Introduction

Juvenile idiopathic arthritis (jia) is a chronic inflammatory condition defined by the International League of Associations for Rheumatology (ILAR) as arthritis that begins before the age of 16 years and persists for at least 6 weeks with exclusion of other known conditions.¹ JIA is divided into systemic arthritis, oligoarthritis, polyarthritis, psoriatic arthritis, enthesitis-related arthritis, and undifferentiated arthritis (Table 60–1).²

Epidemiology

In a systematic review, incidence rates varied from 1.6 to 23 per 100,000 persons and prevalence from 3.8 to 400 per 100,000 persons.³ Pooled incidence and prevalence were about doubled for girls.

Pathophysiology

Inflammation of the joints is thought to be related to polymorphisms in human leukocyte antigens that lead to antigen-activated T cells that release cytokines.⁴ This stimulates chondrocytes, osteoclasts, and fibroblasts to release metalloproteinases, leading to the erosion of bone and cartilage, synovial joint inflammation, and pannus formation.⁴

History and Physical Examination

In addition to a detailed history of joint pain, systemic features such as duration of fever, serositis, acute anterior uveitis, and lymphadenopathy are also important to ask about.⁴ A family medical history of psoriasis or rheumatologist conditions, especially ankylosing spondylitis, enthesitis-related arthritis, sacroiliitis with inflammatory bowel disease, Reiter’s syndrome, and acute anterior uveitis, is particularly helpful.^4,11

Objective: Laboratory Tests/Radiology

Laboratory Tests

Leukocytosis, thrombocytosis, and anemia are common in the condition.⁵ Inflammatory markers may be elevated, including the erythrocyte sedimentation rate (ESR), C-reactive protein, or ferritin. Rheumatoid factor (rarely seen in children younger than age 10),⁶ anti-cyclic citrullinated peptide antibodies, HLAB-27, and antinuclear antibody (ANA) determinations should be ordered. Laboratory values that are usually negative include antibodies to double-stranded deoxyribonucleic acid (dsDNA), Smith (Sm) antigen, Sjögren’s syndrome–related antigen A (SSA or Ro), Sjögren’s syndrome–related antigen B (SSB or La), or ribonucleoprotein (RNP).

Imaging

Findings on x-ray include soft tissue swelling, osteopenia, loss of joint space, erosions, growth disturbances (epiphyseal overgrowth), and joint subluxation.⁷ Systemic features such as hepatosplenomegaly and pericardial or pleural effusions may be seen on radiographs.⁷ Magnetic resonance imaging (MRI) shows synovial hypertrophy, joint effusions, and osseous and cartilaginous erosions. On T1-weighted gadolinium contrast studies, active synovitis may show up as enhancements.⁷

General Management Options

Algorithms for management are based on category of JIA, disease activity (low, moderate, and high), and poor prognostic features (present, absent).⁸ Improvement is evaluated based on physician global assessment of disease activity, parent/patient global assessment of well-being, functional assessment, active joint count, restricted joint count, and erythrocyte sedimentation rate (ESR).⁸

Management: Therapies/Modalities/Bracing/Lifestyle Intervention

Exercise therapy in moderation is thought to help with common problems seen in children with JIA including muscle atrophy, bone mass deficits, pain, and decreased aerobic capacity. Generally, low-impact sports and aquatic activities are preferred.⁹ A Cochrane Review pooled analysis showed a trend but no statistical significance of improvement with therapy.⁹ Electrotherapy and ultrasound for patient with tenosynovitis and massage and cold thermotherapy for acute joint inflammation can be used as well.⁹ Bracing is recommended for joint stabilization, axial misalignment, and to encourage proper weight bearing on a case-by-case basis.⁹

Considerations and precautions should include avoidance of weight-bearing exercise when joints are actively inflamed, radiographic screening with cervical flexion-extension views for C1–2 instability before participation in collision/contact sports if the child has neck arthritis, and cardiac evaluation for children with systemic arthritis or enthesitis-related arthritis subtype (HLA-B27–associated arthritis).¹⁰ As with the general population, mouth guards during activities with jaw and dental injury risk, especially if the child has jaw involvement, and eye protection during activities with ocular injury risk, especially if child has uveitis, are recommended.¹⁰

