Clinical and PT Orthopaedics

ORTHOPAEDICS
INDEX
SL.NO TITLE PAGE NO.
1 Syndromes 2–6
2 Soft tissue injuries 7 – 19
3 Regional disorders 20 – 39
4 Neuromuscular disorders 40 – 50
5 Hand injuries 51 – 54
6 Diseases of bone and joints 55 – 82
7 Cervical and lumbar pathology 83 – 97
8 Inflammatory and degenerative conditions 98 – 107
9 Soft Tissue injury and healing 108 - 111
10
11
12
13
14
15
16
17
18
19
1|Page Viresh – Orthopaedics

CHAPTER 13: SYNDROMES
1. THORACIC OUTLET SYNDROME

• Outlet is bordered medially by the scalenus anterior, medius,
and posterior and the first rib;
• Posteriorly by the upper trapezius and scapula;
• Anteriorly by the clavicle, coracoid, pectoralis minor, and
deltopectoral fascia; and laterally by the axilla.
CAUSES OF TOS
• COMPRESSIVE NEUROPATHY
• Faulty posture: Forward head with increased thoracic
kyphosis, protracted scapulae, and forward shoulders
• Entrapment of the neural tissue from scar tissue or pressure
• Respiratory patterns that continually use the action of the
scalene muscles
• Congenital factors such as an accessory rib, a long transverse process of the C-7 vertebra
• Traumatic injuries, such as clavicular fracture.
Common disabilities due to TOS
• Sleep disturbances that could be from excessive pillow thickness or arm posture
• Inability to carry briefcase, suitcase, purse with shoulder strap, or other weighted objects on the
involved side
• Inability to maintain prolonged overhead reaching position
• Inability to do sustained computer or desk work, cradling a telephone receiver between head and
involved shoulder, or prolonged periods driving a car
Test for diagnosis
- Adons test
- ROOS TEST
ADONS TEST:
Starting position: The test can be performed with the patient in either sitting or standing with their elbow in
full extension.
Procedure
• The arm of the standing (or seated) patient is abducted 30 degrees at the shoulder and maximally
extended.
• The radial pulse is palpated and the examiner grasps the patient's wrist.
• The patient then extends neck and turns the head toward the symptomatic shoulder and is asked to
take a deep breath and hold it.
• The quality of the radial pulse is evaluated in comparison to the pulse taken while the arm is
resting at the patient's side.
Positive Test
• The test is positive if there is a marked decrease, or disappearance, of the radial pulse
• It is important to check the patient's radial pulse on the other arm to recognize the patient's normal
pulse.
• A positive test should be compared with the non-symptomatic side.
ROOS TEST:
Starting position:
• The patient has both arms in the 90° abduction-external rotation position
• Shoulders and elbows are in the frontal plane of the chest
Execution: The patient is to open and close the hands slowly over a 3-minute period
Results if normal:
• Only forearm muscle fatigue and minimal distress.
Location of Compression
• Interscalene triangle
• Costoclavicular space

• Axillary interval.
INTERSCALENE TRAINGLE
• Bordered by the scalenus anterior and medius muscles and the first rib
• If these muscles are hypertrophied, tight, or have anatomical variations, they may compress
the proximal portion of the brachial plexus
• Symptoms from dysfunction in this area are reproduced with Adson’s maneuver.
COSTOCLAVICULAR SPACE
• Between the clavicle superiorly and the first rib inferiorly.
• Compression of the neurovascular bundle can occur between the clavicle and first rib,
especially if the clavicle is depressed for periods of time like in carrying a heavy suitcase
or shoulder bag or with a faulty, slouched posture, fractured clavicle, elevated first rib.
AXILLARY INTERVAL
• Between the anterior deltopectoral fascia, the pectoralis minor, and the coracoid process.
• Compression if the pectoralis minor is tight owing to faulty posture with the scapula tipped
forward or to repetitive overuse
• Holding the arms in an elevated position places a stretch on the lower branches of the brachial
plexus and blood vessels
• Roos test also produce the symptoms
• Pectoralis minor palpation also produces symptoms
Common Impairments in TOS
• Intermittent brachial plexus and vascular symptoms of pain, paresthesia, numbness, weakness,
discoloration, and swelling
• Muscle length–strength imbalance in the shoulder girdle with tightness in anterior and medial structures
and weakness in posterior and lateral structures
• Faulty postural awareness in the upper quarter
• Poor endurance in the postural muscles
• Shallow respiratory pattern characterized by upper thoracic breathing
• Poor clavicular and anterior rib mobility
• Nerve tension symptoms when the brachial plexus is placed on a stretch.
NON - OPERATIVE MANAGEMENT

- Educate the patient
• Teach posture correction
• Teach how to modify provoking stresses
• Teach safe exercises for home exercise program
- Mobilize restricted neurological tissue
- Mobilize restricted joints, connective tissue, and muscle
- Improve muscle performance
• Develop control and endurance in postural muscles
• Progress strengthening exercises
Correct faulty breathing patterns
• Relax upper thorax
• Teach abdominodiaphragmatic or bi-basalar breathing patterns
Progress functional independence
• Involve patient in all aspects of program.
2. CERVICAL RIB:
It is a fibrous or bony over development of the costal process of the seventh cervical vertebra. It may be
unilateral or bilateral. It is congenita and generally asymptomatic in the early years.
Symptoms:
Neurological Symptoms: Usually lowest nerve trunk of the brachial plexus may be pressed against the rib.
1. There may be complete sensory anaesthesia in the forearm and hand over the area supplied by the lowest
trunk of brachial plexus.

2. Pain and paraesthesiae may be present on the ulnar aspect of the forearm and hand; occasionally relieved
by changing the position of hand.
3. Weakness of the finer movements of hand may be present.
4. Atrophy may be present in the interossei, and the muscles of the thenar and hypothenar eminence at a
later stage.
Vascular symptoms:
1. Absence or feeble radial pulse.
2. Dusky cyanosis of the forearm and hand.
Differential diagnosis
It is important to rule out peripheral vascular diseases such as Raynaud’s disease. Certain other conditions
such as syringomyelia, motor neuron disease, poliomyelitis and muscular dystrophy should also be kept in
mind.
Treatment:
Surgery is indicated in patients with established progressive vascular and neurological signs. It consists of
removal of the pressure – causing elements, i.e., cervical rib and the associated fibrous band and occasionally
dividing the scaleni group of muscles.
PT Management:
Choice of therapeutic method depends upon the symptoms:
1. Postural guidance
2. Thermotherapy modality for pain relief
3. Exercises to improve distal circulation of hand and fingers.
4. Exercises to improve tone, power and endurance of the whole arm in general and small muscles of the hand
in particular.
Specific exercises develop these muscle groups are extremely important:
1. Self – resisted scapular elevation.
2. Self – resisted scapular adduction (shrugging).
3. Improving endurance of the muscles of the shoulder girdle by endurance training exercise.
4. Progressive resistance exercise (PRE) for the shoulder girdle muscles with weight belt.
5. Maximum isometric holds.
3. SCALENEUS SYNDROME
A symptom complex characterized by brachial neuritis with or without vascular or vasomotor disturbance in
the upper extremities.
Also called scalenus anticus syndrome.
Symptoms
Pain, tingling, and numbness anywhere from the shoulder to the
fingers. Deltoid or other muscles of the arm atrophy.
Treatment
The posture should be corrected, and sometimes the arm and
shoulder are immobilized. When relief is not obtained, surgical
correction may be required.
4. COSTOCLAVICULAR SYNDROME
The Costo-clavicular passage is formed by the clavicle
antero-laterally, the first rib medially, and the scapula
Posteriorly.
The brachial nerve plexus, subclavian artery and subclavian

vein run within the costoclavicular space between the first rib
and the clavicle.

The neurovascular bundle is vulnerable to compression in this space.
Mechanism of syndrome
• In soldiers with loaded knapsacks, who developed pain, numbness, and fatigue ability of the arms as
they stood at attention.
• The mechanisms of compression involved downward movement of the clavicle against the first rib with
a resultant tendency to shearing of the neurovascular bundle
It can occur by
• The clavicle depresses toward/against the first rib like in slumping shoulders
• A tight subclavius like obese, middle aged or elderly women.
• The first rib elevates toward/against the clavicle like in labored breathing. Tight anterior and middle
Scalenes and subclavius.
Presenting complaints
• Pain or ache sometimes accompanied by stiffness in the neck and shoulders, pain, paresthesia, and
fatigue ability of the upper limbs are the main presenting complaints.
• Symptoms are usually bi-lateral, though more pronounced on the dominant side.
• They are aggravated by work and exercise, particularly carrying heavy shopping bags.
• Symptoms are relieved by rest and sleep, are minimal or absent in the morning, and become pronounced
as the day progresses.
• Patients occasionally complain of puffy blue hands.
• Tight, narrow straps have cut deeply into the underlying soft tissues
• Direct downward pressure with a forefinger in the groove reproduces symptoms.
• Tenderness over the acromioclavicular joint
• Paranesthesia when present are likely to involve the thumb and all fingers and sometimes the whole
limb.
• Some patients complain of puffy blue hands.
• Patients with this form of costoclavicular syndrome are usually younger
• Firstly, the goal is to open the space between the clavicle and first rib.
• After placing moist heat on the costoclavicular space itself
• The costoclavicular space should now be stretched by passively bringing the client’s arm back into
extension and up into abduction
• Attention to posture directed at avoiding stooping and shoulder girdle exercises helps.
5. LEVATOR SCAPULE SYNDROME

• Levator scapulae syndrome is a condition in which the Levator scapulae muscle becomes irritated
and inflamed.
• The main cause of Levator scapulae syndrome is sitting for long periods at a time,
particularly when you sit with poor posture.
• Sports collisions, falls, and car accidents can all cause this condition.
6. CERVICOBRACHIAL SYNDROME
• Pain and stiffness of the cervical spine with symptoms in the shoulder girdle and upper extremity
• Tingling, numbness or discomfort in the arm, upper back and upper chest with or without an associated
headache.
• When there is a combination of neck complaints and (radiating) complaints in the arm, we can call it a
cervicobrachial syndrome or cervico brachialgia.
• The occupation of most patients is manual work with continuous, repetitive tasks like computer work,
writing, manipulating or moving objects and lifting or overhead work
• Tasks that require holding the same neck position for a long period are provocative
Differential Diagnosis
• Shoulders and arms (painful shoulder)
• Cervical radiculopathy
• Levator scapulae syndrome
• Polymyalgia rheumatica (painful shoulder)
• Early stage of rheumatic diseases (RA (any age) or ankylosing spondylitis (30 years)).
• Due to infections or bone lesions of the cervical spine (e.g. Spondylodiscitis, metastases).

How to reproduce the pain:
Adson maneuver
• the head is placed in extension and bent to the side while the patient holds his breath and the
physician observes for symptoms
• The elevated arm stress test: hyperabduction of the arm may produce symptoms
• A loss of pulse during these tests indicates the thoracic outlet syndrome
Spurling test.
7. VERTIBROBASILAR SYNDROME
• Vertebrobasilar insufficiency is defined as transitory ischemia of the vertebrobasilar circulation
• Dizziness, vertigo, headaches, vomit, diplopia, blindness, ataxia, imbalance, and weakness in both
sides of the body are the most common symptoms.
TEST
• In this patient, the physical examination procedures were performed with the patient in supine.
• The patient’s head was supported by the therapist in a neutral position, and baseline resting
symptoms of vertigo, visual disturbances, and headache were absent.
• The patient’s head was passively turned into right
rotation and held at end range for 30 seconds while the
therapist monitored for symptoms of VBI.
• The patient’s head was returned to neutral and
remained in this position for 30 seconds to allow for a
potential latent response.
• No symptoms were provoked, and nystagmus was not
observed and repeat same for left cervical rotation.
• When the patient’s cervical spine was passively placed
into extension, familiar symptoms of vertigo were
produced and persisted as long as the head was
maintained in extension.
• The patient’s head was immediately repositioned into
neutral and remained.
• There (approximately 60 seconds) until the symptoms
abated.
8. PIRIFORMIS SYNDROME
• Caused when the piriformis muscle
compresses the sciatic nerve
• Pain is usually felt in one buttock -radiation
of pain down the back of the leg (sciatica).
• Pain aggravated by hip activity, Eg. walking,
or prolonged sitting.
• To avoid pain and pressure in the area you
may sit
• Sometimes, you’ll walk with the foot turned
out due to shortening of the piriformis
muscle.
TEST: Piriformis test in side-lying position:
• Patient is positioned in side-lying on the
unaffected side.
• FAIR test
(Flexion Adduction and Internal Rotation).

CHAPTER 6: SOFT TISSUE INJURIES
DEFINITIONS:
1. SPRAINS:
A Sprain is a stretching or tearing of ligaments – the tough bands of fibrous tissue that connect two
bones together in your joints. The most common location for a sprain is ankle. Sprains can be either a mild
sprain or a severe sprain.
Symptoms: Pain, Swelling, Bruising, Limited ability to move the affected joint, Hearing or felling a “pop” in
the joint at the time of injury.
2. STRAINS:
Strain is an acute or chronic soft tissue injury that occurs to a muscle, tendon, or both (Contractile
components).
Signs and Symptoms: Pain, functional loss of the involved structure, muscle weakness, contusion and
localised inflammation.
3. CONTUSION:
Also called as a Bruise. It is caused when blood vessels are damaged or broken as the result of a blow
to the skin. It is an injury caused to muscle fibers and connective tissues. They are typically caused by trauma
or by blunt force to a body part. This trauma crushes the muscle fibers, but doesn’t break the skin tissue.
4. TENDINITIS:
Tendinitis is an inflammation or irritation of a tendon – the thick fibrous cords that attach muscle to
bone. The condition causes pain and tenderness just outside a joint. Common sites: Shoulders, elbows, wrists,
knees and heels.
5. TENDON RUPTURE:
Tendon rupture is a condition in which a tendon separates in whole or in part from tissue it is attached,
or is itself torn or divided in whole or in a part. Common areas of tendon rupture include: Quadriceps, Achilles
tendon, Rotator cuff and biceps.
6. TENOSYNOVITIS:
Inflammation of the thin synovial lining of a tendon sheath is termed Tenosynovitis. It may arise from
mechanical irritation or from bacterial infection.
Two types of Tenosynovitis:
a) Irritative tenosynovitis: Commonly seen in the tendons of the hand and results in pain and swelling.
b) Infective tenosynovitis: It is an infection of the synovial lining of the tendon by pyogenic or tubercular
bacteria.
7. TENDINOSIS:
It is a condition that is characterized by swelling and pain of a tendon. It occurs when tendons
degenerate to break down. Tendons have small tears or disorganized collagen fibres instead of straight
collagen fibers. This condition is most common in elbow, shoulder, knee, hip and Achilles heel tendons.
8. BURSITIS:
Inflammation that occur in a normally situated bursa or in an adventitious bursa. It may arise from
mechanical irritation or from bacterial infection.
Two types of Bursitis:
a) Irritative bursitis: It is caused by excessive pressure or friction, occasionally due to a gouty deposit.
b) Infective bursitis: A bursa get infected by a pyogenic or tubercular infection. It occurs commonly in
trochanteric bursa or prepatellar bursa.
Common Bursitis: Prepatellar bursitis (Housemaid’s Knee), Infrapatellar bursitis (Clergyman’s Knee),
Olecranon bursitis (Student’s elbow), Ischial bursitis (Weaver’s bottom), On lateral malleolus (Tailor’s ankle),
On great toe (Bunion).

