Thursday, July 3, 2014

Progress and Significance of Current Concussion Research - Developing a Blood Biomarker for Brain Injury

If you read my post on Concussions in the NHL, you'll know that a concussion is considered to be among the most complex injuries to diagnose in sports medicine. A concussion is a clinical diagnosis based largely on the observed injury mechanism (point of contact, force on head area, etc.), signs, and symptoms. Due to the fact that there is no true [perfect] diagnostic test for a concussion, physicians must rely on patient-reported symptoms and neurological testing to make a diagnosis. Additionally, unlike other neurological injuries, most concussions cannot be identified by advanced neuroimaging techniques such as CT scans or MRIs.

In this post I'll highlight some current research on concussion.


Concussion is still an injury that is largely debated. Most debate surrounds the long-term effects of the injury. What isn't debated is that a player suffering from a concussion should never return to play (RTP) the same day as the injury and should take a minimum of a few days off to recover and rest. Concussion in athletes practicing contact sports is a growing problem worldwide and new research has highlighted some important facts about the injury:

  • The underlying pathophysiology of a concussion is an acute disturbance of neuronal function combined with damage to neuronal and glial (neuronal support) cells. This acute disturbance may eventually present chronic consequences (Blennow et al.). 
  • Most concussions resolve after 7 days or within a couple weeks; however studies have revealed that 10-15% of concussions remain symptomatic more than a year after the injury. The chronic and sometimes even progressive symptoms of concussion have been linked to repeated injury occurring before the brain has properly recovered (Baugh et al.).
  • Cerebrospinal fluid (CSF) can show biochemical changes in the central nervous system (CNS). CSF biomarkers such as total tau (T-tau) and neurofilament light (NFL), show elevated levels of axonal damage after acute damage to the brain (Hesse et al. and Nylen et al.) 
    • The levels of these biomarkers correlate with the severity of the brain damage and eventually return to normal after a period of rest (Zetterberg et al. Neselius et al.).
    • CSF is obtained via a lumbar puncture, a sometimes painful procedure that is invasive and not optimal for routine testing.
A simple biomarker for concussion which can be used routinely and accurately as a diagnostic tool would be extremely useful for team physicians. This test could not only help diagnose a concussion, but also be useful in follow-up for concussed athletes and aid RTP decisions.

A recent study published in the JAMA Neurology Journal had the objective of "determining if sports-related concussion is associated with elevated levels of blood biochemical markers of injury..." The researchers collaborated with the Swedish Hockey League to conduct the research. 


In the study Blood Biomarkers for Brain Injury in Concussed Professional Ice Hockey Players, Dr. Pashtun Shahim et al. researched an objective biomarker to help in clinical decisions regarding concussion. The study examined three biomarkers to determine their significance: 
  • Neuron-specific enolase (NSE) - a biomarker for neuronal injury (elevated levels found in boxers that had been repeatedly hit in the head (Zetterberg et al).
  • S-100B - a glial cell biomarker named S-100 calcium-binding protein B, elevated levels found in boxers who took head shots compared with boxers who only took body shots (Graham et al.).
  • Plasma T-tau - elevated levels found in Olympic boxers, which then normalized after rest (Neselius et al.).
The research was approved by the Swedish Ice Hockey Association and ran through the University of Gothenburg. With player's consents, team physicians of all 12 teams in the Swedish Hockey League would collect pre-season data, asking all players to take the Standardized Assessment of Concussion. Two of the consenting teams, Frölunda and Lülea, collected baseline blood samples from all their players prior to the start of the season. 

The study asked physicians to document signs and symptoms of concussion as well as any other examination findings when making their diagnosis. For players who suffered a concussion during the season, blood samples were collected at 1, 12, 36, 48, and 144 hours post-injury (or when the player returned to full-contact). 

