Clinical Evaluation

Cold Abscess Causes, Presentation and Treatment

The term cold abscess refers to an abscess [An Abscess is a collection of liquefied tissue(pus) in the body] where typical signs of abscess [warmth, redness, tenderness,] are absent. The prefix cold indicates that the abscess is not hot because that is the usual case.

Thus a cold abscess is not accompanied by the classical signs of inflammation- heat, redness, fever, pain etc., which are usually found with the pyogenic abscess.

The only conditions when a cold abscess shows sign of inflammation are

When it is about to burst out of the skin
When there is a mixed infection with pyogenic organisms.

A cold abscess is typically seen in tubercular infection but can be encountered in actinomycosis, blastomycosis, and leprosy.

Cold abscesses are most commonly associated with osteoarticular tuberculosis and lymph node tuberculosis.

Pathogenesis of Cold Abscess Formation

The characteristic microscopic lesion in tuberculosis is the tuberculous granuloma– a collection of epithelioid and multinucleated giant cells in the periphery. Within the tubercle, small patches of caseous necrosis appear. These may coalesce into a larger yellowish mass and the center may break down to form an Abscess.

Thus cold abscess is formed by a collection of products of liquefaction & the reactive exudates.

After formation of the abscess, continuous disease activity may build up the pressure further and the cold abscess breaks its boundaries, penetrates the ligaments in articular disease, bone & periosteum in osseous disease.

Further buildup makes the cold abscess to migrate in various directions following the path of least resistance along fascial planes, blood vessels and nerves to appear superficially at distant sites away from the site of the lesion.

In the lymph nodes, periadenitis results in matting and fixity of lymph nodes. The lymph nodes coalesce and breakdown to form caseous pus which may perforate the deep fascia and present as fluctuant swelling on the surface.

The overlying skin becomes indurated, breaks down and leads to the formation of a sinus.

The cold abscess is composed of

Serum
Leucocytes
Caseous material
Bone debris
Tubercle bacilli

Sometimes, the cold abscesses may get secondarily infected by pyogenic bacteriae and present as a hot abscess.

Sites of Cold Abscess

Cold abscesses are most commonly seen in

Neck & Axilla
Back
Side of chest wall

Majority of the cold abscess are in relation to spinal tuberculosis.

Majority of the spinal cold abscesses trickle down distal to the site of the disease But in a bedridden patient, the pus can migrate proximally to the site of the spinal lesion as well.

Clinical Features

There would be a painless swelling of insidious onset without any history of high fever. The slight rise of temperature is seen in tuberculosis and is due to disease activity.

On examination, there would be a mass of soft and cystic consistency. The swelling would have fluctuations and there would be no transillumination. By large the swelling is not compressible though in some cases where the apparent abscess communicates with an underlying cavity, the size may reduce on the application of pressure.

Often the patient has other features suggestive of tuberculosis. If not, location of the abscess could indicate as a rough guide to the region involved.

Additional sinuses may be present.

Sometimes, the only presentation of tuberculosis is a cold abscess and work up to find underlying lesion may be required.

The abscess would cause local Pressure effects too especially the deep cold abscesses.

For example in the cervical spine, the exudate collects behind prevertebral fascia & protrude forward as retropharyngeal abscess which may cause dysphagia, dysphonia, dyspnoea and/or hoarseness of voice

Laterally, it may spread into the sternomastoid muscle & present as swelling in the neck.

The abscess may trickle down to mediastinum to along trachea or esophagus.

In the thoracic spine, the collection may cause the formation of a paravertebral abscess. It also may enter into spinal canal & cause extradural compression of the cord.

It can penetrate the anterior longitudinal ligament to form a mediastinal abscess or through the medial arcuate ligament to form a lumbar abscess.

IT may appear anywhere along the course of intercoastal nerve too.

In the lumbar spine, the pus can track along the psoas muscle towards the groin & presents as psoas abscess. It might lead to flexion of the hip, a condition termed as pseudo flexion deformity of hip>

It can travel along the iliopsoas tendon to appear on the medial aspect of the thigh.

It can spread laterally beneath iliac fossa to emerge at the iliac crest near the anterior superior iliac spine. The pus can also form an abscess in Scarpa’s triangle or gluteal region.

Differential diagnosis

Lipoma
Cyst
Soft tissue tumors

Diagnostic Work Up

Most of the cold abscesses are evident from their history, location and examination findings. The workup should include finding the tubercular lesion.

Routine blood works will show increased lymphocytes, raised ESR and CRP.

Antigravity aspiration and study for tuberculous bacteria are initiated which include PCR and culture of the aspirate. Stain for acid-fast bacilli is not positive often due to paucibacillary nature of osteoarticular tuberculosis.

X-ray and MRI are useful imaging studies. CT is able to assess bone destruction better.

In the cervical region, retropharyngeal abscess may be seen on lateral x-ray [Soft tissue shadow thickness in front of C3 vertebra >4mm].

Normal limits are shown in x-ray.

Paravertebral shadow on AP view indicates paravertebral abscess in the thoracic spine. Psoas shadow may be obliterated on x-ray in case of psoas abscess.

MRI gives a better assessment of extradural abscesses / subligamentous spread. It can also reveal skip lesions and spinal cord compression.

Treatment of Cold Abscess

The cold abscess is not the primary culprit. Underlying tuberculosis is. Therefore the treatment is for underlying tuberculosis. As underlying tuberculosis heals, the cold abscess would reduce at first and then go away.

The treatment of tuberculosis is by use of antitubercular drugs.

[Read more on the treatment of tuberculosis]

Some cold abscesses are large and would need a reduction of the fluid load for drugs to reach the site.

The aspiration is done in an antigravity fashion in a zig-zag method, so as to avoid fistula formation from continuous gravitational drainage through the puncture site.

For very large cold abscess, ultrasound-guided Pigtail catheter drainage or open surgical drainage is considered.

Ankle Pain Causes and Treatment

By Arun Pal Singh

Ankle pain can originate in ankle joint or surrounding tissues. The ankle joint is a weight-bearing hinged joint and ankle pain can be caused by injury or disease of the ankle joint or surrounding tissues.

The present article is a general overview of causes and treatment of ankle pain.

Relevant Anatomy

[Read detailed anatomy of ankle joint]

The ankle joint anatomy is formed by the meeting of three bones.

The end of tibia including the medial projection called medial malleolus.
The lower end of fibula also called lateral malleolus
Dome of the talus bone

The stability of the ankle joint is provided by lateral and medial ligaments. The ankle joint is surrounded by a fibrous

joint capsule.

Tendons passing through all around the ankle and fibrous structures also contribute to the stability. Notable are

Achilles tendon behind the ankle attaching at the back of the heel.
Posterior tibial tendon passing behind the medial malleolus.
Peroneal tendon passes behind the lateral malleolus to attach into the foot.

Causes of Ankle Pain

Ankle Injuries

Ankle sprains are one of the common musculoskeletal injuries. Sprains are partial or complete ligament tears. Both medial and lateral ligament can get injured.

The typical injury is caused by twisting of the ankle. There might be a popping sensation.

Fractures around the ankle occur as a result of greater force. This could be due to twisting of the ankle, falls or motor vehicle injuries.

Depending on the type of force the ankle can get dislocated too.

Ankle injuries result in immense pain and are associated with swelling. Movements of the ankle are painful.

Tenderness would be present over the injured part.

With a severe ankle injury, such as from a motor vehicle accident, dislocation of the ankle joint can occur. Ankle dislocation is a serious injury and generally requires a surgical repair. A dislocated ankle occurs when there is complete damage and disruption of the ligaments that support the ankle joint.

Tendinitis

Tendinitis or tendonitis) is inflammation of the tendon. Common tendons around the ankle to be involved by tendinopathy [a better term which includes both tendinosis and tendinitis] are the Achilles tendon, the posterior tibial tendon, or the peroneal tendon.

Tendinitis can result from trauma or underlying inflammatory diseases or illnesses such as rheumatoid arthritis, ankylosing spondylitis, and other seronegative spondyloarthropathies.

All forms of tendinitis cause pain, swelling, and tenderness in the tendon area involved. Depending upon the causation, the development may be rapid or slow.

Tendinosis can lead to tendon rupture. Achilles tendon rupture is quite common in middle-aged recreational athletes. It occurs without much trauma and often spontaneously. There is a popping sound and the patient walks awkwardly as there is a loss of strength of plantar flexion.

The treatment is often Surgical.

Achilles-tendon-rupture and gap is seen — Achilles Tendon Rupture

Bursitis

Two main bursae that can cause ankle pain are

Retrocalcaneal or subtendinous bursa [which is located between the Achilles tendon and the calcaneus]. This bursa is anterior to Achilles tendon.
Subcutaneous calcaneal bursa, superficial to the Achilles tendon. Also called the Achilles bursa. This bursa is located between the skin and posterior aspect of the distal Achilles tendon.

Inflammation of either or both of these bursae can cause pain at the posterior heel and ankle region. Retrocalcaneal bursitis is fairly common.

Arthritis

Primary osteoarthritis of the ankle is less common in the ankle than knee or hip. Presence of degenerative changes in ankle joint may occur in the knee or hip malalignment or muscular imbalances.

Valgus or varus ankles can give rise to secondary osteoarthritic changes. But ankle joint can be involved in rheumatoid arthritis, psoriatic arthritis, reactive arthritis or pseudogout.

Malunion of ankle fractures may also lead to degenerative changes.

Osteochondritis Dissecans

Osteochondritis dissecans is a condition in which a segment of articular cartilage with its underlying subchondral bone gradually separates from the surrounding osteocartilaginous tissue.

The separation of the fragment may be partial or complete.

Osteochondritis dissecans affects two forms. Juvenile which affects children between age 5-15 years and adult form that affects adolescents with closed physes and adults.

In the ankle, it affects the posteromedial aspect of the talus 56% of the time and in the anterolateral aspect 44%.
Osteochondritis dissecans has a male-to-female ratio of 2-3 to 1.

The exact cause is not known.

Osteochondrosis

Sever Disease refers to osteochondrosis of apophysis of the calcaneum.

Sever disease or calcaneal apophysisits was first described by JW Sever in 1912. Sever disease is a painful inflammation of the calcaneal apophysis. It is considered as an adolescent nonarticular osteochondroses.

The repetitive pull of the tendocalcaneus on its insertion is thought to be responsible for this entity. The problem occurs in growing age and occurrence is more in children who actively participate in sports.

The typical pain is behind the ankle.

Plantar fasciitis

Plantar fasciitis is a common cause of heel pain and occurs due to degenerative changes at the insertion of the plantar fascia on calcaneal tuberosity. The plantar fascia is the most common cause of heel pain for which professional help is sought.

Pain on weight bearing is a typical complaint.

