Sever’s Disease

Sever’s disease is a common cause of heel pain in children between the ages of 9 and 12 years. The pain is due to calcaneal apophysitis occurring due to repetitive and continuous traction on the calcaneus from the Achilles tendon. The apophysis is not part of a joint and has muscle or tendon attachments. This traction apophysitis may lead to stress fractures, pain and tenderness over the heel.

Sever’s disease is similar to Osgood-schlatter disease of the tibial tubercle.

Patients are usually young athletes presenting with heel pain that increases with activities. Upon examination there could be swelling, tenderness, warmth and/or redness on the back of the heel where the Achilles tendon inserts.

Plain lateral X-rays may show sclerosis or fragmentation of the calcaneal tuberosity. Sclerosis is not specific for this condition.

Fragmentation of the calcaneal tuberosity on the other hand, is more common in patients with Sever’s disease relative to the general population.

Remember that Sever’s disease is a clinical diagnosis. X-rays may show other causes of pain such as tumors, fractures, infections or cysts. MRI is not commonly used, but can help rule out calcaneal stress fractures or osteomyelitis.

Sever’s disease is a self-limiting condition that usually resolves with time. Treatment usually consists of NSAID, Achilles tendon stretching exercises, and activity modifications and in severe condition a short leg walking cast can be used.

Osteoporosis

Osteoporosis is a decrease in bone strength. The strength of the bone depends on mineral density and bone quality. Osteoporotic bone is at risk of fracture at the hip, wrist and spine.

If fracture of the vertebral spine occurs, the patient will have a fivefold increased risk for having a second vertebral fracture or hip fracture. A second vertebral fracture means you may have more compression fractures in the future.

With one hip fracture, there will be a tenfold increase of another hip fracture occurring. Men with hip fractures have a higher mortality rate than women.

Lifetime risk of fractures of the hip, spine and wrist is 40 %. The decrease of bone strength and bone mass clearly predicts fracture risk.

Osteoporosis affects 45% of women aged 50 or older. There is some correlation between osteoporotic fracture and risk of death. This is logical since 25% of patients with hip fracture die within one year. The lifetime risk is high with senile osteoporosis. There are about million osteoporosis related fractures that occur per year.

Men and women both begin to start “spending” or losing bone at a certain point in their lives. Banking or building up of bone during youth has benefits during the later years. Most individuals obtain their peak bone mass between ages of 16 and 25 years. Men begin to lose bone mass after the age of 25 years at a rate of 0.3% per year. Women begin to lose bone at a rate of 0.5% per year. After menopause there is an accelerated rate of bone loss at the rate of 2-3% of total bone loss per year for about 10 years.

Osteoporosis has bone mineralization but abnormal osteoclast function. There are two types of osteoporosis:

1. Type I: postmenopausal which occurs 15-20 years after menopause. It has increased risk of vertebral and wrist fractures. It is due to estrogen deficiency.
2. Type II: senile which occurs in men and women over the age of 70 years. Vertebral and hip fractures are a risk. It occurs more in females than males with a ratio 2:1. It is due to aging and long term calcium deficiency.

20-25% of elderly patients could die within one year suffering of a hip fracture.

Risk factors for osteoporosis include: thin, north European descent, people who live sedentary lifestyles, smoker and drinkers, and anti-seizure medications as phenytoin (Dilantin) and phenobarbital.

The bone mineral density is measured by T- score which is relative to normal age, young, matched control (25 year old women) and Z-score which is relative to similar aged patients.

How is osteoporosis measured? It is measured by DEXA scan at the hip through the T –score. DEXA scan is important in predicting fracture risk.

Lab findings as albumin, calcium, phosphate, vitamin D, parathyroid hormone and bone specific alkaline phosphatase are usually normal.

Vitamin D levels are low in about 70 % of patients with fracture. Vitamin D absorbs calcium from the intestines. With aging, the stomach acidity decreases and the calcium absorption decreases and vitamin D requirements increase. Elderly need more vitamins D to absorb the same amount of calcium.

Treatment of osteoporosis include: bisphosphonates, Denosumab and calcitonin. Bone stimulation can be achieved by parathyroid hormone, calcium and vitamin D.

When to initiate therapy? If T-score is less than -2 with no risk factors, if T-score is less than -1.5 with at least one risk factor as prior vertebral fracture or hip fracture.

What decides if you develop osteoporosis or not? Your savings: you can control this by adding more bone when you are young before the age of 25 years. You begin spending your bone after 25 years.

What is Brachial Neuritis?

Brachial Neuritis is a condition of severe shoulder pain that usually radiates down the arm and up to the neck and scapula. It can also be referred to as neuralgic amyotrophy (NA) and/or parsonage-turner syndrome. The pain is sudden, severe and may last for a few weeks. This pain may disturb sleep! It usually occurs on its own without a history of trauma. The condition occurs more in males and it may occur at any age.

The position of comfort is the shoulder adducted with the elbow flexed. Neck movement and Valsalva’s maneuver do not increase the pain. Pain is increased by movement of the arm. Although the pain is severe and sudden, lasting at least a few weeks, the condition is usually under diagnosed or not diagnosed at all.

Weakness may be absent in the acute phase, however as the pain resolves, weakness of certain muscles will remain. The degree of weakness correlates with the severity of the initial pain.

