Monday, November 21, 2011

Diagnosis of knee instability

According to Rossi et al, for knee; clinicians should have own series of exams with whom he is more confident and on whom he relies on for diagnosis. Usually, three sets of series are used:

1. One for patello-femoral/extensor mechanism pathologies
2. Another for meniscal and chondral (articular) lesions
3. The other one for instability evaluation

Among the above said to assess the 3rd category is difficult to diagnose. Often the diagnosis becomes more difficult because there are more than one tissue involved.

Following are clues to diagnose them:

1. Anerior medial instability (AMI):

AMI occurs due to: ACL + MCL + medial meniscus injury.

Test series to diagnose it are: valgus stress, anterior drawer, Lachman tests

2. Anterior lateral instability (ALI):

ALI occurs due to: ACL + lateral capsule + lateral meniscus injury.

Test series to diagnose it are: valgus stress, anterior drawer, Lachman, pivot shift tests

3. Posterior lateral instability (PLI):

PLI occurs due to: Injury to posterior lateral corner of the knee.

Test series to diagnose it are: external rotation, dial, recurvatum, posterolateral drawer tests

4. Posterior medial instability (PMI):

PMI occurs due to: MCL + ACL + Posterior medial corner.

Test series to diagnose it are: valgus stress, posterior drawer, Lachman tests

5. AMI + ALI instability:

Occurs due to: ACL + MCL + lateral capsule ( But PCL is intact)

Test series to diagnose it are: anterior drawer, Lachman, pivot shift, valgus stress
6. PMI + PLI instability:

Occurs due to: ACL + MCL + lateral capsule (But PCL is intact)

Test series to diagnose it are: anterior drawer, Lachman, pivot shift, valgus stress, varus stress tests


Rossi et al. Sports Medicine, Arthroscopy, Rehabilitation, Therapy & Technology 2011, 3:25 (

Sunday, November 20, 2011

Type of SLAP lesions & The dead arm syndrome

The SLAP lesions:
Superior labrum tears were first described by Andrews. Further SLAP lesions as described by Snyder are subdivided into 4 types (I-IV) & this classification is according to their severity of tear. For best diagrams of the SLAP lesions refer to the following site:

Type I SLAP lesion:
This is a partial tear and degeneration to the superior labrum, where the edges are rough and fray along the free margin, but the labrum is not completely detached.
Type II lesion:
Type II is the comonest type of SLAP tear. The superior labrum is completely torn off the glenoid, due to an injury (often a shoulder dislocation). This type leaves a gap between the articular cartilage and the labral attachment to the bone. Type 2 SLAP tears can be further subdivided into (a) anterior (b) posterior, and (c) combined anterior-posterior lesions.
Type III lesion:
A Type III tear is a 'bucket-handle' tear of the labrum, where the torn labrum hangs into the joint and causes symptoms of 'locking' and 'popping' or 'clunking'. 

Type IV lesion:
The Type IV SLAP tear is one where the tear of the labrum (bucket handle tear) extends into the long head of biceps tendon.

Dead arm syndrome (DAS) &; Type II SLAP lesion:

Now the most important part of the article is which of the SLAP lesion presents with “Dead arm syndrome”.
Dead arm syndrome is clearly a subjective phenomenon (see the definitions below). The sufferer is mostly an athlete whose work involves lot of throwing for example base ball or cricket. The athlete will often say "I just can't throw anymore, and / or the shoulder just doesn't feel right". This type of injury tends to progress gradually over time, slowly creeping up on the overhead athlete until severe pain and subjective instability limits his or her ability to perform.

Dead arm syndrome: Definition

1. Sensory diminution or loss in the arm after anterior shoulder dislocation or subluxation. (Stedman's medical dictionary)

2. The Dead Arm Syndrome has been defined as the inability to throw, spike or serve at pre-injury level secondary to subjective pain and instability.

Description & progression of DAS:

Dead arm syndrome starts with repetitive motion and thus force exerted on the posterior capsule of the shoulder. Overuse can lead to posterior capsule hypertrophy. The next step is tightness of the posterior capsule called posterior capsular contracture. This reduces the shoulder internal rotation. If shoulder activities are still continued then over time, with enough force, a tear may develop in the labrum. The shoulder is unstable and dislocation may come next. Dead arm syndrome won't go away on its own with rest—it must be treated. If there's a SLAP lesion, then surgery is needed to repair the problem. If the injury is caught before a SLAP tear, then physical therapy with stretching and exercise can restore it. Before hand how to know then a SLAP lesion or a dead am syndrome may occur? The answer is shoulders at risk for the dead arm syndrome have a marked loss of internal rotation caused by contracture of the posteroinferior capsule such that less than a 180 degrees arc of rotation is achieved with the arm abducted 90 degrees (the 180 degrees rule).

What is the cause of DAS?
According to Buckhart et al root cause of the dead arm syndrome is the Type II SLAP lesion.
Type 2 SLAP lesions that cause the dead arm syndrome in overhead-throwing athletes are most likely acceleration injuries that occur in late cocking rather than deceleration injuries in follow-through.

