Osteonecrosis of the Hip

Osteonecrosis or avascular necrosis of the hip is death of a segment of bone in the femoral head due to disruption of the blood supply. The etiology of this condition is not fully understood. There are several risk factors associated with osteonecrosis of the hip.

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The condition is bilateral in about 80% of the patients. Check the other hip even if it is asymptomatic.

Early diagnosis is important. In early stages of osteonecrosis, a femoral head preserving procedure may be done.  In late stages of osteonecrosis, the femoral head collapses and cannot be saved. The femoral head may need to be replaced.

Obtain AP frog leg lateral views of the hip. The frog leg lateral view will show the crescent sign. MRI is the study of choice especially when the patient has persistent hip pain, radiographs are negative and the diagnosis of osteonecrosis is suspected.

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The Ficat classification is a commonly used system to stage osteonecrosis of the hip.

  • Stage I: normal appearing X-ray. MRI will detect the lesion (changes in the marrow).
  • Stage II: sclerosis and cyst formation
  • Stage III: subchondral fracture. Crescent sign and flattening of the femoral head.

Stage IV: advanced lesions with arthritis, osteophyte formation and loss of the joint space.

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Treatment

For early stages of osteonecrosis of the hip, initial trial of non surgical treatment is usually done. Surgery may be needed if non surgical methods are not successful.

Non-operative treatment includes:

  • Bisphosphonates: may also be used before the femoral head collapses. Still experimental.

Traditional surgical treatment: when the lesion is small, a head preserving procedure can be done.

  • Core decompression for stages I and II: can make a single large hole or multiple holes in the femoral head. It decompresses the head and stimulates a healing response. The lesion is anteriorly and superiorly.
  • Core decompression with bone graft: debride the necrotic area and place the bone graft. Some lace this much bone graft.
  • Traditional fibular graft: is done in younger patients.

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Complications:

  • Donor site pain and leg dysfunction
  • Tibial stress fracture form side the graft is taken.
  • Total hip arthroplasty (cementless cup and stem) or total hip resurfacing. Resurfacing is not commonly used.

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  • Total hip replacement (predictable): is considered to be the traditional procedure for advanced stages of osteonecrosis of the hip.
  • Total hip resurfacing (controversial): need adequate bone stock to support the femoral component. The result is not as good when compared with a patient with osteoarthritis (older group).

 

 

 

Pediatric Cervical Spine Injuries

Cervical spine injuries are generally not common in children. Blow 8 years of age, cervical spine injuries usually occur in the upper cervical region. Above 8 years of age, cervical spine injuries occur in the lower cervical region. The prevertebral soft tissue shadow may appear widened on lateral x-ray of a crying child with no injury. Cervical spine injuries should be suspected in multiple trauma patients. Rule out cervical injuries in all patients with head or facial trauma.

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Spinal cord injury without radiological abnormality (SCIWORA) is due to ligamentous elasticity and flexibility of the pediatric vertebral column which can withstand injuries without the evidence of deformity, however the spinal cord will be damaged. It should be suspected in a child with neck injury and neurological symptoms with no radiological bony abnormalities. Common in spinal cord injuries below 8 years of age and usually occurs in the cervical or thoracic spine. SCIWORA usually resolves with no neurological deficiencies but there is high risk of reoccurrence. Investigation of choice is MRI and treatment is cervical immobilization.

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Atlanto-occipital dislocation

It is a fatal injury due to major trauma. It is more common in children than adults due to:

Increased head-body ratio in children.

The occipital condyles of children are smaller than those of adults.

There are three classifications for Atlanto-occipital injuries:

  1. Anterior displacement of the occiput
  2. Longitudinal distraction of the occiput from the atlas ( avoid traction)
  3. Posterior displacement of the occiput.

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Diagnosis is by x-ray. CT scan and MRI that shows ligamentous injury.

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Treatment: reduction should be urgently done with early immobilization by halo vest. Avoid traction in type II. Post reduction radiograph should be obtained to ensure adequate reduction. Cervical spine x-ray should be done daily to ensure maintained reduction.  Atlanto-occipital dislocation is a ligamentous injury that is usually unstable and may need atlanto-occipital fusion.

Os odontoid

Os odontoid is due to congenital or unrecognized fracture of the odontoid. It is accidently discovered on radiological investigation. It should be differentiated from acute odontoid fractures.

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Treatment is conservative if no pain, no neurological deficiency and no cervical spine instability. Surgical treatment is done in patients with progressive symptoms as neck pain, neurological deficiency or cervical spine instability. In young children without progressive deficits, it is better to delay surgical treatment until six to seven years of age. By that time the child will have sufficient bony development of the cervical spine.

Odontoid fracture

Odontoid fractures occur in young children usually around 4 years of age. Treatment includes reduction and immobilization in extension. Complete reduction is usually obtained but it is not necessary, 50% reduction is satisfactory. Growth disturbances are rare.

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Persistence of the basilar odontoid synchondrosis is seen in one half of children up to age eleven and may mimic an odontoid fracture. This line appears sclerotic unlike acute fractures and is located well below the base of the odontoid where most adult fractures occur.