Of the 288 players in the SHL, 35 had a sports-related concussion for the duration of the study. 28 of these players' samples were used in data analysis, as the remaining 7 players either withdrew consent or had an uncertain diagnosis. Of these 28 concussions,
  • Three (10.7%) suffered a loss of consciousness (LOC)
  • 25 (89%) experienced symptoms such as headaches, confusion, dizziness, or nausea. 
  • 15 (53.5%) had symptoms lasting longer than 6 days.
T-tau levels were significantly higher in post-concussion samples compared with the pre-season samples. Unfortunately, the S-100B and NSE post-concussion samples were not significantly different from the pre-season samples. However, the samples collected immediately after injury (1 hour) showed elevated levels of both T-tau and S-100B when compared with the pre-season samples. The levels of these two biomarkers peaked at this timepoint (1 hour post-concussion). The levels of T-tau 144 hours after injury remained significantly elevated when compared to baseline samples; however, this did not occur in S-100B and NSE samples.

Assessing the severity of a concussion is important in the management of the injury and determination of when to RTP. The level of T-tau was not significantly different post-concussion for different grades of concussion; however, players whose concussions had symptoms for > 10 days or experienced a LOC had some higher levels. The levels of S-100B 1 hour post-concussion were significantly higher in players that experienced a LOC and those players that had symptoms for > 10 days when compared to players whose symptoms resolved in 6 days.

The T-tau biomarker displayed a significant diagnostic accuracy level, where T-tau concentrations at 1 hour post-concussion could accurately predict the number of days it took for concussion symptoms to resolve and the players to experience a safe RTP. Plasma T-tau, while highly specific to the Central Nervous System (CNS), is a promising biomarker which can be used in the diagnosis of a concussion and RTP decisions.

The NHL and NHLPA should consider participating in more studies with researchers. The wealth of information that could be learned from just basic investigation on a few blood samples is highly valuable and could not only aid current players experiencing concussion but also help determine the NHL's future plan for limiting injury.


  1. Baugh CM, Stamm JM, Riley DO, et al. Chronic traumatic encephalopathy; neurodegeneration following repetitive concussive and subconcussive brain trauma. Brain imaging Behav. 2012;6(2): 244-254. 
  2. Blennow K, Hardy J, Zetterberg H. The neuropathology and neurobiology of traumatic brain injury. Neuron. 2012;6(5);886-899. 
  3. Hesse C, Rosengren L, Vanmechelen E, et al. Cerebrospinal fluid markers for Alzheimer's disease evaluated after acute ischemic stroke. J Alzheimers Dis. 2000;2(3-4): 199-206. 
  4. Nylen K, Csajbok LZ, Ost M, et al. CSF-neurofilament correlates with outcome after aneurysmal subarachnoid hemorrhage. Neurosci Lett. 2006; 404(1-2); 132-136. 
  5. Zetterberg H, Hietala MA, Jonsson M, et al. Neurochemical aftermath of amateur boxing. Arch Neurol. 2006;63(9): 1277-1280. 
  6. Neselius S, BRisby H, Theodorsson A, Blennow K, Zetterberg H, Marcusson K. CSF-biomarkers in Olympic boxing; diagnosis and effects of repetitive head trauma. PLoS One. 2012;7(4):e33606. 
  7. Zetterberg H, Tanriverdi F, Unluhizarci K, Selcuklu A, Kelestimur F, Blennow K. Sustained release of neuron-specific enolase to serum in amateur boxers. Brain Inj. 2009:23(9): 723-726. 
  8. Graham MR, Myers T, Evans P, et al. Direct hits to the head during amateur boxing is associated with a rise in serum biomarkers for brain injury. Int J Immunopathal Pharmacol. 2011;24(1): 119-125. 
  9. Neselius S, Zetterberg H, Blennow K, et al. Olympic boxing is associated with elevated levels of the neuronal protein tau in plasma. Brain Inj. 2013;27(4): 425-433.