More about Type II SLAP lesions form Buckhart et al’s article:

Clinical presentations of all 3 types of Type II SLAP lesion are different. Following are few points to remember about them.
1. Posterior and combined Type 2 SLAP lesions can be disabling to overhead-throwing athletes because of posterosuperior instability and anteroinferior pseudolaxity.
2. The Jobe relocation test is positive with posterosuperior pain in patients with posterior or combined anterior-posterior Type 2 SLAP lesions and is negative in patients with anterior Type 2 SLAP lesions.
3. Rotator cuff tears are frequently associated with posterior or combined anterior-posterior SLAP lesions, are lesion-location specific, and typically begin from inside the joint as undersurface tears.
4. The peel-back mechanism is a likely cause of posterior Type 2 SLAP lesions.

•    Two categories
o    Aware of subluxation
o    Unaware of subluxation
•    Often misdiagnosed as other shoulder pathology or cervical lesion

Associations with other diseases
•    Thoracic Outlet Syndrome
o    30% of patients had coexistent TOS
o    Due to altered kinetics of the Scapulothoracic Joint
o    Resultant neurovascular compromise

Treatment of DAS:

A. Surgical:
1. Repair of posterior SLAP lesions can return overhead-throwing athletes to full overhead athletic functioning.
2. To securely repair the posterosuperior labrum to resist torsional peel-back, suture anchors must be placed posterior to the biceps at the corner of the glenoid. The repair must be protected against external rotation past 0 degree for 3 weeks to avoid undue premature torsional stresses on the repair from the peel-back mechanism.

B. Physiotherapy:
Rehabilitation of athletes with the dead arm syndrome must include the entire kinetic chain.

1. Burkhart SS et al;  Clin Sports Med. 2000 Jan;19(1):125-58.
2. Wikipedia

Friday, November 18, 2011

What is metabolic fitness (MF)?

In previous years, fitness was commonly defined as the capacity to carry out the day’s activities without undue fatigue. These days, physical fitness (PF) is considered a measure of the body’s ability to function efficiently and effectively in work and leisure activities, to be healthy, to resist hypokinetic diseases, and to meet emergency situations.

Physical fitness comprises two related concepts: general fitness (for the purpose of health), and specific fitness (a task-oriented definition based on the ability to perform specific aspects of sports or occupations). Physical fitness is generally achieved through correct nutrition, exercise, and enough rest.

PF can be measured as an out come of physical activity and also as a moderator on morbidity and mortality. Physical fitness for purposes of health, is best defined by the specific components that relate to improved health or reduced disease. The components of Health-Related Fitness are:
–    Morphological
–    Muscular
–    Motor
–    Cardiorespiratory
–    Metabolic
For the discussion of our topic metabolic fitness is more important. Metabolic fitness is the newest component if fitness.

Metabolic fitness:

Physical inactivity is strongly associated with an increased risk of premature disease and death, and the falling level of physical activity. Both aerobic fitness (maximum oxygen uptake) and metabolic capacity of the muscles are important in this matter. The role of the metabolic capacity/fitness of muscle, appears to be especially critical for the development of metabolic-related diseases and thus for the health of the individual.

Definition: A definition of metabolic fitness is proposed as the ratio between mitochondrial capacity for substrate utilisation and maximum oxygen uptake of the muscle.
Indirect means of determining metabolic fitness is Glucose tolerance, blood lipid & cholesterol profiles (especially HDL & triglyerisdes) & finally lipid oxidation.

Skeletal muscle is an extraordinarily plastic tissue and metabolic capacity/fitness changes quickly when the level of physical activity is altered. High metabolic fitness includes an elevated use of fat at rest and during exercise. The capacity for glucose metabolism is also enhanced in trained muscle.

There are many adaptations to physical activity. Exercise-induced activation of genes coding for proteins involved in metabolism is described as an underlying mechanism for some of these adaptations. The increased gene expression is of relatively short duration, which implies that a certain regularity of physical activity is required to maintain high metabolic fitness. Thus, metabolic fitness is directly related to how much the muscle is used, but even low levels of physical activity have a beneficial effect on metabolic fitness and the overall health of the individual.
Subcomponents of metabolic fitness include:
–    Glucose Tolerance
–    Blood Lipid and Cholesterol Profiles
–    Lipid Oxidation

Glucose Tolerance
1. Regular exercise can be used to treat glucose intolerance in Type II diabetics.
2. Effects of exercise include normalizing insulin and glucagon production by the liver, increasing insulin sensitivity by the exercising muscle, thus enhancing glucose uptake.

Blood Lipid and Cholesterol Profiles
1. Exercise decreases total blood cholesterol, increases HDL-Cholesterol, and decreases blood triglycerides.

Lipid Oxidation
1. High lipid oxidation alters cholesterol metabolism and reduces body fat to reduce risk of cardiovascular disease. Thus, chronic aerobic exercise spares glucose stores and uses more fat oxidation for fuel.