In terms of lifestyle, it is important to monitor and consider supplementing calcium and vitamin D, especially for patients on corticosteroids. Providing psychological and social integration support is helpful.⁹ Periodic ophthalmologic examinations are recommended to screen for uveitis.¹

Management: Medication

Medications are used to control disease and thus limit disability while minimizing the damage and debility that can be caused by side effects of these immune-modulating agents.^2,8,12 Nonsteroidal anti-inflammatory drugs (NSAIDs) are the most commonly used analgesic likely because they are also anti-inflammatory. Patients respond differently to different NSAIDs. Glucocorticoids are used intraarticularly and systemically. Non–biologic disease–modifying antirheumatic drugs (DMARDs) include methotrexate, the first-choice agent for children with JIA (FDA approved),² sulfasalazine, and leflunomide. Biologic DMARDs include interleukin 1 (IL-1) inhibitors, tumor necrosis factor (TNF) inhibitors, and monoclonal antibodies. Drug safety monitoring includes a complete blood count (CBC), liver function tests (LFTs) and serum creatinine determinations.⁸ Tuberculosis screening and in some cases hepatitis B and C screening are recommended prior to initiation of methotrexate or TNF-α.⁸

Management: Procedural/Surgical Interventions

Synovectomy can be helpful on a case-by case basis as a last resort.¹

Introduction

Juvenile spondyloarthropathy (JSpA) is characterized by arthritis and abnormal new bone formation in axial joints,¹³ leading to ossification.¹ Ankylosing spondylitis (AS) is the prototype, which requires radiographic sacroiliitis; however, in children, hip and peripheral arthritis with enthesitis is more likely to be present.¹⁴ JSpA is a subtype of either enthesitis-related arthritis (ERA) or undifferentiated arthritis.¹⁴

Epidemiology

Spondyloarthropathy accounts for about 2% to 11% of cases of juvenile arthritis.¹⁴

Pathophysiology

This is an inflammatory autoimmune response in which HLA-B27 is thought to play a critical role.¹⁴

Diagnosis

Juvenile spondyloarthropathy is diagnosed when a child prior to 17 years of age meets the European Spondyloarthropathy Study Group (ESSG) criteria for the classification of spondyloarthropathies.¹ Criteria include inflammatory spinal pain or synovitis that is asymmetrical or predominantly in lower extremities.¹³ Additionally, patients must have at least one of the following: psoriasis, inflammatory bowel disease (IBD), buttock pain alternating between buttocks, enthesopathy, plain-film radiographic evidence of sacroiliitis, family history, or having one of the following—acute diarrhea, urethritis, or cervicitis—within 2 months of the diagnosis of arthritis.¹⁵

History and Physical Examination

Flares and remission of arthritis, enthesitis, and/or back pain are common.¹⁶ Typical progression is arthritis/enthesitis in peripheral joints followed by hip, sacroiliac, and spine.¹³ Musculoskeletal complaints or acute anterior uveitis may precede the diagnosis.¹³ Examine the patient for enthesitis, sacroiliitis, dactylitis, acute anterior uveitis (presents as pink, painful eye), nail pitting, and psoriasis.¹³ Peripheral joint examination with external rotation of the hip observing for asymmetry, as well as shoulder and temporomandibular joint (TMJ), should be included. Pediatric Schober’s test is valid for patients over 10 years of age when compared with normal values.¹³

Objective: Laboratory Tests/Radiology/Biopsies

Laboratory Tests

Laboratory tests are as in JIA. Also, on CBC, microcytic anemia or an elevated platelet count is seen.¹³ The major marker for JSpA is HLA-B27.¹⁴ A stool guaiac test can be done if IBD is suspected.¹³ Radiographs and ANAs are typically unremarkable.¹³