A heel spur is commonly found in plantar fasciitis patients, but many asymptomatic persons also have heel spurs.

Plantar fasciitis could be bilateral in almost one-third of cases. It is usually seen in people aged 40-60 years. Early incidence is noted in people with spondyloarthropathies.

Infectious Arthritis

Infection of the ankle joint can be caused by many organisms and is common in children than adults.

A typical bacterial arthritis presents with immense pain, immobility, and welling of the joint. The joint is swollen and red. High-grade fever is often associated.

Tuberculosis of the ankle joint is less common and does rarely has an acute presentation. the typical presentation is the pain on weight bearing and swelling of the joint.

Posterior Tibial Tendon Dysfunction

Posterior Tibial Tendon Dysfunction is often called adult acquired flatfoot. Usually, it occurs in one foot but some people may develop it in both feet. Untreated, It is usually progressive.

It is generally caused by overuse of the posterior tibial tendon by activities that involve the tendon, such as running, walking, hiking or climbing stairs.

Pain, swelling, a flattening of the arch and an inward rolling of the ankle are usual symptoms.

The pain is the inside of the foot and ankle along the course of the tendon.

Later, as the arch begins to flatten, there may still be a pain on the inside of the foot and ankle.

The foot and toes begin to turn outward and the ankle rolls inward.

Lab Studies in Ankle Pain

CBC, ESR, CRP, Rheumatoid factor, antinuclear antibodies, and HLA B-27etc would help to differentiate between inflammatory and infectious causes. Aspiration and culture of the organism from the joint fluid would further help to confirm the infectious causes. PCR for tuberculosis may suggest the presence of mycobacteria.

Imaging

X-rays are the basic imaging required. Anteroposterior and lateral views are done. X-rays are able to show bony injury, joint subluxation or dislocation. They can also show advanced infection of the bone.

Reduction of joint space would be seen in chronic arthritis.

In soft tissue injuries, the x-rays would be normal.

In complex periarticular injuries like pilon fractures, CT with 3D reconstruction would help.

MRI is able to reveal soft tissue injuries better and grade them. Joint pathologies, talar lesions, and tendon ruptures would be better revealed by MRI. It is also able to differentiate between inflammatory and infectious pathologies.

Treatment

The actual specific treatment would depend on the cause of ankle pain.

Mild ankle injuries are initially treated with ice, rest, and limiting the amount of walking and weight-bearing on the injured ankle. The leg can be elevated to reduce swelling, and crutches are often recommended to avoid further trauma to the injured ligaments.

Anti-inflammatory medications can be given to reduce local inflammation. Ice packs help decrease further swelling of the area and can reduce pain.

Patients with severe injuries are placed in immobilization casts or may require surgical repair.

[More on the treatment of sprains ]

[More on the treatment of ankle fractures.]

Immediate treatment of tendinitis involves immobilizing the area, elevation, and limiting weight-bearing, applying ice, and using nonsteroidal anti-inflammatory drugs (NSAIDs) to decrease inflammation.

Achilles tendon ruptures require orthopedic surgical repair.

[More on the treatment of Achilles tendinosis ]

[More on the treatment of Achilles rupture]

A patient with bursitis is also treated by rest and anti-inflammatory drugs.

[Read more about the treatment of bursitis]

Plantar fasciitis may require modification of shoe wear, heel cushion, and anti-inflammatory drugs.

[More on the treatment of plantar fasciitis]

Arthritis requires rest and NSAIDs. Weight relieving assistance like stick or walker may be prescribed.

Specific treatment may be initiated for rheumatoid arthritis and other inflammatory arthritides.

[More on the treatment of rheumatoid arthritis]

Bacterial arthritis is treated by the use of antibiotics and drainage of pus if required. Antitubercular treatment is given for tubercular arthritis of the ankle. For resting the joint, a splint may be applied.

Osteochondrosis is treated by the rest of the ankle joint, avoidance of activity and NSAIDs.

Osteochondritis dissecans may be treated with rest and medication or need arthroscopic removal.

Lumbosacral Plexopathy – Causes and Management

By Arun Pal Singh

Lumbosacral plexopathy is an injury to the nerves in the lumbar or sacral plexus.

Lumbosacral plexopathy can be caused by many disorders. The prevalence of lumbosacral plexopathies is unknown and is much less common than brachial plexopathies.

Risk factors vary based on cause.

Relevant Anatomy

The lumbar and sacral plexuses together make lumbosacral plexus which is formed from the anterior (ventral) rami of the L1 through S4 nerve roots

The lumbar plexus is derived from the anterior rami of the L1 through L4 nerve roots. These rami pass downward and laterally along the psoas major muscle where they eventually form the plexus.

While within the psoas, they divide into anterior and posterior branches.

The posterior branches of anterior rami, L2-L4, become the femoral nerve, which exits from the lateral aspect of the psoas, traveling through the iliacus and under the inguinal ligament to the anterior thigh.

The anterior branches become the obturator nerve, that exits through the obturator foramen to the medial thigh. The lumbar plexus also gives off the lateral femoral cutaneous nerve of the thigh, iliohypogastric, ilioinguinal, and genitofemoral nerves.

The lumbar plexus and sacral plexus are united via the lumbosacral trunk, which is comprised of a part of L4 nerve root anterior rami, and all L5 anterior rami. The lumbosacral trunk passes over the sacral ala and joins the anterior rami of the S1-4 nerve roots to complete the sacral plexus.

The sacral plexus lies more inferiorly and posteriorly within the pelvic outlet. It is made up of ventral primary spinal nerve branches from L4 to S4, which form several branches including the following:

Proximal branches to the pelvic musculature and buttock region, including nerves to the quadratus femoris, Gemelli, obturator internus, piriformis, and superior and inferior gluteal nerves.
Posterior femoral cutaneous nerve, which has multiple sensory branches to the genitals and thigh.
Sciatic nerve

Read detailed anatomy of Lumbosacral Plexus

Causes of Lumbosacral Plexopathy

Structural

Retroperitoneal hemorrhage (anticoagulation, hemophilia)
Pelvic or abdominal tumor
Aneurysm (common or internal iliac artery)
Endometriosis
Trauma

Nonstructural

Inflammatory (plexitis)
Infarction
Postpartum [during childbirth]
Diabetes (diabetic amyotrophy – most common non-structural cause)
Radiation
Postsurgical (retractor injury)

Pattern of Injury or Plexopathy

Lumbosacral plexus lesions usually are divided clinically into

Upper lumbar plexus [anatomical lumbar plexus]
Lower lumbosacral plexus [anatomical sacral plexus]

Lumbar plexopathies

It predominantly affects the L2–L4 nerve fibers. Pain, if present, usually is located in the pelvis with radiation into the anterior thigh. Quadriceps, iliopsoas, and hip adductor muscles ( femoral and obturator nerves) are the affected muscles.

The knee reflex is frequently depressed or absent.

Sensory loss and paresthesias occur over the lateral, anterior, and medial thigh and may extend down the medial calf

Sensory abnormalities are

Over the lateral thigh (lateral femoral cutaneous nerve)
Anterior thigh (the intermediate cutaneous nerve of the thigh from femoral nerve
Medial thigh (the femoral branch of the genitofemoral nerve, the medial cutaneous nerve of the thigh [femoral branch] and obturator nerve)
Medial calf (saphenous nerve [femoral]).

Lower Lumbosacral Plexopathy

It predominantly affects the L4–S3 nerve fibers.

There is a complaint of a deep boring pain in the pelvis that can radiate posteriorly into the thigh with extension into the posterior and lateral calf.

The ankle reflex may be depressed or absent.

Sensory symptoms and signs may be seen over the posterior thigh and posterior-lateral calf and in the foot.

Muscles affected are

Hip extensors (gluteus maximus)
Hip abductors and internal rotators (gluteus medius and tensor fascia latae).
Hamstrings
All leg muscles supplied by the peroneal and tibial nerves.

Nerve fibers that would go to form the peroneal nerve often are preferentially affected in lumbosacral plexopathies. Therefore the patient may have foot drop and sensory disturbance over the dorsum of the foot and lateral calf. In some cases, the pattern of weakness and numbness may be difficult and electrodiagnostic studies are needed to differentiate.

Clinical Presentation

The patient typically presents with unilateral weakness, sensory loss, and pain.

The presentation may be acute or subacute depending on the cause

The Plexopathy is generally unilateral but the bilateral disease is possible (massive traumas, autoimmune diseases, or radiation-induced).

The symptoms of plexopathy would be accompanied by other symptoms of the associated conditions. For example in autoimmune disease, the skin lesions or other symptoms and signs suggestive of autoimmune disease may be present.

Systemic symptoms like weight loss, fever may be present in some conditions.

The affected limb would have signs suggestive of lower motor neuron injury.

There would be decreased muscle bulk in the distribution of the affected nerves. Muscle tone is decreased in the affected muscles, and reflexes are usually absent or greatly diminished.

[Patellar reflex is present in intact lumbar plexus whereas hamstrings reflex and Achilles reflex are affected [ supplied by the sacral plexus.]

The pattern of weakness would indicate root affected and thus guide to the part of the plexus involved.

Differential Diagnoses

Radiculopathy
Cauda equina syndrome [in bilateral plexopathy]
Peroneal nerve palsy

Lab Studies

Lab studies would depend on the causation.

In general

Blood glucose and glycosylated hemoglobin in diabetic lumbosacral plexopathy
Erythrocyte sedimentation rate
White blood count if an abscess is suspected
Prothrombin time and platelets to know blood disorders

Imaging

X-rays would reveal any bony trauma.

MRI/CT can identify space occupying lesions (eg, cancer, hematoma, abscess) that may be compressing the plexus. MRI neurogram can be done evaluate if nerve root avulsion has occurred.

Neural Studies

Electrodiagnostic testing is used to localize the nerve injury and characterize the process.

Nerve Conduction Studies

Fibular and tibial motor nerve conduction studies with F waves would be absent or of low amplitude in sacral plexus involvement.

Sural, saphenous, and lateral femoral cutaneous sensory nerve conduction studies would be expected to be absent or of low amplitude, with normative distal latency unless the amplitudes are very low, in which case there may be prolonged distal latencies.too.

It must be noted that sensory nerve conduction would be normal in root avulsion too because the dorsal root ganglion cell body remains intact.

Comparison with an opposite limb or upper limb may help.

Needle electromyography

Multiple muscles innervated from L2 to S1 with multiple peripheral nerves are tested. Lumbar paraspinals should also be tested to search for radiculopathy. No motor recruitment will be seen in case the plexus is severely damaged or there is root avulsion.

Management of Lumbosacral Plexopathy

The management of plexopathy would depend on the cause. Following options are available

Pain management
- Drugs
- Spinal cord stimulators
- Intrathecal therapies.