Saturday, April 19, 2014

Reviewing the David Backes injury, diagnosing a concussion


Also known as a mild traumatic brain injury, the concussion is the most common type of traumatic brain injury. At the 4th International Conference on Concussion in Sport (Zurich, November 2012), a panel discussion took place to obtain a consensus-based definition of a concussion. The Concussion in Sport Group (CISG) defined a concussion as follows:
Concussion is a brain injury and is defined as a complex pathophysiological process affecting the brain, induced by biomechanical forces. Several common features that incorporate clinical, pathologic and biomechanical injury constructs that may be utilised in defining the nature of a concussive head injury include:
In essence, a concussion is a head injury with a temporary loss of brain function that may result in a variety of physical, cognitive, and emotional symptoms.

Right now, a concussion is a clinical diagnosis based largely on the observed injury mechanism (point of contact, force on head area, etc.), signs, and symptoms. The first step towards a diagnosis of a concussion is actual recognition of the injury.

The hallmark signs of acute sports concussion include:
  • Loss of consciousness (LOC)
  • Problems with attentional mechanisms
    • Manifested as (but not limited to): slowness to answer questions and follow directions, easily distracted, poor concentration, vacant stare/glassy eyed. 
  • Memory disturbance
  • Balance disturbance
Over the course of the first 24 hours following a concussion injury, other signs and symptoms may manifest. However, it's important to note that there is a large range of these symptoms and they often vary, not all of these symptoms are seen in every case of sports concussion. The most common symptoms reported in concussion literature include:
  • Somatic symptoms such as headache
  • Cognitive symptoms such as feeling like in a fog
  • Emotional symptoms such as lability
  • Physical symptoms such as LOC and amnesia
  • Behavior changes such as irritability
  • Cognitive impairment
  • Sleep disturbance (insomnia)
  • Dizziness and balance problems
  • Blurred vision
  • Fatigue
If any one or more of these symptoms is recognized, a concussion should be suspected and a management plan should be implemented.

Since concussions are often hard to recognize and to diagnose, the Zurich Consensus on Concussion in Sport proposed diagnostic criteria for sideline evaluation. An athlete shows any of the following, they need to be removed from play and assessed.
  • Initial obvious physical signs consistent with concussion (LOC, balance problems)
  • Teammates, trainers, coaches observe cognitive or behavior changes in functioning consistent with concussion symptoms reported
  • Any concussion symptoms reported by the athlete injured
  • Abnormal neurocognitive or balance examination
Following a removal from play:
  • Physician evaluated the player using standard emergency management principles, most notably to exclude  severe head trauma or cervical spine injury
  • Once first aid issues are addressed, assessment of the concussive injury should be made using the SCAT3 or other sideline assessment tools (NHL uses ImPACT concussion testing, read here:
  • The player should not be left alone following the injury and serial monitoring for deterioration is essential over the initial few hours following injury
  • A player with diagnosed concussion should not be allowed to return to play on the same day. 
    • It has been unanimously agreed that an athlete should not return to play on the same day of the injury. Studies have shown that athletes allowed back into play following a concussion may demonstrate neuropsychological deficits post injury. 

The graduated return to play protocol following a concussion is a stepwise process and is outline below: 

In this stepwise progression, an athlete only proceeds to the next level if they are asymptomatic at the current level. Each step should take at least 24 hours, making the minimum amount of time to proceed through the full rehabilitation protocol one full week. Athletes should never return to play on the same day as an injury.


St. Louis Blues captain David Backes left Game 2 today with 4:51 to play after a brutal check to the head by Chicago Blackhawks defenseman Brent Seabrook. Backes was behind the Blackhawks' net and overskated the puck, as he attempted to curl back towards the puck, Seabrook approached from the circles and leveled Backes with a check to the head.