Radiology

An anteroposterior (AP) x-ray of the pelvis is used to detect structural damage, which appears late in the disease, usually in adulthood.¹³ MRI, particularly the STIR sequence, and gadolinium enhancement can be used to detect early inflammation/lesions.¹³ Gadolinium use is critical in children because unlike adults, synovial enhancement may be detected without accompanying bone marrow edema.¹⁷

Management: Therapies/Modalities/Bracing/Lifestyle Intervention

Stretching to prevent loss of range of motion of joints, including the spine, is often a key component of therapy.^9,13,18 Patients with enthesitis in their feet may benefit from orthotics, especially those that cushion and support the heel and metatarsal joints.¹³ Lifestyle interventions are as per JIA.

Management: Medication

First-line treatment is NSAIDs, which, in addition to managing pain, may slow new bone formation.¹³ Tolmetin and sulindac are thought to be particularly effective.¹³ In refractory cases, anti-TNF agents are used.

Management: Procedural/Surgical Interventions

Orthopedic surgery has a limited role in the management of pediatric SpA, but joint replacement can be done in adults with long-standing disease.¹³

Introduction

Hemophilia is an X-linked recessively inherited bleeding disorder.¹⁹ Bleeding into joints can lead to chronic joint disease and pain, bleeding in the head can cause paralysis and death, and bleeding into the skin, muscle, or soft tissue can cause hematoma.²⁰ The most common hemophilias are hemophilia A (classic hemophilia) and hemophilia B (Christmas disease).²⁰

Epidemiology

Hemophilia occurs in about 1 in every 5,000 male births.²⁰ About 200,000 males in the United States currently have hemophilia.²⁰ Hemophilia A is about four times as common as hemophilia B.²⁰ Patient’s with hemophilia have a normal lifespan if they receive treatment.²¹

Pathophysiology

Hemophilia is caused by a mutation in a factor gene on the X chromosome causing absence or decrease in clotting factor VIII in hemophilia A (classic hemophilia) or in clotting factor IX in hemophilia B (Christmas disease).²⁰ Iron released from blood in the joints leads to inflammation and articular cartilage damage.²² Young children’s cartilage is especially sensitive.²²

Diagnosis

The definitive diagnosis and severity are based on the percentage levels of factors VIII and IX.²³ Babies can be tested soon after birth via blood test, and prenatal genetic testing is also available.²⁴

History and Physical Examination

Clues in the newborn include excessive duration of bleeding with circumcision or heel stick blood draw, as well as an intracranial bleed after delivery with forceps or vacuum.²³ When the child is older, hematuria, prolonged nose bleeds, heavy menstrual bleeding, and bleeding after dental work, surgery, or trauma is described.²⁵ Hemarthrosis usually develops within a few hours and is often felt as a burning sensation.²⁶ Family history of hemophilia is present in about 70% of patients.²⁷

Signs of hemophilia on physical examination include evidence of bleeding such as raised bumps, bruises, bleeding mucous membranes, signs of gastrointestinal (GI) bleed, hematomas, and hemarthrosis.²⁸ Hemarthrosis causes an inflamed, tense, warm, join, and the skin becomes bright red.²⁸ The affected joint is held in an antalgic flexion position with painful and limited mobility.²⁹

Objective: Laboratory Tests/Radiology

Laboratory tests should include levels of factors VIII and IX. The activated partial thromboplastin time (APTT), prothrombin time (PT), fibrinogen, von Willebrand factor (vWF) assay, and platelets are usually normal. CBC may show anemia.²³ Genetic testing is done for clinical phenotype and to determine the need for genetic counseling.³⁰ MRI of large and symptomatic joints is the most reliable imaging method to evaluate the presence and progression of hemophilia-related joint destruction.³¹