Physical therapy
- Strengthening of partially affected muscles
- Correction of address muscular imbalances
- Maintain flexibility
- Improve balance and gait.
Assistive devices and braces like AFO to correct foot drop and weakness
Surgery in selected cases of severe nerve injury
- Preferred in root avulsions and sharp lacerations

Prognosis

The clinical course depends on the cause.

Except in root avulsion, traumatic plexopathies partial recovery normally, and many patients will have a full or nearly full recovery.

Recovery may take about 18 months after injury.

For lumbosacral plexopathy caused by compression such as (eg, retroperitoneal hematomas), outcomes can be excellent but patients may have lingering symptoms.

Similarly, for diabetic lumbosacral plexopathy, significant improvement with time occurs through some non-progressive deficits may remain.

In radiation-induced plexopathies, unfortunately, a slow but progressive loss of function is expected.

Patients of plexopathy may be left with decreased function and an abnormal gait related to muscle weakness including foot drop. There could be sensory deficits [ insensate skin].

Chronic pain may also be present.

Neoplastic plexopathy generally has a very poor prognosis when they are not resectable and resistant to radiotherapy.

Needle electromyography may be used to monitor the progress.

Common Lumbosacral Plexopathies

Retroperitoneal Hemorrhage

Retroperitoneal hemorrhage is most commonly seen in

Complication of anticoagulation
Hemophilia
Aortic aneurysm rupture.

Such hemorrhages usually are located within the psoas muscle itself, where they can compress the lumbar plexus.

The presentation is of acute severe pain where the hip is flexed and slightly externally rotated.

The major neurologic deficit usually is in the femoral nerve territory, with the weakness of hip flexion and knee extension and a reduced or absent knee-jerk. However, the examination would reveal some dysfunction in the obturator or lateral femoral cutaneous nerve or both.

The treatment would depend on the cause but a decompression is almost always required.

Mass Lesions

Tumors from the bladder, cervix, uterus, ovary, prostate, colon, or rectum may compress the lumbosacral plexus leading to lumbosacral plexopathy.

Lymphoma and leukemia can directly infiltrate nerves, even in the absence of a mass lesion on imaging studies.

Aneurysms or pseudoaneurysms of the internal iliac or common iliac artery have been reported to compress the lumbosacral plexus.

In women, endometriosis can cause implantation of abnormal tissue on the plexus and cause compression. These lesions more often affect the lower lumbosacral plexus.

Endometriosis may result in intermittent symptoms but other lesions are usually slowly progressive.

Idiopathic Lumbosacral Plexitis

Idiopathic plexitis pathology is not completely known. It is thought to be inflammatory, often occurring within a few weeks of a possible inciting immunologic event, such as a cold, flu, or immunization.

There is a severe deep pain in the pelvis or in the upper leg. It characteristically persists for 1 to 2 weeks but may last many months. Because both the upper and lower plexus may be involved leading to different patterns of weakness and sensory loss.

The weakness recovers over many months to years.

Postpartum Plexopathy

Other names for this compression injury to the lumbosacral plexus during labor and delivery are maternal peroneal palsy, maternal birth palsy, neuritis puerperalis, and maternal obstetric paralysis. Although most large series place the incidence of this disorder at one in 2600 births, there are likely many milder cases that never reach medical attention.

The mechanism involves compression of the fetal head against the underlying pelvis and lumbosacral plexus. The compression primarily occurs at the lumbosacral trunk which is vulnerable as it crosses the pelvic outlet and no longer protected by the psoas muscle as they rest against the sacral ala near the sacroiliac joints.

The origin of the superior gluteal nerve lies which is close can also get compressed.

As the fibers that eventually form the peroneal division of the sciatic nerve lie posteriorly, closest to the bone, and are more vulnerable. It should be kept in mind when women present with foot drop after delivery [It can be misdiagnosed as peroneal palsy at the fibular neck.]

Weakness may be noticed immediately or within the first few days after delivery.

In addition to peroneal weakness, the examination would reveal mild weakness hamstrings; hip abduction, extension, and internal rotation indicating a higher lesion than just foot drop.

A sensory deficit is marked over the dorsum of the foot and lateral calf but may be patchy.

Diabetic Lumbosacral Plexopathy

Diabetic lumbosacral plexopathy is most common non-structural lumbosacral plexopathy. Patients develop severe aching or burning and lancinating pain in the hip and thigh, followed by weakness and wasting of the thigh muscles

It occurs in type 1 and 2 diabetes mellitus.

Often, the root and nerve levels are also involved and the disorder is called lumbosacral radiculoplexus neuropathy.

Control of sugar by adjustment of diabetes medication is important.

The management includes neuromodulator medications like gabapentin or pregabalin for neuropathic pain and selective norepinephrine reuptake inhibitors such as duloxetine.

References

Jaeckle KA. Neurological manifestations of neoplastic and radiation-induced plexopathies.Semin Neurol.2004;24:385-393.
Laughlin RS, Dyck JB. Electrodiagnostic testing in lumbosacral plexopathies.Phys Med Rehabil Clin N Am. 2013;24:93-105.
Garozzo D, Zollino G, Ferraresi S. In lumbosacral plexus injuries can we identify indicators that predict spontaneous recovery or the need for surgical treatment? Results from a clinical study of 72 patients.J Brachial Plex Peripher Nerve Inj.2014;9:1.
Kent KC, Moscucci M, Gallagher SG, DiMattia ST, Skillman JJ. Neuropathy after cardiac catheterization: incidence, clinical patterns, and long term outcome. J Vasc Surg.1994;19:1008-1013.

Thoracolumbar Junction and TLTV

By Arun Pal Singh

Thoracolumbar junction is the junction between the Thoracic spine and the Lumbar spine. The junction consists of the part of the vertebral column from the eleventh thoracic vertebra to the first lumbar vertebra. Here the spinal curvature changes from kyphosis to lordosis, and the orientation of the facet joints changes from coronal to sagittal. 12th thoracic vertebra to 2nd lumbar vertebra.

The thoracic spine contains 12 vertebrae and lumbar spine 5. The change in vertebral anatomy adapting to lumbar anatomy can be noticed in last two thoracic vertebrae.

Thoracolumbar junction is important because it marks the change of region. To identify different junctional vertebrae different counting methods are applied.

A thoracolumbar transitional vertebra or tltv is defined as a vertebra with partially retained features of the thoracic and lumbar segments at the thoracolumbar junction.

For example, there may be 13 thoracic and 4 lumbar vertebrae.

TLTV also makes necessary to count the vertebrae in the right manner

The issue of counting arises on the images. For certainty, either the image of the whole spine should be available or thoracic and lumbar vertebra should be identifiable by marked landmarks in the given image. SO it is important to identify correct vertebral levels in thoracolumbar x-ray by just looking at that x-ray, to avoid cost ineffective whole spine imaging.

Different Methods of Vertebral Counting in Thoracolumbar Junction

Counting Down from C2 or T1

This method is commonly used.

The last thoracic vertebra is defined by counting down from the second cervical vertebra (C2) or the first thoracic vertebra (T1) under the assumption that there are 12 thoracic vertebrae.

The cervical spine has a relatively stable morphology and a fixed vertebral count of seven.

But, the number and distribution of thoracic and lumbar segments exhibit considerable variation,[ There could be 22, 23 or 25 presacral segments, there could be 13 rib-bearing thoracic vertebrae with 4 lumbar-type vertebra or 11 rib-bearing thoracic vertebrae with 6 lumbar-type vertebrae.

Identification of Ribs

By labeling the rib-bearing vertebra as the thoracic vertebra, one does not need whole spine images and allows segmentation of the lumbar and thoracic vertebra. But there is a lack of definite criteria by which ribs can be differentiated from rib equivalents.

Differentiating Thoracolumbar Transitional Vertebrae

Differentiation of vertebral segments at the thoracolumbar junction as the TLTV or non-TLTV (thoracic or lumbar) segments through definitive criteria for differentiating the most caudal ribs also enable the surgeon to identify without whole spine images.

An axial image that shows the relationship between the vertebra and most caudal ribs is required for it.

Types of Caudal Ribs

Two of the counting methods and classification of TLTV involves identification of caudal ribs.

A rib articulates with the facet at the body or pedicle of the vertebra.

Most caudal ribs can be classified into one of four types

Normal rib – >3.8 cm length rib
Hypoplastic rib (short rib)- A separated bone <3.8 cm
Unfused transverse process (accessory ossification center or lumbar rib) – A structure articulating with a shortened lumbar costal process or as a structure that was linearly adjacent to such processes
Mixed type – Does not meet any of the above criteria. it appears as a separated bone articulating with the facet on both the pedicle and transverse process.

Thoracolumbar transitional vertebra

A thoracic vertebra is identified by the presence of paired ribs that are 3.8 cm or more in length and originate from the facet at the pedicle (or the body of the vertebra). By contrast, a lumbar vertebra is defined as a vertebra without articulating ribs, the absence of facets for a rib on the pedicle (or the body of the vertebra), with fused transverse processes.

A transitional vertebra is defined as one with characteristics of the corresponding superior and inferior segments, whereas the TLTV is defined as a vertebra with partially retained features of the thoracic and lumbar segments at the thoracolumbar junction.

Five types according to the length of the separated bones, the presence or absence of a facet at the pedicle (or body) of the vertebra and the presence or absence of articulation with separated bones.

Type I

Includes paired ribs with more than one short rib

Type IIA

A 3.8-cm or longer rib on one side and an accessory ossification center or transverse process on the contralateral side

Type IIB

Short rib on one side and an accessory ossification center or transverse process on the contralateral side

Type III

Unilateral or bilateral mixed type rib

Type IV

Unilateral or bilateral accessory ossification center.

References

Farshad-Amacker NA, Lurie B, , Herzog RJ, Farshad M. Is the iliolumbar ligament a reliable identifier of the L5 vertebra in lumbosacral transitional anomalies? Eur Radiol 2014; 24: 2623–30. doi: 10.1007/s00330-014-3277-8
Tureli D, Ekinci G, Baltacioglu F. Is any landmark reliable in the vertebral enumeration? A study of 3.0-Tesla lumbar MRI comparing skeletal, neural, and vascular markers. Clin Imaging2014; 38: 792–6. doi: 10.1016/j.clinimag.2014.05.001
Thawait GK, Chhabra A, Carrino JA. Spine segmentation and enumeration and normal variants. Radiol Clin North Am2012; 50: 587–98. doi: 10.1016/j.rcl.2012.04.003
Carrino JA, Campbell PD, Jr, Lin DC, Morrison WB, Schweitzer ME, Flanders AE, et al. Effect of spinal segment variants on numbering vertebral levels at lumbar MR imaging. Radiology2011; 259: 196–202. doi: 10.1148/radiol.11081511 12 . Wigh RE. The thoracolumbar and lumbosacral transitional junctions. Spine (Phila Pa 1976) 1980; 5: 215–22. doi: 10.1097/00007632-198005000-00003
Malanga GA, Cooke PM. Segmental anomaly leading to wrong level disc surgery in cauda equina syndrome. Pain Physician 2004; 7: 107–10.
Singer KP, Breidahl PD. Accessory ossification centers at the thoracolumbar junction. Surg Radiol Anat 1990; 12: 53–8.