MENISCAL INJURIES OF KNEE:
Common in males and these constitutes a common group of
injuries peculiar to the knee, frequently being reports with
increasing sporting activity.
Mechanism of Injury:
The injury is sustained when a person, standing on a semi-flexed
knee, twists his body to one side. The twisting movement, an
important component of the mechanism of injury, is possible
only with a flexed knee.
During this movement the meniscus is 'sucked in' and nipped as
rotation occurs between the condyles of femur and tibia. This
results in a longitudinal tear of the meniscus.
Pathoanatomy
The meniscus is torn most commonly at its posterior horn. With every subsequent injury, the tear extends
anteriorly. The meniscus, being an avascular structure, once torn does not heal. If left untreated, it undergoes
many more sub-tears, and damages the articular cartilage, thus initiating the process of osteoarthritis.
Types of meniscal tear
1. Bucket handle tear 4. Radial tear
2. Anterior horn tear 5. Posterior horn tear
3. Complex tear 6. Longitudinal tear
Bucket handle tear: Most common type
The bucket handle is displaced towards middle of the joint so
femur rolls upon tibia through meniscus. It limits full extension
and also called as ‘Locking of knee’.
Clinical Features:
• Occurs in young males
• Recurrent episodes of pain and locking of the knee
• Sudden jerk while walking
• Swelling after few hours of injury and last for days.
• Swelling appears overnight and knee in 10° flexion.
• History of classic twist injury.
On Examination:
• Knee swollen
• Tenderness in region of knee joint line
• Gentle full extension cause pain
• Pain localized
• Wasting of quadriceps
Special test:
1. McMurray’s test:
Patient supine with testing knee in maximal flexion. Passively internally rotate and extend the knee.
This tests lateral meniscus. Test medial meniscus with same procedure except rotate tibia into lateral rotation.
Positive finding is reproduction of click and/or pain in knee joint.
2. Apley’s test
Helps to differentiate between meniscal tears and ligamentous lesions. Patient prone with testing knee
flexed to 90°. Stabilize patient's thigh to table with your knee. Passively distract the knee joint then slowly
rotate tibia internally and externally. Next step is to apply a compressive load to knee joint and once again
slowly rotate tibia internally and externally. Pain or decreased motion during compression indicates a
meniscal dysfunction. If pain or decreased motion occurs during the distraction then it is most likely a
ligamentous dysfunction.

3. Thesalay test
Patient standing injured leg and hold the arms of the therapist for support. Bend the knee to 20° and
rotate over the tibia three times on each side. Test is positive if the pain is present of the joint line.
Radiological examination:
With meniscal tears there are no abnormal X-ray findings. X-rays are taken to rule out any associated
bony pathology. MRI is a non-invasive method of detecting meniscus tears. It is a very sensitive investigation,
and sometimes picks up tears which are of no clinical significance.
Arthrography: It is a technique where X-rays are taken after injecting radiopaque dye into the knee.
The dye outlines the menisci, so that a tear, if present, can be visualized. Being an invasive technique, it is no
longer used.
Arthroscopy: This is a technique where a thin endoscope, about 4-5 mm in diameter – the arthroscope,
is introduced into the joint through a small stab wound, and inside of the joint examined.
Management or treatment:
Treatment of acute meniscal tear: Conservative management:
If the knee is locked, it is manipulated under general anaesthesia. No special maneuver is needed. Once
knee relaxes, torn meniscus falls into place and the knee is unlocked.
Immobilize knee in Robert Jones Compression Bandage for 2 – 3 Weeks.
Treatment of chronic meniscal tear: Surgical Management
Excision of displaced fragment (torn meniscus)
Meniscorraphy: Preserve meniscus by suturing
CRUCIATE INJURIES IN KNEE

1. ANTERIOR CRUCIATE LIGAMENT:
This ligament is most commonly ruptured, often hyperextension in association with the tears of medial
and lateral collateral ligaments.
Mechanism of Injury: Occur due to twisting force on semi-flexed knee
O’ Donoghue Traid: MCL, Medial meniscus and ACL tear occur
Pain is Diffuse and tenderness is vague.
Special test:
1. Anterior drawer test
This is a test to detect injury to the anterior cruciate ligament. A similar test in which anterior glide of
the tibia is judges with the knee in 10 – 15 degrees of flexion.
2. Lachman test:
Patient supine with testing knee flexed 20°- 30°. Stabilize femur and passively try to glide tibia
anterior. Positive finding is excessive anterior glide of tibia.
Diagnosis:
Clinical Examination: Pain and swelling of the knee. The patient is able to give a history of having
sustained a particular type of deforming force at the knee (valgus, varus etc.), followed by a sound of
something tearing. The pain may be localised over the torn ligament (in cases of injury to collateral
ligaments), but there is vague pain in cruciate ligament injuries. The swelling (haemarthrosis) is variable, but
appears early after the injury.
Radiological examination: A plain X-ray may be normal, or a chip of bone avulsed from the ligament
attachment may be visible. It may be possible to demonstrate an abnormal opening-up of the joint on stress
X-rays. MRI is a non-invasive method of diagnosing ligament injuries, and may be of use in doubtful cases.
Management or Treatment:
Conservative: knee immobilsed in cast or Robert jones bandage for 3-6 weeks in Garde I and II
• Once swelling decrease PT
• Robert Jones Bandage: bandaging with 3 successive layers of cotton with help of crepe bandage to
provide compression.
Surgical: Done for Grade III: Repair of the ligament or Reconstruction.
Complications: Injury to common peroneal nerve, adhesions, ossification in the ligament, Instability and OA.
2. POSTERIORI CRUCIATE LIGAMENT:
This ligament is damaged if the anterior aspect of the tibia is struck with the knee semi – flexed so as
to force the tibia backwards on to the femur.
Mechanism of Injury: Occur due to backward force on tibia.
Pain is Diffuse and tenderness is vague.
Special test:
Posterior drawer test: Indicates integrity of posterior cruciate ligament.
Patient supine and testing hip flexed to 45° and knee flexed to 90°. Passively glide tibia
posteriorly following the joint plane. Positive finding is excessive posterior glide.
Diagnosis:
Clinical Examination: Same as ACL
Radiological examination: Same as ACL
Management or Treatment:
Conservative: Same as ACL
Surgical: Same as ACL
MEDIAL AND LATERAL COLLATERAL INJURIES OF KNEE

1. MEDIAL COLLATERAL LIGAMENT:
It ruptures most commonly from its femoral attachment.
Mechanism of injury: Valgus force/Abduction of femur
Rupture from femoral attachment.
Pain: Medial Side
Swelling: Medial Side
Tenderness: Medially on the femoral condyle
Test: Valgus Stress test (Abduction) positive.

Procedure: Patient supine. Stabilize ankle and apply
medial pressure (valgus stress) to knee joint at 0° and
then at 20 - 30° extension.
Positive sign: Excessive movement compared with
opposite knee.
Treatment: Same as ACL.
2. LATERAL COLLATERAL LIGAMENT:

Mechanism of injury: This ligament is damaged by a mechanism just the reverse of above i.e., adduction of
the tibia on the femur (varus force).
The ligament is avulsed from head of the fibula with a piece of bone. Lateral collateral ligament injuries are
uncommon because the knee is not often subjected to varus force (the knee is not likely to be hit from the
inside).
Pain: Lateral Side
Swelling: Lateral Side
Tenderness: Laterally on the fibular head.
Test: Varus Stress (Adduction) test

Procedure: Patient supine. Stabilize ankle and apply lateral pressure (varus stress) to knee joint at 0° and then
at 20 - 30° extension.
Positive sign: Excessive movement compared with opposite knee.
Treatment: Same as ACL.
10 | P a g e Viresh – Orthopaedics
LATERAL LIGAMENT OF ANKLE
This is the weakest ligament and is often injured. It has three parts:
i) Anterior talo – fibular
ii) Calcaneo – fibular in the middle and
iii) Posterior talo – fibular
Mechanism of injury: Occur in inversion force
Grade Signs & Symptoms
Grade I Ankle sprains are painful, but they have no increased laxity when compared with the
uninjured side. This correlates with mild stretching of the ATFL.
Grade II Ankle sprains are painful and have an increased laxity on testing. This correlates with a
complete tear of the ATFL and a partial tear of the CFL.
Grade III Ankle sprains are usually painful and have an unstable ankle joint on examination. This
correlates with complete ruptures of both the ATFL and CFL.
Diagnosis:
• History of twisting leading to pain and swelling
• Weight Bearing causes increase pain
• If complete tear then patient say giving way at time of injury
• Swelling and tenderness at LCL site
• If inversion and neutral position pain: LCL ligament
• If eversion and neutral position pain: MCL ligament
• Inversion and PF pains: Anterior TF ligament
Radiological Features:
• X-Ray ankle
• Stress X-rays
• If talus is titled more than 20° on forced eversion or inversion: complete LCL or MCL tear.
Treatment:
• Grade 1: Below knee plaster for 2 weeks then mobilization
• Garde 2: plaster for 4 weeks and mobilization
• Garde 3: plaster 6 weeks and mobilization
Complications: a) Stiffness of the ankle b) Osteoarthritis
WRIST SPRAINS
A wrist sprain is an injury to the ligaments of the wrist region, including the ligaments
connecting the carpal bones and the ligaments connecting the proximal row of carpal bones with the
radius and the ulna. By injury we mean that the ligaments are partially or completely torn.
There are three grades:
1. A mild overstretching of the ligaments, without joint instability.
2. A partial rupture of the ligaments, with no or mild joint instability.
3. A complete rupture of a ligament with severe joint instability.
Mechanism of injury: is a fall on an outstretched arm/hand, with an important impact on the thenar
eminence, combined with a dorsiflexion, an ulnar deviation and intercarpal supination -stress.
Treatment or Management: Conservative Management:
1. Rest: 2. Ice
3. Compression: Wrap the wrist with an elastic compression bandage and limit swelling.
4. Elevate: Try to keep the wrist above heart level as often as possible, during two days. This will help
drain fluid and reduce swelling around the wrist.
5. Nonsteroidal anti-inflammatory drugs are recommended.
Surgical Management:
In case of a severe wrist sprain it can be recommended to immobilize the wrist. In some rare cases a
surgery may be needed to repair a ligament that was torn completely.
STRAINS
1. QUADRICEPS
A quadriceps muscle strain is an acute tearing
injury of the quadriceps due to an acute stretch of the
muscle, forceful contraction or repetitive functional
overloading.
Acute injuries are usually the result of a single
traumatic event and cause a macro-trauma to the
muscle. They mostly occur in contact sports such as
rugby, soccer and basketball because of their dynamic
and high collision nature.
Overuse, chronic or exercise-induced injuries
are subtler and usually occur over a longer period of
time. They result from repetitive micro-trauma to the
muscle.
Mechanism of injury:
There are generally three mechanisms of injury for a quadriceps strain.
1. Sudden deceleration of the leg (e.g. kicking),
2. Violent contraction of the quadriceps (sprinting) and
3. Rapid deceleration of an overstretched muscle (by quickly change of direction).
Characteristics/Clinical Presentation
Grades of quadriceps strain:
Grade 1 symptoms: A twinge felt in the thigh, tightness, Mild discomfort on walking and running.
Grade 2 symptoms: Sharp pain when running, jumping or kicking and be unable to play on. Pain while
walking and swelling or mild bruising, unable to fully bend the knee.
Grade 3 symptoms: Symptoms consist of a severe, sudden pain in the front of the thigh, unable to walk
without the aid of crutches. Bad swelling appears immediately and significant bruising within 24 hours.
Medical Management
• NSAID's (Nonsteroidal anti-inflammatory drugs).
• Surgical Intervention is done to complete quadriceps muscle rupture.
• The use of hyperbaric oxygen therapy.
Indications for Surgery

• Large intramuscular hematoma(s),
• A complete (III degree) strain or
• Tear of a muscle with few or no agonist muscles, or
• A partial (II degree) strain if more than half of the muscle belly is torn.
2. HAMSTRINGS
• A hamstring strain, sometimes called a pulled hamstring, happens when one or more muscles gets
stretched too far and starts to tear.
• Getting a hamstring strain is also more likely if:
• You don't warm up before exercising.
• Tight quadriceps which pull your pelvis forward and tighten the hamstrings.
• Weak glutes. Glutes and hamstrings work together. If the glutes are weak, hamstrings can be over
loaded and become strained.
Symptoms:
• Sudden and severe pain during exercise, along with a snapping or popping feeling
• Pain in the back of the thigh and lower buttock when walking, straightening the leg, or bending over
• Tenderness
• Bruising
Diagnosis:
• Grade 1; mild strain. You may experience some pain when you use your leg, but it will be minor
and there will be minimal swelling.
• Grade 2; partial tear of one or more of the hamstring muscles. limp when you walk and feel
some pain during activity.
• swelling and bruising, and you might not be able to straighten your leg all the way.
• Grade 3; complete tear of one or more of the hamstring muscles.
• You'll feel pain and not be able to straighten your leg all the way, and you'll notice swelling right
away
• Walking will be very difficult and may require crutches.
Treatment:
• Use the RICE formula as soon as possible after the injury
• Take pain medicine. Ibuprofen and other non-steroidal anti-inflammatory drugs (NSAIDs) can help
relieve pain and reduce swelling in the leg.
• Do stretching and strengthening exercises.
3. CALF
Calf muscle strain injuries (CMSI) occur commonly in sports involving high-speed running or
increased volumes of running load, acceleration and deceleration as well as during fatiguing conditions
of play or performance. Muscle strains commonly occur in the medial head of the gastrocnemius or close
to the musculotendinous junction.
Grading of calf strains
Grade Symptoms Signs Average time to
return to sport
I Sharp pain at the time of activity or after Pain on unilateral calf raise or hop 10 - 12 days
Tightness, able to continue activity,
without pain or with mild discomfort
Post activity tightness and/or aching
II Sharp pain at the time of activity in calf Pain with active plantarflexion 16 - 21 days
Unable to continue activity, Significant Pain & weakness with resisted
pain with walking afterwards, swelling Plantarflexion, Loss of
in muscle, Mild to moderate bruising dorsiflexion, Bilateral calf raise
present pain
III Severe and immediate pain in the calf, Inability to contract calf muscle 6 months after
often at musculotendinous junction May have palpable defect surgery
Unable to continue with activity, Thomson's test positive
considerable bruising and swelling
within hours of injury
Characteristics:
1. Gastrocnemius Strains 2. Soleus Strains 3. Plantaris Strains
Treatment:
Conservative Management: Rest, ice, compression and elevation; Compression bandage to help to stop
swelling, to avoid creating a gait imbalance.
Prevention: Regular stretching ensures good joint mobility.
4. BICEPS
A bicep tear is a tear in the bicep muscle that can occur in the shoulder or elbow. The tear can be
complete (the tendon has torn completely away from the bone) or partial.
Bicep tears or strains are classified as grades 1 – 3 depending upon severity of the injury.
Types of bicep tears or strains
Grade 1 — minor injury that involves overstretching the biceps muscle or tendon, typically without a loss
of strength or mobility.
Grade 2 — causes moderate tearing in the biceps or tendon with some loss of mobility or strength.
Grade 3 — a complete rupture of the biceps muscle or tendon, may require surgery to repair.
Causes of a bicep tear or strain
There are a variety of causes for a bicep tear or strain including:
• Constant overuse — sports that require repetitive movement on the bicep in the shoulder or elbow
can cause a bicep tear or strain.
• Acute injury — moving or twisting your elbow in an unfamiliar way can cause a bicep tear or
strain, for example, falling on an outstretched arm.
Treatment: Nonsurgical treatment options include rest, ice and anti-inflammatory medications.
5. TRICEPS
A triceps strain is a relatively uncommon condition that typically causes pain in the back of the upper arm
and is characterised by partial or complete tearing of the triceps brachii muscle. Triceps strains can range
from a minor partial tear provoking minimal pain and loss of function, to a complete rupture.
The severity of injury can range from a grade 1 to a grade 3 tear and are classified as follows:
• Grade 1: A small percentage of fibres are torn resulting in some pain, but allowing full function.
• Grade 2: A significant percentage of fibres are torn with moderate loss of function.
• Grade 3: All muscle fibres are ruptured resulting in major loss of function.
Most triceps strains are classified as grade 2 tears.
Causes of a triceps strain
A triceps strain typically occurs due to a sudden, forceful contraction (or less commonly, a stretch) of the
triceps muscle. Occurs during heavy pushing or straightening of the elbow against resistance (such as
performing explosive dips, push-ups, bench presses, cable triceps exercises etc.
Diagnosis of a triceps strain
X-Ray, Ultrasound, CT scan or MRI scan may be required to confirm diagnosis, rule out other conditions
and assess the severity of the tear.
Treatment: Same as that of Biceps
CONTUSIONS
1. QUADRICEPS
Definition: Charley horse/cork thigh/dead leg.
A quadriceps contusion is a traumatic blow, a deep bruise to the anterior lateral or medial aspect of the
thigh.
Swelling and tenderness with (terrible) pain on passive stretch and active contraction
The diagnosis is a Quadriceps contusion is with resultant hematoma.
The contusion is the result of an external force that can damage the muscle but can’t eliminate its
function completely. Quadriceps contusions can lead to two serious complications: Compartment
Syndrome and myositis ossificans.
Mechanism of injury: A contusion is the most common acute thigh injury in contact sport such as
football, rugby and basketball. Contusions are caused by external forces like a direct blow from an
opponent's knee. Thus, muscle contusions are classified as acute direct muscle injuries. The most
frequently injured muscles are the exposed rectus femoris and the intermediate vastus, lying next to the
bone, with limited space for movement when exposed to a direct blunt blow.
Risk factors:
• Contact sports and sports that require quick starts, i.e. running races and other track events.
• Warm up and cool down habits.
• Off season/preseason/season training habits.
• Poor muscle conditioning.
• Playing position.
• Level of competition.
• Protective equipment use.
• Playing experience.
• Injury history, especially to the thigh, hip and/or knee.
• Medical history of any bleeding disorder.
• Age.
• Poor nutrition.
• Smoking history.
• Obesity.
Clinical Features:
A massive blunt force mostly to the anterior or lateral thigh causes rupture to the muscle fibers.
In the beginning there are negligible symptoms, but after 24 hours this will lead to hematoma
formation within the muscle causing: pain, swelling, stiffness and impairment of functional quadriceps
excursion.
Pathophysiology
• Broken blood vessels resulting in bleeding (hematoma) into the injured area
• Crushed muscle tissue resulting in hip and knee dysfunction.
If there is major untreated and/or unresolved bleeding deep in the muscle tissue, a serious condition
known as myositis ossificans can occur.
Contusion injury can lead to either diffuse or circumscribed bleeding that displaces or
compresses muscle fibres causing pain and loss of motion. It happens that muscle fibres are torn off by
the impact, but typically muscle fibres are not torn by longitudinal distraction. Therefore, contusions
are not necessarily accompanied by a structural damage of muscle tissue. For this reason athletes, even
with more severe contusions, can often continue playing for a long time, whereas even a
smaller indirect structural injury forces the player often to stop at once.
Classification
Pain Active knee flexion Gait Description Average loss of activity
Mild > 90° Normal Capillary rupture: Blood into 6 days

