Concussion in Athletes

A concussion is a transient impairment of the brain function occurring due to a violent shake of the brain. A concussion is a function impairment, not a structural brain injury, therefore a CT scan will be normal. In the United States alone, sports injuries lead to 1.6-3.8 million concussions annually. In head to head collisions in football, a player’s head may experience G forces ranging from 100-190Gs. These forces and rapid deceleration speeds exerted on the brain are similar to being hit on the head with a sledge hammer. A sudden blow to the head leads to bouncing of the brain back and forth in the skull cavity. The shaking motion of the brain within the skull cavity may lead to a concussion.


Only 10% of concussions are associated with loss of consciousness (LOC). Therefore, LOC is not necessary to diagnose a concussion. Symptoms of concussions include: headache and dizziness (most common), confusion, imbalance LOC, vomiting, and convulsions or seizures. Other symptoms include:

  • Amnesia
  • Slurred speech
  • Feeling sluggish or foggy
  • Double/blurry vision
  • Light sensitivity
  • Sensitivity to noise
  • Decreased playing ability

When managing a concussion, one must first assess airway, breathing, and circulation. The cervical spine should also be assessed in case of an injury. Assessment of sensory and motor functions. Diagnosing a concussion depends on careful clinical examination and asking questions to assess the patient’s attention, memory, orientation, concentration, balance, and reaction time. When a concussion is diagnosed, the player must NOT return to play.

Concussion assessment tools such as the Standard Assessment of Concussion Test (SAC) or Immediate Post-Concussion Assessment and Cognitive Test (impact) may be used on the sidelines and at later follow-ups to assess the patient’s brain function and compare the pre-injury scores. It is worth noting that the SAC test does not include a neurologic exam and does NOT measure reaction time, coordination or balance. When concussion assessment tools are not available on the sidelines, the following questions can be used to quickly assess orientation, anterograde and retrograde amnesia, concentration, and the patient’s ability to recall word lists (adopted from the CDC with minor modifications):

  1. Concentration
    1. Ask the patient to repeat days of the week backwards
  2. Orientation
    1. What stadium are we in?
    2. Who scored last?
    3. What is the name of the opposing team?
  3. Retrograde Amnesia
    1. Do you remember the hit?
    2. What was the score prior to the hit?
  4. Anterograde Amnesia
    1. Choose any three words and ask the patient to repeat them
  5. Ability to recall word list
    1. Ask patient to recall the three words you asked earlier


It is worth noting that remote memory loss is more worrisome than recent memory loss. Patients who demonstrate any of the following signs and symptoms should be taken to the emergency room immediately: worsening headaches, repeated vomiting, seizures or convulsions, prolonged LOC, focal neurological sign, disorientation to time, place, and person, neck pain, increasing irritability and confusion, and upper or lower limb weakness or numbness. Red flags that may indicate the need to acquire head imaging such as CT scans include: A prolonged LOC, post-traumatic amnesia, persistently altered mental status, focal neurological deficits, and continued deterioration of clinical signs.

It is important to remember that the following are contraindications to return to play:

  • Symptoms lasting more than 15 minutes
  • Prior concussion within the same season
  • Loss of consciousness
  • Amnesia
  • Development of complications such as post-concussion syndrome
  • Recurrence of symptoms on exertion

Complications include conditions such as second impact syndrome. Second impact syndrome occurs after sustaining a second head impact, even if minor, before achieving recovery from the first concussion may be potentially fatal. The mortality rate associated with second impact syndrome is approximately 50%. It occurs due to loss of autoregulation of the brain’s blood supply leading to vascular engorgement and herniation of the lower brain. Treatment usually consists of close observation, intubation, hyperventilating the patient and administration of IV osmotic diuretics.

Post-concussion syndrome occurs when persistent symptoms such as headaches, dizziness, and confusion lasting for weeks or even months after a concussion. Treatment is symptomatic and the patient will return to play is contraindicated. Epidural bleeding is associated with a lucid interval during which the patient feels find, followed by sever neurological decline. Seizure prophylaxis and surgical decompression are usually indicated. Cumulative effects may occur whether or not repetitive concussions have a cumulative effect remains a controversial topic.

Even though players may be eager to return to the game quickly, they must be advised to follow a stepwise strategy in order to achieve complete recovery and avoid potentially life threatening complications. The recovery strategy should include the following steps: a period of complete physical and mental rest until the symptoms subside. This should be followed by a return to light aerobic activities. Sports-specific training (still no contact). The recovery strategy should include non-contact drills and full-contact drills.

MRSA Screening & Decolonization

The best way to prevent surgical site infection, is optimizing the patient prior to surgery. The physician will want to make sure that the patient is nutritionally fit. Specific protocols will need to be followed for patients with conditions such as diabetes, are overweight, or who smoke. It is also important to improve the skin and soft tissue condition (area where the incision will be). The physician should try to reduce the bacterial burden that the patient is carrying. Immediately before surgery, the patient should be given prophylactic preoperative antibiotics and try to decrease the contamination in the operating room. The patient may bring organisms on themselves into the operating room (about 80% of these organisms are brought in by the patient). A screening for Methicillin-Sensitive Staphylococcus Aureus (MSSA) or Methicillin Resistant Staphylococcus Aureus (MRSA) and decolonization. Identifying the patients carrying diseases and treating the condition prior to going into the hospital will reduce the infection rate. Once patients are in the hospital, it is possible for them to spread bacteria to other patients. The best way to prevent the spread of bacteria is with PROPER HAND WASHING PRACTICES!