Immune Response to Orthopedic Implants

By Arun Pal Singh

Immune response to orthopedic hardware after implantation could be due to metal sensitivity or against other components, usually of bone cement.

The condition though rare, metal hypersensitivity should be considered.

In cases of recurrent pain and aseptic loosening related to implanted hardware.

The first report of cutaneous hypersensitivity caused by a metallic orthopedic implant was a 1966 case report by Foussereau and Laugier, which described a patient with eczematous dermatitis overlying the site of a metallic plate used for fracture fixation.

The metal hypersensitivity could also be seen in cardiovascular, dental, plastic and surgical implants and is not limited to the orthopedic device.

Most of these manifest in for of allergic skin reactions, impaired wound healing, infection-mimicking reactions, effusions, pain, and implant loosening.

Metal sensitivity may also be associated with chronic fatigue syndrome, fibromyalgia, and autoimmune syndromes.

But, it could be difficult to reach at the diagnosis in a particular case.

Different metals in the implants, different manufacturing methods, small numbers of patients in the studies, and difficulty in achieving adequate diagnosis add to the confusion.

Moreover, the clinical spectrum overlaps with more frequent causes of allergy and the diagnosis in question can be reached at only by exclusion further adds to the difficulties.

Once the more common causes of implant failure have been excluded [Infection, non-union, aseptic loosening, other inflammatory conditions, mechanical failure of the implant, and malalignment issues] the possibility of allergic reaction to the metal must be considered, evaluated, and if present, managed.

Screw Pull Out and Nonunion of Fracture Humerus — Screw Pull Out and Nonunion in Fracture Humerus

Metal Sensitivity and Implant Failure

In metal sensitivity, patients report hypersensitivity reactions to metals found in costume jewelry, belt buckles, or watches. The most common metal sensitivity in humans is against nickel. The others are beryllium, cobalt, chromium, tantalum, titanium, and vanadium.

The overall prevalence is estimated to be between 10% and 15%, higher in women than in men.

In contrast to cutaneous exposure to metals in the day to day life, metallic orthopedic implants are inserted deep but these metals can sensitize the body and provoke an immune reaction.

It has been found that circulating metal ions increase following joint replacement, especially in patients who have experienced implant loosening and is attributed to the continuous release of metal ions into the tissue surrounding the implant. This release occurs as a result of the corrosive process.

It is theorized that the accumulation of metal ions may trigger a localized inflammatory response that can lead to implant failure.

This proposed etiology is controversial though.

Metal hypersensitivity in patients with a failed implant is approximately six times more common than in the general population, and three times higher than in all patients with a metallic implant.

It is not known, however, whether this hypersensitivity is the cause or the result of implant failure, or whether separate autoimmune mechanisms may be responsible

Pathophysiology of Immune reaction of Implant

The hypersensitivity reaction is typically in an immune response mounted against metallic particles that are released as a result of implant wear or corrosion [it was seen more in metal on metal prostheses].

Loose metallic degradation products are known as haptens. These can complex with proteins and become capable of acting as antigens for circulating lymphocytes and induce an immediate humoral hypersensitivity response (type I, II, and III hypersensitivity reactions).

More commonly, these induce a cell-mediated delayed-type (type IV) hypersensitivity response via the activation of CD4+ T_H1 lymphocytes in the peripheral lymphoid tissues which release. pro-inflammatory cytokines (i.e., TNF-?, IFN-?, IL-1, and IL-2). These cytokines recruit macrophages to the site of the implant.

Significant levels of metal ions have been found in the periprosthetic tissues, the liver, spleen, lymph nodes, and urine/serum of hip arthroplasty patients. This shows that it is not just a local phenomenon.

As noted before, the hypersensitivity reaction can be to non-metallic components of the implant as well [even when metal hypersensitivity is not present], including allergens in the bone cement such as acrylates, benzoyl peroxide, N, N-dimethyl-p-toluidine, and gentamicin.

Another theory suggests that aseptic joint loosening may involve the proliferation of osteoclasts on metals such as titanium and vanadium and their subsequent degradation, uptake, and release of the metals from the device. This accounts for the high serum levels of metal in the systemic circulation and would serve as a potential mechanism for implant loosening.

This also induces a hypersensitivity reaction that exacerbates the loosening process.

Another proposed mechanism involves the haptenogenic stimulation of toll-like receptors in the periprosthetic tissue.

Still, others maintain implant loosening is primarily the result of a cytotoxic process in response to prolonged wear on the joint.

The nature of the implant alloy and the local exposure of the implant are important.
For example, implant-grade 316L (low carbon) stainless steel releases far less nickel than low-grade stainless steel suture.

Implant properties may alter the amount of surface area available for metal ion release.

Plasma-spray coatings and grouting agents decrease ion release from the implant. Roughened, grit-blasted or grooved surfaces increase the surface area available for ion release from and thereby increase the local levels of dissolved metal.

Clinical Presentation

The patients may present with symptoms suggestive of non-union and hardware failure, including pain and motion at the fracture

Patients with joint replacements have symptoms of loosening, including pain and instability.

Local signs may be normal or very subtle. Sometimes, warmth, erythema, and swelling over the implant may be present [as in infection], though systemic complaints (eg, fever) are unlikely.

Metal hypersensitivity may also present as a skin rash at the site of the implant. The manifestations are usually subtle.

In the usual course of true postimplantation metal hypersensitivity, the symptoms develop over months to years. In the case of fracture fixation, this may be long after the union renders the device dispensable.

In multipart devices, like prosthetic joints may be associated with periods of increased activity

There is also evidence that metal sensitivity may play a role in causing the conditions of chronic fatigue syndrome, fibromyalgia, and autoimmune/inflammatory syndrome induced by adjuvants (ASIA).

Differential Diagnosis

Infection should be ruled out.

Osteolysis due to implant loosening is always in the differential diagnosis.

The mechanism of osteolysis is primarily a local reaction to particulate debris, which leads to a cascade of cellular reactions that eventually lead to increased osteoclastic activity around the prosthesis. Osteolysis is a reaction to local irritation, not an immune hypersensitivity response.

Diagnostic Workup

No workup is required in asymptomatic patients with a stable implant. The purpose of the workup is to confirm hypersensitivity to be a cause of implant failure.

In most of the fracture fixations, the hypersensitivity or implant loosening, if presents usually seen after a long time after union.

So the workup is required in cases of implant failure with non-union and prosthetic loosening.

It is important also to rule out non-allergic causes of implant failure which include aseptic osteolysis, infection, recurrent dislocation, and fracture.

Blood Tests

Routine blood tests may show inflammatory mediators (eg, platelet count, C-reactive protein [CRP] level, and erythrocyte sedimentation rate [ESR]) are normal or mildly elevated.

Serum Levels of Metal

Concentrations of metal ions increase due to corrosion of the implant. These concentrations increase in loose implants.

Monitoring chromium and cobalt concentrations [every 6-12 months] have been suggested for patients with painful metal-on-metal hip replacements

The reference range for blood levels of cobalt and chromium are not defined but in the unexposed population, normal ranges are below 10 nmol/L and below 5 nmol/L, respectively.

They are in the range of 30 and 45 nmol/L, respectively, in unilateral well-functioning hip prostheses but increase to 6550 and 3400 nmol/L in failed prostheses.

Aspiration/Swabs

The peoperative aspiration for cultures, to rule out infection. Tissue culture and swabs from the affected area would help to rule out infection as the cause but false positives and false negatives are common.

Biopsy

Biopsy of the synovial membrane at is the most accurate method for differentiating between infection and hypersensitivity reaction to the implant.

An arthroscopic biopsy with an intraoperative frozen section of the periprosthetic membrane is ideal for diagnosis.

There is an appearance a diffuse collection of perivascular lymphocytes, plasma cells, localized bleeding, necrosis, fibrin exudation, and presence of macrophages with drop-like inclusions

Imaging

X-rays may show

Radiolucencies around the hardware
Screw migration
Change in position of the implant
Cystic changes may be seen. [as seen in osteolysis]

Computed tomography (CT) is not especially helpful.

Magnetic resonance imaging may help to evaluate the status of the implant. Ultrasonography can also detect fluid but is nonspecific.

Tests for Hypersensitivity

Skin Patch Test

Skin patch testing has for metal hypersensitivity is cost-effective but the result of test needs to be considered in the context of a patient’s medical history and physical findings.

Many patients with implanted metal hardware have a positive skin test for those but are asymptomatic.

Patients who have a clear history of contact dermatitis to metal should be evaluated by patch testing prior to device implantation. But a positive patch test alone should not be used to justify the removal of the device. That decision to explant a device should be made on the basis of clinical factors and a risk-benefit analysis.

Patch testing in patients with a history of metal allergy helps to choose a less immunogenic device for implantation.

No causal relationship can be made between patch test reactivity and implant performance.

Lymphocyte transformation test

Some authors consider the lymphocyte transformation test to be the most reliable test.

The test involves measuring the proliferative response of T lymphocytes upon 7-day incubation with and without the addition of metal antigen.

Lymphocyte transformation test is a helpful test in doubtful or questionable cases.. LTT more directly tests the immune components responsible for the hypersensitivity reaction in the periprosthetic tissue than the patch test

Lymphocyte transformation test has yet to earn widespread adoption among providers evaluating cases of suspected metal yet to be used widespreadly.

It is also technically sophisticated and expensive.

Lymphocyte transformation test is still not widely available, is not well standardized and some authors recommend against its routine use.

Lymphokine Migration Inhibition Factor Test

This test selectively detects lymphokine migration inhibition factor, which, when present, indicate an active immune response and metal sensitivity.

[Lymphokine migration inhibition factor acts to prevent lymphocytes from leaving a site where foreign antigens are present.]

The test is performed by isolating the lymphocytes and mixing with solutions of specific metal ions, such as nickel, chromium, cobalt, or titanium

The test result is considered positive if the lymphocytes stay in the metal ion solution, indicating a cellular reaction to the metal dissolved in that solution. (No migration means positive test)

The test result is negative if the lymphocytes migrate away from the particular metal ion solution [This indicates that lymphocytes are not reacting to the dissolved metal.]

The lymphokine MIF is considered as the most useful clinical test for diagnosis of hypersensitivity reaction to orthopedic implants.