Credit to @myregularface

The principal point of contact is Backes' head. Not only does Seabrook's shoulder hit Backes' head directly, but the back of his head hits the boards immediately after. Backes laid motionless on the ice following the hit, although he didn't lose consciousness, this isn't a good sign. When he tried to get up, Backes had balance issues and clearly looked dazed. As the Blues' athletic trainer held him back, Backes struggled to stay on his skates and needed help getting to the locker room. 

As bolded above, Backes clearly exhibits signs of a concussion with balance issues, a vacant stare and the inability to follow the athletic trainer's directions of staying out of the scrum following the hit. Backes left the game and didn't return for overtime which is the right move. Following a hit to the head, especially this severe, the player should never return to play the same day.

Backes will need a lot of rest. The Blues doctors will make a detailed management plan after an assessment today and tomorrow morning. Backes will want to play Monday night undoubtedly, but it probably isn't the best move following a hit like this. Concussions require a minimum of 6 days of recovery as detailed above, but this isn't often followed. Backes shouldn't be rushed back, especially considering the Blues are up 2-0 in the series. 

Tuesday, April 15, 2014

On-ice evaluation and management of head and neck injuries

In last night's final regular season game for the Vancouver Canucks, a scary incident occurred towards the end of the second period. While going to retrieve the puck in the defensive zone, Daniel Sedin skated towards the end boards and took a hit from behind from Calgary Flames forward Paul Byron, going head-first into the glass.

Sedin lay still on the ice for several minutes before the Canucks physician and medical staff were able to complete the thorough neurological protocol. Sedin was taken to Vancouver General Hospital in stable condition on a stretcher and underwent further evaluation. Byron was assessed a five-minute major for boarding and a game misconduct.

The video below recaps the whole situation, including Sedin being stretchered off the ice:

The good news is that Sedin was released from the hospital later that night. He acquired a CT scan and is apparently injury free. He recaps the situation here on Canucks clean-out day:

Following a head or neck injury like Sedin's last night, there is strict protocol medical staff must follow.  I'll try to detail that as much as possible.

Head and neck injuries are usually the result of either direct (hit to the head) or indirect contact (hit causing the head/neck to be injured, a la Sedin). Head and neck injuries are the most serious in all of sports, as consequences of neurological injuries have a potentially high incidence of morbidity and mortality. Studies have estimated that 70% of traumatic deaths and 20% of permanent disability in sports-related injuries are due to head and neck injuries (Van Camp et al, Mueller et al.).

Head and neck injuries require immediate assessment and action. The initial assessment of an injury is important, but challenging for physicians. If an injury is fatal, it causes immediate neurological consequences that are easy to identify (ex: Professor Sid Watkins account of Aryton Senna's death from the documentary Senna). The most challenging aspect of assessing a neurological injury is identifying athletes with a 'mild' injury without immediate symptoms. Often, it takes concussion symptoms up to 24 hours to manifest. When initially assessing the injury, the mechanism and amount of force are considered in the diagnosis.

There are five steps to managing a head or neck injury that occurs during play. Physicians will always err on the side of caution. They are:

  1. Preparation for any neurological injury (assembling paramedics, equipment, worst-case scenarios)
  2. Suspicion and recognition (no official diagnosis made, based on observation and patient reporting)
  3. Stabilization and safety (depending on severity, could mean securing the body on a stretcher or just moving to a better location off-ice in a safe manner).
  4. Immediate treatment and possible secondary treatment (CPR if necessary, etc.)
  5. Evaluation for return to play (long-term...players suffering a possible concussion should NOT return to play the same day)

A physician will start with a basic safety evaluation which includes the ABC (Airway, Breathing and Circulation) evaluation. If the athlete doesn't have the normal ABC's (not breathing, no pulse) CPR should be initiated immediately (this is what happened with Peverley a few months ago).

Additionally, if there is any suspicion of a head or neck injury, the athlete should immediately be assessed for level of consciousness. The most extensively used tool that provides a prognostic indicator for recovery is the Glascow Coma Scale:

A score of >11 is associated with a good prognosis for recovery, while <7 is quite serious with a less favorable prognosis. These 'scales' are debated among the neurological community, however. Is there such a thing as 'mild' head injury if it has lifelong effects?