Management

Prophylaxis with factor from an early age, generally started after the first or second joint bleed,²² can prevent spontaneous bleeding and the severe joint damage to which children are especially prone.^21,22 Prophylaxis in adults is controversial.²² Unfortunately, patients may develop antibody against clotting factor.²¹ Current advances include clotting factors with extended half-lives that require decreased frequency and dosing and various recombinant factors created to decreased immunogenicity.²¹ Under development are nonfactor replacements, including new proteins and gene therapies.²¹ Desmopressin is also used to help boost levels of factor VIII and vWF.²¹

Hemarthrosis is treated promptly with factor replacement, followed by rest, compression, elevation, and commonly ice.²⁹ Once pain and swelling subside, progressively there is typically improvement in range the joint, strengthening of periarticular muscles, and proprioception.²⁹ For pain, NSAIDs are generally avoided, although evidence exists that COX-2 inhibitors may be safe in patients over 12 years of age.³² General athletics are encouraged and are especially beneficial for both musculoskeletal and social health.²² Collision, high-contact, and high-velocity sports should be avoided unless the patient receives adequate prophylaxis.³³ Orthoses are helpful for immobilization (during an active bleed), motion control, offloading stress and weight, and modifying stance.³⁴ Orthoses also can be used at night to prevent inadvertent injury during sleep.³⁴

Procedural/Surgical Interventions

Arthrocentesis is considered for large, voluminous, tense, and painful joints²⁸ within the first 12 hours.²⁸ However, it is controversial because it increases the risk of infection and may cause more bleeding by not allowing the blood to tamponade.²⁸ In cases of recurrent hemarthrosis, radioactive synoviorthesis or surgical synovectomy is recommended.²⁸ Surgical joint replacement is a treatment for significant degeneration and pain in a joint in later life.³⁵

Epidemiology

According to the World Health Organization (WHO), about 5% of the world’s population carries a hemoglobin (Hgb) mutation.³⁶ People from Africa, the Caribbean, Central and South America, India, the Mediterranean, and the Middle East have a higher rate of sickle cell trait.³⁷ This may be explained by the fact that sickle cell trait confers protection against certain species of malaria that are endemic in those regions.³⁸ In the United States, 90,000 to 100,000 people are affected.³⁸

Pathophysiology

In sickle cell disease, HgbS has a mutation in which hydrophilic glutamic acid is replaced by hydrophobic valine, causing the protein to polymerize. This leads the red blood cells to become “sickled” and “stiff,” which can result in vasoocclusion (VOC) as well as intravascular and extravascular hemolysis.³⁸

Diagnosis

Diagnosis is made by newborn screening, most commonly with Hgb electrophoresis and sometimes confirmed by DNA sequencing.³⁸ Diagnosis can also be made by chorionic villus sampling (first trimester) or amniocentesis (second trimester).³⁸

History and Physical Examination

The history should focus on signs and symptoms of common complications, including painful VOC (commonly in the lower back, legs, and arms, peaking in the twenties), acute chest syndrome (incidence highest between 2 and 5 years of age), stroke, cholecystitis/lithiasis, splenic sequestration, anemia, pulmonary arterial hypertension, and impaired growth/maturation. Chronic pain may be from arthritis, arthropathy, leg ulcers, or vertebral body collapse. Neuropathic pain may occur due to nerve compression by bone or iron-overload neuropathy.³⁹ Common musculoskeletal complications include bone marrow hyperplasia,³⁹ infarction/osteonecrosis,³⁹ osteomyelitis, septic arthritis³⁹ (commonly Salmonella),^39,40 osteopenia, and osteoporosis.

Physical examination may show erythema, edema, joint effusions, or point tenderness, signs of VOC. In children under age 2, VOC commonly presents in the hand or foot, termed “dactylitis.” Neurologic examination for occult stroke (present in up to 39% of patients with sickle cell disease)⁴¹ is critical.

