Duda will likely have an MRI today to determine the extent of his injury.
We’ve all heard much about the dangers of football and the alarming incidence of concussions in the sport. Also about the NFL’s initial resistance to acknowledging the probable relationship of concussions to Chronic Traumatic Encephalopathy (CTE), which currently can only be diagnosed on autopsy.
CTE – as defined by the Boston University CTE Center16 – is “a progressive degenerative disease of the brain found in athletes (and others) with a history of repetitive brain trauma, including symptomatic concussions as well as asymptomatic subconcussive hits to the head… This trauma triggers progressive degeneration of the brain tissue, including the build-up of an abnormal protein called tau. These changes in the brain can begin months, years, or even decades after the last brain trauma or end of active athletic involvement. The brain degeneration is associated with memory loss, confusion, impaired judgment, impulse control problems, aggression, depression, and, eventually, progressive dementia.”
The concern many have is not only for the health and safety of the athletes. Others who have suffered mild traumatic brain injury want to know if they are susceptible to CTE as well. No one really has that answer yet. However, lets look carefully at the information that is out there and how it can be interpreted.
First, scary as it may be, recognize that the high incidence of CTE reported in studies reflects several biases. The most significant of these is self-selection. The brains that have been examined on autopsy are primarily those of athletes who have donated their brains for research due to symptoms they’ve experienced, or those whose family has suspected the diagnosis. This clearly inflates the percentages of athletes diagnosed with the condition.
One such study done by Boston University and the US Department of Veteran’s Affairs17 established that 87 of 91 football players had signs of CTE on autopsy, while Boston University also found the condition in 79% (131 of 165) of football players across all levels.17
These frightening results are mildly contrasted by another study18 that looked at 60+ former NFL players – all aged 60-69 – to try to identify symptoms of CTE in living people. Their age range indicates that these were players who played before heightened concussion awareness and before protocols were initiated by the NFL. The results showed that 60% had completely normal age-appropriate cognitive decline. Of the remaining 40%, 6% met the criteria for dementia. It would be interesting – and possibly revealing – to be able to correlate the findings on these men with how their brains subsequently present on autopsy.
Though this group also played before helmets were improved, the sturdier helmets may even have encouraged harder hitting. The NFL’s response has included recent rule changes to modulate direct hits to the head, though the game will likely see an even greater proportion of debilitating but less threatening lower body injuries as a result. The players of today are also typically stronger, bigger and faster than those in the era of those tested in this study. This too likely influences the frequency and outcomes of traumas that they experience.
Though the brain has the ability to recover from one injury, long-term effects are more likely after multiple incidents.
However, keep in mind that football players sustain blows to the head (direct and/or indirect) on almost every play. This cumulative subconcussive microtrauma may be as much or more of a factor in causing CTE than one or few isolated incidents of concussive trauma. Not at all good for football or soccer players, but an encouraging note for others who fear the long term effects of having sustained a concussion, or even several of them.
Vulnerability differs amongst athletes on the field. Dr. Steven Erickson noted that offensive linemen face forces “that are generally linear and the players know they are coming. Consequently, the head doesn’t move very much, so the brain doesn’t move very much. This may still represent brain trauma, but less often to the degree of causing concussion.”
He contrasted this with receivers. Though the “magnitude of the forces they sustain may be lower, the rotational component to the trauma, the player not being able to anticipate the nature of the hit and the degree of subsequent brain motion all make it more likely they will sustain a clinical concussion.”
A study by the Mayo Clinic, published in December 2015, found that one in three amateur athletes who participated in contact sports while in school developed CTE. 19 That statistic will likely cause even more scrutiny of the games and cause some to weigh the risk-reward of participation differently than before. Again though, this study also reflected issues of self-selection.
I asked Dr. Erickson about the cheating (underperforming) on baseline screening that we have read about occurring in the NFL, and whether this effort by some players to lessen the likelihood that a subsequent concussion will be diagnosed can be detected.
His response was that “though it may be possible, there are internal checks with ImPACT™ whereby validity scores can generally identify when an individual is cheating.”
Dr. Erickson commented that “this is another advantage of the vestibular test (see Part 2 of this series) advocated at the Banner Concussion Center, because a non-physiologic response is detected with intentional underperformance or anxiety responses to testing, We benefit from the fact that athletes don’t know how to cheat to underperform on the test.”
He added that “of course, best medicine is for an athlete to put in best effort at baseline as well as post injury. The motivation factor is very real. Sometimes those not particularly motivated in baseline testing are very motivated to achieve in order to return to play,”
Hopefully more athletes and their coaches are acknowledging that playing through will not serve them well either in the short or long term.