After checking the ABCs, if an athlete is conscious and alert, the physician will caution them to remain still; they will also ask them what is wrong and if they feel any pain. If an athlete has any head, neck, or back pain, they should not be moved until the spine is stabilized. The player's helmet and padding should not be removed; removal can cause unwanted motion or worsening of the fracture which could result in permanent nerve damage/paralysis. Players should not be moved until trained paramedics are able to assist. If players are in the prone position, proper log rolling technique is used to move them into a supine position for better assessment.

A hard cervical collar and a spine board should always be used to prevent further injury until a cervical injury can definitely be excluded. As seen in the image below from last night, Sedin is completely immobilized. He is strapped securely to the spine board, is wearing a neck brace (after having his helmet carefully removed by a trainer), and his head is strapped down.

Unlike in Sedin's situation, if a cervical spine injury is excluded but there is still fear of a head injury, the player can be slowly assisted to a sitting position which could help decrease intracranial pressure. If the athlete is stable while sitting, they can be assisted to help stand and then escorted to the locker room for further evaluation. During this time, the physician should conduct a complete neurological exam and evaluation. If a head injury is suspected, the player should not return. If the athlete is in unstable condition or is at risk for a deterioration in condition, they should be transported to the hospital.


Mueller FO, Cantu RC. Catastrophic injuries and fatalities in high school and college sports, fall
1982 – spring 1988. Med Sci Sports Exerc 1990;22(6):737 – 41.

G. Ghiselli et al. / Clin Sports Med 22 (2003) 445–465.

Van Camp SP, Bloor CM, Mueller FO, et al. Nontraumatic sports death in high school and
college athletes. Med Sci Sports Exerc 1995;27(5):641 – 7.

Sunday, April 13, 2014

Collection of posts at Sports Injury Alert

Lately I've been writing a few short-form articles for Sports Injury Alert's NHL Division when I have the spare time. They don't go as in-depth as some of my posts on my personal site as I aim for a quick analysis of an injury. You can find them here:

Sunday, March 16, 2014

An in-depth analysis of Rich Peverley's heart condition: What is atrial fibrillation and what does it mean for Peverley's hockey career?

Rich Peverley was a part of the huge Boston Bruins - Dallas Stars trade this past summer that sent Tyler Seguin to Dallas and Loui Eriksson and Reilly Smith to Boston (among other pieces). Peverley only missed one game last season and the Stars were happy to add the veteran to their otherwise young forward core.


As part of regular preseason testing, Peverley had an electrocardiogram (ECG/EKG), a simple test that records the heart's electrical activity. Unfortunately, Peverley's EKG was abnormal, showing that the player had atrial fibrillation (afib) - the most common cardiac arrhythmia (heart rhythm disorder/irregular heartbeat), present in about 5 million Americans.

EKG showing atrial fibrillation (top) compared with a normal sinus rhythm (bottom).
The bottom purple arrow shows a P wave (represent depolarization of the atria), which are absent in afib EKGs.
As described in the caption above, atrial fibrillation can be detected by certain abnormal characteristics on an EKG. One of the most common findings is the absence of P waves, which represent depolarization of the atria. Instead of a regular P wave, the EKG shows disorganized electrical activity before the Q wave and the large R waves. Another characteristic of afib is irregular R-R intervals, caused by an irregular conduction of impulses to the ventricles. The R-R interval on a EKG is shown below.


To understand afib, you need to understand the heart's anatomy and electrical system. Your heart has four chambers - two atria (top) and two ventricles (bottom). The atria are small pumps that act as a primer, pushing blood into the ventricles which then pumps the blood out to the rest of the body. The electrical system is what causes the myocardium (muscle of the heart) to be stimulated and cause contraction in the chambers. 