Objective: Laboratory Tests/Radiology/Biopsies

CBC may show anemia, leukocytosis, and thrombocytosis. In VOC crisis, HgbS percentage; reticulocyte count, type, and screen³⁸; and ESR help to rule out osteomyelitis.⁴⁰

Chest x-ray is used to diagnose acute chest syndrome. MRI is used to diagnose stroke. Infarcts of vertebral end plates can lead to “codfish vertebra” (biconcave).⁴² For screening, transcranial Doppler is recommended annually for patients aged 2 to 16 years.³⁸ Some centers screen using radiographs for avascular necrosis of femoral heads, echocardiography for pulmonary arterial hypertension (PAH; standard in adults only), and MRI for silent stroke/vasculopathy.³⁸

Management: Medications/Prophylaxis/Therapies

Hydroxyurea is used to increase expression of fetal Hgb. Prophylactic transfusion are used to suppress patient’s red blood cell (RBC) production.⁴³ Emerging treatments to increase HgF include gene therapy and hematopoietic precursors.³⁸ Treatment of VOC crisis includes intravenous (IV) fluids, aggressive pain management, and blood transfusions. Treatment of acute chest syndrome includes the preceding plus empirical antibiotics, respiratory support, and, in severe cases, corticosteroids.³⁸

Vaccinations with pneumococcal polysaccharide, Haemophilus influenzae type b, pneumococcal conjugate (PCV13) vaccines as well as prophylactic penicillin are recommended. An annual ophthalmologic examination is needed to screen for sickle retinopathy.³⁸ In terms of therapy, the strongest support exists for cognitive-behavioral therapy.⁴⁴

Procedural/Surgical Interventions

Hematopoietic bone marrow transplantation is the only cure, but it is reserved for severe sickle cell disease (SCD) given the morbidity and mortality of possible infection, graft versus host disease, and graft failure. Perioperative transfusion is recommended for all major surgeries.³⁸

Introduction

Musculoskeletal infections can be divided into bone, joint, and soft tissue infections, including discitis, flexor tenosynovitis, and abscess in a muscle.⁴⁵ This section focuses on bone infections (acute bacterial osteomyelitis [ABO]) and joint infections (acute bacterial arthritis [ABA]).⁴⁶

Epidemiology

In the United States and other first-world countries, the incidence of ABA is 4 to 10 per 100,000 children, and ABO is estimated at 10 to 80 per 100,000 children.⁴⁶ The majority are spread hematogenously (vs. traumatically), and methicillin-susceptible Staphylococcus aureus (MSSA) and methicillin-resistant S. aureus (MRSA) are generally considered the most common pathogens,⁴⁷ although a study looking at polymerase chain reaction (PCR) in addition to culture found Kingella kingae to be the most common agent in children aged 1 to 2 years.⁴⁸ Peak incidence occurs in children around 2 to 6 years of age.⁴⁶ Hips and lower extremities are most commonly affected.⁴⁶ Complications include sepsis (most common cause of death), endocarditis, deep vein thrombosis (DVT), infected pulmonary emboli, limb-length discrepancy, avascular necrosis (AVN), and pathologic fractures.⁴⁶

Pathophysiology

Occult bacteremia occurs in the setting of anatomic susceptibility to bacterial invasion.⁴⁹

Diagnosis

Diagnosis is based on the criteria of four of the following: fever, refusal to bear weight, leukocytosis >12,000/mm³, and ESR >40 mm/h were found in one study to have diagnostic specificity for ABO of 93% and sensitivity of 99%.⁵⁰ Joint fluid is inoculated into a blood culture bottle for growth of fastidious organisms.⁴⁶

History and Physical Examination

The typical presentation of ABO is fever coinciding with the decreased use of the affected extremity or refusal of weight bearing.⁴⁶ Pelvic, sacroiliac, or vertebral infections can masquerade as vague abdominal or flank pain.⁴⁶ In the hope of identifying the likely organism, the history should include recent travel, animal exposures, ingestion, immunization status, SCD, and recent illnesses.⁴⁶

Typical examination is significant for a tender, swollen, erythematous, warm area in a joint or over bone.⁴⁶ Associated signs such as erythema in mucous membranes, conjunctival injection, murmur or rub on heart examination, abnormal breath sounds on lung examination, abdominal pain or organomegaly, decreased range of motion of a joint, skin trauma or rash, or neurologic deficits such as weakness or abnormal reflexes should be noted.⁴⁶ Vital signs should be monitored for any signs of possible sepsis.⁴⁶

