Sports Medicine for Special Groups
[…] secondary to overuse and accommodation. Rotator cuff and bicipital tendinopathies, for example, represent common types of pathology seen in the spinal cord injury (SCI) population due to wheelchair usage. Disorders of these tendons typically result from impingement or as an isolated traumatic injury. Given that this population requires their shoulders for mobility, it is common for disease to progress. The presentation over time varies from acute to slowly progressive pain and dysfunction.6 Specific secondary or associated conditions and complications Amputee Athlete Following amputation and prosthetic fitting, the skin of the distal portion of the residual limb becomes a weight-bearing surface where it had not previously been, resulting in increased risk for abrasions, blisters, and skin rash.7 Skin breakdown may occur when pressure is applied disproportionately to a pressure-sensitive area of skin on the residual limb. Skin may also develop verrucous hyperplasia; a wart-like lesion at the distal end of the residual limb.8 Sweating with athletic activity can increase moisture at the skin-socket interface and make skin breakdown more likely. Skin breakdown can be particularly disabling in an amputee, who relies on weight bearing through the residual limb for ambulation.8,9 A neuroma may occur at the distal end of a transected nerve in the residual limb of an amputee. When a neuroma is exposed to pressure, it creates paresthesias, dysesthesia, and radiating pain in the phantom distribution of the transected nerve. When a neuroma occurs on a weight-bearing structure, it can create severe pain with ambulation, limiting an athlete’s ability to train and compete. Unwanted socket pressure and irritation in the below-knee amputee can also lead to prepatellar, infrapatellar, and pretibial bursitis.7 Heterotopic ossification (HO) has been reported to develop frequently in joints and muscle adjacent to trauma with the residual limbs of traumatic amputees, which may increase risk of skin breakdown or stimulate pain with weight bearing.10 HO typically develops within the first 6-12 months after amputation, often while an amputee is beginning prosthetic training. This allows for modifications of the socket prior to athletic competition.10 Spinal Cord Injury Athlete Autonomic dysreflexia (AD) is a condition that occurs when sympathetic outflow increases in response to a noxious stimulus that is unregulated. Spinal cord injuries at the level of T6 and above are at risk for AD. Symptoms include paroxysmal hypertension, bradycardia, facial flushing, and headache. If hypertension continues to increase without treatment, stroke or death may occur. Common noxious stimuli that lead to AD include tight clothing, urinary or fecal retention, renal or bladder stones, pressure ulcers, infections, or intra-abdominal pathology.9 When AD is intentionally induced to gain a competitive advantage, it is referred to as “boosting”. Consequently, the subject exhibits increased BP and blood flow to working muscles, thus improving performance.11 Examples of self-induced noxious stimuli may include drinking large amounts of fluids, strapping legs tightly, or clamping their catheters to induce bladder distention.7 Studies have shown that more than 15% of athletes with SCI above T6 have voluntarily induced AD to boost their performance.11 It is important to recognize boosting poses serious health risks for the athlete and is considered an ergogenic aid that is not sanctioned by sports-governing bodies.7 Temperature regulation is impaired in athletes with SCI, especially with lesions above T8.7 Impaired sweating below the lesion level reduces the effective body surface area available for evaporative cooling. This can lead to hyperthermia. Cool temperatures can also pose a risk when there is an inability to sense wet clothing and decreased shiver response below the level of injury. Impaired vasomotor and sudomotor neural control, decreased muscle mass below the lesion, and possible impaired central temperature regulating mechanisms all contribute to the development of hypothermia.7 Other complications seen in athletes with SCI include pressure skin ulcers, increased spasticity, and stress fractures. Cognitively impaired athlete Common musculoskeletal issues in the Down syndrome population include joint laxity, poor muscle tone, scoliosis, pes planus/cavus, hallux varus/valgus, patellofemoral syndrome, slipped capital femoral epiphysis (SCFE), plantar fasciopathy, tendinopathy, and osteoarthritis. Atlanto-axial instability diagnosed with flexion and extension radiographs for instability (>4-5 mm of odontoid-atlas separation), may be present in these individuals. Some individuals may have instability but remain asymptomatic. In […]
Post-Traumatic Syringomyelia
[…] sensation, and loss of bladder and bowel functions2. Post-traumatic syringomyelia (PTS) occurs as a delayed complication in patients with traumatic spinal cord injury (SCI). Congenital causes of syringomyelia will not be covered here. Etiology PTS is more common after complete SCI but […]