The heart's electrical system controls the rate and rhythm of the heartbeat. With each heartbeat, an electrical signal spreads from the top of the heart in the atria to the bottom, causing the heart to contract and pump blood. In normal hearts, the electrical signal begins in the sinus node (or sinoatrial - SA node) which is located in the right atrium. The signal travels through the right and left atria, causing the atria to contract and pump blood into the ventricles, then moving to the atrioventricular (AV) node and slowing down slightly to allow the ventricles to fill up with blood. After the electrical signal leaves the AV node and travels down to the ventricles, causing them to contract and pump blood to the lungs and the rest of the body. This process is shown in the gifs below: 
A normal sinus rhythm
In atrial fibrillation, the electrical system is flawed. The signal doesn't begin in the SA node but rather at a different part of the atria or in several parts of the atria. The signals can clash and cause different impulses and don't travel normally, spreading throughout the atria in a rapid and disorganized manner. This causes the atria to fibrillate (quiver) and and the atria/ventricles to no longer beat in a coordinated way as the ventricles don't completely fill with blood.
Haywire electrical signals that occur during atrial fibrillation
As the electrical signal passes to the ventricles, they can beat too quickly (rapid ventricle response tachycardia) and the ventricle is pumping without completely filling with blood. With the heart beating so fast beyond normal range (tachycardia) and not pumping enough blood to the rest of the body, you become dizzy and nauseous. Eventually your blood pressure drops rapidly (hypotension) , your brain and muscles aren't receiving as much oxygen as they should, and you can pass out/collapse (syncope). 

Additionally, Afib increases the likelihood of a stroke because blood clots can form while swirling around the atria and not properly flowing through to the ventricles. 


Normally, afib resolves on it's own and the heart is able to reset and start pumping blood normally. Afib is fairly common and generally not life-threatening. The condition can be controlled with medications, starting with blood-thinners to prevent clots. It's highly unlikely Peverley was on an intense blood thinner such as warfarin but could have been taking low doses of aspirin. Doctors can also prescribe medications which can help control heart rate, such as beta blockers and calcium channel blockers. However, even with these medications, Peverley (as an NHL athlete) still faced huge risks due to the intense nature of the game which requires short bursts of activity.

Afib can also be treated with a procedure known as a cardiac ablation. Peverley had an ablation earlier during the preseason, however, even following a successful ablation, almost a 1/3 of patients will have recurring symptoms. An ablation is a procedure where a catheter is threaded up into the heart through vessels in the leg and to the problem location of the heart.  Once the catheter is in place, electrodes on the end measure the electrical activity (detect an arrhythmia), detect the problem area, and they are then ablated either using radiofrequency pulses (which burn the area) or through cryoablation (freezes).

UPDATE: Peverley apparently did not undergo an ablation this past preseason. Peverley underwent a cardioversion procedure. There are two forms of cardioversion; synchronized electrical cardioversion and pharmacologic (chemical) cardioversion. Synchronized electrical cardioversion uses two electrode pads to deliver a therapeutic reversion shock that is timed at a certain point in the cardiac cycle (synchronization). This differs from defibrillation which is supposed to re-start the rhythm of the heart. Pharmacological cardioversion uses agents such as sodium channel blockers, beta blockers and calcium channel blockers to stabilize the heart (rhythm control).


Not even halfway through the first period, Peverley finished a shift and collapsed suddenly on the Stars bench. In a chaotic scene, the Stars players were frantic to get the refs attention and stop the game. The trainers and medical staff immediately picked Peverley up and hustled him down the tunnel. Information was very limited and the press, announcers and fans were confused as to what just happened.
Amazing, no? The Stars then released this bit of information:
And everyone started worrying. Eventually, people connected the dots that Peverley had missed the preseason due to his afib, and even missed a game last week due to "feeling strange," a possible recurrence of his condition.