Cement wear particles are immunologically inert and have specifically been found not to cause a lymphocyte response in vitro. Thus, the lymphokine MIF result should be negative in osteolysis.

Other Tests

Luminex cytokine assays may more accurately reveal the qualitative and quantitive involvement of different cell types. Increased cytokine levels are found in patients with aseptic loosening.

Phase-contrast and laser scan confocal microscopy (LSCM) is another method of quantifying the number of positive cells involved in the immune reaction.

Treatment

There is no medical treatment is available. However, in patients where surgery is not to be done, a 21-day course of topical corticosteroids may sometimes control symptoms. Analgesics including nonsteroidal anti-inflammatory drugs may control the symptoms.

Options for surgical treatment are

Revision Surgery

This is considered in joint replacement prosthesis or fracture implant that is still necessary for fracture stability.

An implant with titanium alloy or zirconium coating may be successful. Ceramic implants are chosen over the metal on metal implants. Use of implants with polytetrafluoroethylene-coated bearing surfaces is currently being investigated

Removal

For implant that is no longer necessary – Removal

Surgical removal of the culprit metal in these cases results in a clearing of the hypersensitivity reaction.

Prevention

In selected patients with known metal hypersensitivity, alternative prostheses or fracture fixation implants during preoperative planning may be considered for prevention of hypersensitivity.

However, routine preoperative screening in patients with no symptoms of metal hypersensitivity.

Testing is indicated in patients with known hypersensitivity reactions though there is no agreement on which specific patients require testing

Patients with known nickel allergy who, for example, may best be treated with titanium implants when such devices are available either in primary or revision surgery.

Before routine total hip or knee replacement, in patients suspected of having metal allergies, alternative prostheses may also be indicated, including ceramic implants, implants composed of different alloys, and coated implants.

References

Deutman R, Mulder TJ, Brian R, Nater JP. Metal sensitivity before and after total hip arthroplasty. J Bone Joint Surg Am. 1977 Oct. 59(7):862-5.
Goldring SR, Clark CR, Wright TM. The problem in total joint arthroplasty: aseptic loosening. J Bone Joint Surg Am. 1993 Jun. 75(6):799-801. .
Merritt K, Brown SA. Metal sensitivity reactions to orthopedic implants. Int J Dermatol. 1981 Mar. 20(2):89-94.
Lachiewicz PF, Watters TS, Jacobs JJ. Metal Hypersensitivity and Total Knee Arthroplasty. J Am Acad Orthop Surg. 2016 Feb. 24 (2):106-12.
Wawrzynski J, Gil JA, Goodman AD, Waryasz GR. Hypersensitivity to Orthopedic Implants: A Review of the Literature. Rheumatol Ther. 2017 Jun. 4 (1):45-56.
Swiontkowski MF, Agel J, Schwappach J, et al. Cutaneous metal sensitivity in patients with orthopaedic injuries. J Orthop Trauma. 2001 Feb. 15(2):86-9.
Donati ME, Savarino L, Granchi D, et al. The effects of metal corrosion debris on immune system cells. Chir Organi Mov. 1998 Oct-Dec. 83(4):387-93
Lützner J, Hartmann A, Dinnebier G, Spornraft-Ragaller P, Hamann C, Kirschner S. Metal hypersensitivity and metal ion levels in patients with coated or uncoated total knee arthroplasty: a randomised controlled study. Int Orthop. 2013 Oct. 37 (10):1925-31.

Neurogenic Claudication – Risks, Pathophysiology and Treatment

By Arun Pal Singh

Neurogenic claudication, also called pseudoclaudication, is a common symptom of lumbar spinal stenosis due to causing impingement or inflammation of the spinal nerves

Claudication refers to an impairment in walking or pain, discomfort, numbness, or tiredness in the legs that occurs during walking or standing and is relieved by rest.

The word claudication comes from the Latin claudicare meaning ‘to limp’. Thus, it is a form of claudication due to neurogenic causes.

The feeling is typically described as a painful cramping or weakness or heaviness in the legs after a certain distance has been walked [few hundred meters or even less in severe cases].

Typically the distance that a patient may walk without symptoms of claudication gets reduced over the time.

Claudication is most commonly is due to vascular causes and that is what the word “claudication” refers mostly to. To differentiate it from the vascular claudication, the term neurogenic is used along with claudication.

Risk Factors for Neurogenic Claudication

Neurogenic claudication is usually caused by spinal stenosis (narrowing of the spinal canal) in the lumbar spine (lower back). The narrowing of the spinal canal is generally degenerative changes, disc herniations.

The risk factors for narrowing of spinal canal [spinal stenosis] and thus neurogenic claudication are-

Age

It is something which we cannot avoid. As we grow older, arthritic changes [bone spurs or osteophytes] and degenerative disc disease [disc buldges] occur leading to a narrowing of the canal.

Obesity

A greater weight puts a greater load on the spine and hence increases the degenerative changes

Previous Spinal Deformities

Previous trauma or congenital abnormalities may lead to a reduction of canal space and hence neurogenic claudication. Many arthropathies or calcium deposition diseases can contribute to the reduction of space.

[ Read more on spinal stenosis ]

The pain is usually worse when standing and can often be temporarily relieved by sitting down or flexing forward.

Pathophysiology of Neurogenic Claudication

In the setting of decreased canal space, the symptoms of spinal stenosis become prominent when a further reduction of the space leads to compression of the neural structures. Erect position leads to the extension of the spine causing overlapping of laminar edges of adjacent vertebral bodies, with resultant relaxation and inward buckling of the ligamental flavum. There is also the movement of the superior facets in the anterior direction.

The claudication occurs because of increased metabolic demands of compressed nerve roots because of the ischemia resulted from compression [Oxygen demands of the spinal nerve roots may exceed the available blood flow].

Pain is relieved when the patient flexes the spine leaning forward, stooping, sitting] because flexion of the canal increases canal size by stretching the protruding ligamentum flavum, reduction of the overriding laminae and facets, and enlargement of the foramina.

This relieves the pressure on the exiting nerve roots and, thus, decreases the pain.

Clinical Presentation

Neurogenic claudication may present in one or both legs. It usually presents as some combination of discomfort, pain, numbness and weakness in the calves, buttocks, and/or thighs.

Patients are typically in their 50s and report intermittent, crampy, diffuse radiating thigh or leg pain with associated paresthesias.

It is often precipitated by walking and prolonged standing. The pain is classically relieved by a change in position or flexion of the waist.

The patients typically have a lesser disability in climbing steps, pushing carts and cycling where the lumbar spine is flexed and the vertebral foramen widens.

Downhill ambulation worsens the pain as lumbar spine is kept in extension.

[Lumbar spinal canal and lateral recess cross-sectional area increases with spinal flexion and decreases with extension.]

Patients may compensate for symptoms by flexing forward, slowing their gait, leaning onto objects (eg, over a shopping cart) and limiting the distance that a patient could walk.

Differentiation Between Vascular and Neurogenic Claudication

Distinguishing between neurogenic and vascular claudication is important because the treatments, as well as the implications, are quite different.

Vascular claudication is a manifestation of peripheral vascular disease and arteriosclerosis. Other vessels, including the coronary, vertebral, and carotid, are also often affected.

In some patients, neurogenic and vascular claudication may occur together and it is important to identify them both

Vascular claudication may be accompanied by changes in skin color, turgor, and temperature. The distal lower extremity pulses or arterial bruits may be absent.

Classic five Ps of vascular claudication are

Pulselessness
Paralysis
Paresthesia
Pallor
Pain

A patient with vascular claudication also complains of cramping pain in the buttocks, thighs, which stops quickly with rest, even in the standing position.

But the pain of neurogenic claudication is not relieved by standing alone but with postures that cause flexion of the spine. Thus pain in neurogenic claudication may continue for as long as you remain standing. Bending forward or sitting down usually relieves the pain, but even then it does not stop as quickly as pain resulting from insufficient blood flow.

If the patient is able to differentiate, vascular claudication pain starts in their feet or calves and radiates up toward their back and buttock.

Neurogenic claudication often starts in their back and buttock and radiates down toward their feet.

Neurogenic pain is increased with walking, walking downhill/downstairs, and extension of the back whereas relieved with walking flexed with a cart, and sitting/lying.

Vascular claudication increases with walking, walking both up or downhill, and both with extension and flexion of the back. It is not relieved with walking flexed with a cart.

Diagnosis and Treatment of Neurogenic Claudication

Neurogenic claudication is a symptom in itself and leads to the disease causing it. The most common cause is spinal stenosis.

The workup includes clinical examination and imaging for spinal stenosis.

Treatment of neurogenic claudication involves the treatment of the condition causing the narrowing of the canal. the narrowed space generally needs to be decompressed

Read more on spinal stenosis for different treatment approaches.

Prevention of Neurogenic Claudication

While we cannot absolutely stop this from happening, maintaining a healthy lifestyle helps.

There are various lifestyle choices that one could choose and follow to stay with the healthy spine and reduce the pace of stenosis.

These include

Maintain healthy weight
Flexibility exercises
Quitting smoking
- Smoking reduces oxygen availability to the disc and surrounding tissues.
Maintaining good posture

Allen Test – Details and Uses

By Arun Pal Singh

Allen test or the modified Allen test is a sign that is used to determine the flow of the blood to the hands. The Allen Test was first described by Edgar Van Nuys Allen in 1929.

In 1952, Irving S Wright suggested a modification of the test which has replaced the original test universally.

The alternative method is often referred to as the modified Allen’s test or modified Allen test. As this is the test now mostly used, the term Allen test may suggest this only.

The Allen test is used to assess the arterial blood flow to the hand and determine the patency of the radial or ulnar artery.

It is reported to have a sensitivity of 73% and a specificity of 97%.

Original Test

The original test as proposed by Allen is performed as follows

The patient is asked to clench both fists tightly for 1 minute at the same time.
Pressure is applied over both radial arteries simultaneously so as to occlude them.
The patient then opens the fingers of both hands rapidly, and the examiner compares the color of both. The initial pallor should be replaced quickly by rubor [redness]
The test may be repeated, this time occluding the ulnar arteries.

The test looks for abnormal circulation. If color returns quickly as described above, Allen’s test is considered to demonstrate normal circulation. If the pallor persists for some time after the patient opens their fingers, this suggests a degree of occlusion of the uncompressed artery.

Modified Allen Test

Instruct the patient to clench his or her fist; if the patient is unable to do this, close the person’s hand tightly.
Using your fingers, apply occlusive pressure to both the ulnar and radial arteries, to obstruct blood flow to the hand.
While applying occlusive pressure to both arteries, have the patient relax his or her hand, and check whether the palm and fingers have blanched. If this is not the case, you have not completely occluded the arteries with your fingers.