So, does the Banner Concussion team advocate keeping kids from playing sports? Most definitely not… Each member acknowledges the many benefits of sport, such as exercise, physical development and emotional growth. Developing mental toughness and learning life lessons such as teamwork and how to deal with adversity while enjoying a healthy social outlet that is fun, challenging and productive trumps fear.
They stress that concussion can happen almost any time – even to those who don’t play sports – and that sports can be made safe. The key to addressing concussion is education and diligence. It is important to be able to identify concussion if/when it happens and seek appropriate assessment and care. By managing the symptoms, recovery is accelerated and the likelihood of recurrence minimized. The value of baseline testing cannot be stressed enough nor can the importance of not allowing an athlete of any age to return to play after sustaining a head trauma resulting in symptoms without undergoing an evaluation.
Though most who suffer a concussion recover fully and within a four-week period, the caution is to understand that symptoms left untreated – can result in long lasting consequences.
As for those who sustain multiple head traumas and, quite possibly – or especially – those who have also suffered repeated microtrauma, the long term effects are coming into better focus with the further study of CTE.
References for Parts 1-3 of the Concussion Series:
- Centers for Disease Control and Prevention (CDC), National Center for Injury Prevention and Control. Report to Congress on mild traumatic brain injury in the United States: steps to prevent a serious public health problem. Atlanta (GA): Centers for Disease Control and Prevention; 2003.
- Lescohier I, DiScala C. Blunt trauma in children: causes and outcomes of head versus intracranial injury. Pediatrics 1993;91(4):721-5.
- Langlois JA, Rutland-Brown W, Wald M. The epidemiology and impact of traumatic brain injury: a brief overview. Journal of Head Trauma Rehabilitation 2006;21(5):375-8
- Finkelstein E, Corso P, Miller T and associates. The Incidence and Economic Burden of Injuries in the United States. New York (NY): Oxford University Press; 2006.
- Fung M, Willer B, Moreland D, Leddy J. A proposal for an evidence-based emergency department discharge form for mild traumatic brain injury. Brain Injury 2006;20(9):889-94.
- Alexander, Andrew L., Lee, Jee Eun, Lazar, Mariana, Field, Aaron, S.
Diffusion Tensor Imaging of the Brain. Neurotherapeutics. 2007 Jul; 4(3): 316–329.doi: 10.1016/j.nurt.2007.05.011
- Field M, Collins M, Lovell M, Maroon J. Does age play a role in recovery from sports-related concussion? A comparison of high school and collegiate athletes. The Journal of Pediatrics 2003;142(5):546-53.
- Bryan Kolb, PhDand Robbin Gibb, PhD: Brain Plasticity and Behaviour in the Developing Brain . J Can Acad Child Adolesc Psychiatry. 2011 Nov; 20(4): 265–276.
- Guskiewicz K, et al. Cumulative effects associated with recurrent concussion in collegiate football players: the NCAA Concussion Study. JAMA 2003;290(19):2549-55.
- Pellman EJ, Lovell MR, Viano DC, Casson IR. Concussion in professional football: recovery of NFL and high school athletes assessed by computerized neuropsychological testing–Part 12. Neurosurgery 2006;58(2):263-74;discussion 263-74
- Kashluba S, Casey JE, Paniak C. Evaluating the utility of ICD-10 diagnostic criteria for postconcussion syndrome following mild traumatic brain injury. Journal of the International Neuropsychological Society 2006;12(1):111-8.
- Dean PJ, O’Neill D, Sterr A. Post-concussion syndrome: prevalence after mild traumatic brain injury in comparison with a sample without head injury. Brain Inj. 2012;26(1):14-26. doi: 10.3109/02699052.2011.635354.Epub 2011 Nov 22
- McManus, C. Stress-Induced Hyperalgesia: Clinical Implications for the Physical Therapist Orthopedic Physical Therapy Practice. 2012;24(3):165-168. (http://carolynmcmanus.com/publications/mcmanus-stress-induced-hyperalgesia.pdf)
- UPMC Sports Medicine Website
- Boston University CTE Center: http://www.bu.edu/cte/about/what-is-cte/
- Hart, J.J., JAMA Neurology 2013
- Mayo Clinic Press Release: Mayo Clinic: Evidence suggests contact sports played by amateurs increase risk of degenerative disorder http://newsletter.carehubs.com/t/ViewEmail/j/2B6E3073A3AD413C/59F3204D88C0AFA89A8E73400EDACAB4
- Aubry M, et al. Summary and agreement statement of the first International Conference on Concussion in Sport, Vienna 2001. Clinical Journal of Sports Medicine 2002 Jan;12(1):6-11