connective tissue
Mild ecchymosis, feels soreness
after cooling down or the following
day, the injured area may be tender
to touch, Ability to stretch the
muscle may be reduced slightly. The
strength of the muscle may also be
slightly affected.
Moderate 45 - 90° Antalgic Crushing of the muscle fibres with 56 days

vasomotor reaction, Minimum
stiffness after rest, Swelling, Pain &
tenderness
Severe < 45° Severely Rapid swelling and bleeding, the > 60 days
antalgic patient will be unable to walk
properly without the aid of crutches,
Pain
& Tenderness
Diagnostic: Physical examination:
Palpation along the injured muscle: to localize the pain and exact site of muscle damage and also to
determine if there is any associated injury.
Muscle firmness testing was performed with fingertip palpation, with the muscle firmness at the site
of the injury compared with the firmness of the same site on the uninjured leg.
Circumference measures were taken at the suprapatellar border, and at 10 and 20 centimeters proximal
to this site on both thighs, using a purpose-made device which was designed to ensure that the
distances above the suprapatellar border were constant for all subjects.
Test: 1. Passive knee range of motion testing
2. The brush-swipe and tap tests
3. Strength testing of the quadriceps
4. Measurement of knee flexion
Medical Management
NSAIDs can be useful short term for decreasing pain, but their long-term effect on muscle healing is
not known.
Rest, ice, compression. Compression is important in order to limit the hemorrhage for the first
24 to 48 hours. If the patient rests with his knee flexed, it helps to avoid muscle stiffness.
Active and passive quadriceps muscle stretching with emphasis on knee flexion. After 24 h, the brace
or wrap should be removed and gentle, active, pain-free range of motion at the knee should be
instituted along with stretching and isometric quadriceps strengthening. The active phase of treatment,
including functional rehabilitation, can begin when pain-free, active knee flexion of at least 120° is
attained. Improve the functionality and a return to sport when full motion and strength are achieved.
Return to sports criteria

Criteria are similar to muscle strains for return to sports in contusions of the quadriceps. The athlete
should be pain free, attain 120° of knee flexion with hip extended, and perform all aspects of functional
field testing without limitations. Protective thigh padding is recommended prior to resuming sports in
order to reduce recurrence.
2. GLUTEAL
Bruising of the skin and underlying tissue anywhere on the body is caused by a direct blow to the
body. Contusions can cause bleeding form ruptured capillaries. They cause tenderness to the surrounding
tendons, nerves, and other soft tissues. They occur in contact sports such as football, ice hockey, and
baseball.
Symptoms:
• Swelling and a hard lump in the injured buttock.
• Pain and tenderness in the injured area.
• Feeling of firmness when pressure is exerted on the buttock.
• Bruising or discoloration under the skin.
Treatment:
• See your physician for a precise diagnosis unless the injury is minor.
• Use the first three steps of the R.I.C.E. method (Rest, Ice, Compress, Elevate).
• Ice the area and massage the area with ice.
• After 48 hours, apply heat instead of ice if it feels better.
• Take a whirlpool bath if available.
• Protect the area with a bandage.
• Massage very gently to reduce swelling.
Prevention:
• Wear protective equipment such as hip pads, when appropriate.
• Begin a muscle strengthening program.
• Don't take any major chances during play to protect your body.
3. CALF
A calf contusion is a condition characterized by a bruise or ‘corky’ to the back of the lower leg,
usually as a result of a direct impact.
The muscle group at the back of the lower leg is commonly called the calf. The calf comprises of 2
major muscles one of which originates from above the knee joint
(gastrocnemius) the other of which originates from below the knee joint
(soleus). Both of these muscles insert into the heel bone via the
Achilles tendon.
Mechanism of injury: Following a direct impact to the calf, damage to
the muscle fibres, connective tissue and small blood vessels of the muscle
may occur. This results in a ‘bruise’ to the calf and is known as a calf
contusion.
Calf contusions can range from minor contusions resulting
in minimal pain and allowing ongoing activity, to severe contusions
resulting in significant pain and loss of function.
Causes of a calf contusion

Calf contusions occur following a direct impact to the calf muscle from an object or person. This
most commonly occurs due to a collision with another player during contact sports, such as football or
rugby, or from an impact from a ball in sports such as hockey or cricket.
Signs and symptoms of a calf contusion
Sudden pain in the calf muscle at the time of injury.
In minor calf contusions, pain may be minimal allowing continued activity.
In more severe cases, patients may experience severe pain, muscle spasm, weakness and an inability to
continue activity. Patients with a severe contusion may also be unable to walk without a limp.
Swelling, tenderness and bruising may also be present in the calf muscle, along with an inability to stretch
the calf as far as usual.
Diagnosis of a calf contusion: MRI scan or ultrasound
Treatment for a calf contusion
Treatment may comprise:
Soft tissue massage (after the initial 72 hours period), Electrotherapy (e.g. ultrasound), Dry needling, Joint
mobilization, Stretches, Anti-inflammatory advice (NSAID’s), The Use Of Crutches , Achilles tendon
taping, Calf taping, the use of heel wedges applying a compression bandage , the use of protective padding
to the calf muscle to prevent re-injury, ice or heat treatment, exercises to improve the strength and flexibility
of the calf, education, activity modification advice, hydrotherapy, establishment of an appropriate return to
activity or sport plan.
4. DELTOID
DELTOID CONTUSION
A deltoid contusion is a bruise in the deltoid muscle which is situated on the side of the shoulder. This
occurs after a direct impact to the muscle, usually from a hard, blunt object such as a hard ball or an
opponents elbow
Symptoms of a Deltoid Contusion

• Pain in the muscle after impact.
• Pain and difficulty when lifting the arm to the side.
• Tender to touch the muscle.
• Bruising appears.
• There may be some swelling.
Treatment
• Rest the arm, apply a sling if necessary, to relax the muscle.
• Apply ice or cold therapy products as soon as possible and regularly to ease the pain, bleeding, and
inflammation.
• In most cases, a deltoid contusion will heal naturally within 1-2 weeks.
• If symptoms persist visit a doctor to rule out further damage.
Also look out for neural signs such as tingling, numbness, and weakness in the arm or hand which may
indicate nerve damage.
TENDON RUPTURES
1. ACHILLES TENDON
• Occurs when tendon is degenerated and occurs above 40 years
• While pushing off → calf muscle contracts → contraction resisted by body weight--- unable to tip
toe → a gap is seen at TA tendon insertion.
SIMMONDS TEST:
• Patient prone: squeeze the calf muscles
• If tendon intact: foot do PF
• If tendon rupture: foot remain still
Differential diagnosis:
INCOMPLETE TEAR: Gap not seen, Patient able to stand on tip toe
Tear of soleus muscle: Cause pain and tenderness halfway up till calf and relieved by increase heel of shoe
2. ROTATOR CUFF MUSCLES (for detail – refer chapter 17 )

Causes:
• Overuse injury
• Overload injury
• Age related changes
• Decreased vascularity at attachment
Consequences of RC Tear:
3. BICEPS
• Localised tenderness in bicipital grove

• Pain in front of shoulder with any arm movement
• Pain occurs more if arm is extended
• Radiation of pain till shoulder
• Pain worse at night or once patient got up in morning’
• Occurs due to any unprepared movement or sudden jerk to the shoulder
• How to prevent: Proper warm up before the exercise
Diagnose:
Speed test/Biceps or Straight arm test
• Patient in sitting position
• The arm to be tested should be in about 60 degrees of front flexion with the
forearm supinated and the elbow fully extended.
• In the starting position the examiner forcefully presses
down on the patient’s arm at the forearm. The patient
attempts to resist the pressure of the examiner.
Alternatively, the patient attempts to forward flex the
shoulder while the examiner resists.
• Test is considered positive if pain is reported in the
bicipital groove.
Biceps load test

• This test is used to check the ability of the transverse humeral ligament to hold
the biceps tendon in the bicipital groove
• Patient sits while examiner stands in front. The patient’s elbow is flexed to 90
degrees and the forearm is in a pronated position while maintaining the upper
arm at the side. Patient is instructed to supinate arm while examiner
concurrently resists forearm supination at the wrist
• Localized pain at the bicipital groove indicates a positive test.
Yegarson test
• The patient should be seated or standing, with the humerus in
neutral position and the elbow in 90 degrees of flexion.
• The patient is asked to externally rotate and supinate their arm
against the manual resistance of the therapist.
• Yergason's Test is considered positive if pain is reproduced in the
bicipital groove during the test.
Management: Goal: to return to sports

Treatment:
• Ice compression for 5-10 min for two times/day
• Electrotherapy modalities
• When pain reduced then strengthening of biceps
4. PECTORALS
Pectoralis major tendon rupture is a rare shoulder injury, most commonly seen in weight lifters. This
injury is due to the increased emphasis on healthy lifestyles.
Mechanism of Injury: Pectoralis tendon ruptures are most commonly seen in weight lifting, ruptures have
also been reported in many other sporting activities such as boxing, football, rodeo, water skiing, and
wrestling.
Clinical Presentation: Bruising can be seen over the anterior lateral chest wall or in the proximal arm.
Pain generally is not intense. An isometric contraction will reveal asymmetry to the chest wall. This
asymmetry can be easily confirmed by looking for medial movement of the nipple on the chest wall. Loss of
strength is particularly notable to internal rotation of the arm when testing at neutral.
Diagnostic Procedures: Radiography, Magnetic resonance imaging (MRI) can be especially helpful where
a partial tear is suspected
Management / Interventions
- Conservative treatment
- Surgical treatment
CHAPTER 17: REGIONAL CONDITIONS
SHOULDER
1. PERIARTHRITIC SHOULDER (ADHESIVE CAPSULITIES, FROZEN SHOULDER)
• Term given by Codman
• A Disease of unknown aetiology where the gleno – humeral joint becomes painful and stiff because of
the loss of resilience of the joint capsule, possibly with adhesions between its folds.
• Defined as clinical syndrome having painful restriction of both active and passive shoulder movements
due to cause within the shoulder or by other part of the body
Ex: fracture clavicle and diabetes
• Characterized by progressive pain and stiffness of shoulder which usually resolves in 18 months
• Mainly occur due to: diabetes, hyperparathyroidism, hemiplegia.
Causes:
1. Primary: Idiopathic
2. Secondary: Tendinitis of RC, Bicipital tendinitis, fractures, dislocation, diabetes, CVD
Clinical Features
In 1934, Codman gave diagnostic criteria for frozen shoulder. They are:
• Pain in shoulder with slow in onset
• Pain at deltoid insertion
• Inability to sleep on affected side
• Atrophy of supraspinatus and infraspinatus
• Local tenderness
• Restriction of active and passive range of motion
• Painful and restricted elevation and external rotation
Classification:
• The capsular pattern of Cyrix was also used to describe frozen shoulder where the external rotation
will be more affected than abduction and medial rotation.
Hanafin and Chiaia stated 4 stages
Stage 1: By Nevasier the preadhesive stage or pre freezing stage from 0 to 3 months where there is mild pain
increases with all movement at end ranges.
Stage 2: “The Acute adhesive” or “freezing” stage from 3 to 9 months the acute adhesive or freezing stage
where thickened synovitis with high level of pain at end ranges and significant limitation in forward flexion,
abduction, internal rotation, external rotation.
Stage 3: “The Fibrotic “or “frozen stage” from 9 to 15 months with minimal pain, significant limitation in all
ranges having rigid end feel.
Stage 4: “Thawing phase” from 15 to 24 months with minimal pain and range of motion improves.
Diagnosis on the basis of tissue irritability levels which will reflect tissue ability to handle physical stress
and related to physical status and inflammatory activity that are present.
• Diagnosis of tissue irritability helps in deciding treatment frequency, intensity, duration and optimal
dosage of rehabilitation protocol.
• On the basis of history, the irritability level can be determined by knowing ability to sleep through night,
which is predominant symptom pain or stiffness and the symptoms become worse or has improved in last
3 weeks.
High Irritability:
• High pain VAS (>6/10)
• Consistent night or resting pain
• High disability on self-reported outcomes
• Pain before end range of active or passive ROM
• Active ROM is less than Passive ROM
Moderate irritability:
• Moderate pain VAS (>4-6/10)
• Intermittent night or resting pain
• Moderate disability on self-reported outcomes
• Pain at end range of active or passive ROM
• Active ROM is same as Passive ROM.
Low irritability:
• Low pain (VAS<3/10)
• No night or resting pain
• Low disability on self-reported outcomes
• Minimal pain at end range of active or passive ROM
• Active ROM is same as Passive ROM
TREATMENT:
Conservative Treatment:
• Stage I: NSAIDS and Intraarticular steroids, hot fermentation.
• Stage II and III: Rehabilitation
Surgical Treatment:
• Release of rotator interval and coracohumeral ligament by arthroscopy
Stiffness can be prevented by continuous shoulder mobilizing exercises.
2. ROTATOR CUFF TENDINITIS