Objective: Laboratory Tests/Radiology/Biopsies

Laboratory tests should include CBC, blood culture, ESR, and C-reactive protein (CRP) determination. Procalcitonin at a cutoff at 0.4 ng/mL is another sensitive and specific marker.⁵¹

X-ray, followed by ultrasound and then MRI, is recommended.⁴⁶ X-ray helps to rule out fracture.⁴⁶ MRI detects cortical and bone marrow edema/inflammation and associated soft tissue infections important for surgical planning.⁴⁶ Ultrasound is used for suspected deep joint infections.⁴⁶

Management: Medication and Procedural/Surgical Interventions

Drainage and irrigation of joints are preformed immediately for source control, preservation of function, and microbiologic diagnosis/confirmation of pathogen to select the most appropriate antibiotic.⁴⁶ CRP level should be trended and expected to decrease in the first 48 hours to a level less than 5 mg/dL; otherwise, there is likely a focus of infection that was missed.⁵² Initial empirical therapy should include IV antibiotics against common pathogens: S aureus, streptococci, and ideally K. kingae.⁴⁶ Increasingly, research recommends switching from IV to oral antibiotics sooner^53,54 and using CRP,^52,55 fever, and pain⁵² to determine when to switch.

General Overview

History and Physical Examination

The history includes mechanism of injury and typical pain questions of intensity, type, onset, duration, timing, associated symptoms, exacerbating and alleviating factors, previous treatments tried, history of previous injury, and any red flags. Careful physical examination includes inspection of the location of the pain, joint above and below the affected area for referred pain, and the spine for radicular pain, as well as relevant vascular and neurologic examination.

Imaging

X-ray is used for bones (at least two views, i.e., anteroposterior [AP] and lateral), and computerized tomography (CT), and MRI are used for soft tissue and cross-sectional anatomy. Imaging is especially useful when the clinical diagnosis is unclear, objective measurement of the degree of injury affects management, and to rule out associated injuries. Ultrasonography is especially valuable in children because there is no need for sedation. Radiographs are undesirable in the pediatric population because of radiation exposure and the high ratio of cartilage to bone in a child’s skeleton.² Matching radiographic findings with clinical history and physical examination is critical because there are many incidental findings, such as spondylolysis and herniated discs, that are often asymptomatic.

Acute Trauma: Fractures, Strains/Sprains

Epidemiology of Acute Trauma

In children under age 15, falls are the leading cause of nonfatal injuries, followed by being struck by or against an object.¹ In children aged 15–19, the leading causes are being struck by or against an object, falls, and motor vehicle injuries.¹ Child abuse must also be considered.

Fractures

Epidemiology

The most common fractures in children are in the upper extremities. Forearm fractures account for 40% of childhood fractures, with 75% of these being at the distal radius.⁴

Pathophysiology

Pediatric bones are different from adult bones in a variety of ways. First, there is the existence of a physis (growth plate) that can be disrupted, leading to complete or partial growth failure.⁵⁶ Physis fractures are generally classified using Salter-Harris classification (Fig. 60–1).56 Types I and II do not cross the epiphysis and so generally do not cause growth disturbance.⁵⁶ Approximately 15% to 30% of all childhood fractures are growth plate fractures.³ Second, pediatric bones are not fully ossified, making them weaker and softer, which can lead to bowing of the bone and easier fracture.⁵⁶ Because pediatric bone is weaker than ligaments, fracture is generally more common than ligament injury in this age group.⁵⁶ The same mechanism that would cause a muscle or tendon strain in an adult may cause an apophyseal avulsion in an adolescent.⁵⁶ Examples of bending types of fractures include a torus or buckle fracture, in which one side of the bone bends and the other side remains intact, and a greenstick fracture, in which one side is bent and the other side has a partial fracture. Third, ossification centers in pediatric bone make radiologic diagnosis more difficult.⁵⁶ Fourth, pediatric bones have a faster and better ability to heal, remodel, and self-correct angulation.⁵⁶ Important principles include time-appropriate management depending on bone age, potential of bone to remodel based on contacting elements and forces, and risk for degenerative joint disease later in life. Early detection is critical.