How can we decrease the bacterial burden of the patient bringing these organisms to the operating room? What are the tests that we should do? How can we help the situation when the patient is in the clinic or in the office?

areasThe patient should be screened for MSSA or MRSA and then a decolonization should be done. Some patients have large reservoirs of bacteria (carriers) and these are the patients who will have an increased risk of surgical site infection. These reservoirs are located in the nose, axilla, groin, and perianal area. These patients will need to be identified so the bacteria can be eradicated and the risk of surgical site infection can decrease. Being a MRSA carrier will increase the chances of infection (about 10x more risk for surgical site infection). You wouldn’t know that the patient is a MRSA carrier unless you test them. It is important to identify these MRSA carriers so that proper antibiotics can be given. A MRSA “carrier” is an individual who can carry the bacteria without necessarily becoming ill. About 2% of the population are MRSA carriers.

MRSA is a contagious bacteria that is difficult to treat because it is resistant to most commonly used antibiotics. In the bacteria cell wall, there is a penicillin binding protein. When penicillin is able to bind to the binding protein of the cell wall, disruption of the cell wall and destruction of the bacteria is possible. However, if the staph aureus acquires the mecA gene, then it can alter the penicillin binding protein, making the bacteria resistant to all penicillin. The primary way of transmitting MRSA is through direct contact from another person, an object that has it, or from sneeze droplets of an infected person. 30% of staph bacteria lives in the nose. About 25-30% of the population is colonized with S. aureus.


This means that the bacteria is present; however, it is not causing an infection with S. aureus. Ironically, if you are a carrier, you are only 6 times as likely to receive an infection, while non-carriers are 10 times as likely. MRSA carriers are diagnosed by examining a swab or culture of the nose. The physician will want to identify these patients before bringing them to the hospital, and eradicate or decolonize the organisms by using a 2-4% chlorhexidine bath for 5 days. The patient should leave the chlorhexidine on the surface of the skin (it works better if kept on for a longer time), so it is better not to wash it off. A 2% nasal mupirocin for five days may also be used. By the screening and eradication program, you can drop the infection rate by about 40-60% or more depending on the compliance of the patient. Our institution showed that empiric treatment is less costly than S. aureus screening and decolonization in total joint arthroplasty patients. They find that the cost is much less than the cost of the standard screening and decolonization of the S. aureus. They found that the empiric treatment allows for more efficient workflow without compromising the patient.


Distal Biceps Tendon Repair & LAC Nerve Vulnerability

The biceps muscle is attached to the bone at the elbow. The biceps muscle is inserted into the radial biceps rupturetuberosity by the distal biceps tendon. The biceps muscle is responsible for some elbow flexion and is the primary supinator of the forearm. Supination is the function used when turning a key or a door knob. The biceps muscle is responsible for over 50% of forearm supination. Rupture of the distal biceps tendon involves flexion of the elbow against resistance with eccentric loading and sudden tearing of the tendon. The muscle may retract into the upper arm causing a bump or “Popeye” sign. If the ruptured tendon is not repaired, the patient will lose the ability to supinate the forearm adequately. Injury to the lateral antebrachial cutaneous nerve may occur when treating a distal biceps tendon rupture. The lateral antebrachial cutaneous nerve lies between the brachialis and biceps muscles. The nerve can become injured from aggressive retraction. The lateral antebrachial cutaneous nerve originates cutaneous nerve originates from the musculocutaneous nerve. Injury to the nerve results in loss of sensation along the radial aspect of the forearm.

Treatment of a distal biceps tendon injury usually requires surgery due to the important supination function of the biceps muscle. Surgery may be done in the form of a single anterior incision or a two incision technique. Both of these techniques have their advantages and disadvantages. The anterior approach is easier with minimal risk of synostosis; however, there is a risk of injury to the posterior interosseous nerve. The two incision approach has less risk of injury to the posterior interosseous nerve, however there is a risk of synostosis. The lateral antebrachial nerve is the nerve most commonly injured during repair of a distal biceps tendon rupture regardless of the technique that is used. When treating the distal biceps tendon rupture, identify and protect the lateral antebrachial cutaneous nerve. Diffuse pain and paresthesia in the forearm after distal biceps tendon repair should be investigated for lateral antebrachial cutaneous nerve injury. In this situation, the nerve may need to be explored.

injury to LCN


AVN of the Femoral Head- Causes, Trauma to the Hip

AVNAvascular necrosis (AVN), or osteonecrosis, is death of a segment of bone due to disruption of the blood supply. Extraosseous or intraosseous interruption of the venous or arterial blood flow. AVN may be caused due to fractures of the femoral neck or dislocations of the hip, or due to mechanical disruption of blood vessels. Trauma to the deep branch of the Medial Femoral Circumflex Artery may occur with antegrade rod placement during piriformis entry in children. Posterior dislocation of the femoral head should be reduced in an expedited way to decrease the risk of thrombosis of the vessels which supply the femoral head. Osteonecrosis develops in about 2-20% of hips that are reduced within 6 hours. The risk of osteonecrosis will increase with delay in reduction of the hip. Osteonecrosis appears within two years after the injury. It is evident within one year in most patients.

acute femoral neck fracture

With a Pipken fracture, the patient should be informed about the complications of AVN preoperatively. Fixation failure is associated with osteonecrosis or nonunion. The effect of the anterior approach on osteonecrosis is not known. Stress fractures should be pinned before displacement occurs. Displacement will have a bad result. Osteonecrosis can be clinically significant when followed by lateral segmental collapse. The more vertical the fracture line, the greater the chance of AVN occurring. In acetabular fracture fixation, during intraoperative dissection for acetabular fracture reduction and fixation, avoid injury to the ascending branch of the Medial Femoral Circumflex Artery (MFCA). Fractures of the hip in children are associated with a high rate of osteonecrosis.