The tendinous fibres of the rotator cuff muscles at or near their insertion into the tuberosity undergo
degenerative changes with advancing age. Disintegration changes predisposes to rupture.
Mechanism of injury: A fall of the shoulder or an attempt at lifting a heavy object
• Overuse injury
• Overload injury
• Age related changes
• Decreased vascularity at attachment
Pathology:
Consequences of RC Tear:
Special test:
Neer impingement test, Hawkins Sign
Treatment:
Tendon should be repaired immediately in a case of fresh rupture. After which active exercises are instituted.
A chronic tear can be treated either by conservative methods or by surgical repair. Anterior acromioplasty
(open or arthroscopic) is performed as an adjunctive procedure to rotator cuff.
3. SUPRASPINATUS TENDINITIS
A Complete tear of the supraspinatus results in total loss of
active abduction at the glenohumeral joint.
Mechanism of injury:
• Occur due to rubbing of supraspinatus tendon below the
coracoacromial arch
• Also called as “Painful syndrome or rotator cuff
tendinitis”.
Pathology:
Normally when arm abduct → Supraspinatus tendon slides
below the arch → At 90° Abduction the ER of humerus occur
so that rotator cuff occupies sub acromial space →
But if arm is continuously in Abduction and IR, ER causes
compression of rotator cuff and as it come to anterior edge of
acromion process leads to tendinitis.
So, position of Abduction, Flexion and IR is called as

Impingement Position
Other factors causing tendinitis:
1. Osteoarthritic thickening of ACJ
2. Osteophytes on anterior edge of acromion
3. Swelling of rotator cuff
4. Rheumatoid arthritis
Clinical Features:
1. Subacute tendinitis (Painful arc syndrome)
2. Chronic tendinitis
3. Cuff disruption
1. Subacute tendinitis (Painful arc syndrome)

Symptoms:
• Pain on 60° to 120° arm abduction
• Disturbance of scapulohumeral rhythm
• Tenderness present on Anterior edge of acromion
• Occur due to vigorous activities like competitive swimming
Lesion that causes painful arc syndrome
• Minor tear of supraspinatus tendon
• Supraspinatus tendinitis
• Subacromial bursitis
• Crack fracture of GT of humerus
Treatment:
• Rest
• Sling to elevate arm with elbow flexed
• Ice compression to reduce inflammation
• Relaxed passive movements
• Codman's passive pendular exercise
• Active pendular exercises
• Strengthening exercise to arm
• After immobilsation of 2-3 weeks: vigorous exercises, relaxed passive pendular flexion and extension
in sling, strong isometric abduction
2. Chronic tendinitis
• History of recurrent attack of subacute tendinitis
• Pain increases when vigorous activity
• Pain worse at night
• Patient cannot sleep on affected side
• More comfortable in sitting
• Restriction on activities like hair grooming or dressing due to pain and stiffness
• Crepitation of rotator cuff when shoulder is passively
Test for identification:
• Empty can test/Jobes test
• Full can test
• Painful arc
• Impingement sign: Therapist stabilizes scapula with one hand and other hand is used to move affected
arm in Flexion, Abduction and Internal rotation leading to Gt directly under coracoacromial arch
3. Cuff disruption
• Most advance stage disorders
• History of refractory shoulder pain with increasing stiffness and weakness
• Can lead to partial or full thickness tear’
• Identification of tear
• Partial tear: Abduction active
• Complete tear: No active abduction
Complete tear
• Pain subsides
• Active abduction not possible
• Patient will do shrug of shoulder as trick movement
• Abduction paradox: passive abduction is full and once arm above 90° patient do abduction by deltoid
and when lowering arms sideways the arm drops suddenly also called as “Drop arm sign”
4. INFRASPINATUS TENDINITIS
A complete rupture, strain or tendinitis in the muscle. Painless weakness and painful arc with loss of 30 degree
of lateral rotation at the shoulder are the salient features of a complete rupture.
If the lesion is deep and distal, full passive elevation will be painful because the tendon is caught between the
tubercle of the humerus and the acromion.
Diagnostic Test:
1. Active test of the ROM of the shoulder external rotation with slight over pressure at the terminal point of
range. Pain appearing at the end of the range of external rotation is indicative of tendinitis of infraspinatus.
2. Active resistive test of the external rotation of shoulder: degree of resistance will be good but considerable
pain will limit the force of muscular contractions.
3. Passive test of ROM of external rotation will not reveal much limitation or pain.
Treatment:
Injection therapy: Hydrocortisone may be given.
Others same as supraspinatus management.
Physical therapy.
5. BICIPITAL TENDINITIS
• Localised tenderness in bicipital grove
• Pain in front of shoulder with any arm movement
• Pain occurs more if arm is extended
• Radiation of pain till shoulder
• Pain worse at night or once patient got up in morning’
• Occurs due to any unprepared movement or sudden jerk to the shoulder
• How to prevent: Proper warm up before the exercise
Diagnose:
Speed test/Biceps or Straight arm test
• Patient in sitting position
• The arm to be tested should be in about 60 degrees of front flexion with the
forearm supinated and the elbow fully extended.
• In the starting position the examiner forcefully presses
down on the patient’s arm at the forearm. The patient
attempts to resist the pressure of the examiner.
Alternatively, the patient attempts to forward flex the
shoulder while the examiner resists.
• Test is considered positive if pain is reported in the
bicipital groove.
Biceps load test

• This test is used to check the ability of the transverse humeral ligament to hold
the biceps tendon in the bicipital groove
• Patient sits while examiner stands in front. The patient’s elbow is flexed to 90
degrees and the forearm is in a pronated position while maintaining the upper
arm at the side. Patient is instructed to supinate arm while examiner
concurrently resists forearm supination at the wrist
• Localized pain at the bicipital groove indicates a positive test.
Yegarson test
• The patient should be seated or standing, with the humerus in
neutral position and the elbow in 90 degrees of flexion.
• The patient is asked to externally rotate and supinate their arm
against the manual resistance of the therapist.
• Yergason's Test is considered positive if pain is reproduced in the
bicipital groove during the test.
Management:
• Goal: to return to sports
Treatment:
• Ice compression for 5-10 min for two times/day
• Electrotherapy modalities
• When pain reduced then strengthening of biceps
6. SUBACROMIAL BURSITIS
The subacromial bursa is situated under the upper part of the deltoid muscle and the acromion process. It
reduces the friction and thereby permits internal rotation of the greater tuberosity of the humerus under the
acromion in movements of abduction and internal rotation of the shoulder.
It always occurs following a lesion of neighboring structures. The patient complains of pain in the shoulder
on abduction and internal rotation of the humerus. The tenderness is over the greater tuberosity which
disappears on abduction.
Treatment:
Analgesics and rest to relieve pain. Injection therapy in moderately severe cases. Hydrocortisone is infiltrated
into the area of the bursa.
In patients with intense pain, surgical excision of the inflamed bursa may be done.
Physical therapy
ELBOW
1. TENNIS ELBOW
• Also called as “Lateral epicondylitis”.
• Pain and tenderness over lateral epicondyle of
humerus
• Pain on insertion of ECRB tendon
• Mainly occur in tennis players because of
wrong strokes, improper bat, flexibility less
• Also occur in people who do repeated wrist
extension activities.
Pathology: → refer flow chart
Clinical features:
• Pain on activities with wrist extension
• Pain on forceful gripping activities
• Pain localized on lateral epicondyle
• Pain increases with activities like pouring tea,
shaking hand, lifting with forearm pronated
Clinical test:
COZENS TEST:
Therapist: Stabilize lateral epicondyle
• Patient makes a fist
• Pronate forearm
• Radial deviation
• And therapist do extension
• Pain on lateral epicondyle (+ve)
MILLS TEST:
• Grasp lateral epicondyle
• Pronate Forearm
• Flexion of wrist
• Extension of elbow
• If pain present test is positive
WRINGING TEST:
• When patient is asked to wring a towel
• Pain present on lateral epicondyle
MAUDSLEYS TEST:
• Resisted extension of middle finger leads to pain at lateral
epicondyle
DIFFERENTIAL DIAGNOSIS:
• Note possible sensory paresthesia in the superficial radial nerve distribution to rule out Radial tunnel
syndrome.
• The cervical nerve roots should be examined to rule out cervical radiculopathy.
• Other conditions: bursitis of the bursa below the conjoined tendon, chronic irritation of the radio
humeral joint or capsule, Radio capitellar chondromalacia or arthritis, radial neck fracture
osteochondritis dissecans of the elbow.
Treatment:
• Conservative: Rest and ultrasound
• Change of Equipment
• Local anesthesia and steroid injection
• Mills Maneuver: done before surgery if all methods fail.
• Forceful extension of a fully flexed and pronated forearm after injection
• Surgical treatment
• Done when pain more than 6 weeks
• Fail to respond on conservative management, restriction of activities for 2 weeks
• Percutaneous release of epicondylar muscles
• Excision of proximal portion of annular ligament,
• Excision of bursa and synovial fringes.
2. GOLFER’S ELBOW/ MEDIAL EPICONDYLITIS

• Pain and tenderness at medial epicondyle
• Pain at origin of flexor tendons of elbow
Clinical test:
1. Supinate the elbow and do wrist extension
2. Resisted wrist flexion in pronated hand
3. Resisted pronation
Treatment same as Tennis Elbow.
3. STUDENT’S ELBOW/OLECRANON BURSITIS/MINERS ELBOW/DRAUGHTSMAN ELBOW

• Chronic inflammation of olecranon bursa
• Due to repetitive injuries, injections
• It occurs when student keep elbow repeatedly over table for long time while reading and writing
Treatment same as Tennis Elbow.
4. TRICEPS TENDINITIS
• Tendonitis of the triceps is an inflammation of the muscle tendon who usually occurs on the triceps
tendon attachment (the olecranon) this is often accompanied by microtraumas
• The patient has pain and tenderness in the triceps tendon insertion into the olecranon
• This pain exacerbates by a forced extension of the elbow, Swelling around the elbow
• The patient is no longer able to do some activities of his daily living like for example to lift a heavy
box
• Not overuse your upper arm and elbow.
• use functional braces to prevent injury and warm up and stretch before an activity
• Lateral epicondylitis
• Medial epicondylitis
• Posterior Elbow Impingement
• Elbow Arthritis
• Olecranon Bursitis
• Synovial Plica Syndrome
• Snapping triceps
• Radio capitellar Arthritis
Examination: Active or passive movement of the elbow also gives pain to the
patient.
Milking maneuver test:
• the patient grasps the thumb of the affected arm and pulls downward,
with the affected elbow positioned as shown, stressing the ulnar collateral
ligament.
• Elbow pain or apprehension is positive for UCL injury.
WRIST AND HAND
1. DE QUERVAIN’S TENOSYNOVITIS
• Pain and swelling over radial styloid process
• Occur by inflammation of APL and EPB
• Tenderness at tip of radial styloid process
Causes:
• Menopause
• Direct trauma
• Forceful gripping
• Wringing of clothes
Test:
• FINKELSTEINS TEST: Thumb adducted across palm and do ulnar deviation --- leads to pain
• Resisted radial deviation: leads to pain
Treatment:
• Rest in crepe bandage
• Analgesic and ultrasound
• Immobilization: wrist in 15 *extension, CMC joint in 40* abduction and thumb at MCPJ in 10*
flexion for 8 weeks
2. GANGLION/CYSTS
• Cystic swelling on dorsum of wrist
• Result from mucoid degeneration of tendon sheath
• Mild discomfort
• Cyst is multiloculated
• Arise from leakage of synovial fluid
• Painless lump
• Lump well defined and not move
3. TRIGGER FINGER/THUMB/ STENOSING TENOSYNOVITIS

• Flexor tendon are trapped at entrance to its sheath
• When a forced extension of fingers is done the tendon passes from
narrow space and SNAP of A1 pulley occurs
• Also leads to locking of fingers
• Occur due to thickening of fibrous sheath
• More common in diabetic and gout, tailors, farmer, typist or those who
have more thumb movement
Clinical features:
• Ring and middle finger affected
• Patient feels click as they bend the finger
• When hand unclenched affected finger remains in flexed
• Tender nodule in front of MCPJ
• Locking of finger occurs
Treatment:
• Cured by injecting methyl prednisolone into tendon sheath
• Refractory cases need operation by incision over distal palmar
crease
• Flexor synovectomy
4. MALLET FINGER/HAMMER FINGER/BASEBALL FINGER

• Occurs due to injury to extensor tendons
• This results in the inability to extend the fingertip without pushing it
• There is generally pain and bruising at the back side of the farthest away
finger joint
• Usually results from over bending of the finger tip
• Typically, this occurs when a ball hits an outstretched finger and jams it
• This results in either a tear of the tendon or the tendon pulling off a bit of
bone
• The diagnosis: on symptoms and supported by X-rays
• Treatment is generally with a splint that holds the finger straight
continuously for 8 weeks.
• This should be begun within a week of the injury, If the finger is bent
during these weeks, healing may take longer.
• If a large piece of bone has been torn off surgery
• Without proper treatment a permanent deformity of the finger may occur.
• Splints are used.
5. CARPAL TUNNEL SYNDROME

• Carpal tunnel syndrome (CTS) is most common entrapment neuropathy
• CTS is a neuropathy caused by entrapment of median nerve at the level of the carpal channel,
delimitated by carpal bones and by the transverse carpal ligament
• Incidence and prevalence:
▪ More common in females than males
▪ Prevalence rates: Females → 9.2%, Males → 6%
▪ Incidence rates: 276:1,00,000/year
Anatomy and pathophysiology:
Causes:
Anatomic:
• Dislocation of lunate
• Ganglionic cysts
• Recent or mal healed fracture
• Lipoma
Systemic:
• Myxedema
• Amyloidosis
• Leukemia
• DM
• Pregnancy
• CHF
• RA
Occupational:
• Repetitive stress injury leading to flexor tenosynovitis
• Hand-arm vibration syndrome
Clinical diagnostic criteria for CTS:
• Numbness and tingling in the median nerve distribution
• Nocturnal numbness
• Weakness and/or atrophy of the thenar musculature
• Tinel’s sign
• Phalen’s test
• Loss of 2-point discrimination
• Ameliorating/exacerbating factors
• Improvement by splinting and/or steroid injection
• Worsening with activities such as driving and strenuous hand use
• Coexisting medical conditions: Pregnancy; Diabetes; Hypothyroidism
CLASSIFICATION OF CTS
First stage:
Patients have frequent awakenings during the night with a sensation of swollen, numb hand
• severe pain that irradiates from the wrist to the shoulder,
• annoying tingling in their hand and fingers (brachialgia paraesthetica nocturna)
• Hand shaking brings relief.
• At morning, a sensation of hand stiffness usually persists.
Second stage:
Presence of symptoms also during the day, mostly when the patient remains in the same position for a long
time, or performs repeated movements with hand and wrist.
• When motor deficit appears, the patient reports that objects often fall from his/her hands
Third stage:
Final stage, hypo-/atrophy of the thenar eminence.
• In this phase, sensory symptoms may diminish.
Differential diagnosis that mimic CTS:

• Pronator syndrome
• Flexor digitorum superficialis muscle
• Anterior interosseous nerve syndrome
• Cervical radiculopathy (especially C6–C7)
• Brachial plexopathy (in particular of the upper trunk)
• Thoracic outlet syndrome
• CNS disorders (multiple sclerosis, small cerebral infarction)
Physiotherapy management:
• Ultrasound therapy
• Low level Laser therapy
• Carpal bone mobilization
• Soft tissue mobilization
• Neural mobilization
• Splint
6. DUPUYTREN’S CONTRACTURE/SUPERFICIAL PALMAR FASCITIS

• Palmar fascia fans out from wrist towards fingers leading to extension across MCPJ
• Hypertrophy and contracture of palmar fascia leads to
puckering of palmar skin and fixed flexion of fingers
• Is an autosomal dominant trait
• More in males, rock drilling, epileptics, smokers.
Clinical Features:
• Nodular thickening in palm and extending distally to ring
and little finger
• Pain present
• Bilateral appearance with palm puckered, nodules
• Garrod’s pads: Dorsal knuckle pads are thickened
• Lederhosen disease: Nodules present on sole of feet
Treatment:
• Operation: Excision of fascia and cords
• Splintage done and removed after few days for active motion exercise
PELVIS AND HIP