Management

Treatment depends on severity and type of fracture, open (bone fractures puncture skin) or closed, bone affected, alignment, and whether the fracture goes through a growth plate. Conservative treatment involves immobilization with a cast or splint to decrease pain and movement and traction for alignment. Surgery with internal or external fixation is common. Internal fixation is when hardware is under the skin and may include a metal plate or screw on the outside of the bone, a metal rod going through the marrow, or wires for small bone pieces. Hardware is removed after healing in some cases. Alternatively, external fixation can be done, where pins or screws are placed above and below fracture site and then attached to metal bars on the outside of the skin (later removed).

Distal radius fracture is the most common and is divided into buckle/torus fracture (very common, the fracture is managed with a short-arm cast for 3–4 weeks followed by return to normal activity) and greenstick fracture, complete fracture (transverse), comminuted fracture (multiple pieces), and physeal fracture (Salter-Harris I–V).⁵⁷ Other common fractures in the upper extremity include clavicular fractures (generally managed conservatively with a sling for 2–3 months and return to play about 3–4 months after injury) and supracondylar fractures (generally treated surgically with closed reduction followed by percutaneous pin fixation and long-arm cast).⁵⁷ Common lower extremity fractures include fractures of the pelvis, femoral shaft, femoral neck, tibial eminence, tibia, ankle, and metatarsal phalanx, as well as “triplane fracture” of the ankle.⁵⁸

Sprains/Strains/Bursitis/Contusions

General Overview of Management

A “sprain” is an injury to a ligament, whereas a “strain” is defined as an injury to muscle or tendon. “Contusions” are direct tissue injury to muscles and connective tissue leading to muscle hemorrhage and bruising. Strains can also be chronic from repetitive movements.^59,60 Contusions are generally due to acute injuries. When considering a soft tissue injury in children, it is critical to rule out a fracture because fractures are more common in children. Sprains, strains, and contusions are generally treated conservatively with ice, compression, elevation, NSAIDs for pain, relative rest, and protection of the area. Immobilization, with casting or bracing, is recommended if symptoms or injury is severe or the child is unable to comply with rest. Significant sprains require immobilization, generally for 10 days.⁶¹ Assistive devices such as a wheelchair or crutch may be used to allow the injured area to rest. In severe soft tissue injury to muscle, tendon, or ligament, surgery may be needed to align, stabilize, or reattach anatomy to allow for improved function of the injured area or prevent worsening or complications of injury such as AVN. A rehabilitation program is critical to successful return to play and previous level of function and to prevent further injuries.

The most common strains occur in the low back and hamstring muscles.⁶² The time for healing is quite variable and may take several weeks to months.

Contusions are common in sports after blunt trauma, especially in contact sports such as football and hockey, commonly on the quadriceps. After muscle hemorrhage, granulation tissue forms that can mature into a dense collagenous scar and lead to significant disability.⁶³ Active range of motion (ROM) is encouraged, and once the patient is able to achieve 90 degrees of flexion, progressive strengthening can be started.⁶³ Passive ROM may cause increased hemorrhage and is not recommended.⁶³ Severe contusions take 4 to 6 weeks to heal.⁶³ Special thigh guards can be employed to protect from further injury.⁶³ Complications of quadriceps contusions include the very rare situation of compartment syndrome of the thigh and myositis ossificans.⁶³

