October 26, 2011

Fatal Brain Injury In H.S. Football Game

Ridge Barden, a 16 year old Phoenix, New York high school football player, died on October 14, 2011 after suffering a concussion and traumatic brain injury (TBI) during a game for Homer High School. Barden was a defensive tackle for the team, and died a few hours after falling to the turf in the 3rd quarter of the game following a blow to the head. The coroner determined the cause of death to be subdural hematoma, and massive swelling of the brain.

A subdural hematoma occurs when blood vessels rupture between the brain and the outermost of three membranes that cover the brain, (the dura) resulting in a collection of blood. Subdural hematomas can occur acutely, from a severe blow to the head, subacutely, in which the signs and symptoms can occur days or weeks later, or chronically, in which the precipitating cause might not even be known or remembered by the person suffering the condition. (Additionally, the elderly, people taking aspirin daily, or alcohol abusers can also suffer a subdural hematoma).

Coaches and school administrators watched a video of the game to determine if they noted a particularly violent collision which caused the fatal injury to Barden. Also under scrutiny was the helmet that Ridge was wearing, known as a Riddell “Revolution”. There are lawsuits pending by former NFL players against the league and Riddell Sports, Inc., the manufacturer of football helmets, alleging that former players now suffer from severe injuries from repeated collisions and concussions, including dementia, and CTE, meaning chronic traumatic encephalopathy. Chronic traumatic encephalopathy is a progressive debilitating disease suffered by people who have had multiple concussions or other head injuries. The brain tissue deteriorates from the blows and a protein called “tau” accumulates on the brain. CTE is also known as “dementia pugilistica”, since until recently the huge majority of these cases were diagnosed in boxers.

Teenagers are considered to be more at risk for concussions and traumatic brain injuries as the brain tissue is not completely developed. The National Center for Catastrophic Sports Injury Research notes that Ridge Barden was the 13th high school football player to die from a brain injury since 2005 and the third in 2011. An additional 5 college football players have suffered fatal brain injuries during a game in that same 6 year span. In Ridge Barden’s case, there was apparently no prior history of head trauma or concussion, and the autopsy did not reveal any previous brain injury.

During a recent Senate Commerce Committee Hearing, the topic being addressed was whether manufacturers of sports equipment made misleading statements and claims about their products. Several neurosurgeons and sports concussion experts testified who specialize in traumatic brain injury and sports concussions. Dr. Kevin Guskiewicz, the chairman of the department of Exercise and Sports Science at the University of North Carolina testified that Ridge Barden’s life could only have been saved if he had undergone an immediate operation to relieve the pressure on his brain as a result of the subdural hematoma. However, the problem is that in order to diagnose the issue, a CAT Scan must be ordered, and Barden’s condition deteriorated to quickly allow him to undergo a CAT Scan.

Dr. Robert Cantu, a neurosurgeon at Boston University and well known expert in the field of sports related head trauma and injuries, explained that when a person is conscious immediately after a trauma, and then deteriorates quickly as in Ridge Barden’s case, the cause of death is not the subdural hematoma, but massive brain swelling. Frequently, the fatal injury is due to a previous trauma to the brain compounded by a second impact in close proximity in time to the first. Dr. Cantu calls this “second impact syndrome” in association with subdural hematoma.

After a House Judiciary Committee hearing in October of 2009 in which NFL Commissioner Roger Goodell was pounded with questions about the NFL’s concussion policies, the NFL changed its rules to require that a player diagnosed with a concussion would not be permitted to return to that same game even if he was not experiencing any symptoms.

In the wake of the truly tragic death of Ridge Barden, numerous other high school and college football players like him, and the continuing litigation by former NFL players against the league and Riddell, changes must be contemplated and hopefully implemented. One possibility would be to terminate the three point stance for linemen, (with one hand on the ground as well as two feet), and go to a two point stance, in the expectation that this would limit helmet to helmet contact and result in more blocking with arms and hands. Another possibility would be to eliminate the purposeful helmet hit whereby running backs lower their heads into a defender to garner some additional yardage, and defenders respond by lowering their heads as well. Something else to consider would be fewer full contact drills, which undoubtedly contribute to the long term problem—after all, there are no referees blowing a whistle for helmet on helmet contact, and it is certainly unlikely that a head coach or assistant coach at any level would lecture a player for being too aggressive with an opposing teammate in practice.