1. IT BAND SYNDROME
• It’s an overuse injury to physically active people as a result of technical errors, anatomical factors
and muscular tightness
Training errors:
1. Abruptly increasing running mileage
2. Running on uneven surfaces
3. Running on slippery surfaces
4. Running too many hills
5. Improperly using a varus wedge
- Varus heel wedges can be used to reduce pronation and supination by angling heel bone either
medially or laterally and when running.
Anatomical factors:
1. Prominent lateral femoral epicondyle
2. Tight iliotibial band
3. Excessive genu varum
4. High arch in foot.
5. High Q angle
6. Restricted range of motion
7. Difference in leg lengths
DIAGNOSIS:
NOBLES TEST:
Procedure: The patient is supine or side-lying with the injured side up. Grasp just above the ankle and
slowly bend the knee back and forth several times from 0-90° while palpating and applying firm pressure on
the lateral epicondyle of the femur for crepitus with the thumb of the other hand.
Interpretation: Palpable snapping, rubbing or “squeaky hinge-like” crepitus or localized pain that increases
with pressure at or above the epicondyle (often at 30° of flexion) indicates ITB syndrome
OBERS TEST:
• Extend and abduct the hip joint.
• Slowly lower the leg toward the table -adduct hip- until motion is
restricted.
• Ensure that the hip does not internally rotate and flex during the test and
the pelvis must be stabilized
• As allowing the thigh to drop in flexion and internal rotation would
'give in' to the tight TFL and not accurately test the length
Treatment:
- Stage one involves resting the knee, stretching the band, applying ice and taking NSAID’s.
- Stage two includes a local steroid injection, phonophoresis and podiatric evaluation.
- Stage three involves surgical intervention for refractory cases.
2. PIRIFORMIS SYNDROME
• Caused when the piriformis muscle compresses the sciatic nerve
• Pain is usually felt in one buttock -radiation of pain down the back of the leg (sciatica).
• Pain aggravated by hip activity, Eg. walking, or prolonged sitting.
• To avoid pain and pressure in the area you may sit
• Sometimes, you’ll walk with the foot turned out due to shortening of the piriformis muscle.
TEST: Piriformis test in side-lying position:
• Patient is positioned in side-lying on the unaffected side.
• FAIR test
(Flexion Adduction and Internal Rotation).
Treatment same as above.
3. TROCHANTERIC BURSITIS
• Trochanteric bursitis is inflammation (swelling) of the bursa
(fluid-filled sac near a joint) at the outside i.e at greater
trochanter
• When this bursa becomes irritated or inflamed, it causes pain in
the hip. This is a common cause of hip pain.
Causes:
• Injury to the point of the hip: falling onto the hip, bumping the
hip into an object, or lying on one side of the body for an
extended period.
• Play or work activities that cause overuse or injury to the joint areas like running up stairs,
climbing, or standing for long periods of time.
• Incorrect posture. caused by scoliosis, arthritis of the lumbar (lower) spine, and other spine
problems.
• Stress on the soft tissues as a result of an abnormal or poorly positioned joint or bone (such as leg
length differences or arthritis in a joint).
• Other diseases or conditions. gout, psoriasis, thyroid disease or an unusual drug reaction.
• Previous surgery around the hip or prosthetic implants in the hip.
• Hip bone spurs or calcium deposits in the tendons that attach to the trochanter.
Symptoms:
• Pain on the outside of the hip which is worst after running for a while and after a run.
• The pain sometimes radiates down the outside of the thigh and it is often tender to press into the
outer / back hip area.
• climbing stairs and laying on that side may cause a problem
• Pain that gets worse during activities such as getting up from a deep chair or getting out of a car.
Preventions:
• Take it slow at first and gradually build up your activity level.
• Use limited force and limited repetitions.
• Stop if unusual pain occurs.
• Avoid repetitive activities that put stress on the hips
• Get a properly fitting shoe insert for leg length differences.
• Maintain strength and flexibility of the hip muscles.
• Use a walking cane or crutches for a week or more when needed.
KNEE
1. OSTEOCHONDRITIIS DISSECANS
• Small avascular bone fragment and cartilage get separated
from femoral condyle and appear loose in the joint.
• Due to trauma, impact at patella or microtrauma of tibial ridge
• Mainly affect lateral part of medial femoral condyle and leads
to avascular fragment and later to lose body in joint.
Clinical Features:
• Male more affected
• Quadriceps wasting
• Small effusion
• Tenderness at femoral condyle
• Wilson sign: knee flexed 90* then rotated medially and
straight leads to pain
• But with lateral rotated knee no pain
Radiological features:
• X - Ray: Lesion will be seen mainly at lateral pad of medial femoral condyle
• MRI
• BY avascular necrosis due to corticosteroid injection or alcohol abuse
• In this lesion will be on femoral condyle not the lateral part
Treatment:
Early stages: If cartilage intact and no lesion visible only pain: no treatment
If fragment is unstable: Small fragment: arthroscopy
Large fragment: fixed with screws
Detached fragment:
• Detached but in one piece: screw fixation
• Detached and in many pieces: remove all pieces, knee in cast for 6 weeks
2. A) PREPATELLAR BURSITIS/HOUSEMAIDS KNEE

B) SUPRAPATELLAR BURSITIS
• Swelling in front of patella and
joint
• Uninfected bursitis due to
constant friction
• Mainly occur in carpet cleaners,
floor cleaners and miners who do
not protective knee pads
C) INFRAPATELLAR BURSITIS/CLERGYMANS KNEE

• Swelling below patella, superior to patella ligament
• Mainly occur for people who prays on knees
Treatment
• Avoid kneeling
• Firm bandaging
• Severe pain then aspiration
3. POPLITEAL TENDINITIS
• Popliteus tendon tenosynovitis is a gap in the tendon of the popliteus
• Injury occurs in athletes and people with a history of other knee
ligament injuries after trauma
• It is a relatively unusual condition in non-athletes without a history
of Knee traumas.
Symptoms:
• Pain that occurs at the posterolateral part of the knee joint
• Inflammation, acute onset of pain, localized swelling, redness and marked tenderness over the lateral
side of the knee
• From the fossa popliteal to the outside of the knee joint will be very sensitive and painful
• A crackling sound (crepitation) when the tendon is moved is also generally heard
painful resisted knee flexion (15-30°) or internal rotation and the knee cannot be fully extended
• If the patient continues to load his knee, symptoms will get worse and scar tissue can form
• Popliteus tendinopathy is often diagnosed in professional runners and triathletes
• D/D by intraarticular pathology
• Osteochondritis dissecans
• Iliotibial band Syndrome: which is an overuse condition. Tenderness is palpable at the lateral side of
the knee joint. The pain becomes worse during activity, particularly running downhill and climbing
stairs.
• The popliteal cyst: The patient reports insidious onset of mild to moderate pain in the popliteal area
of the knee.
4. PATELLAR TENDINITIS
- It is also called as “Jumper’s Knee”.
- Repetitive microtrauma to the tendon – bone interface as in jumpers, is the causative factor for patellar
tendinitis. There is pain over the inferior pole of patella.
- On examination, tenderness is felt over bone – tendon without swelling or instability.
- During the acute phase, medication, rest, cryotherapy, diapulse or ultrasonics is applied. Gentle isometrics
to quadriceps are initiated.
- Gradual mobilization of the knee is begun, when the pain and tenderness are reduced.
5. CHONDROMALACIA PATELLA
• Also called as “Patellar pain syndrome/Patellofemoral
overload syndrome”.
• Anterior knee pain and patellofemoral tenderness
• Mainly occur due to overload of patellofemoral joint
Causes:
• Injury like direct impact on front knee which damage
articular cartilage
• Overload due to malalignment of extensor mechanism
• Overload due to weakness of vastus medialis
• Overload causes change in both articular cartilage and
subchondral knee
Clinical Features:
• Teenage girl or young adult athlete complain of pain over
front of knee
• H/O injury /recurrent displacements
• Symptoms aggravated by activity or climbing stairs /standing for long time
• Knee give way and swells up
On Examination:
• Quadriceps wasting
• Fluid in knee
• Tenderness under patella
• Crepitus on moving the knee
• Patellofemoral pain elicited by pressing the patella against femur and asking patient to contract
quadriceps
• Patellar tracking: Ask patient to sit on edge of couch and ask to flexion and extension of knee
• Measure Q angle of knee
• Skyline view of patella to check tilting or subluxation
• Lateral view of knee for patella alta and baja
• Arthroscopy to know cartilage softening
• All causes of anterior knee pain has to be D/D
• Patellar instability: patella subluxation or tilt
• Infra-articluar pathology: plica syndrome, osteochondritis dissecans
• Referred pain form hip in SCFE (Slipped Capital Femoral Epiphysis)
Treatment:
• Conservative: adjustment with activity causing pain
• Exercises to strengthen medial quadriceps
• Check for valgus foot and corrections
• Operative measures:
• Lateral release of knee capsule and extensor retinaculum
• Chondroplasty: Shaving of patellar articular surface
• Patellectomy: Only done when no treatment works and severe pain
6. PLICA SYNDROME
• Failure to absorb synovial membrane leads to persistent folds in
specific regions of membrane c/a patellar plica.
• When plica becomes irritated and inflamed leads to pain c/a
Plica syndrome.
Can be present at:
INFEROPATELLAR PLICA
• Also called as ligamentum muscosum
• Located anterior to ACL in the intercondylar area and attaches
to inferior pole of patella
SUPRAPTELLAR PLICA
• It lies superior to patella
• Connects post aspect of quadriceps above to synovial pouch
MEDIAOPATELLAR PLICA
LATEROPATELLAR PLICA
Clinical Features:
• Young adult complains of pain in front of knee with clicking episode
• H/O trauma
• Symptoms increased by exercise or climbing stairs
• Muscle wasting and effusion present
• Tenderness near upper pole of patella
• Snapping voice
Treatment: Conservative management includes routine knee rehabilitation program. Transverse massage
over plica and sessions of hamstrings stretching are important.
Arthrotomy and orthoscopic surgery to excise plica.
7. FAT PAD SYNDROME (HOFFA’S SYNDROME)

• The knee fat pad, or infrapatellar fat pad, is a soft tissue structure which lies
just below and under the kneecap (patella) and consist of sensitive structures
in the knee.
• If irritated cause pinching or “impingement” on the fat pad
• Fat pad syndrome is also known as Hoffa's Syndrome.
Causes:
• Forceful blow to the front of the knee (i.e. fall, motor vehicle accident,
football tackle)
• Tight quadriceps
• Genu Recurvatum (excessive extension of the knee)
• Forward tipping pelvis
• History of osteoarthritis in the knee
• Scarring and subsequent fibrosis (hardening) of the fat pad
Symptoms:
• Pain in the front of the knee
• Swelling below and around the knee
• Pain with fully straightening the knee
• Pain with prolonged walking, squatting and kicking activities
• Pain with wearing high heels
Diagnosis:
• On examination: check for symptoms
• In addition, they will perform a clinical test called Hoffa’s test which involves moving the kneecap
after you contract your quadriceps muscles.
• An MRI may also be used to diagnose fat pad inflammation
Treatment:
• Reduce your pain and inflammation by electrotherapy, cryotherapy, therapeutic taping, acupuncture
and gait education.
• Check joint and muscle range of motion.
• Strengthen your knee and leg muscles.
• Optimize your patellofemoral (kneecap) alignment.
• Improve your proprioception, agility, dynamic balance, landing technique and function eg walking,
running, squatting, hopping and landing.
ANKLE AND FOOT

1. ANKLE SPRAIN
This is the weakest ligament and is often injured. It has three parts:
i) Anterior talo – fibular
ii) Calcaneo – fibular in the middle and
iii) Posterior talo – fibular
Mechanism of injury: Occur in inversion force
Grade Signs & Symptoms
Grade I Ankle sprains are painful, but they have no increased laxity when compared with the
uninjured side. This correlates with mild stretching of the ATFL.
Grade II Ankle sprains are painful and have an increased laxity on testing. This correlates with a
complete tear of the ATFL and a partial tear of the CFL.
Grade III Ankle sprains are usually painful and have an unstable ankle joint on examination. This
correlates with complete ruptures of both the ATFL and CFL.
Diagnosis:
• History of twisting leading to pain and swelling
• Weight Bearing causes increase pain
• If complete tear then patient say giving way at time of injury
• Swelling and tenderness at LCL site
• If inversion and neutral position pain: LCL ligament
• If eversion and neutral position pain: MCL ligament
• Inversion and PF pains: Anterior TF ligament
• X-Ray ankle
• Stress X-rays
• If talus is titled more than 20° on forced eversion or inversion: complete LCL or MCL tear.
Treatment:
• Grade 1: Below knee plaster for 2 weeks then mobilization
• Garde 2: plaster for 4 weeks and mobilization
• Garde 3: plaster 6 weeks and mobilization
Complications: a) Stiffness of the ankle b) Osteoarthritis
2. PLANATR FASCITIS
• When plantar fascia gets pathological degeneration then called a plantar
fasciitis
• Origin of plantar fascia: arises from medial process of calcaneal
tuberosity
• Insertion: distally in 5 slips to plantar aspect of fore foot, medial and
lateral intermuscular septa
Plantar fascia fibers direction:
• Arranged from proximal to distal direction
• Arranged longitudinally
• Collagen type 1 fibers
Parts of Plantar fascia:
1. Medial
2. Central
3. Lateral
Central portion: Thickest, 12 to 29 mm in width
: Triangular shape
: Arises on medial tuberculum of calcaneus and extending forward to cover plantar of FDB
: Divides into 5 digitation which inserted on MTP Joint
Lateral Portion:
Distally thin → proximally thick to form a strong band which have abductor digiti muscle and continued
inferiorly to peroneal retinaculum → Distally inserted in 5 MT joint capsule.
Medial portion: Thinner

❖ Covers plantar surface of abductor halluces muscle
❖ Extend to flexor retinaculum of foot and medially to dorsal fascia of foot
❖ Inserts finally on 5 MTJ
Plantar fascia consists of:
1. Collagen type 1 fibers
2. Presence of hyaluron: It helps in glide the fibrous muscle, efficient shock absorber, anti-inflammatory
3. Nerve endings of Ruffini and pacini corpuscles (mechanoreceptors)
4. Inner surface of plantar fascia is innervated more than outer area
Risk factors of plantar fasciitis:

1. Limited ankle dorsiflexion
2. High body mass index
3. Running
4. Work related WB activities
5. Cavus foot
Limited ankle dorsiflexion
If Achilles tendon is short → Limited ankle DF → Excessive pronation of foot to compensate limited DF →
Increased tensile loads on plantar aponeurosis → Plantar fasciitis
High body mass index: Of more than 25 to 30 kg/m2
Running: Plantar fascia has degenerative process causing heel pain during weight bearing activities
• So, failure of plantar fascia to support load of body leads to plantar fasciitis
Plantar fasciitis is common in runners → In heel strike of running heel first contact with ground →
Absorb impact up to 3 times body weight → Ability to transfer impact depends on plantar fascia, plantar fat
pad, intrinsic foot muscle → With aging or repetitive over use the absorption power decreases → more
susceptible to plantar fasciitis
Work related weight bearing activities
1. Work under poor shock absorption
2. Time spent on hard surfaces
3. Time spent in walking
4. No of times jumping in and out of vehicle
5. 4 to 7 years of factory work
Cavus foot
1.It leads to poor flexibility
2. Arches shape of foot puts tension over plantar fascia leading to plantar fasciitis
Diagnosis of plantar fasciitis:

❖ Pain over plantar medial heel region
❖ More pain with initial steps after a long time of inactivity. Like: getting up in morning initial steps
❖ More pain with prolonged weight bearing
❖ Pain on palpation of proximal insertion of plantar fascia
Test:
❖ Positive windlass test
❖ Negative tarsal tunnel test
❖ Limited ankle dorsiflexion
❖ Abnormal FPI score
❖ High body index
Examination:
1.Outcome measures: LEFS, FDI, VAS
2.Activity and functional limitation measures:
• No direct measure present to assess it
• Pain present on heel, foot is how much since 24 hours
• Pain on taking initial steps after lying or sitting for long hours
• Pain level with single stance
3.Physical impairment measures:
1. Ankle dorsiflexion range:
Patient position: prone lying with knee extension and ankle out of couch
Ask to do active and passive dorsiflexion
Measure by: goniometer stationary arm over shaft of fibula
Moving arm over shaft of 5th metatarsal
2. Dorsiflexion eversion test
Used to diagnose tarsal tunnel syndrome
Patient sitting in Non-WB position
Examiner will dorsiflex ankle and evert the foot, extend the toes
Maintain this position for 5 to 10 seconds
Taping over tarsal tunnel region to elicit sign
Will lead to numbness or Tinel’s sign positive
3. Windlass test
Use to measure impairment in fascia and ligament (Wind glass effect→)
4. Longitudinal arch angle
Windlass test done in Weight Bearing and Non-Weight Bearing to produce windlass effect of plantar
fascia and to see heel pain is produced or not
Test done in 2 position: Weight Bearing and Non- Weight Bearing
Weight Bearing: Patient stand on step stool → Side to be tested position those MT head over edge
of step and equal weight Bearing on both sides → Examiner passively extends MTPJ to end range
and IP flexion → Do till pain is reproduced
Non-Weight Bearing: Patient sitting → Examiner Stabilizes
ankle joint in neutral by one hand just behind 1 MT head →
Examiner extends 1 MTPJ till end range → See for heel pain
to reproduce.
• Normal longitudinal arch angle formed by
• 1 line: From midpoint of medial malleolus to navicular
tuberosity
• 2 line: Medial prominence of 1 MTP head to navicular
tuberosity
• Patient standing with equal WB on both feet → See midpoint
of medial malleolus, navicular tuberosity, medial prominence of 1 MT head are marked → By
goniometer measure by 3 points with navicular tuberosity as axis point → Normal angle is 150-170*
Interventions in plantar fascia:
1. Manual therapy (A)
2. Stretching (A)
3. Taping (A)
4. Foot orthoses(A)
5. Night splints (A)
6. Physical agents
7. Electrotherapy(D)
8. Low level laser therapy(C)
9. Phonophoresis(C)
10. Ultrasound(C)
11. Footwear (C)
12. Education and counselling for weight loss (F)
13. Therapeutic exercise and neuromuscular reeducation(F)
14. Dry needling(F)
3. CALCANEAL SPUR
• Spike of bone at anterior edge of calcaneal tuberosity
• Occurs usually at posterior aspect of calcaneum and also c/a
retrocalcaneal bursitis/spur
Causes:
• Repeated plantar fasciitis
• Repeated trauma
• Constant pull of shortened plantar fascia
• Hill heel Footwear
• Fibromatosis of plantar fascia
Clinical Features:
• Pain over ball of heel
• Tenderness over plantar aspect of heel
• Swelling at attachment of plantar fascia
• X-Ray heel lateral view: show prominent bone spike from calcaneus
Treatment:
Conservative:
• Rest, NSAIDS, contrast bath, local corticosteroid, microcellular rubber for sole of footwear
Surgery:
• Osteotomy of calcaneal spur
• Decompressing operation with multiple drill holes in calcaneus
• Lateral release of plantar fascia
4. TARSAL TUNNEL SYNDROME

- Pain, burning sensation or paresthesia may occur in the toes and sole of the foot in the distribution of the
medial plantar nerve. This occurs as a result of compression neuropathy of the medial plantar nerve in the
tarsal tunnel under the flexor retinaculum on the medial aspect of the heel. This situation is analogous to the
compression of the median nerve in the carpal tunnel at the wrist.
- This compression neuropathy may be precipitated by previous sprains, fracture, tenosynovitis of the tibialis
posterior or flexor hallucis longus tendon or exaggerated medial or lateral deviation of the calcaneum.
Treatment:
- Surgical decompression of the tarsal tunnel by excising the flexor retinaculum relieves the
symptoms.
- Non-operative treatment includes steroid infiltrations at the compression site, corrective orthosis,
thermotherapy, ultrasonics and TENS.
5. ACHILLES TENDINITIS
• Occurs when tendon is degenerated and occurs above 40 years
• While pushing off → calf muscle contracts → contraction resisted by body weight--- unable to tip
toe → a gap is seen at TA tendon insertion.
SIMMONDS TEST:
• Patient prone: squeeze the calf muscles
• If tendon intact: foot do PF
• If tendon rupture: foot remain still
INCOMPLETE TEAR: Gap not seen, Patient able to stand on tip toe
Tear of soleus muscle: Cause pain and tenderness halfway up till calf and relieved by increase heel of shoe
6. METATARSALGIA
• Defined as pain beneath metatarsal head or shafts
• Due to trauma /inflammation or constant pressure at particular point
Causes:
• Weakness of intrinsic muscles of foot
• Pes cavus
• High heel shoes
• Obesity
• Arthritis
TYPES:
1.STATIC METATARSALGIA
• Due to hallux valgus, obesity
2.RELAXATION METATARSALGIA
• Failure of interosseous muscles to draw metatarsal together leads to
• Extra weight taken by metatarsal head leads to strain on ligament and cause pain
3. Compression metatarsalgia
• Due to clowded footwear
4.Fracture of II Metatarsal bone
7. MORTON’S NEUROMA
• Sudden onset of pain with burning sensation over outer border of forefoot and between 3 and 4 th
toes in walking
• Due to thickened digital nerve between 3 and 4 MT bone
CHAPTER 14: NEUROMUSCULAR DISORDERS
1. CEREBRAL PALSY (Syn: Static Encephalopathy)
This is a disorder of movement and posture caused by a non-progressive lesion in the immature brain, leading
to global dysfunction.
Lesions
In cerebral palsy, the lesion could be in either the brain or the upper cervical cord, and the lesion is static.
Incidence is 0.6–5.9/1000 live birth.
Classification:
Cerebral palsy is classified based on various clinical types and based on the degree of severity.
Based on clinical types (Minear’s) Based on severity
Spastic (65%) (Commonest type) Mild (25%) Independent in daily activities
Dyskinesia (25%) Moderate (50%)
The following varieties are described: Needs help in daily activities and
Athetosis ambulation
Tremor Severe
Choreiform
Dystonia Patient is bedridden and has a wheelchair
Rigidity existence
Ataxia
Mixed
Lesions in the Brain

In cerebral palsy, the lesions in the brain can occur in the following four areas:
􀁸 Cerebral cortex (spastic type)
􀁸 Midbrain (dyskinesia)
􀁸 Cerebellum (ataxic)
􀁸 Widespread brain involvement (rigidity and mixed).
Causes:
Pre – Natal Natal Post – Natal Peri – Natal (0 – 7 days)
Rubella infection Birth trauma Trauma Most lesions causing CP occur
Fetal anoxia Anoxia Encephalitis during this period
Maternal diabetes Prematurity Meningitis
Clinical Features
This depends on the location of lesions in the brain. Single muscle involvement is rare as in polio and
entire portion of the body supplied by that area of brain is involved, the patients show delayed mile stones and
primitive reflexes are usually preserved. Clinical features depend on the geographic distribution of cerebral
palsy and the associated handicapping situations.
Geographic distribution of cerebral palsy Associated handicapping conditions
Monoplegia (0.3%) Sensory deficit in hand (50-60%)
Hemiplegia (50%) Speech problems
Paraplegia (21%) Mental retardation
Triplegia (3.1%) Deafness
Quadriplegia (25%) Visual defects
Diplegia Seizures
Double hemiplegia Perceptual problems
Tetraplegia Emotional problems – most important
Total Body Involvement Scoliosis
Orthopedic Deformities
The following are the common orthopedic deformities encountered in cerebral palsy
Upper Limb
- Pronation contracture of the forearm - Flexion deformities of the wrist and fingers.
- Thumb in palm deformity - Swan neck deformity.
- Shoulder adduction and internal rotation deformity.
Lower Limb
- Adduction deformity (most common). - Flexion and internal rotation deformity.
- Dysplastic and subluxated hip. - Dislocated hip.
- Pelvic obliquity.
Spine
- Scoliosis - Kyphoscoliosis.
Knee
- Genu recurvatum - Genu valgum
- Patella alta - Subluxation or dislocation of patella.
- Knee flexion contracture — (most common).
Foot
- Equinus deformity - Varus or valgus
- Talipes equinovarus - Calcaneus deformity
- Talipes cavus - Hallux valgus
- Claw toes.
Treatment
There is no cure for cerebral palsy. Hence, the aim of treatment is to increase the patient’s assets as much
as possible and minimize his or her defects.
To improve the quality of life in cerebral palsy is as follows:
􀁸 Education and communication is the first priority.
􀁸 Activities of daily life.
􀁸 Mobility
􀁸 Ambulation.
The role of orthopedic surgeon starts when the child is 12 months of age and seldom before.
Methods
􀁸 Motor age test.
􀁸 Physiotherapy, occupational therapy, speech therapy, etc.
􀁸 Use of braces to:
– Improve function.
– Control unnecessary movements.
– Prevent and correct deformities.
Drug therapy: The role of drug therapy is disappointing. Muscle relaxants, antiepileptic may have a role.
Surgery
􀁸 Not done till the child reaches five years of age.
􀁸 Indicated to correct deformity in an ambulatory patient and to make him or her socially more acceptable.
􀁸 Commonly indicated in spastic type of cerebral palsy.
Choice of Surgery
Operation on nervous system: Sympathectomy, rhizotomy (anterior or posterior).
Operation on muscles and tendons:
􀁸 Tenotomy, tendon lengthening and tendon transfers.
􀁸 Myotomy and muscle transposition.
Operation on bones and joints:
􀁸 Bone lengthening or bone shortening to equalize the limb lengths.
􀁸 Osteotomies to correct knock knee, and other bone deformities.
􀁸 Arthrodesis of wrist, hip and foot to correct deformity, provide stability and to improve functions.
PHYSIOTHERAPY ASSESSMENT
Subject assessment:
Name: Age: Sex: Address:
Information taken from care taker/mother:
Chief complaints (Taken when the mother notice the dysfunction)
History: Review of complications of pregnancy and delivery, birth weight, gestation, any neonatal and
perinatal difficulties and developmental milestones.
Pre – natal history: Age of mother, consanguity marriage, any drugs taken during pregnancy, any addiction
– smoking/alcohol, history of torch infection/previous abortion, still born or death after birth, multiple
pregnancies, status and cast of the mother.
Peri – natal history: Place of deliver, history of preterm or post-term delivery/asphyxia at birth/ prolonged
labour pain, type of delivery (forceps, vacuum delivery), presentation of child (breech), legs or head comes
first, condition of mother at the time of delivery (chances of eclampsia → seizures in mother during delivery).
Post – natal history: Delayed birth cry, weight of the child at birth, History of trauma to brain during first 2
years of life/neonatal meningitis, jaundice, hypoglycemia, hydrocephalus or microcephaly.
Nutritional habits of the child (malnutrition), feeding difficulties
Any medical, surgical or PT treatment taken before:
- Treatment was used/ effective or not
- Ability level of child at that time, obstructs the child from progress, APGAR score from the case sheet.
Objective Assessment:
On Observation:
Behavior of the child and Communication of the child, Attention span, Position of the child, postural
control and alignment.
• Use of limbs and hands: Attitude of limbs during playing and in all positions, secondary aspects,
forms of locomotion’s.
• Deformities: In LL and UL
• High cognitive function
• Attention deficit disorder
• Cranial nerve integrity
• Special senses
On Examination:
• Sensory assessment
• Motor integrity
• Reflex integrity
• ROM and flexibility
• Anthropometric measurements
• Growth parameters
• Developmental milestones
• Joint Range of motion (Active and Passive)
• Posture
• Balance and gait
• Bowel and bladder involvement
• Functional capacity
PT MANAGEMENT:
INFANCY (1ST STAGE – 3 YEARS)
Aim: family education, handling and care, promote infant and prevent interaction, establish head and neck
control, attain and maintain upright position promote sensory motor development, encourage development of
functional skills and play.
Visual Development: integrated with control of head, neck, etc.
Language development
Facilitating motor developments
Acceptance of prone position
Postural stability of the shoulder joints
Maintaining an upright position
PRE – SCHOOL PERIOD

Increase force generation (strengthening)
Reduce Spasticity
ROM Exercise, splinting and serial coasting, MFR, Rhythmic rotations, stretching of tight structures,
dorsal rhizotomy, botox injections
Increase mobility and flexibility
ROM exercise, strengthening exercises of prime moves of a joint, main length of muscle by regular
stretching and splinting
Prevent deformity
Orthosis and night splints, Lycra splinting and tapping techniques
Improve physical activity
CIMT – function in hemiplegic CP
Exercise → intensive challenging and meaningful and involve integration of skills, note function.
Oraotor rehabilitation: ice, sucking water bottle.
Improve ambulatory capacity
Improve play activity (play therapy)
SCHOOL AGE AND ADOLESCENCE