Burn Rehabilitation
[…] the most destructive stress response on the body when compared to sepsis and other forms of trauma, including brain injury, spinal cord injury, and polytrauma.6 Burn injuries ignite local and systemic responses throughout the body. In local responses, there are three zones of a burn: coagulation (irreversible tissue loss due to coagulation of proteins), stasis (decreased tissue perfusion that if managed appropriately prevents irreversible damage), and hyperemia (outermost zone, good recovery except with prolonged hypoperfusion or severe sepsis).7 Systemically, burn injuries induce a prolonged hypermetabolic state and massive inflammatory response that can cause multiorgan system dysfunction. The hypermetabolic state can last for years after the initial burn. 8 A surge in proinflammatory cytokines (IL-6, IL-1b, TNF alpha), catecholamines (dopamine, epinephrine, norepinephrine), and hormones (cortisol, glucagon) after a burn injury perpetuate the hypermetabolic state9 and lead to organ dysfunction. Cardiovascular changes after burn injury include elevated heart rate, increased cardiac output, and increased capillary permeability leading to loss of intravascular proteins and extravasation of fluids into the interstitial compartment.8 Myocardial contractility is decreased, possibly due to release of Tumor Necrosis Factor- α (TNF- α). These changes result in systemic hypotension and end organ hypoperfusion. Burns can cause pulmonary dysfunction including bronchoconstriction and respiratory failure. Skeletal muscle breakdown and proteolysis after burn injury occurs as a response to ameliorate the hypermetabolic state and due to prolonged immobilization. Adipose tissue is altered after burn injury and lipolysis is activated to help meet the energy demands of the body. Patients with burn injury are at risk for cachexia due to the hypermetabolic state.7 Additionally, non-specific down regulation of the immune response can occur after burn injury, which in turn affects both cell mediated and humoral pathways.7 Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time) Initial phase (resuscitation): 1-3 days. Interdisciplinary team at a dedicated burn center, with focus on the burn’s pathophysiology, inhalation injury, and edema formation.10 Fluid resuscitation serves as the mainstay of systemic treatment in moderate and severe burns to maintain organ and tissue perfusion. The Parkland formula is used to calculate the initial fluid requirements of a patient within 24 hours after acute burn injury. 11 Acutely, goals are promotion of wound healing, scar suppression, pain reduction and prevention of complications.12 Second phase (wound care): The objective here is excision of nonviable tissue and biological closure, infection prevention, facilitation of wound healing while ensuring adequate pain control. Local wound management includes topical antibiotics and various biologic and non-biologic dressing as means of protection from the environment, drainage absorption, and providing a moist environment for wound healing.12 Third phase (definitive wound closure): This involves replacing temporary wound covers with a definitive cover. Skin grafts are used in treating partial thickness and full thickness burns. Early surgical removal of burned skin followed by skin grafting reduces the number of days in the hospital and usually improves the function and appearance of the burned area.12 Final stage (rehabilitation, reconstruction, and reintegration): Rehabilitation for patients with burn injuries starts from the day of injury, lasting for several years and requires multidisciplinary efforts. It also emphasizes preparing the patient for the psychological and social challenges the patient may face once integration to society occurs.1,2 Specific secondary or associated conditions and complications Skin and joint contractures, neuropathies, heterotopic ossification, septic arthritis, joint subluxations/dislocations, hypertrophic scarring, pruritus and dry skin, abnormal gait or postures (e.g., scoliosis), critical care myopathy/neuropathy and heat intolerance are all possible complications that may arise after a burn injury.14 Essentials of Assessment History After initial assessment, it is important to obtain a history of the event either from the patient or a bystander. An adequate history will help determine the potential of an inhalation injury, concomitant trauma and any preexisting medical conditions that may influence the patient’s outcomes or physical exam. It is crucial to obtain the patients chief complaint, circumstances of the injury (enclosed space, related trauma, non-accidental injuries, etc.) the source of the burning agent (thermal, chemical, electrical, etc.) medications patient is taking, status of tetanus immunization and if there was loss of consciousness at any time during the