The muscles that are commonly involved are the supraspinatus and the infraspinatus muscles. The suprascapular nerve is the most commonly involved followed by the deltoid, which is the abductor of the s shoulder innervated by the axillary nerve.

The condition may occur bilaterally and may occur subclinically (only seen on an EMG). Muscle weakness may continue for a significant period of time. Sensory changes may be variable. If there is no sensory loss, this is a classic finding that confirms the diagnosis. There is a decreased sensation in a lot of cases. The lateral antebrachial cutaneous nerve is usually involved.

Motor changes predominantly occur over sensory changes and can involve the brachial plexus from C5-T1 with a variable degree of weakness. It can affect more than one nerve branch with certain patterns of involvement can be seen on the MRI.

It is a benign, self-limiting problem with 90% of patients returning to near normal condition in about 3 years. Only about 1/3 of the patients will recover at about 1 year. The etiology of brachial plexus neuritis is unknown.

Hyperintense muscles involved in the sagittal plane (supraspinatus, infraspinatus, and deltoid). In advanced cases, the muscles will either be atrophied or have fatty infiltration.

EMG and Nerve studies are helpful for the diagnosis and the prognosis. In the first 4 weeks, there will be acute denervation in the roots and the peripheral nerves. EMG may be abnormal for up to 7 years after the diagnosis.

Rule out other conditions such as radiculopathy from a herniated disc. This can be excluded from imaging of the cervical spine. Other conditions that may be considered differential diagnoses are adhesive capsulitis and lyme disease. There are two particular conditions that are very interesting with acute brachial neuritis. The first is bilateral interosseous nerve palsy, which is caused by viral brachial neuritis. The patient has the inability to do the Ok sign. It is motor loss that follows intense shoulder pain and usually the condition resolves with time.

The second condition is winging of the scapula. The serratus anterior muscle involvement may cause dull aches and pain. Acute, sudden severe pain consider with acute brachial neuritis that involves the C7 nerve root. C7 nerve root gives the long thoracic nerve, which innervates the serratus anterior muscle. If the patient has severe shoulder pain and winging of the scapular rule out brachial neuritis!

The treatment includes rest, observation and steroid injections. Avoid using a sling, a sling will cause flexion and internal rotation contracture of the shoulder. The sling may also cause a stiff elbow.

What is Rheumatoid Arthritis?

Rheumatoid arthritis involves the synovium of the joints. The condition of rheumatoid arthritis will result in deformities. Rheumatoid arthritis occurs in females more than males.

There may be a hereditary component with rheumatoid arthritis. Rheumatoid arthritis has spontaneous remissions and exacerbations. The disease can have a systemic nature. Pain and stiffness of joints especially in the morning (morning stiffness). Rheumatoid arthritis is typically poly-articular, bilateral, and symmetrical and most commonly affects the hands and feet.

X-rays show periarticular erosions at the time of diagnosis. Osteopenia and minimal osteophyte formation favors the diagnosis of rheumatoid arthritis.

Pathogenesis

Rheumatoid is an auto immune disease. The disease has two important components: immunological reactions and increased degradative enzymes. The IgM (rheumatoid factor) is produced by the plasma cell as an antibody to the native IgG, which is altered in RA. 70% of the patients with RA have rheumatoid factor positive. Leukocytes are attracted to the immune complex forming deposits over the inflammatory surface of the synovium. These leukocytes ingest fibrin and immune complex and is called the rheumatoid cells. The leukocytes release lysosomal enzymes that causes acute inflammatory response and tissue necrosis as well as inflammatory mediators (IL-1, IL-6, and TNFα). The chondrocytes respond to stimulation by TNFα, IL-1 and other inflammatory mediators causing cells to become activated and secrete more metalloproteinases which lead to cartilage damage. The synovium becomes hypertrophied (Pannus), showing intimal hyperplasis and infiltration by plasma cells and lymphocytes.

Stages of Rheumatoid Arthritis

Early stages (acute) include hot, swollen, tender joints (synovitis), wrist swelling, MCP swelling and Flexor Sheath Synovitis. Complicated rheumatoid arthritis include digital vasculitis, ecchymosis, skin atrophy and nodules. Advanced rheumatoid arthritis includes swelling of the MCP joints, lateral slippage of extensor tendons and tendon ruptures and ulnar deviation of fingers. X-rays show destruction of MCP with subluxation, ulnar deviation and wrist destruction.

Finger deformities include mallet, boutonniere, and swan neck.

The thumb is also involved. These changes occur due to proliferation, inflammation and hypertrophy of the synovium. Involvement of the distal radioulnar joint is usually associated with rupture of the extensor digiti minimi.

Rheumatoid Nodules

25% of patients with RA will have subcutaneous nodules on extensor surfaces of elbow and forearm. Nodules are often multiple and seen along the ulnar margin of the forearm or pulp of the digits. Vasculitis is more common in patients with SC nodules, it is a strongly seropositive disease (aggressive) with a less than favorable prognosis.

Treatment

If the patient has synovitis, it should be treated by a splint and medical treatment. If the patient has joint space narrowing, bone erosions and osteopenia the patient will need a synovectomy. If the patient has joint destruction/fixed deformity or loss of hand function, surgery is based on the conditions.

Before operating on RA patients, x-ray of the cervical spine is needed because the patient may have subluxation of C1-C2. Metacarpophalangeal joint arthroplasty of the fingers usually results in decreased extensor lag and improvement of the ulnar drift.