Release the occlusive pressure on the ulnar artery only to determine whether the modified Allen test is positive or negative.

Negative modified Allen test

If the hand flushes within 5-15 seconds it indicates that the ulnar artery has good blood flow. This normal flushing of the hand is considered to be a positive test.

Positive modified Allen test

If the hand does not flush within 5-15 seconds, it indicates that ulnar circulation is inadequate or nonexistent. In this situation, the radial artery supplying arterial blood to that hand should not be punctured.

Basis of Test

The hand has a complex and rich vascular network, which is mostly supplied by the radial and ulnar arteries.

The radial artery runs between the brachioradialis and flexor carpi radialis muscles and splits into a superficial branch to contribute to the superficial palmar arch and the other branch crosses dorsally deep to the tendons of the anatomic snuffbox to form the deep palmar arch.

The ulnar artery lies under flexor carpi ulnaris. At the wrist, it enters the Guyon’s canal, where it splits into a deep palmar branch and a superficial palmar branch. The superficial palmar branch forms the superficial palmar arch, while the deep branch contributes to the deep palmar arch.

Thus the hand is supplied by two arteries. If the blood supply from one of the arteries is cut off, the other artery can supply adequate blood to the hand.

While most of the people have this dual arterial supply, a minority of people lack this.

The test aims to establish ts fact especially before an intervention involving the arteries. This could be a simple sampling for arterial blood gas or an arm surgery. [See Uses]

Video of Allen Test

Following video explains well the performance of Allen test.

Uses of Allen Test

Arterial Blood Gas Analysis

Arterial blood gas analysis requires a sample from an arterial blood. The radial artery is one of the common arteries used for this purpose. An uncommon complication of radial arterial blood sampling/cannulation is disruption of the artery (obstruction by a clot), placing the hand at risk of ischemia where the people lack dual blood supply.

Using the Allen test before sampling may help to screen this issue.

People who have a single blood supply in one hand often have a dual supply in the other, allowing the practitioner to take blood from the side with dual supply.

Heart Bypass Surgery

The radial artery is occasionally used as a conduit for bypass surgery as its patency lasts longer in comparison to the saphenous veins. Before removal of radial artery removal, Allen test is performed to assess the suitability of the radial artery to be used as a conduit.

A result of fewer than 3 seconds is considered as good and suitable. A result of between 3–5 seconds is equivocal.

The artery is not considered for grafting if the result is longer than 5 seconds.

Wrist Surgery

Before operating the wrist it is important to ensure if both arteries supply the hand especially in situations where an artery has a chance of getting damaged.

Diagnostic Tool

Allen test can be used as a diagnostic tool for a number of disorders, such as any diseases with reduced vascularization in the arm, i.e. thoracic outlet syndrome or compartment syndrome.

Genu Recurvatum or Knee Hyperextension

By Arun Pal Singh

Genu recurvatum is a deformity in the knee where the knee angulates backwards because of hyperextension occurs in the tibiofemoral joint [the knee goes further into extension beyond the neutral]

Genu recurvatum is also called knee hyperextension and back knee.

Depending upon hyperextension, the recurvatum could be mild, moderate or severe.

The normal range of motion of the knee joint is from 0 to 135 degrees in an adult. Genu recurvatum is operationally defined as knee extension greater than 5°[Also labeled as -5 and implies 5 degrees beyond zero.]

Genu recurvatum may cause knee pain, an extension pattern gait and have poor proprioceptive control of terminal knee extension.

The condition can be congenital or acquired.

Congenital genu recurvatum is apparent at birth. It can occur as an isolated entity or can be associated with other musculoskeletal anomalies, or part of a syndrome. [see the list of causes]

Isolated congenital genu recurvatum is thought to be associated with include breech positioning and oligohydramnios.

Congenital dislocation of the knee is the major cause of pathological genu recurvatum and some authors consider them entities in the continuum.

Genu Recurvatum in a child, Image Credit- JOCR

Factors Causing Genu Recurvatum

The following factors may be involved in causing this deformity

Laxity of the knee ligaments
Muscle Weakness

- Biceps femoris muscle
- Hip extensor muscles
- Gastrocnemius muscle
- Popliteus muscle weakness

Malalignment of the tibia and femur as in malunion
Instability of the knee joint due to ligaments and joint capsule injuries
Deficit in joint proprioception
Lower limb length discrepancy

Conditions Associated with knee recurvatum

Spastic lesions
Lower motor neuron lesions like Polio
Congenital genu recurvatum
Cerebral palsy
Multiple sclerosis
Muscular dystrophy
Plantar flexion contracture
Arthrogryposis multiplex congenita
Congenital knee dislocation
Connective tissue disorders (e.g. Ehlers-Danlos disease, Larsen syndrome)
Connective tissue disorders
- - Marfan syndrome
  - Ehlers-Danlos syndrome
  - Benign hypermobile joint syndrome
  - Osteogenesis imperfecta disease
Proximal growth plate injury
Osgood-Schlatter disease
osteomyelitis)
Ligament injury as in sports
- Cruciate ligament injury
- Posterolateral corner injury
- Superficial medial collateral knee
- Posterior oblique ligament.

Clinical Presentation

Knee recurvatum may be asymptomatic or may cause

Knee giving way into hyperextension
Difficulty with endurance activities
Pinching in the front of the knee

An assessment of a patient for ligament hypermobility should be made.

Imaging

X-rays rule out bony injuries or subluxation.

Assessment of knee alignment must be performed via a long leg x-ray. Their posterior tibial slope must also be calculated on a lateral knee x-ray.

Patients who have a decreased posterior tibial slope tend to have more problems with knee hyperextension.

Treatment for Genu Recurvatum

Positional congenital knee recurvatum gets resolved spontaneously.

For other types of congenital recurvatum treatment may include watchful waiting, flexion exercises, splinting, casting, or surgery. The treatment is guided by severity.

Treatment of acquired genu recurvatum would depend on the cause. Not all causes would be curable though and treatment may aim at functional improvement.

For example, ligament reconstruction should be done in cases of ligament injury and osteotomy may improve the knee in case of malalignment.

Proximal tibial osteotomy in cases where the tibial slope is increased may be done.

Patellar Instability – Causes, Presentation and Treatment

By Arun Pal Singh

Patellar instability or Patellofemoral instability is a frequent cause of symptoms of anterior knee pain and episodes of mechanical instability.

It is also called patellar subluxation syndrome.

There is a difference between symptoms of instability and patellar dislocation, though the former may cause the latter to happen.

The term can denote a sign on physical examination or can be a symptom when the patient gets a feeling of the knee giving way.[The patella slips out of the trochlear groove.]

As instability is a subjective symptom, the objective elements included are patellar maltracking, subluxation or dislocation.

Patellar instability occurs due to morphologic abnormalities in the patellofemoral joint where the patella is prone to recurrent lateral dislocation.

It can develop, also, after traumatic dislocation of the patella in which the medial stabilizers are stretched or ruptured, which eventually can result in recurrent dislocations of the patella.

Chronic patellar instability of the patellofemoral joint and recurrent dislocation may lead to progressive cartilage damage and severe arthritis.

Most patients with patellar instability are young and active individuals [second decade].

Redislocation risk is reported to be highest amongst girls aged 10-17 years.

Prevalence is 6-77 per 100,000 population.

Anatomy and Biomechanics of Patellar Instability

The patella is the largest sesamoid bone and is located between the quadriceps and patellar tendon. It serves as a biomechanical lever, magnifying the force exerted by the quadriceps on knee extension.

It also functions to centralize the divergent forces of the quadriceps muscle and thus transmitting the tension around the femur to the patellar tendon.

Patellofemoral joint stability is maintained by static as well as dynamic stabilizers.

Static Stabilizers

[read anatomy of Patella]

Retinacular Structures

These are medial and lateral retinacular structures. They are most effective within the range of 20° flexion and full extension. During this, the patellofemoral joint is most vulnerable as other stabilizing forces are not active yet.

Medial structures

These include three ligaments

Patellofemoral ligament
Patellomeniscal ligament
Patellotibial ligament

Medial patellofemoral ligament is the most important of all. It is a continuation of the deep retinacular surface of the vastus medialis obliquus. It runs transversely between the proximal half of the medial border of the patella to the femur between the medial epicondyle and the adductor tubercle.

Patellofemoral joint stabilizers — Patellofemoral joint Stabilizers, Image credit: Physiopedia

Lateral Structures

The superficial layer consists anteriorly of the fibrous expansion of the vastus lateralis and posteriorly it is formed by superficial oblique retinaculum further posteriorly.

Deep layer Consists of following ligaments

Epicondylopatellar ligament [also called lateral patellofemoral ligament]
Deep transverse retinaculum
Patellotibial band

The epicondylopatellar ligament is indirectly attached to femur via the proximal and distal attachments of the iliotibial band. Thus tightness of iliotibial band would influence the lateral stability force inferred

Trochlear geometry

Patella enters trochlea at 20-30 degrees of flexion, after which the bony anatomy of trochlea offers inherent stability.

Trochlea is concave to accommodate convex patellofemoral joint. [Normal sulcus angle of 138?±?6° on Merchant view].

The lateral femoral trochlea extends further anteriorly than the medial side, providing a buttress to lateral patellar subluxation.

Moreover, the lateral ridge of the trochlea extends further proximally than it does on the medial side, thus engaging the patella in early knee flexion and deflecting it medially. [Thus providing a lateral check.]

Decrease in trochlea depth or trochlear dysplasia is an important risk factor for recurrent patellar dislocation

Patella geometry

Congruity between the patella and the trochlea provides some degree of constraint to the patellofemoral joint. On knee bending, the initial contact area is the distal and lateral patella facet initially and with further flexion, the contact area on the patella articular surface moves more proximally until in deep flexion when medial facet makes contact. The shape of the patella and more importantly the cartilage may impact the stability..

Patella Height

With patella alta, engagement of patella into the trochlear does not occur in the early phase of knee flexion, thus potentiating instability at the patellofemoral joint.

Limb Alignment

Q angle is an important determinant of limb alignment. It is defined as [8 to 10° and in females, it is 15 ± 5°].

An increase in the “Q” angle results in an increased valgus vector to the patella femoral joint. Genu valgum, increased femoral anteversion, external tibial torsion and/or a lateralized tibial tuberosity can all ultimately affect patella tracking.

Dynamic Stabilisers

Vastus medius oblique and vastus lateralis muscles are the important dynamic stabilizers.

The vastus medius obliquus overlies and merges with the medial patellofemoral ligaments to provide active and passive stabilization of the patella.

