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.
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.
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.
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.
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.
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).
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:
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.
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.
Gait is the pattern of how a person walks. We will be discussing different gait abnormalities.
Antalgic gait is a painful gait. A patient with antalgic gait does not want to spend time on the one leg due to pain. A patient wants to get their weight off the affected extremity. When pain is increased by walking, it leads to an antalgic gait (Figure 1).
An antalgic gait can be caused by multiple factors due to pain in any part of the lower extremity. It is usually caused from hip or knee pathology or from severe disc radiation symptoms (Figure 2).
The pain can be helped by using a cane on the opposite side of the painful extremity.
Trendelenburg gait is an abnormal gait that is usually found in people with weak abductor muscle of the hip which is supplied by the superior gluteal nerve. The patient cannot abduct the affected hip due weakness of the abductor muscles on the affected side. If the patient has weakness on one side of the pelvis and when the patient stands on that side, the pelvis on the contralateral side will drop. This is called Trendelenburg sign. A positive Trendelenburg sign occurs when there is dysfunction of the abductor muscles and the body is unable to maintain the center of gravity on the side of the stance leg (Figures 3, 4). The patient will show an excessive lateral lean to keep the center of the gravity over the stance leg.
Weakness can also occur in patients with L5 radiculopathy or avulsion of the abductor muscle tendon (Figure 5) which occurs with increasing frequency after hip replacement surgery.
The superior gluteal nerve injury is a major factyor in this gait. With bilateral weakness of the abductor muscles, the patient will have dropping of the pelvis on both sides during walking which leads to a waddling motion. This gait is seen in patients with myopathies.
Slap gait occurs due to weakness of the foot and ankle dorsiflexors which allows the foot slap down on the floor with each step. Slap gait is a heel gait abnormality that can be diagnosed by hearing the patient walk with a normal walking gait, the heel strikes the ground first followed by controlled relaxation of the foot and ankle dorsiflexors in order to allow the forefoot to come in contact with the ground
Foot drop gait or steppage gait is due to total paralysis of the ankle and foot dorsiflexors (Figure 6). it is sometimes called neuropathic gait. A common symptom of foot drop is a high steppage gait that is often characterized by raising the thigh up in an exaggerated fashion while walking. The patient must externally rotate the leg or flex the hip or knee to raise the foot high enough to avoid dragging the toes along the ground. If the patient has foot drop then they have to have a high steppage gait or else they will trip on the foot and fall forward.
Conditions causing foot drop include L4-L5 disc herniation, a herniated disc compressing the L5 nerve root may cause foot drop, lumbosacral plexus injury due to pelvic fracture (Figure 7), hip dislocation leading to injury of the common peroneal nerve (Figure 8) and injury to the knee as knee dislocation (Figure 9).
Wide based gait
A wide based gait occurs due to myelopathy and neurological disorders. This gait disturbance is described as clumsy, staggering movements. It can be associated with cervical or thoracic spine pathology. Patient example of myelopathy with significant cervical spine disc compression of the spinal cord can be seen in Figure 10.
Patient will have a slow, wide, broad based ataxic gait. The patient will have a wide stance as they try to maintain balance. There will be unsteadiness of the trunk with excessive shift in the center of the gravity.
Gluteus maximus gait
When the gluteus maximus muscle (Figure 11) is week, the trunk lurches backwards (extension of the trunk). It occurs at heel strike on the weakened side to interrupt the forward motion of the trunk. This compensates for weakness of hip extension. The function of the gluteus maximus muscle is external rotation and extension of the hip joint.
The sacroiliac joint (Figure1) is the joint that connects the spine to the pelvis. It can be found between the sacrum, (the triangular-shaped bone in the lower portion of the spine) and the ilium of the pelvis. Joining these bones together are strong ligaments.
Unlike other joints in the body, the sacroiliac joint does not have much movement. However, it is essential in transferring the load of your upper body to your lower body. In other words, weight bearing forces go through the sacroiliac joint and acetabulum. Injury to this area affects the weight bearing ability of the joints. Its motion is a combination of rotation, tilting and sliding.