The following day, Dr. Gil Salazar (emergency physician) from UT Southwestern released a statement with the Stars explaining the situation and what the medical staff did with Peverley:
"We provided oxygen for him. We started an IV. We did chest compressions on him and defibrillated him, provided some electricity to bring a rhythm back to his heart, and that was successful with one attempt, which is very reassuring."
So, within a matter of minutes, Peverley got almost instantaneous CPR and a shock from an automated external defibrillator (AED). The fact that he needed to be shocked means his arrhythmia turns from a fib into vfib. It's excellent news that Peverley was conscious and talking after just one shock which probably re-started his normal heart rhythm.

Peverley will undergo a battery of tests including another EKG and probably an echocardiogram. It was revealed that Peverley now has a device that can detect his heart rhythm and deliver a shock if necessary.
This device is probably an implantable cadioverter defibrillator, which uses electrical pulses or shocks to help control life-threatening arrhythmias. The ICD has wires with electrodes that connect to the heart chambers and has the ability to detect an abnormal rhythm. ICDs aren't the same as pacemakers which can only give low-energy electrical pulses to correct certain irregular heartbeats. ICDs can give high-energy pulses which are needed to correct dangerous arrhythmias in the ventricles. The image below displays the difference:

UPDATE: Peverley hasn't had an ICD implanted yet, nor has he had an ablation. It's likely that the procedure he'll undergo in Cleveland will be an ablation or another cardioversion.It's unlikely Peverley will get an ICD since it would be nearly impossible to play in the future with one (getting hit would dislodge the leads). 

 Two days after the chaotic event, the Stars announced that Peverley is out for the season and will undergo a procedure on his heart and pursue other treatments.
It's probably best that Peverley isn't playing. He'll probably undergo an ablation. Another surgical option is the maze surgery, an open-heart surgery that is usually only done if absolutely necessary (such as for heart valve disease). During this procedure, the surgeon makes small cuts and burns in the atria to prevent the spread of disorganized electrical signals. Considering Peverley's condition (NHL athlete) it's very unlikely he'll undergo this procedure.

It's unclear what this means for the rest of his career. Everyone in the NHL wishes Pevs the best in this scary situation and we're glad he's doing well.

Saturday, March 15, 2014

Injury history of the deadline's traded players

A few huge moves were made at the NHL trade deadline. Below I'll list some of the major players traded their respective injury history so fans of the new player's team can understand what type of player they acquired and their accompanying injury history.

Monday, March 10, 2014

Quick Take: Dallas Stars Rich Peverley collapses on bench during 1st period, taken to hospital

Something went wrong during tonight's Columbus Blue Jackets @ Dallas Stars game as Stars players were frantic to get the referees attention and halt the game. After collapsing on the bench, Stars center Rich Peverley was rushed down the tunnel on a stretcher by the Dallas Stars trainers and medical staff. Peverley reportedly has an irregular heartbeat (arrhythmia) which could have contributed to his collapse. It is unclear at this time whether Peverley suffered a heart attack.

Sunday, March 9, 2014

Stars' Kari Lehtonen "not doing well" after last night's collision

After last night's Dallas Stars 4-3 win over the Minnesota Wild, Stars coach Lindy Ruff was upset about the hit that took his star goaltender out of the game at 6:37 of the third period. The Wild's Erik Haula came barreling over Lehtonen, causing the goaltender to lose his helmet and fall backwards, hitting the back of his head against the crossbar. Lehtonen immediately left the ice, looking very dazed as he was bleeding from his head.

Credit to u/crazy_canucklehead on r/hockey

In addition to stitches for the wound, it's probable Lehtonen suffered a concussion. Haula recieved 15 minutes in penalties, a major for charging and a 10 minute game misconduct.  