The most common sprain (and athletic injury in general) occurs at the ankle.^63,64 Ligament injuries are classified accordingly. Grade I sprains (mild) have no appreciable disruption of tissue, and there is minimal loss of function, and they involve only the anterior talofibular ligament.⁶¹ Grade II sprains (moderate) have some disruption of tissue and partial loss of function with involvement of the anterior talofibular and calcaneofibular ligaments.⁶¹ Grade III sprains (severe) have significant or complete disruption of tissue with involvement of all the lateral ligaments and even the deltoid medially.⁶¹ Grade III sprains and interosseous ligament injuries are more prone to develop osteochondral fractures and chronic instability.⁶¹ Anterior talofibular injury is most common and occurs during ankle inversion injuries.⁶¹ Physical examination includes the anterior drawer test, in which laxity is felt when the heel is translated forward while holding leg still. Stressing the foot in inversion and eversion is also helpful to determine the cause of pain.⁶¹ A syndesmosis sprain occurs when there is injury to the membrane between the tibia and fibula and is diagnosed by the tibia-fibula squeeze test, in which the tibia and fibula are squeezed at midcalf, and the patient feels pain in the anterior and slightly proximal to the ankle joint.⁶¹ Ottawa ankle rules suggest that x-rays should be performed if there is acute blunt injury with pain in the malleolar zone, bony tenderness to palpation at the posterior edge or tip of the malleoli or inability to bear weight immediately after the injury; these rules are validated for children over 6 years of age.⁶¹ Rehabilitation must include proprioceptive training. Some athletes may benefit from ankle stabilization with a brace or taping.⁶³ Chronic ankle instability in skeletally immature athletes is uncommon.⁶³

The most common sprain in the knee is caused by injury to the anterior cruciate ligament, which may require surgical management.⁶³ The incidence of this type of injury is approximately 0.01%.⁶⁴ In the shoulder, acromioclavicular (AC) separation is the most common ligament injury. Physical examination may be significant for pain with shoulder flexion, adduction, or abduction; tenderness to palpation over the AC joint; and AC joint separation (compared with the noninvolved side). Treatment is with conservative management using a sling for 3 to 7 days or surgery depending on severity.

Chronic Injuries: Bursitis/Tendinopathy

Children are susceptible to overuse injuries because they are skeletally immature.⁶³ This includes a number of injuries such as bursitis and tendinopathy.

Bursitis

Bursitis is caused by inflammation of the bursa, a fluid-filled sack that functions to cushion joints. Common areas for bursitis are subacromial, olecranon, prepatellar, and infrapatellar bursae and ischial and trochanteric bursae.⁶⁵ Chronic bursitis is caused by exposure to prolonged pressure, repetitive overuse, microtrauma, or inflammatory arthropathies.⁶⁵ Superficial joints should be aspirated and analyzed for crystals and infection. The typical natural history of bursitis is that it is self-limited and will improve, but some cases become chronic.⁶⁵ Treatment is to protect the joint and manage pain with NSAIDs.⁶⁵ An inflamed bursa can be injected with an anesthetic or glucocorticoids for therapeutic and diagnostic reasons.⁶⁵ If the pain resolves, this supports a diagnosis of bursitis.^63,65

Trochanteric bursitis is often associated with iliotibial band tendonitis or “snapping hip syndrome.” Treatment is conservative, focused on stretching the iliotibial band and hip abductors, in addition to vigorous icing. Corticosteroid injection into the greater trochanteric bursa may provide substantial benefit in cases refractory to more conservative management.

Tendinopathy

“Tendinopathy” is a chronic tendon injury that can occur from a variety of causes. “Tendinitis” refers to acute tendon injury with inflammation. Patients are often treated with NSAIDs and physical therapy with an eccentric bias as well as manual therapy, including soft tissue mobilization and stretching.⁶⁶ Steroids, lidocaine, and platelet-rich plasma (PRP) injections are also used. However, in the long run, there is evidence that corticosteroids are less effective than more conservative management.⁶⁷ This may be due to steroids weakening the tendon.⁶⁶ There is limited evidence for PRP yet, but smaller, limited studies have shown some improvement.⁶⁶ Future developments include stem cell therapy, growth factor treatment, and gene transfer.⁶⁶ Extracorporeal shock-wave therapy (ESWT) can be beneficial, especially in insertional and calcific tendinopathy.⁶⁶