Risk Factors for Patellar Instability

On MRI, the primary contributing findings to patellar instability are trochlear dysplasia (85% of abnormal cases), quadriceps dysplasia/patellar tilt ( 83% of abnormal cases), patella alta (present in 24% of abnormal cases) and tibial tuberosity–trochlear groove distance (increased in 56% of abnormal cases).

The following are the risk factors for patellar instability –

Trochlear dysplasia – trochlear joint surface is flattened
Patella alta
Lateralization of the tibial tuberosity
- Femorotibial malrotation
- Genu recurvatum
Increased femoral anteversion
Medial Retinaculum injury
Ligamentous laxity
Abnormal muscle tone
Medial patellofemoral ligament insufficiency
Increased Q-angle
- Genu valgum
Inadequate vastus medialis obliquus

Clinical Features

Patients may complain of anterior knee pain and episodes of mechanical instability. The patient may complain of buckling of the knee under certain circumstances.

The pain is aggravated activities such as stair climbing/getting down, running, hopping and jumping, and changing direction.

Patellar dislocation may take place as a direct traumatic event in some cases.

Another thing that may occur is patellar subluxation. Subluxation or lateral translation will involve the transient lateral movement of the patella.

In general, it is early in knee flexion such that the patient will experience a feeling of pain or instability.

Joint stiffness and creaking or cracking sounds during movement may be reported.

Joint swelling which persists or occurs recurrently may be reported.

A physical examination would vary with the presentation.

In an acute dislocation, deformity and swelling are assessed and the patient is taken for a reduction on an emergency basis.

Palpation of the patella may reveal a palpable defect at the medial patellar margin and tenderness along the course or at the insertion of the medial patellofemoral ligament. Muscle atrophy may be seen in vastus medialis obliquus if there is a disruption of the muscle.

There would be of hypermobility of patella in the lateral and medial directions

In chronic cases, apart from knee inspection and palpation, physical examination includes assessment of

Lower limb alignment in coronal, sagittal and axial planes
Any evidence of joint hyper laxity
Q angle
Special Tests

Special Tests

Patellar glide test

In this test, the patella is forced to glide by the examiner by pushing it first medially and then laterally. The test is done in 30 ° knee flexion.

The normal movement is less than two quadrants in a medial and lateral direction.

A medial/lateral displacement of the patella greater than or equal to 3 quadrants indicates incompetent lateral/medial restraints.

Less than one quadrant movement indicates tightness of the structures.

Lateral patellar instability is more frequent than medial instability.

Apprehension test

The examiner holds the relaxed knee in 30 ° of flexion and manually subluxes the patella laterally. When the test is positive, the patient complains of pain and anxiety, resisting any further lateral motion of the patella [defensive contraction of muscles]

This may be so positive that the patient pulls the leg back when the therapist approaches the knee with his hand, preventing so any contact, or the patient grabs the therapist’s arm.

The test carries almost 100% sensitivity.

Patellar-gravel test or Clarke Test

The patient is positioned in a supine or sitting position with the involved knee extended. The examiner places the web space of his hand just superior to the patella while applying pressure. The patient is instructed to gently and gradually contract the quadriceps muscle.

Another variation of the test involves pushing down on the patella directly.

A positive sign on this test is a pain in the patellofemoral joint.

J-Sign

This sign checks for lateral patellar tracking and is not very specific for patellar instability. The patient sits with knee bent 45°. Examiner instructs the patient to straighten knee while observing patellar tracking

If the examiner observes patellar deviation laterally [makes the shape of the letter “J”]

It probably shows dysfunction of patellar tracking dysfunction, vastus medialis oblique deficiency or increased Q-angle.

Imaging

Standard x-rays include anteroposterior and lateral views of the knee.

X-rays may reveal osteochondral fractures, osteoarthritis of the tibiofemoral joint and loose bodies.

Lateral view x-rays can tell about patellar height and calculation of different indices.

Trochlear depth can be known from lateral views as well.

Crossing sign is present in trochlear dysplasia. The “crossing sign” represents abnormally elevated floor of the trochlear groove rising above the top of the wall of one of the femoral condyles, assessed on lateral radiographs. The base of the trochlear crosses the line of the lateral femoral condyle.

“Double contour sign” is a double line at the anterior aspect of condyles, and seen if medial condyle is hypoplastic.

Skyline view can show decreased trochlear depth and large sulcus angle (>144º).

Sulcus angle defined as the angle formed between lines joining the highest points of the bony medial and lateral condyles and the lowest bony point of the intercondylar sulcus.

Congruence angle of Merchant

Bisect the sulcus angle to establish the zero reference line.
Identify the lowest point on the articular ridge of the patella
Draw a line from the vertex of sulcus angle to the lowest point on the ridge.
Angle between this line and the reference line is the angle of congruence
If an angle is medial to a reference line, it carries a negative value
If lateral it carries a positive value
Normal angle is defined as < – 16 deg;

CT

Computed tomography is able to provide a three-dimensional view of the patellofemoral joint.

CT scans are reported to be more accurate and sensitive in detecting abnormal tracking, tilt, and subluxation.

They are also helpful in the assessment of lower limb alignment, femoral anteversion, and lateralization of the tibial tubercle

A tibial tubercle to trochlear groove distance of greater than 20 mm [patellar translation] is virtually always associated with patella instability.

MRI

MRI is considered as the gold standard investigation. It provides reliable images of soft tissue and articular surface.

Measurements similar to those made with CT scans can be easily accomplished.

MRI can be helpful in demonstrating chondral defects, patellar and trochlear dysplasia, patellar tilt, tibial tubercle offset, patellar height, avulsion fragments, and the integrity of the retinacular or patellofemoral ligamentous structures.

Articular cartilage contour can be different from that of the underlying bony contour, therefore MRI a useful adjunct especially when planning surgery.

Associated radiological findings can be in patellar instability are

knee joint effusion
Medial patellofemoral ligament tear
Bone contusion in patella and lateral condyle
Osteochondral defects in patella
Edema/hemorrhage of vastus medialis
Intra-articular loose bodies
Internal derangement of knee

Chronic patellar instability, if not treated, may lead to severe arthritis and chondromalacia patellae.

Treatment of Patellar instability

Conservative Treatment

For patellar instability, conservative treatment should be attempted first. Surgical intervention should be reserved until conservative measures have failed.

In the acute phase, includes anti-inflammatory analgesia, ice therapy, elevation and a period of immobilization. The treatment aims at reduction of inflammation and relief of pain.

Bracing and taping have been recommended but more evidence is required.

In acute dislocation of patella, immobilization for a period followed by physical therapy is chosen as treatment. The duration of immobilization may be up to six weeks.

In acute circumstances, indications for surgery include complicated dislocations with associated osteochondral fractures.

The physical therapy includes closed-chain exercises and passive mobilization followed by muscle strengthening exercises.

It is very important in the rehabilitation program to strengthen the quadriceps muscle and VMO.

Surgical Treatment

Surgery may address either bony or soft-tissue components, in a proximal or distal procedure

Lateral release

It was commonly performed in the past but most studies have shown disappointing mid and long-term results. Overzealous or inappropriate lateral release can lead to further medial patellar instability.

Lateral release should only be used as an adjunct to proximal or distal realignment procedures or medial retinacular repair.

Medial repair

Repair, imbrication (reefing) or plication of the medial retinacular structures are designed to strengthen the medial structures. These procedures can be performed in an open, arthroscopic or as an open-arthroscopic technique.

Thermal reefing has been also reported. Usually, the procedure is done in conjunction with a lateral release..

Medial Patellofemoral Reconstruction

MPFL reconstruction offers an appropriate treatment modality in a chronic situation.

This is a relatively newer interest. The construction of medial patellofemoral ligament can be done using grafts have from semitendinosus, gracilis, quadriceps tendon or adductor magnus.

Mesh-type artificial ligament has also been reported.

Bony realignment procedures

Tubercle Realignment Procedures

A common form of malalignment is a large Q angle or increased tibial tubercle to trochlear groove offset. Reducing the Q angle by medialising the tibial tubercle insertion has a role in patellar realignment surgery.

The Elmslie-Trillat procedure

It consists of

Lateral retinacular release
Medial capsule reefing
Medial transposition of the anterior tibial tubercle

This procedure is effective in resolving patellar instability but it is not as successful for patients whose main complaint is anterior knee pain. This may lead to overloading of the medial patellar articular causing patellofemoral arthritis.

Distalization of tibial tubercle

Distalisation in cases of patella alta with instability. Distalisation of the tibial tubercle during the procedure can inherently induce medialisation due to tibial torsion, and thus can result in over medialisation

Fulkerson Procedure

This entails medialisation of the tibial tubercle in order to correct the Q angle with anteriorisation of the tubercle. The anteromedialisation of the tibial tubercle elevates the distal pole of the patella, which in turn reduces contact on the distal patella during early knee flexion, thus potentially alleviating anterior knee pain symptoms and preventing arthritic progression.

Potential disadvantages of this procedure, however, include the more invasive nature of the operation, a larger osteotomy, more reports of tibial fracture, and a prolonged rehabilitation.

Trochleoplasty

In most cases, trochlea dysplasia is mild and well tolerated by patients.

This technique is indicated in severe dysplasia with a trochlear bump of greater than 6 mm, trochlear dome, abnormal patellar tracking and/or failed previous surgery.

The methods for deepening trochleoplasty include lateral facet elevating and sulcus deepening) among others. have been shown to prevent recurrent instability, but may cause ongoing pain due to damage of the articular cartilage, trochlear necrosis, arthrofibrosis and incongruence of the patella.

Patellar osteotomy

With a dysplastic patella, the possibility of conducting a longitudinal patella osteotomy exists. Lateral positioning of the patella can result in increases in patellar pressure. By performing a lateral osteotomy the medial facet can improve the medial contact of the facet in the trochlear groove and has been reported to have a good analgesic effect in the literature

It is rarely performed.

References

Dejour H, Walch G, Nove-Josserand L, Guier C. Factors of patellar instability; an anatomic radiographic study. Knee Surg Sports Traumatol Arthrosc. 1994;2:19–26. doi: 10.1007/BF01552649
Conlan T, Garth WPJ, Lemons JE. Evaluation of the medial soft-tissue restraints of the extensor mechanism of the knee. J Bone J Surg Am. 1993;75:682–693.
Grelsamer RP, Klein JR. The biomechanics of the patellofemoral joint. J Orthop Sports Phys Ther. 1998;28:286–298.
Tecklenburg K, Dejour D, Hoser C, Fink C. Bony and cartilaginous anatomy of the patellofemoral joint. Knee Surg Sports Traumatol Arthrosc. 2006;14:235–240.
Beaconsfield T, Pintore E, Maffuli N, Petri GJ. Radiological measurements in patellofemoral disorders. Clin Orthop Relat Res. 1994;308:18–28.
Stanciu C, Labelle HB, Morin B, Fassier F, Marton D. The value of computed tomography for the diagnosis of recurrent patellar subluxation in adolescents. Can J Surg. 1994;37(4):319–323.
Sillanpaa P, Mattila VM, Visuri T, Maenpaa H, Pihlajamaki H. Ligament reconstruction versus distal realignment for patellar dislocation. Clin Orthop Relat Res. 2008;466(6):1475–1484.
Arnbjornsson A, Egund N, Rydling O, Stockerup R, Ryd L. The natural history of recurrent dislocation of the patella: long-term results of conservative and operative treatment. J Bone J Surg Br 74(140–2)
Fulkerson JP, Becker GJ, Meaney JA, Miranda M, Folcik MA. Anteromedial tibial transfer without bone graft. Am J Sports Med. 1990;18:490–496.
Bollier M, Fulkerson JP. The role of trochlear dysplasia in patellofemoral instability. J Am Ac Orthop Surg. 2011;19(1):8–16.