Assessment of metabolic fitness:
The direct measurement of metabolic fitness and/or aerobic demand is the means that can be used as an index of the efficacy of an exercise training program or other therapeutic intervention; as medical risk factor for predicting the risk of cardiovascular disease, diabetes, death or other health outcome; or as an aid to pharmaceutical companies for drug discovery in the area of metabolic fitness, deconditioning, and oxidative biology.

1. Ugeskr Laeger. 2002 Apr 15;164(16):2156-62.
2. Kennedy RA et al; Journal of Sports Science and Medicine (2007) 6, 448-454

Saturday, November 12, 2011

Clinical classification of Erb’s palsy & it’s physiotherapy

Narakas classified babies with obstetric palsy into four groups
I. Upper Erb's palsy (C5, C6 injury)
II. Extended Erb's (C5, C6, C7 injury)
III. Total palsy (C5, C6, C7, C8 & T1 injury)
IV. Total palsy with Horner’s syndrome (C5, C6, C7,C8 & T1 injury)

Clinically however Narakas Group II can be sub-classified into two groups according to this 'early recovery of wrist extension.'

II a. recovery of Gr 3 wrist extension before 2 months of age.
II.b. recovery of Gr 3 wrist extension after 2 months of age.

II a recovers the UL function much faster than the II b group.

Muscles paralysed in Group I are: Biceps, Deltoid, Brachialis, Brachioradialis, partly supraspinatus, infraspinatus, Supinator.

Extended erbs palsy involves the elbow & wrist

Intrinsic muscles of hand & ulnar flexors are paalysed in total palsy

Horner’s syndrome comprise of: Ptosis, Miosis, Anhydrosis, Enopthalmus, Loss of ciliospinal reflex.

Sensory loss in Gr I & II may be in little area over deltoid.

Physical therapy approach in nut shell:

Therapy is the cornerstone in the management of the symptoms of a child with BPP brachial plexus palsy. Popular or conventional physiotherapy approaches include exercise therapy, tactile stimulation, soft tissue manipulation techniques and functional splinting. Recently functional stimulation is found better than common electrical stimulation (2).

Galvanic stimulation to the paralysed muscles. Libile method is used with faradic stimulation.

Exercise therapy:
A comprehensive program that includes stretching exercises, safe handling and early positioning techniques, developmental and strengthening activities, and sensory awareness should be developed and updated as needed.
For the first 2 weeks, the child may have some pain in the affected shoulder and limb, either from the injury or from an associated clavicular or humeral fracture. The arm can be fixed across the child's chest by pinning of his/her clothing to provide more comfort. However, some authors have discouraged this pinning in favor of immediate institution of gentle ROM exercises. Parents should be instructed in techniques for dressing the child to avoid further traction on the arm.
A comprehensive therapy program should consist of ROM exercises, facilitation of active movement, strengthening, promotion of sensory awareness, and provision of instructions for home activities. Overall goals should focus on minimizing bony deformities and joint contractures associated with BPP, while optimizing functional outcomes.

Splinting & taping:
Often a wrist extension splint is necessary to maintain proper wrist alignment and reduce the risk of progressive contractures even at 2 weeks period.
Static and dynamic splinting of the arm is useful to reduce contractures, prevent further deformity, and in some cases, assist movement. Commonly prescribed splints include resting hand and wrist splints, elbow extension splints, dynamic elbow flexion and supinator splints. Careful selection and timing of splint use is essential to optimization of the desired effect.

Taping techniques may be used by the therapist to control scapular instability and hence to promote improved shoulder mobility.

Contractures &stretching:
Severe contractures should be avoidable with consistent therapeutic exercises, including passive and active stretching, flexibility activities, myofascial release techniques, and joint mobilization.

Over time, these contractures can lead to progressive bony deformity and shoulder dislocation. Early and consistent stretching of internal rotators should minimize the risk of this problem. External rotation, performed with the shoulder adducted alongside the chest and with the elbow flexed to 90°, provides maximum stretch of internal rotators (specifically, the subscapularis) and the anterior shoulder capsule.
The scapula should be stabilized while stretching shoulder girdle muscles to maintain mobility and preserve some scapulohumeral rhythm. Early development of flexion contractures at the elbow is common and can be exacerbated by radial head dislocation caused by forced supination. Aggressive forearm supination, therefore, should be avoided.

Sensory awareness:
Sensory awareness activities are useful for enhancing active motor performance, as well as for minimizing neglect of the affected limb. Use of infant massage and drawing visual attention to the affected arm can be incorporated easily into play and daily activities. Weight-bearing activities with the affected arm in all positions not only provide necessary proprioceptive input but also can contribute to skeletal growth.


1. Al-Qattan MM et al; J Hand Surg Eur Vol. 2009 Dec;34(6):788-91. Epub 2009 Sep 28.
2. Okafor UA et al; Nig Q J Hosp Med. 2008 Oct-Dec;18(4):202-5.