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October 3, 2011

Metal Hips Failing At An Alarming Rate

In an article written by Barry Meier in the New York Times on October 1, 2011, there has been a significant failure rate of metallic artificial hips of late, which has led to recalls and defective product lawsuits. Across the United States and in Europe as well, numerous patients are looking to have metal on metal artificial hips removed and replaced. The problems stem from small pieces of metallic debris that break off the devices causing tissue damage and loss of muscle surrounding the artificial hip.

It appears that many when patients sought out their original surgeons to complain of substantial pain and muscle problems, they were informed they were fine, (normal diagnostic scans and/or blood tests) which allowed the issues to be exacerbated, with the possibility of lasting tissue damage.

The failure process is generally seen as occurring in the following manner:

1. Metal fragments get released into the body;

2. Scavenger cells try to engulf them and to digest some of the fragments;

3. The metal fragments are broken down into ions, which react with tissues;

4. Ions react chemically with tissue, causing some tissue to die and the possibility of early failure of the hip.

The research at present points to only a small percentage of the 500,000 people who received all metal hips that are now encountering problems. However, since some patients may not report pain, tissue damage could be occurring without them knowing it. The article discusses Dr. Young-Min Kwon, an orthopedic surgeon at Massachusetts General Hospital, who has been treating many patients with failed metallic hips, and who is seeing increasing numbers of patients with failures. Dr. Kwon noted that: "what we are seeing is a complex phenomenon."

A study in England determined that all metal hips failed 3 times as often as metal hips that contained plastic components as well. The Food and Drug Administration (FDA) reported more than 5,000 complaints about all metal hips in the first six months of 2011. There have been recalls in the Johnson and Johnson Depuy division of artificial hips due to the significant early failure rate. Further, there have been numerous product liability lawsuits, including one mentioned in the article by Cyndi Lafuente, an IRS advisor who found out in 2010 that the artificial hip she received in 2007 was being recalled by Johnson and Johnson.

Often, the problem is not determined by diagnostic examinations or blood tests, which can be normal despite the ongoing tissue damage engendered by the metallic debris turning into ions in the body. The FDA has ordered manufacturers of artificial hips to institute studies to determine how often the metal artificial hips are failing and the effects on patients from that failure. However these studies will not be completed for several years while the failures continue. Interestingly, there have been patients with high level of metallic debris that nevertheless do not have tissue damage, and some patients with tissue damage yet normal metal blood levels.

In Ms. Lafuente's situation, she was having occasional groin discomfort and excessive subluxing, or partial dislocation, of the hip joint. As is typical in these cases, her physician referred her for an MRI and CAT Scan, which both came back as normal, as did a blood test. She was concerned that metallosis was causing permanent injury to the bone and muscle surrounding her hip joint, and not satisfied with the "wait and see" approach of her physician.

Fortunately for Ms. Lafuente, an Internet search resulted in an informal consultation with Dr. David Langton, an orthopedist in England who recommended that she undergo a hip aspiration. Hip aspiration involves the removal of synovial fluid from the hip joint to determine if there is an infection or other ongoing process. In the U.S., aspiration is not generally performed until radiological and blood tests have been completed, although metallic debris initially accumulates in the synovial fluid rather than the blood. Ms. Lafuente returned to her surgeon, he aspirated her hip, and the results showed that she had a full 10 times the normal amount of metal in the synovial fluid. Based on this significantly high metal count, the surgeon performed hip revision surgery shortly thereafter, and fortunately for Ms. Lafuente, there was no permanent damage to the bone or muscle surrounding the artificial hip. She is still recovering, albeit the process has apparently been slow and arduous. The conclusion from this seems to be that in artificial hip cases, do not simply rely on normal MRI, CAT scan, and blood tests, nor should you accept a surgeon's "wait and see approach", especially in cases where the artificial hip has been recalled.

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