event.1 If meeting the patient for the first time during the final rehabilitation phase, it is important to inquire about potential sequelae that may result from burn injuries; for example, pruritus, sleep disturbance, change in mood, pain, and impairments in mobility, self-care, activities of daily living, and instrumental activities of daily living. Physical examination Post critical-care examination includes: General: Evaluate mental status, cognition, appearance, vital signs and pain level.1 Cardiovascular: Auscultate heart and evaluate heart rate and rhythm. Respiratory: Auscultate lungs. Evaluate oxygen requirement. If patient has tracheostomy, assess trach and evaluate secretions. Skin: Describe burn location, size, depth and burn pattern. Body surface area may be calculated using the Rule-of-Nines and the Lund and Browder chart (takes into account changes in body surface area with age and growth). Evaluate for cyanosis, circulation, edema, redness, warmth, scarring, ulcerations, document skin graft location and status, and assess donor sites.1,2 Musculoskeletal: Range of motion (ROM), atrophy, muscle wasting, strength, joint deformity (contractures), bony abnormality (heterotopic ossification (HO).1,2 Extremities: if burn injury resulted in amputation, evaluate residual limb shape, length, ROM, strength, skin, and incision. Neurological: Evaluate cranial nerves, changes in sensation, reflexes, tone, proprioception and coordination).1,2 Psychiatric: evaluate affect and mood for anxiety, depression, post-traumatic stress disorder, and adjustment disorder. Functional assessment A multidisciplinary team composed of a physiatrist, speech therapist, occupational therapist, physical therapist, nurse, rehabilitation psychologist, social worker, and case manager can be helpful to comprehensively evaluate the function of a patient who has sustained a severe burn injury. Various functional assessment tools exist that can aide the multidisciplinary team. The Borg Exertion Scale and vital signs (heart rate, respiratory rate, and blood pressure) assess tolerance to daily activities and exercise. The Functional Independence Measure and the Care Item Set are tools that are used to measure self-care and mobility. Psychological distress occurs in many burn patients for whom adequate evaluation needs to be performed in order to identify depression (PHQ-9, Beck Depression Scale), anxiety (Depression Anxiety Stress Scale, Beck Anxiety Scale), PTSD and/or body image issues (Rosenberg Self-Esteem Scale).15 Laboratory studies Pre-albumin and albumin are useful for assessing protein/nutritional status. White blood cell (WBC) count, neutrophil percentage, erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP) may help detect the presence of infection, although early on they may have a low yield because of the inflammatory response associated with the burn itself. Imaging Heterotopic ossification (HO) can be a sequela of a burn injury. Triple phase bone scintigraphy is sensitive for detecting HO, and the gold standard for diagnosing HO. Xray If concern for limb ischemia, assessment of peripheral pulses in burn patients can be performed with a Doppler ultrasound.1 Supplemental assessment tools The Burn Specific Health Scale (BSHS) is as a specific outcome measure for burn injuries including physical, psychological, and social aspects. Jebsen Hand Function Test helps assess a broad range of uni-manual hand functions required for activities of daily living (ADLs). The West-Haven-Yale Multidimensional Pain Inventory may be used in conjunction with behavioral and psycho-physiological strategies to help assesses chronic pain in individuals. Craig Handicap Assessment and Reporting Technique is a simple objective measure of the degree to which impairments and disabilities result in handicaps.15 Electrodiagnostic test may be performed to evaluate for neuropathy or myopathy. Sequential photography can be taken to help assess burn and scar progression. Early predictions of outcomes The progress that has been made in burn care over the past few decades has dramatically increased survival rates for burn victims such as; antibiotic therapy, techniques to excise burn eschar and new technology/clinical skills in the management of burn wounds, resuscitation and nutrition.16 Outcomes are poorer as burn depth and TBSA increase (>40%).2 Associated injuries, such as head injury, inhalation injury, and comorbidities, such as diabetes have been shown to worsen outcomes. Increase mortality after burn injury is associated with age less than 2 years or older than 60.13 Environmental Healed burn skin is fragile and sensitive to the sun and chemicals. With a deep partial thickness or full thickness burn, sweat glands are destroyed and are not replaced when the skin heals. This type of damage can lead to problems with thermoregulation in hot and humid conditions because sweating is crucial in controlling body temperature. Precaution with certain forms of exercise, recreation, or