Normal Alignment of Lower Limb – Axes and Orientation

By Arun Pal Singh

To understand the deformities of the lower limb, it is important to grasp and establish the parameters defining normal alignment. The normal alignment of lower limb is governed by the arrangement of the femur, tibia, hip, knee, and ankle.

To understand it better, the complex three-dimensional shapes of bones and joints can be simplified to basic line drawings in frontal, sagittal, or transverse anatomic planes.

axes of lower lib — Image credit: Current Revisions in Musculoskeletal Medicine

Anatomical and Mechanical Axes of Lower Limb

Each long bone has a mechanical and an anatomic axis. The mechanical axis of a bone is the straight line connecting the joint center points of the proximal and distal joints in the frontal or sagittal plane. Most of the mechanical axes are considered in the frontal plane.

The anatomic axis of a bone It is the line passing through the midpoint of the diaphysis.

Thus mechanical axis is always a straight line in both frontal or sagittal plane but the anatomic axis line may be straight in the frontal plane but curved in the sagittal plane, as in the femur.

As the mechanical axis is considered mostly in the frontal plane, we need to define only the frontal plane joint center points of the hip, knee, and ankle.

Midpoint of Joints

Hip Joint

For the hip, the joint center point is the center of the circular femoral head [ Can be identified with Mose circle or goniometer]

Knee Joint

Center of the knee joint can be found by [All methods almost approximate to the same point.]

Marking a point at the top of the femoral notch
Midpoint of the femoral condyles
Center of the tibial spines
Midpoint of the tibial condyles

Using the top of the femoral notch or tibial spines is the quickest method.

Ankle Joint

The ankle joint center point can be marked by

Mid-width of the talus
Mid-width of the tibia and fibula at the level of the plafond
Mid-width of the soft tissue outline

The mid-width of the talus or the plafond is the easiest to use.

Orientation of Joints and Line Denoting Them

A line that represents the orientation of a joint in a plane is called a joint orientation line. Different joints have different orientations.

Ankle

In the frontal plane

Across the flat subchondral line of the tibial plafond in either the distal tibial subchondral line
The subchondral line of the dome of the talus.

In the sagittal plane

From the distal tip of the posterior lip to the distal tip of the anterior lip of the tibia

Knee

The frontal plane

Across the flat or concave aspect of the subchondral line of the two tibial plateaus.
Tangential line to the most distal points on the convexity of the two femoral condyles.

In the sagittal plane

The proximal joint line of the tibia is drawn along the fiat subchondral line of the plateaus
The distal femoral articular shape is circular
- .The distal femoral joint orientation can be drawn as a straight line connecting the two points where the femoral condyles meet the metaphysis of the femur.
- In children, this can be drawn where the growth plate exits anteriorly and posteriorly.
- Blumensaat’s line [represents the intercondylar notch, can be used as the joint orientation line]

Hip

There are two lines and both show orientation in different directions

A line from the proximal tip of the greater trochanter to the center of the femoral head represents the hip joint orientation line of the hip joint in the frontal plane.
Alternatively, the mid-diaphyseal line of the femoral neck can represent the orientation of the hip joint. It uses the center of the femoral head as one point and the mid-diaphyseal width of the neck as the second point.

Angles

Angles are formed because the joint lines in the frontal and sagittal planes have a characteristic orientation to the mechanical and anatomic axes.

Joint Orientation Angles

The angle formed between the joint line and either the mechanical or anatomic axis is called the joint orientation angle. Prefix m or a signifies if the axis used is mechanical or anatomical.

The angle may be measured medial (M), lateral (L), anterior (A), or posterior (P) to the axis line.

The angle may refer to the proximal (P) or distal (D) joint orientation angle of a bone.

F stands for femur and T for Tibia.

Thus the mechanical lateral distal femoral angle or mLDFA is the lateral angle formed between the mechanical axis line of the femur and the knee joint line of the femur in the frontal plane.

aLDFA is the lateral angle formed between the anatomic axis of the femur and the knee joint line of the femur.

aPPTA is the posterior angle between the anatomic axis of the tibia and the joint line of the tibia in the sagittal plane.

[Frontal plane angles would be medial or lateral and sagittal plane angles would be anterior or posterior]

The prefixes a or m may be omitted in the following situations

Sagittal plane orientation angles usually refer to the anatomic axis because mechanical axis lines are rarely used in the sagittal plane
Because the mechanical and anatomic axes of the tibia are parallel and the angles would have the same value. Prefix m or a may not be
By convention lateral proximal femoral angle [LPFA] uses a mechanical axis and medial proximal femoral angle uses the anatomic axis, the prefixes may not be applied.

Thus prefixes are most important in distal femoral angles.

Hip

Neck-shaft angle (NSA). The normal NSA is 125°-131°.

Lateral Proximal Femoral Angle

A line from the tip of the greater trochanter to the center of the femoral head. It is also called the horizontal orientation angle for the proximal femur

Normal value 89.9± 5.2°.

Knee

The distal femoral joint line is in slight valgus and the tibia is in slight varus to the proximal tibial joint line. [about 3 degrees]

Anatomical Lateral distal femoral Angle – 79-83 degrees

normal mLDFA to be 87.5±2.5°

Medial proximal tibial angle is 85-90 degrees.

In the saggital plane, the posterior slope of the proximal tibia in the sagittal plane is 10.7± 1.8°.

Posterior proximal tibial angle – 80.4± 1.6° [slight difference is seen the angle when measured from medial or lateral tibial plateau].

Posterior distal femoral angle – 83.1±3.6°

Ankle Joint

Ankle joint is in slight valgus [up to 8° of valgus can be seen].

Lateral distal tibial angle is 88.6±3.8 degrees.

In saggital plane there is the anterior tilt of the distal tibia.

Joint Convergence Angles

The angle formed between joint orientation lines on opposite sides of the same joint is called the joint line convergence angle. In the knee and ankle joints, these lines are normally parallel.

Anatomic Axis – Joint Line Intersection Points

Anatomic Axis to Joint Center Distance or aAJCD

This denotes the distance between mechanical and anatomical axes at any given joint. This is calculated in the coronal or frontal plane.

The distance from point of intersection of anatomic axis lines with the joint line can be described relative to the center of the joint line or to one of its edges.

In the frontal plane, the distance on the joint line between the intersection with the anatomic axis line and the joint center point is called the anatomic axis to joint center distance (aJCD).

For hip, the anatomic axis passes through piriformis fossa and the distance between that point and center of the head of the femur gives us aJCD.

In the knee, both anatomic axes of femur and tibia pass appx through medial tibial spine and aJCD becomes the distance between this point and center of joint. For all practical purpose, the medial tibial spine is the reference point.

Normal aJCD for knee is about 10± 5 mm.

For the ankle, the value is 4±4 mm.

Anatomic Axis to Joint Edge distance (aJED)

This value is calculated in the sagittal plane.

aJED is the distance between the point of intersection of the anatomic axis line with the joint line and the anterior edge of the joint.

In distal end of the femur, the anatomical axis divides the joint in anterior one third and posterior two thirds.

Similarly, the tibia is divided into anterior one fifth and posterior four-fifths.

The ankle is divided into two equal halves.

Ratios

The anatomic axis: joint edge ratio (aJER) is the ratio between the aJED and the total width of the joint.

Thus

aJER = aJED/total width of joint

The normal value is 1/3 for the femur and 1/5 for the tibia. The value for the ankle is 1/2 [ Correlate with where axes intersect in lateral view]

Similarly, anatomic axis: joint center ratio (aJCR) is the ratio of the aJCD and the total width of the joint.

Mechanical Axis Deviation

Joint alignment and joint orientation are two considerations in the evaluation of the frontal plane of the lower extremity.

Alignment refers to the collinearity of the hip, knee, and ankle and orientation refer to the position of each articular surface in relation to he axes tibia and femur.

Normally anatomic tibiofemoral angle is 6° valgus.

For alignment and orientation standing AP radiographs of the entire lower extremity on a single film is done.

Mechanical axis passes from center of the femoral head to the center of the ankle and passes almost through center of knee [Although normal alignment is often depicted with the mechanical axis passing through the center of the knee, a line drawn from the center of the femoral head to the center of the ankle typically passes immediately medial to the center of the knee].

When the mechanical axis does not lie close to the center of the knee, it is called mechanical axis deviation.

Malalignment occurs when the center of the knee does not lie close to this line.

The distance between the mechanical axis line and the center of the knee in the frontal plane is the mechanical axis deviation.

It is described as either medial or lateral [also called varus or valgus respectively] malalignment respectively.

9.7±6.8 mm medial deviation is considered a normal variation.

References

https://www.hss.edu/images/newsletters/1uiowety.pdf [includes credit for mentioned images too]
Chao EY, Neluheni EV, Hsu RW, Paley D. Biomechanics of Orthop Clin North Am 1994, 25:379-386.
Hsu RW, Himeno S, Coventry MB, Chao EY. Normal axial alignment of the lower extremity and load-bearing distribution at the knee. Clin Orthop 1990, 255:215-227.
Moreland JR, Bassett LW, Hanker GJ Radiographic analysis of the axial alignment of the lower J Bone Joint Surg Am 1987,69:745-749.
Paley D, Tetsworth K Mechanical axis deviation of the lower limbs: Preoperative planning of uniapical angular deformities of the tibia or Clin Orthop 1992, 280:48-64.
Paley D, Chaudray M, Pirone AM, Lentz P, Kautz D Treatment of malunions and mal-nonunions of the femur and tibia by detailed preoperative planning and the Ilizarov techniques. . Clin North Am 1990, 21:667-691
Paley D, Herzenberg JE, Tetsworth K, McKie J, Bhave A. Deformity planning for frontal and sagittal plane corrective osteotomies. Orthop Clin North Am 1994, 25:425-465.