However, the sacroiliac joint may only slide a couple of millimeters and may tilt and rotate only three or four degrees.
Sacroiliac joint pain is a very common problem and one of the more common causes of low back pain. This type of pain is focused in the lower portion of the back and hip and may radiate out to the buttocks and lower back. In addition, it may radiate down the legs or around to the front, in the groin area. Pain is often worse withstanding and walking and improves with lying down.
When depending on the history and the clinical examination alone, it may be difficult to differentiate between sacroiliac joint pain and other sources of low back pain.
Examination of the sacroiliac joint usually begins with a physician conducting a Faber test. During this test, a physician forces external rotation of the affected hip in the supine position which causes pain in the sacroiliac joint. In addition, there would be tenderness over the sacroiliac joint.
According to Dreyfuss et al, however, sacroiliac joint pain was resistant to identification by 12 clinical examination tests that were standardized against a confirmatory test of intra articular injection.
There are many causes of sacroiliac joint pain including dislocation, sacroiliitis, sacroiliac joint dysfunction, and conditions that alter normal walking patterns. First, sacroiliac pain may be caused by subluxation of the joint. A slightly causes displaced sacroiliac joint places excess stress on the ligaments that hold it together.
Second, sacroiliac joint pain may be caused by sacroiliitis. This is an inflammation of one or both of the sacroiliac joints. It is characterized by pain or stiffness in the lower back, pain that radiates down the leg, decreased range of motion, or pain that worsens when walking or standing.
Another cause of sacroiliac joint pain may be sacroiliac joint dysfunction. This type of sacroiliac joint pain differs from sacroiliitis because its origin is a disruption in the normal movement of the joint. This could either be the result of either too much or too little movement in the joint. When the cartilage is damaged or worn away, bones begin to rub on each other and degenerative arthritis occurs. This is typically the most common cause of sacroiliac joint dysfunction. However, pregnancy may be a cause of sacroiliac joint dysfunction in women. During pregnancy, hormones are released that allow the ligaments to relax. This relaxation of the ligaments holding the SI joints together allows for increased motion of the joints and can lead to increased and abnormal wear on the sacroiliac joint.
Lastly, sacroiliac joint pain may be caused by conditions that alter your normal walking pattern. These conditions include: leg length discrepancy; pain in the hip, knee, ankle or foot; and pregnancy.
While there are a number of ways to determine SI joint pain, the most accurate way is to perform a diagnostic injection of the joint. This type of injection may be done in the office or more accurately using x-ray guidance with a fluoroscope. Once the doctor places a needle in the joint, an anesthetic is injected into the joint to numb the joint. If your pain goes away with the anesthetic, it can be gathered the pain you are experiencing is coming from the SI joint. In a study conducted here, 90 percent of patients that had a CT guided sacroiliac joint injection had sacroiliac joint pain confirmed by the injection.
Treatment for SI joint pain can range from conservative to surgical. First, doctors may suggest conservative measures such as rest, anti-inflammatory medication, phy
sical therapy, and a sacroiliac belt to hold the SI joint together to ease the pain. If these conservative measures are unsuccessful, a series of cortisone injections may be used to reduce the inflammation in and around the joint. If these tactics are unsuccessful, doctors may use one of two surgical approaches: radiofrequency ablation or fusion. Sacroiliac joint pain does remain a diagnostic and therapeutic challenge. In a study conducted here, CT scans were negative in 42 percent of symptomatic sacroiliac joints with a positive sacroiliac joint injection test (Figure2).
Once it has been determined the pain is originating from the SI joint, doctors may perform a procedure called radiofrequency ablation. During this procedure, the nerves that provide sensation to the joint are burned with a needle called a radiofrequency probe. This eliminates sensation from the joint, making it essentially numb. This procedure is a temporary solution, although it can be repeated. The other surgical option available for sacroiliac joint pain is fusion (Figure3).
During this procedure, the articular cartilage from both ends of the Sacroiliac’s bone is removed. The two bones are held together with plates and screws until they fuse into one bone. This will stop the motion between the bones, thus eliminating pain from the joint.