working conditions should be followed to avoid complications such as heat stroke.13 Healed burns, donor sites, and skin grafts are more sensitive to UV light and are risk for sunburn; therefore, patients who experience burn injuries should protect themselves from sun exposure by wearing specialized SPF clothing and utilizing sunscreen with SPF of 30 or higher. Occupational environments should be considered prior to return to work. Patients with inhalation injuries should refrain from working in environments with dust, fumes or respiratory irritants. Social role and social support system Burn patients face social, emotional, vocational and physical challenges. Peer counseling groups for support and mutual problem solving are often helpful.17 See “Patient and Family Education.” Professional issues Employment after burn injury is possible. Mason et al published a systematic review that analyzed return to work outcomes after burn injury and found that 72% of burn patients employed at the time of injury were able to return to work. Risk factors for unemployment include unemployment prior to injury, greater TBSA, longer hospital stay, greater number of surgical procedures, and pre-existing psychiatric conditions.18 Employment outcomes after burn injury vary if the burn injury occurred at or outside of work. For those burned at work, pain (72%), neurologic problems (62%), and psychiatric problems (53%) are the most limiting factors. Those burned outside of work demonstrate limitations secondary to pain (63%), neurologic problems (59%), and impaired mobility (54%) Barriers to return to work early after burn injuries are physical and wound issues, while long term disabilities are secondary to working conditions (temperature, humidity, safety) and psychosocial factors.19 Rehabilitation Management and Treatments Available or current treatment guidelines Surgical treatment guideline is provided by the American Burn Association. Currently, no consensus guideline exists for burn rehabilitation. At different disease stages Initial phase (resuscitation): Critical care services to monitor and correct fluid and electrolyte, metabolic, cardio-pulmonary, hemostatic derangements and infections.17 Second phase (hypermetabolic state, wound care, surgical care, pain management, positioning & splinting): Debridement can be performed to remove eschar and necrotic tissue to prepare a viable base for wound healing, grafting and prevent infections. Escharotomy is indicated in circumferential and partial thickness burns that present with pressure of at least 40mmHgG to prevent necrosis of underlying tissues.20 Topical wound care topical agents (silver sulfadiazine, gauze with bacitracin or mupirocin, mafenide acetate and acetic acid soak). Synthetic dressings with Duoderm, Tegaderm, Xeroform, silver coated gauze (Aquacel, Mepilex, Acticoat) reduce dressing change frequency and patient discomfort.17 Burn injuries induce a systemic response resulting in a hypermetabolic state that can cause multi organ system damage. Propranolol has been shown to modulate the hypermetabolic state, lower heart rate, decrease blood loss during skin grafting procedures, and accelerate wound healing in severely burned adults.21 Oxandrolone is an anabolic steroid shown to decrease protein catabolism, muscle wasting, and hospital stay while improving wound healing, morbidity, and mortality of severely burned patients.22 Maximizing nutrition is critical and early enteral feeding is often necessary. Patients who are severely burned (TBSA >20%) are recommended to have a diet high in protein (1.5-2g/kg/day), low in fat, and supplemented with vitamin C, D, […]
Stingers and Burners
[…] paramount. If bilateral upper extremity or concurrent lower extremity symptoms are present, the athlete should be treated for potential cervical spinal cord injury, including immediate cervical spine immobilization, spinal precautions, and transport by EMS to a trauma center for further evaluation and […]
Traumatic Brachial Plexopathy
[…] assessment plan (IEP) depending on the extent of injury, especially if there is presence of other trauma (traumatic brain injury, spinal cord injury, etc.) In addition, the provider may need to inquire if the pediatric patient has concerns with body image and […]
Pediatric Burns
[…] For example, patients with burn injuries from motor vehicle accidents may have additional injuries such as traumatic brain injuries or spinal cord injuries. If found, focused therapies should be incorporated in the rehabilitation plan to address these conditions. If amputation […]
Orthostatic Hypotension in SCI
[…] smaller drop in blood pressure may be equally important when associated with relevant symptoms that indicate impaired perfusion. OH following spinal cord injury (SCI) is common and well-documented, most often seen with complete lesions above neurological level T6 and most severe during […]
Brachial Plexopathy: Differential Diagnosis and Treatment