Atlanto- Axial rotatory subluxation

Child with rotatory subluxation of C1 on C2 is marked by the direction of head tilt and rotation of the neck.

Atlanto- Axial rotatory subluxation is classified as following:

Type I: unilateral rotatory subluxation with intact transverse ligament.

Type II: unilateral rotatory subluxation with torn transverse ligament

Type III: bilateral rotatory subluxation

Type VI: posterior rotatory subluxation.

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Most common causes of Atlanto-Axial Rotatory Subluxation are:

  • Neck trauma
  • Inflammatory condition as upper respiratory tract infection.
  • Children with congenital anomalies and ligamentous laxity such as Down syndrome.

This injury may be missed due to mild symptoms and signs. The child usually presents with neck pain and torticollis (cock-robin sign). Physician must rule out any neurological deficiencies.

Lateral X-ray shows anterior displacement of C1 over C2. Open mouth view X-ray shows asymmetrical lateral masses of C1. Dynamic CT scan is diagnostic.

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Treatment depends on the duration of injury. For injuries less than 1 week, immobilization by neck collar should be attempted. Halter traction is used in injuries of more than 1 week in duration. Surgical reduction in C1-C2 fusion is used to treat fixed deformities or used in patients with neurological deficits.

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Sub-axial injuries are rare in children and usually occur in adults. These include:

Posterior ligamentous disruption

It is due to flexion or distraction injuries. It may be missed on radiological evaluation due to normal loss of cervical lordosis in children. MRI is diagnostic for the ligamentous injury and treatment by immobilization in extension or posterior arthrodesis if signs of instability are present.

Compression fractures

They occur due to flexion and axial loading injuries. It leads to loss of the vertebral height and usually diagnosed on lateral view x-ray. In children under 8 years of age vertebral height will be regained during growth and kyphosis will be corrected but if kyphosis is more than 20 degrees it might not be corrected with growth.

Burst fractures

It is due to axial loading injuries. Treatment is by traction followed by halo immobilization if there is no neurological deficiency. Surgical fusion is done when neurological deficiencies are present. Anterior fusion leads to kyphotic deformity due to suppression of the anterior growth potential.

Unilateral or bilateral facet dislocation

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Scoliosis in children

Scoliosis is lateral curving of the spine. Pediatric spinal cord trauma will almost always result in scoliosis.

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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.

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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.

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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.

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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.

osteoporosis4.pngRisk 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.osteoporosis5.png

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.

Heat Illness in Athletes

As summer approaches, athletes, coaches and other individuals will need to be aware of heat-related illnesses. Heat illnesses include a spectrum of conditions ranging from heat syncope, heat cramps and heat exhaustion to the more severe heat stroke.

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Heat Syncope (fainting) is a form of orthostatic hypotension that is related to dehydration. It occurs due to inadequate cardiac output and hypotension. It also occurs with standing quickly after sitting or lying down for prolonged durations in the heat. Symptoms include fainting, dizziness and light-headedness. Treatment includes oral rehydration (water, juice or sports drinks) and placing the patient flat on the ground in a cool area with slight elevation of the legs to push the blood back to the vital organs such as the brain.

Heat Cramps are painful muscle cramps that occur due to decreased sodium heat2.pngconcentration in the blood. The patient’s core temperature is usually not elevated. Sodium may decrease when salts are lost in sweat or with excessive water intake that does not include electrolytes leading to a situation called dilutional hyponatremia. Symptoms include painful muscle cramps occurring commonly in the abdominal muscles, arms, legs and thighs. Treatment includes rest, cooling and IV fluids or oral rehydration with fluids rich in electrolytes (sports drinks and juices) to replenish the sodium stores. Prevention could be achieved by consumption of fluids high in electrolytes before strenuous activities.

heat3Heat Exhaustion is the most common heat illness. The body temperature becomes elevated but is less than 40°C. The core body temperature is best measured rectally. The signs and symptoms of heat exhaustion include profuse sweating, core body temperature lower than 40°C, weakness and fatigue, cramping, headaches, nausea and vomiting,  fainting, hypotension, increased heart rate, and fast shallow breathing. Treatment includes rest, IV fluids or oral rehydration and rapid cooling by whole-body immersion in an ice bath.

Heat Stroke is the most severe form of heat illness. It is a medical emergency that needs immediate attention. The patient should be transported to the hospital as soon as possible. Heat strokes occur due to failure of the body’s normal thermoregulatory mechanism. If treatment is not started promptly, end-organ failure and ultimately death may occur. Heat strokes have a high mortality rate and require quick reduction of the patient’s temperature. The three characteristic features of this condition are a lack of sweating, core body temperature above 40°C (best measured rectally) and an altered mental status. Additional signs and symptoms include hot, dry skin, disorientation, confusion and hallucinations, headache and slurred speech. This is a serious medical emergency that requires rapid core body temperature reduction. The patient should have close monitoring of airway, breathing and circulation. The physician should implement basic life support and ACLS protocols. Rapid cooling by whole-body immersion in an ice bath will be utilized as well as IV fluids.

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