Wednesday, February 19, 2014

John Tavares injured in Canada-Latvia game, ruled out for rest of Winter Olympics

John Tavares, star captain of the New York Islanders and 3rd in the NHL in points heading into the Sochi Winter Olympics, left Team Canada's game against Latvia in the second period and did not return for the third period. According to Islanders beat writer Arthur Staple, a source told him that Tavares is done for the Winter Olympics, but it's too early to determine a timeline on whether the injury will impact his NHL time.
Canada's coach Mike Babcock confirmed in a post game injury that Tavares was out for the rest of the tournament with a "leg injury."

Mats Zuccarello's hand injury worse than previously thought

Mats Zuccarello has been an important player for the New York Rangers this season, scoring 43 points in 58 games for the club looking to make the playoffs for the fourth straight season. Zuccarello was named to Team Norway at the Sochi Winter Olympics and was the only NHL player on their roster.

In a game against Austria on the 16th, Zuccarello was injured blocking a shot, the puck injuring his left hand. Zuccarello was able to finish the game against the Austrians, however, missed yesterday's game against Russia due to his injured hand. Originally, Zuccarello's hand injury was considered minor, with only some bruising and swelling. Zuccarello was also noted as having trouble gripping his stick, so he didn't play. However, it was revealed today in the Norwegian media that Zuccarello has a small non-displaced fracture in his left hand. The news was confirmed by NY Post writer Brett Cyrgalis:

The Norwegian news source stated that while Zuccarello is hurt, he should be ready to play when the Rangers return to NHL action on the 27th of February. The bad news is that this is a hand (left) that Zuccarello has previously broken in 2011 while with the Connecticut Whale.

As I wrote in my previous post on hand fractures, hand injuries are fickle and fairly common in the sport of hockey. The most important factor in a hand injury is the location of the fracture. You need to make sure important tissues and ligaments aren't damaged. However, since the fracture is non-displaced, the chances of that are quite slim.

Non-displaced fractures do not require surgery. However, they do produce pain, swelling, bruising, difficultly with movement and grip and also sometimes deformity. Zuccarello's fracture was diagnosed with an x-ray. A regular x-ray is shown below which includes the bone anatomy:

As stated in my previous article, there are four basic types of [hand] fractures:
  • Displaced: the bone breaks into two or more pieces and becomes misaligned. There is a separation between the two fracture faces or the faces are no longer lined up. 
  • Nondisplaced: the bone cracks or breaks but doesn't move and maintains its proper alignment and position (The two fracture surfaces have not moved relative to each other).
  • Comminuted: the bone is broken in several pieces in different places.
  • Open fracture: the bone breaks through the skin (closed is when the bone breaks but there is no puncture or open wound). 
An x-ray showing a displaced fracture of the 2nd, 3rd, and 4th metacarpals. 

The x-ray image below shows a nondisplaced fracture of the 5th (pinky) metacarpal. The dark line (which is circled), is the fracture. This is the best picture of a nondisplaced fracture I can find. 

The good news for Rangers fans again is that Zuccarello's fracture is nondisplaced and will not require surgery. In cases like this when the bone fragments of the fracture haven't displaced much, or if the break is located in the middle (shaft) of the bone, a specially designed cast (or splint) will be used to hold the bone fragments in place and allow them to heal. Follow-up x-rays will be ordered to ensure that the bone is healing in a good position and hasn't slipped out of alignment. The length of immobilization and healing time depends on several factors (location of the fracture, depth of the fracture, possible injury to the surrounding soft/connective tissue and/or ligaments).

Unfortunately, the quick, less than two-week return for Zuccarello honestly seems unlikely. Hand fractures usually take 3-4 weeks to heal at the very least. On top of that, Zuccarello has broken his left hand previously which is not good news. His previous fracture was fairly serious, and finished his season, sidelining him for 4-6 weeks and not letting him participate in the 2011 World Championships for Norway.

Nondisplaced fractures are a common injury and not too complicated. Zuccarello will fly home and probably see a hand specialist after seeing the Rangers doctor. A cast will be placed (if it already hasn't been), and Zuccarello will rest until fully healed.