[…] on the etiology of injury. Traumatic injuries are more common in males aged between 15 and 25 years.5 Like traumatic spinal cord injury, these injuries are most often associated with motor vehicle and often motorcycle collisions.6 In adults, the most common cause of brachial plexus injury is trauma, either by compression or traction.3 Prevalence1,4,6-9 Traumatic: up to 70% from motor vehicle accidents and 22%-49% of athletes in contact sports Compressive: 5.3% in active military (rucksack syndrome), approximately .0001% neurogenic thoracic outlet syndrome Neoplastic: 0.4% Paraneoplastic: 0.5% to 10% Radiation induced: 1% to 14% Obstetrical: 0.4% Patho-anatomy/physiology Traumatic Mechanical injury to the myelin sheath or axon itself resulting from traction, compression, or transection. Burner or stinger syndrome: transient and often mild loss of strength or sensation, most often in the C5-6 distribution, secondary to traction, compression injury or direct blow to the brachial plexus without complete avulsion. Common in contact sports and the most common reported peripheral nerve injury in American Football, occurring in 59-70% of all players1,7,10 Midshaft clavicular fracture: transection or compression injury to the cords or divisions of the brachial plexus sometimes associated with a subclavian pseudoaneurysm.1,11 Shoulder dislocation: compression injury, most commonly affects the axillary nerve, can also affect the posterior cord and musculocutaneous nerve.11,12 Penetrating injuries: by a knife wound, shrapnel, bullet (often a transection), or subsequent hematoma (compression). Commonly affects the infraclavicular plexus.1,11 Compressive/entrapment Thoracic outlet syndrome: typically, a compression injury, commonly affecting the lower plexus. It is caused by narrowed thoracic outlet, possibly because of cervical rib (likely a fibrous band running from a rudimentary cervical rib to the first thoracic rib) or hypertrophied anterior scalene or ischemic injury caused by restricted flow through the subclavian artery.2,13 Rucksack syndrome: compressive/traction injury, commonly of the upper plexus, with painless weakness and numbness caused by depression of the shoulders while wearing a heavy backpack.1,14 Obstetrical Traction or compression injury most commonly of C5-7 nerve roots associated with shoulder dystocia and excessive lateral flexion of the head and neck, malpositioning, and increased birth weight. Primarily an iatrogenic complication at delivery, although there is some evidence for congenital brachial plexopathy related to in utero fetal position.1, 15, 16 Erb palsy: injury to C5-6 (most common) Erb plus palsy: C5-7 Flail arm: C5-T1 with Horner syndrome Klumpke palsy: C8-T1 with Horner syndrome Iatrogenic Postoperative: compressive injury, often of the upper plexus, caused by patient positioning, less commonly a mechanical or ischemic injury caused by axillary anesthetic block, transaxillary arteriography, or postoperative hematoma.1 Poststernotomy: compressive injury, usually affecting C8 and the medial cord, following median sternotomy for cardiothoracic surgery, associated with 1st rib fracture.1 Radiation-induced17-19 Clinical presentation of plexopathy typically delayed from time of radiation by months to years, depending on type of plexopathy (early transient radiation-induced plexopathy v. delayed radiation-induced plexopathy). Plexopathy results from direct axonal damage, demyelination, and microvascular infarction and more indolently because of compression caused by fibrosis, commonly seen following radiation therapy for breast, lung, lymphoma, and head and neck cancer. Concurrent chemotherapy is associated with increased risk for brachial plexopathy especially with increasing total dose (>50 Gy) and fractional dose (>2 Gy) of radiation. The incidence of radiation-induced plexopathies has decreased with tissue-sparing targeted radiotherapy. Chemotherapy:20-22 Multiple chemotherapeutic agents are […]
Heterotopic Ossification
[…] the joint capsule, in planes not connected to periosteum. It is also known as myositis ossificans.1 Etiology HO occurs following spinal cord injury (SCI), traumatic brain injury (TBI), and less commonly after other neurological disorders such as stroke or anoxic encephalopathy. It also occurs after severe burns, fractures (particularly acetabular and elbow fracture), or joint arthroplasty (particularly of the hip).2 Epidemiology including risk factors and primary prevention Risk factors for HO include long bone fracture, immobility, coma >2 weeks, edema, trauma and pressure ulceration. Common locations of HO after injury: SCI patients: Hips and knees commonly affected […]
Cervical Spondylotic Myelopathy (Degenerative Cervical Myelopathy)
[…] Chen YC, Liu L, Tu TH, Lo SS, Cheng H. Epidemiology of cervical spondylotic myelopathy and its risk of causing spinal cord injury: a national cohort study. Neurosurg Focus. 2013 Jul;35(1):E10 Fehlings MG, Skaf G. A review of the pathophysiology of cervical […]