Improve activity, mobility and endurance
School and community participation
TRANSITION TO ADULTHOOD
Improve functional skills
Improve and maintain CV fitness, weight control, maintain integrity of joints and muscles, help prevent
osteoporosis, use fitness clubs etc.
Transition planning: Vocational training and occupational training.
2. POLIOMYELITIS
This is a viral infection of the anterior horn cell of the spinal cord or nerve cells of brainstem, resulting in
temporary or permanent paralysis. Common in children, often attacks young adults.
Viruses
The following Picorna group of viruses is known to cause poliomyelitis:
􀁸 Brunhilde (type I)
􀁸 Leon (type II)
􀁸 Lansing (type III)
Pathogenesis
The virus is transmitted through the feco-oral route, enters the nervous tissue, and destroys the anterior
horn nerve cells because of which the peripheral nerve degenerates resulting in muscle and tendon atrophy.
The bones become small, the joint capsules and ligaments become lax, as there is no protection by the healthy
muscles. All these results in development of various deformities.
Clinical Features
Polio usually affects children less than 12 months. There is a mild episode of fever, headache and
diarrhea. On examination, there could be mild neck stiffness and the child may find it difficult to move the
affected limb (preparalytic). The lower limbs are more commonly affected and the paralysis could be partial
or total (paralytic stage).
The paralysis of the muscles whether spinal (75%) or bulbar (25%) usually lasts until two months.
Then there may or may not be recovery for a period of two years. Any residual paralysis after two years of
affection is permanent with no chance of recovery (Fig. 42.8). Bulbar poliomyelitis is rare and affects the
respiratory muscles. It may be fatal.
Stages and their corresponding features:
Orthopedic deformities:
Foot and ankle: Claw roes, Claw foot, Talipes equinus, Talipes equinovalgus, Flail foot, Pes cavus, Dorsal
bunion, Talipes equinovarus, Talipes calcaneovalgus.
Knee: Flexion contracture of the knee, Quadriceps paralysis, Genu recurvatum, Flail knee
Hip: Flexion abduction contractures of the hip, paralysis of gluteus medius, maximus, Paralytic dislocation
of hip.
Iliotibial band contractures (Results in 9 classical deformities): Lumbar scoliosis, Pelvic obliquity, Hip
flexed and abducted, external rotation of femur, flexion and valgus of knee, posterior and lateral subluxation
of tibia, foot in equinus, shortening
Spine: Kyphosis, Scoliosis and Kyphoscoliosis
Upper limbs: Paralysis of shoulder, elbow, forearm and hand muscles.
Treatment
Broad principles of the treatment
􀁸 To prevent deformities from developing.
􀁸 To assist returning of muscle power by graduated exercises.
􀁸 To reduce disability by appropriate appliance or by operations on joints and muscles.
Treatment Methods
Early stages: During the stages of onset, maximum paralysis and the stages of recovery the following
treatment is recommended, the child is admitted into the hospital, and supportive treatment is given. The child
is put on a ventilator support if there is respiratory para lysis due to bulbar polio. Warm and moist packs are
given to the joints and all intramuscular injections are avoided during this phase. Plaster splints in functional
positions immobilize the affected joints.
Recovery stages: In this stage, the joints are properly splinted through various appliances to prevent or correct
the deformities.
Role of Appliances
The purpose of external appliances is to support joints that have lost their normal control. They are more
often required for lower limbs rather than upper limbs.
External appliances in Poliomyelitis
Spinal brace To support weak spine
Abdominal support To check abdominal protrusion when abdominal muscles are
weak
Hip, Knee, Ankle, Foot orthosis with or without For deformities of the hip, knee and ankle
pelvic support
Knee Caliper To hold knee extended in quadriceps palsy
Below Knee Brace To stabilize a flail ankle or foot
Single below knee (Lateral or medial) To control varus or valgus
Drop foot appliance For mobile equinus deformity
Stage of Post-polio Residual Paralysis (PPRP)
During this stage, the role of orthopedic surgeon is predominant and surgery is the treatment of choice.
Goals of Surgery
􀁸 To obtain muscle balance.
􀁸 To prevent or correct soft tissue contractures.
􀁸 To prevent or correct bony deformities.
Surgical Methods
Soft tissue release for soft tissue contractures, e.g.
􀁸 Soutter’s release: Structures arising from anterosuperior iliac spine are released for hip contractures.
􀁸 Ober-Yount’s procedure consists of sectioning the iliotibial band (ITB) contractures.
􀁸 Tendo-Achilles lengthening for equinus deformity of the foot.
􀁸 Steindler’s release of plantar fascia for cavus foot.
􀁸 Tendon transfers: This is indicated when dynamic muscle imbalance produces deformity requiring brace
protection.
Aims of tendon transfers
􀁸 To replace the function of a paralyzed muscle.
􀁸 To remove the deforming force.
􀁸 To provide stability by improving the muscle balance.
Tendon transfers are not limited to any age group.
Arthrodesis: This is done to:
􀁸 Stabilize a flail joint.
􀁸 Eliminate the need for brace and to improve function.
􀁸 For permanent method of joint stabilization.
Osteotomies to correct deformities like genu valgum, etc.
Ilizarov’s technique for leg length equalization and deformity corrections.
3 Stages of poliomyelitis:
1. Acute Stage:
Generally, lasts 7 days. Symptoms range from mild malaise to generalized encephalomyelitis with widespread
paralysis. Differential diagnosis include Guillain – Barre syndrome and other forms of encephalomyelitis.
Treatment:
Bed rest, analgesics, hot pack and anatomical positioning of the limbs to prevent flexion posturing and
contractures. Padded foot boards, pillows, sandbags and slings can help to maintain position and passive ROM
exercises of all joints.
2. Convalescent Stage:
Begins 2 days after the temperature return to normal and continues for 2 days. Muscle strength should be
assessed after 6 months.
Treatment: Emphasize muscle activity in normal pattern and development of maximal capability of
individual muscle. Vigorous passive strength exercises and wedging casts can be used for mild to moderate
contractures.
3. Chronic Stage:
Begins 24 months after the acute illness. Maximal functional activity.
Treatment: Correct Significant correct balances, soft tissue and bony deformities correction, static joint
stability should be managed by giving orthoses, dynamic joint stability.
POST POLIO SYNDROME:

Name given after late effects of poliomyelitis. Muscle weakness, atrophy etc.
There should be poliomyelitis 2 years back.
Etiology: Caused by decades of increased metabolic demand mode on the body by giant motor units.
These giant motor units were formed.
Clinical features:
Fatigue: Overwhelming tiredness or exhaustion occuring with only minimal effort.
New weakness: Hallmark of PPS
Pain: muscle and joint pain, muscle atrophy
Cold intolerance: Due to sympathetic nervous system involvement, an individual with PPS is intolerant to
COLD. Heat is often not the modality of choice.
Decreased function:
- Fatigue, pain and weakness conspire to produce a cycle of inactivity in the person with PPS.
- Bulbar involvement (Brainstem) damage can lead to vital function such as eating and breathing.
- Sleep may be interrupted.
Medical Management:
- Prednisone (decrease inflammatory response and damage)
- Treatment depends on lifestyle changes
- Healthy diet, exercise in moderative, positive pressure ventilation, treatment of sleep, apnoea, staying
warm.
Physiotherapy management: Goals:
1. Decrease workload on muscle
2. Avoid fatigue
3. Ambulate safely
4. Achieve an optimal level of function independence
Lifestyle modification: Weight loss program required.
Energy conservation: Activity pacing
Exercises: Exercise must strengthen muscle but not induce muscle fatigue.
Aquatic exercises can be beneficial water reduce stress on joints, bone and muscle.
Stretching: Orthosis include shoe lifts, ankle – foot orthosis and knee – ankle – foot orthosis to improve gait
quality.
Pain management: gentle stretching after application of heat is indicated in the presence of cramping.
Surgical management: Post-surgical osteotomy, Tendon transfer.
3. LEPROSY
- It is a chronic granulomatous infectious disease which is caused by mycobacterium leprae.
- Involves peripheral nerves and skin
- Other organs: mucous of mouth, upper respiratory tract, eyes, bones and muscles except CNS, ovary and
lungs are spared.
- Also called as “Hanne’s Disease”.
Bacteriology:
Gram positive obligate intravascular, acid fast strain, affinity to the nerve ends because of Schwann’ cells.
- Grows in cooler regions - Axilla, scalp midline scapular line
- Range from 30 -33° C. - Grow in the nerd mouse.
Reservoir for bacteria: Animals
Source of Infection: Through nasal mucosa → discharged through snizze → droplet nuclei → through
inhalation/cut skin.
Mode of transmission: Droplet infection
Transmission: Skin – to – skin contact, soil contact, in situ vectors, tattooing needles.
Breast feeding and transplacental ways doesn’t transmit. 3 to 5 years’ time to spend. Seen in 2 to 50 years.
Germination period → 12 days. Cell mediated immunity is responsible.
Environmental factors: Humidity, moist soil, poor economic status.
Also called as “Social Disease”.
Classification: Clinico - bacteriological classification
Ridgidlo classification:
1. Tuberculi 2. Borderline tuberculi 3. Borderline borderline type of leprosy
4. Borderline lepromatous 5. Lepromatous leprosy
Indian classification:
1. Indetermine type of leprosy 2. Lepromatous leprosy
3. Tuberculi type of leprosy 4. Borderline type of leprosy 5. Pure neuritic type
Clinical features:
Indetermine type of leprosy:
- One or more hypopigmented maculi
- May progress to tuberculi, borderline/lepromatous leprosy
- Negative type of leprosy.
Tuberculi type:
- Single or few lesions
- Asymmetrical distribution of limbs and sharply designed, dry, flat or a light raised, hypopigmented or
anesthetic region
- Lepromin test => Strongly positive
Borderline tuberculi
- 4 or more lesions asymmetrical distribution maculi satellite lesion.
- Peripheral nerve enlarged in legs and hands
- Hypothesia
- Lepromin test → weakly positive.
Borderline Borderline leprosy
- Symmetrical distribution, equal space between lesion
- Asymmetrical enlargement of nerve
- Sensation may or may not be lost.
- Diagnosis may be doubtful.
Borderline lepromatous
- Hypopigment → maculopupuli
- Nerve symmetrical/asymmetrical enlarged
- Sensation may or may not be lost.
- Lepromin test → negative
Lepromatous leprosy
- Numerous nodules, symmetrical distribution well defined margin
- Lepromin test positive
- Elevated maculi and felt properly
- Involved of ear lobes as seen
- Loss of hair in eyebrows and eye lashes
- Saddle nose deformity
- Collage of nose bridge/ Neo – nine deformity
Course:
Skin → Nerves → thickened → muscle of hands and legs → destruction of nerves → atrophy → toes or fingers
(Loss of digits – auto amputation).
Nerve involvement:
- Superficial nerve involvement
o Contracture of hands and legs are seen
- Most common nerve in upper limb is ulnar nerve
- Cranial nerve – trigeminal nerve → leads to corneal anesthesia.
o Thermal sensation is lost
o Proprioception is pressured
o Facial nerve is also involved.
▪ Difficulty in closure of eyelids.
- Least common nerve in Upper limb is Radial nerve
- In ulnar nerve, medial 1/3rd anesthetic, little fingers involvement, ulnar claw hand deformity.
- Medial nerve: lateral 2/3rd of palm, muscle involvement, claw deformity of middle and index finger,
thumb deformity.
Lower limb:
Common popliteal nerve → foot drop
Posterior tibial nerve → Sole anesthesia
Features to determine of leprosy
Hypopigmented patche/partial or total loss of affected nerve
Thickened nerve, acid – fast bacilli present in smear.
Clinical Examination:
1. Physical:
Exercise of skin → Look for hypopigmentation, palpation of ulnar nerve, lateral popliteal, dorsal
Testing for loss of sensation, Paralysis of hands and legs
Check for MMT
2. Confirmation:
- Nasal smear - Skin Smear - Nasal scrapping
Test: Biopsy of the skin, immunological test - Lepromin test, ELISA.
Isolation of bacteria in mucosa and skin gives confirmation
Treatment:
Multi - drug therapy, chemotherapy
1st Line (12 to within 18 months) – Rifamycin (600 mg/once/month), dapsone (100 mg daily), cholorosomine,
ethinomide, prothinomide.
2nd line – Mycocycline
Multi – drug therapy not contraindicated in HIV, pregnancy.
- Bed rest - Treatment of affected nerve - Suppressors of others
Prevented means:
- Keeping dryness in hands, palm and soles - Use of protective skin by glows
- Prevent joint’s stiffness - Use goggles
Treatment Progression:
Community based rehabilitation is important
1. Wound and ulceration care (in chronic) 2. Orthosis and Splints
3. Passive exercises 4. Maintain the wound in becoming worse
5. In some cases, tendon transfer is done.
4. SPINAL DYSRAPHISM
• It refers to a variety of congenital anomalies resulting from failed fusion of dorsal spinal elements.
• Incomplete closure of the neural tube around third and fourth week of embryonic development.
Aetiology: Family tendency, Nutritional factors, Folic acid use preconception and during pregnancy,
Teratogens e.g. Valproate, phenytoin, alcohol; Homeobox and pax3 embryonic genes.
Pathogenesis
• Occurs between days 20 to 28 of gestation7
• Failure to close of the neural folds at the caudal end of neural tube
• Followed by failure of closure of the caudal somites, resulting in a gap of the spine
• The various varieties of spinal dysraphism are a result of the time and extent of failure of the neural tube
closure.
Open Spinal Dysraphism:
– Most common; 95% cases
– A ratio of 9:1 of OSD to CSD
– Vertebral defect with meningeal or spinal cord as the wall of the extruding cyst
– Almost all OSD are with Chiari II malformation and Hydrocephalus
– Worst form is Rachischisis; associated with anencephaly
– Diagnosed antenatal or at birth
– Neurologic dysfunction is due to;
• Primary defect in development of the nervous tissue
• Exposure to amniotic fluid
• Injury during birth
Closed Spinal Dysraphism:
– 5% of cases; occult;
– With or without a subcutaneous mass
– Intact skin covering
– No meningeal or spinal cord cystic lesion
– Most subcutaneous masses are lipomatous
– Usually identified during investigation of urologic, orthopaedic or dermal and limb problems.
Classification:
1. Open Spinal Dysraphism (95%)
- Myeloleningocele
- Myelocele
- Hemimyelomeniingocele
- Hemimyelocele
2. Closed Spinal Dysraphism (5%)
a) With a subcutaneous mass
Cervical: Cervical myelocystocele, Cervical myelomeningocele, Cervical meningocele
Lumbosacral: Lipomyelomeningocele, Lipomyeloschisis
b) Without a subcutaneous mass
Simple: Tight filum terminale, intradural lipoma, posterior spina bifida
Complex: Diastematomyelia/Diplomyelia, neurentric cysts, derma sinus, caudal regression syndrome,
dorsal enteric fistula.
Myelomeningocele
is another defect, almost always associated with neurological deficit.
The herniated mass arises midline usually in the thoracolumbar region.
It contains: CS, meninges and neural tissue.
1-2/1000 live birth
Failure of complete closure of caudal neural tube
85% occur in lumbar region
Associated conditions include
Chiari malformation, club foot, hydrocephalus, and various cerebral and cerebellar malformations.
Myelomeningocele is subclassified into spina bifida cystica and aperta depending on whether the contents of
the mass communicate with the environment.
Myelocystocele
Refers to a terminal swelling of the neural axis probably secondary to hydromyelia in utero.
The expanding mass contains dilated cord as well as meninges
CSF and fatty/fibrous tissue that herniates midline through a spina bifida defect. This results in a tethered
cord syndrome.
Extrophy of the bladder is a common associated defect.
Sacrococcygeal teratoma should be considered in the differential diagnosis.
Lipomeningocele refers to the fatty contents of a spina bifida lesion.

These may be intradural, extradural, or both.
Present with back mass, bladder problems, paralysis
Cutaneous stigmata
Symptoms are due to tethered cord and cord compression from fatty mass
Treatment is surgical decompression
Anterior Meningocele is an abnormal communication between the spinal subarachnoid space and a pelvic
(or rarely thoracic) mass via a channel in the anterior vertebral column.
Radiological features
Antenatal US
Plain film findings
structural vertebral anomalies such as hemivertebra, butterfly vertebra, or incomplete fusion of posterior
elements; it does not allow imaging of the spinal cord.
CT, MR
Surgical Management:
Careful clinical assessment
– Spina bifida neurological scale
• Pre-op counseling of the parents regarding neurological recovery
• Surgery is for prevention of infection & correcting CSF leak
• Abnormal bladder function persists in most cases
• Lower limbs difficult to assess
– Preservation of L3 → ability to stand
– Preservation L4-L5 → ability to ambulate
• antibiotics if the surgery has to be delayed
• Nursing in prone position or laterally, keeping the defect wet with soaked gauze
• Complete excision of zona epitheliosa and closure of the dural sac and skin is the goal of the surgery
• Failure to achieve the above, results in inclusion cysts and tethered cord
• Closure of the normal skin is done along the long axis of the defect.
Post – operative Care:

• Wound complications, shunt malfunction, hydromyelia, tethered cord or worsening CM II are the common
complication
• Care of the patient with MMC is lifelong requiring pediatric, urologic, physiotherapy, orthopedic, neurologic
and psychologic support
• Stridor, apnoea and bradycardia are signals of poor prognosis and a result of advancing CM II
• Hydrocephalus is either treated simultaneously, before closure of MMC or after clinical appearance.
Post – operative Outcome:

• Ten to 15% of children die in the first 6 years of their lives despite aggressive treatment
• 75 to 80% with normal IQ
• Survival:
– 92% survive to 1 year
– 78% to 17 years of age
– 46% to age > 40 years
• It is to be remembered that surgical treatment aims at reducing disability & death and not the neurological
deficits that has already occurred
• Hydrocephalus and shunt complications tend to affect intelligence.
CHAPTER 7: HAND INJURIES

CRUSH INJURIES:
•With industrialization, the incidence of crush injury to the hand is on the rise
•Cause: Farm injuries, machine injuries and road traffic accidents
•The purpose of treatment in such injuries is to restore function of the hand
INJURIES OF HAND:
Compressive type of force to the tissues.
Most common causes:
- Machine injuries in the industries
- RTA
- Agricultural injuries
- Fall of heavy objects in building collapse, during earthquakes etc.
Crush injuries result in:

• Damage to the overlying soft tissue envelope
• Laceration
• Fracture
• Bleeding
• Loss of vascular integrity
• The neurovascular structures and the bony ligamentous structures
Dangers signs in evaluation of crush injuries:

• Volar swelling, especially in the palm and digits
• Loss of active ROM
• Pain on passive motion of the digits or hand
• Altered neurovascular status
• Increased swelling, even with elevation above heart level
• Profuse bleeding from an open crush injury
CONSIDERATIONS FOR AMPUTATION

• The main aspect in treatment of crushed hand is the assessment of the injury
• The first question faced by the treating doctor is whether the hand or its part is salvageable.
• The only indication for a primary amputation is an irreversible loss of blood supply to the part
• In the absence of such an indication the need for an amputation is advisable based on the following.
1. Age of the patient:
• In children, amputation is indicated only when the part is totally nonviable.
• However, in persons over 50 years of age, amputation of one or two digits, except the thumb, may be
indicated when both digital nerves and both flexor tendons are severed.
2. Cause of crushing:
• High speed, machine injuries produce more crushing
• The causative factor also determines the extent of contamination, and thereby chances of infection; which
in turn influences the decision to salvage the hand or not.
3.Time since injury:
• Patient delay, without proper first-aid have increased risk of infection and poor tissue viability
4. Severity of crushing:
• Examination of the hand, with a viewpoint to evaluate the five tissue areas (skin, tendon, nerve, bone and
joint) helps in judging the severity of crushing
• When three or more of these require special procedures such as grafting of skin, tendon suture, alignment
of bone and joint then amputation is recommended
5.The part of the hand affected:
Every effort should be made to salvage as much of thumb and index finger as possible.
PRINCIPLES OF TREATMENT
1.Assessment of the injury:
• It is done in two stages:
(i) soon after the patient is seen, and
(ii) again prior to the operation
• The purpose of first examination is to assess whether the injury needs care in a specialized hand unit.
• Attention is first directed to the skin and then to bones, tendons and nerves.
2.Treatment priorities:
• The first: Cleaning and debridement of the wound.
• Next is stabilization of fractures and dislocations, and after that is wound closure with or without skin
graft, skin flaps.
3. Individual tissue considerations:
- Skin should be excised conservatively.
• Any enlargement of the skin wound must not cross a skin crease.
•Joshi's fixator (JESS system) is a versatile fixator for stabilizing all types of fractures of the bones of then
hand, with the possibility of adequate soft tissue care.
4. Proper splintage
• Proper splintage of the hand during treatment is necessary, otherwise the ligaments at MP and IP joints
shorten, causing stiffness
• The ideal position of immobilizationis with the MP joints in 90°of flexion and IP joints in extension
(Jame’s position)
5. Supportive care: The following supportive care is required
• Elevation of the hand for first 3-4 days to avoid edema
• Finger movements to avoid edema and stiffness
• Antibiotics, prophylaxis against tetanus and gas gangrene
• Suitable analgesics
• Dressings as necessary
6. Rehabilitation:
• In the initial period, this consists of exercises, wax bath and splintage.
TENDON INJURIES OF HAND
The anatomic Zones

5 Flexor Zones:
Zone 1:
From the insertion of the profundus tendon at the distal phalanx to just distal to the insertion of the FDS.
Flexor digitorum profundus Tendon injury
- Disruption of the FDP tendon, also known as Jersey finger.
- In an athlete’s finger – football or rugby.
- The injury causes forced extension of the DIP joint during active flexion. (Finger lies in slight extension
relative to other fingers in resting position).
- Pain and swelling
Treatment:
- Type 1 injuries (partial rupture of the tendon) can be treated without surgery with rest, ice and elevation.
- A finger splint is often used to hold the digit in place until healed.
- Type II (full tendon rupture) and
- Type III (rupture with bone chip attached)
Zone 2:
Zone II is often referred to as “Bunnell’s no man’s land”, the critical area of pulleys between the insertion of
the FDS and the distal palmar crease.
Both flexor tendons interweave in a complex manner, therefore even minimum swelling can cause adhesions
with pulleys and thereby impair the free motion of the tendon.
Injuries of Zone II: Trigger Finger
- Trigger finger or Flexor tenosynovitis is a condition in which the tendons that flex the fingers become
swollen and inflamed. This results in pain at the base of one or more of the fingers.
- Inability of FDS and FDP tendons to slide smoothly under the A1 pulley.
Zone 3:
Extends from the distal edge of the carpal ligament to the proximal edge of the A1 pulley, which is the
entrance of the tendon sheath.
The distal palmar crease superficially marks the termination of zone III and beginning of Zone II
Injury in this zone leads to Dupuytren’s contracture
Zone 5:
It has carpal tunnel
• 9 content (FDS, FDP, Median nerve)
• Injury here leads to Carpal tunnel syndrome
Extensor Zones:
Zone I • Disruption of terminal extensor tendon distal to or at the DIP joint of the fingers and IP joint of the thumb
(EPL)
• Mallet Finger
Zone II • Disruption of tendon over middle phalanx or proximal phalanx of thumb (EPL)
Zone • Disruption over the PIP joint of digit (central slip) or MCP joint of thumb (EPL and EPB
III • Boutonniere deformity
Zone • Disruption over the proximal phalanx of digit or metacarpal of thumb (EPL and EPB)
IV
Zone V • Disruption over MCP joint of digit or CMC joint of thumb (EPL and EPB)
•"Fight bite" common
• Sagittal band rupture
Zone • Disruption over the metacarpal
VI • Nerve and vessel injury likely
Zone • Disruption at the wrist joint
VII • Must repair retinaculum to prevent bowstringing
• Tendon repair followed by immobilization with wrist in 40° extension and MCP joint in 20° flexion for 3-4
weeks
Zone • Disruption at the distal forearm
VIII
Zone • Extensor muscle belly
VIII • Usually from penetrating trauma
• Often have associated neurologic injury
• Tendon repair followed by immobilization with elbow in flexion and wrist in extension
MALLET FINGER
• A mallet finger is a deformity of the finger caused when the
tendon that straightens your finger (the extensor tendon) is
damaged.
• When a ball or other object strikes the tip of the finger or thumb
and forcibly bends it
• The force of the blow may even pull away a piece of bone along
with the tendon
• The tip of the finger or thumb no longer straightens.
• This condition is sometimes referred to as baseball finger.
• The fingertip droops: it cannot straighten on its own power
• The finger may be painful, swollen and bruised
BOUTONNIERE DEFORMITY
• Flexion deformity of PIPJ
• Occur due to interruption or stretching of central slip of extensor tendon
• Occur due to trauma or RA
• Deformity suspected when: tenderness or cut over dorsum of PIPJ, Active extension of IPJ with MCPJ and
wrist flexion cannot be done
Treatment:
• Early case splinting for PIPJ in full extension for 6 weeks and passive movements for DIPJ
• Open injury of central slip: K wire fixation for 3 Weeks
CHAPTER 11: DISEASES OF BONES AND JOINTS

INFECTIVE CONDITIONS:
1. OSTEOMYELITIS
Infection of the bone by micro – organism is called “Osteomyelitis”.
Osteomyelitis can be acute or chronic.
ACUTE OSTEOMYELITIS
This can be primary (haematogenous) or secondary (following an open fracture or bone operation).
Haematogenous osteomyelitis is the commonest, and is often seen in children.
AETIOPATHOGENESIS
Staphylococcus aureus is the commonest causative organism. Others are Streptococcus and
Pneumococcus. These organisms reach the bone via the blood circulation. Primary focus of infection is
generally not detectable.
The bacteria, as they pass through the bone, get lodged in the metaphysis. Lower femoral metaphysis
is the commonest site. The other common sites are the upper tibial, upper femoral and upper humeral
metaphyses.
Pathology: The host bone initiates an inflammatory reaction in response to the bacteria. This leads to bone
destruction and production of an inflammatory exudate and cells (pus). Once sufficient pus forms in the
medullary cavity, it spreads in the following directions.
a) Along the medullary cavity: Pus trickles along the medullary cavity
and causes thrombosis of the venous and arterial medullary vessels.
Blood supply to a segment of the bone is thus cut off.
b) Out of the cortex: Pus travels along Volkmann’s canals and

comes to lie sub-periosteally. The periosteum is thus lifted off the
underlying bone, resulting in damage to the periosteal blood supply to that part of
the bone. A segment of bone is thus rendered avascular (sequestrum).
Dimensions of this segment vary from a small invisible piece
to the whole diaphysis of the bone. Pus under the periosteum generates sub-periosteal new bone (periosteal
reaction). Eventually the periosteum is perforated, letting the pus out into the muscle or subcutaneous plane,
where it can be felt as an abscess. The abscess, if unattended, bursts out of the skin, forming a discharging
sinus.
c) In other directions: The epiphyseal plate is resistant to the spread of pus. At times it may be affected by
the inflammatory process. The capsular attachment at the epiphysismetaphysis junction prevents the pus from
entering the nearby joint. In joints with an intra-articular metaphysis, pus can spread to the joint, and cause
acute pyogenic arthritis e.g., in the hip, in the shoulder etc.
DIAGNOSIS
The diagnosis of acute osteomyelitis is basically clinical. It is a disease of childhood, more common in boys,
probably because they are more prone to injury.
Presenting complaints: The child presents with an acute onset of pain and swelling at the end of a bone,
associated with systemic features of infection like fever etc. Often the parents attribute the symptoms to an
episode of injury, but the injury is coincidental. One may find a primary focus of infection elsewhere in the
body (tonsils, skin, etc.).
Examination: The child is febrile and dehydrated with classic signs of inflammation – redness, heat, etc.
localised to the metaphyseal area of the bone. In later stages, one may find an abscess in the muscle or
subcutaneous plane. There may be swelling of the adjacent joint, because of either sympathetic effusion or
concomitant arthritis.
Investigations: Investigations provide few clues in the early phase of the disease.
• Blood: There may be polymorphonuclear leucocytosis and an elevated ESR. A blood culture at the peak of
the fever may yield the causative organism.
• X-rays: The earliest sign to appear on the X-ray is a periosteal new bone deposition (periosteal reaction) at
the metaphysis. It takes about 7-10 days to appear.
• Bone scan: A bone scan using Technetium-99 may show increased uptake by the bone in the metaphysis.
This is positive before changes appear on X-ray. This may be indicated in a very early case where diagnosis
is in doubt. Indium-111 labelled leucocyte scan is most specific for diagnosis of bone infection.
Differential Diagnosis:
A) Acute septic arthritis
B) Acute rheumatic arthritis
C) Scurvy
D) Acute poliomyelitis
TREATMENT:
Treatment depends upon the duration of illness after which the child is brought.
a) If the child is brought within 48 hours of the onset of symptoms:

If a child is brought early, it is supposed that pus has not yet formed and the inflammatory process can
be halted by systemic antibiotics. Treatment consists of rest, antibiotics and general building-up of the patient.
The limb is put to rest in a splint or by traction. Choice of antibiotics varies from centre to centre. It broadly
depends upon the age of the child and choice of the doctor. In children less than 4 months of age, a combination
of Ceftriaxone and Vancomycin in appropriate dose is preferred. In older children, a combination of
Ceftriaxone and Cloxacillin is given. Antibiotics are started after taking blood for culture and sensitivity.
Antibiotics are changed to specific ones depending upon the culture and sensitivity report.
The child is adequately rehydrated with intravenous fluids As the child improves, the limb can be
mobilised. Weight bearing is restricted for 6-8 weeks. After 2 weeks, antibiotics can be administered by oral
route for 6 weeks. If the patient does not respond favourably within 48 hours of starting the treatment, surgical
intervention is required.
b) If the child is brought after 48 hours of the onset of symptoms:

If the child is brought late or if he does not respond to conservative treatment, it is taken for granted
that there is already a collection of pus within or outside the bone. Detection of pus is often difficult by clinical
examination because it may lie deep to the periosteum. An ultrasound examination of the affected part may
help in early detection of deep collection of pus. Surgical exploration and drainage is the mainstay of treatment
at this stage. A drill hole is made in the bone in the region of the metaphysis. If pus wells up from the drill
hole, the hole is enlarged until free drainage is obtained. A swab is taken for culture and sensitivity. The wound
is closed over a sterile suction drain. Rest, antibiotics and hydration are continued post-operatively. Gradually,
the inflammation is controlled and the limb is put to use. Antibiotics are continued for 6 weeks.
COMPLICATIONS
This can be divided into two types, general and local:
General complications: In the early stage, the child may develop septicaemia and pyaemia. Either
complication, if left uncontrolled, may prove fatal.
Local complications: Chronic osteomyelitis, Acute pyogenic arthritis, pathological fracture, growth plate
disturbances.
CHRONIC OSTEOMYELITIS
The term ‘chronic osteomyelitis’ is used for chronic pyogenic osteomyelitis.
Causes of chronic osteomyelitis are tuberculosis, fungal infections etc.
There are three types of chronic osteomyelitis:
a) Chronic osteomyelitis secondary to acute osteomyelitis.
b) Garre’s osteomyelitis.
c) Brodie’s abscess.
PATHOLOGY
Acute osteomyelitis commonly leads to chronic osteomyelitis because of one or more of the following reasons:
a) Delayed and inadequate treatment: This is the commonest cause for the persistence of an osteomyelitis.
Delay causes spread of pus within the medullary cavity and subperiosteally. This results in the death of a part
of the bone (sequestrum formation). Destruction of cancellous bone leads to the formation of cavities within
the bone. Such ‘non-collapsing’ bone cavities and sequestra are responsible for persistent infection.
b) Type and virulence of organism: Sometimes, despite early, adequate treatment of acute osteomyelitis, the
body’s defense mechanism may not be able to control the damaging influence of a highly virulent organism,
and the infection persists.
c) Reduced host resistance: Malnutrition compromises the body’s defense mechanisms, thus letting the
infection persist.
The sub-periosteal bone is deposited in an irregular fashion so that the osteomyelitic bone has an
irregular surface. Continuous discharge of pus results in the formation of a sinus. With time, the sinus tract
gets fibrosed and the sinus becomes fixed to the bone. Sequestrum is a piece of dead bone, surrounded by
infected granulation tissue trying to ‘eat’ the sequestrum away. It appears pale and has a smooth inner and
rough outer surface, because the latter is being constantly eroded by the surrounding granulation tissue.
Involucrum is the dense sclerotic bone overlying a sequestrum. There may be some holes in the involucrum
for pus to drain out. These holes are called cloacae. The bony cavities are lined by infected granulation
issue.
DIAGNOSIS
Diagnosis is suspected clinically but can be confirmed radiologically by its characteristic features. The disease
begins in childhood but may present later. The lower-end of the femur is the commonest site.
Presenting complaints: A chronic discharging sinus is the commonest presenting symptom. The onset of
sinus may be traced back to an episode of acute osteomyelitis during childhood. Often sinuses heal for short
periods, only to reappear with each acute exacerbation. Quality of discharge varies from seropurulent
to thick pus. There may be a history of extrusion of small bone fragments from the sinus. Pain is usually
minimal but may become aggravated during acute exacerbations. Generalised symptoms of infection such as
fever etc., are present only during acute exacerbations. A patient with chronic osteomyelitis may present with
complications discussed subsequently.
Examination:
1. Chronic discharging sinus
2. Thickened, irregular bone
3. Tenderness on deep palpation
4. Adjacent joint may be stiff.
Investigations:
1. Radiological examination: The following are some of the salient radiological features seen in chronic
osteomyelitis:
• Thickening and irregularity of the cortices
• Patchy sclerosis
• Bone cavity: This is seen as an area of rarefaction surrounded by sclerosis
• Sequestrum: This appears denser than the surrounding normal bone because the decalcification which occurs
in normal bone, does not occur in dead bone. Granulation tissue surrounding the sequestrum gives rise to a
radiolucent zone around it. A sequestrum may be visible in soft tissues
• Involucrum and cloacae may be visible.
2. Sinogram
3. CT Scan and MRI
4. Blood
5. Pus
1. Tubercular osteomyelitis
2. Soft tissue infection
3. Ewing’s sarcoma
Treatment:
Principles of treatment:
Treatment of chronic osteomyelitis is primarily surgical. Antibiotics are useful only during acute
exacerbations and during postoperative period. Aim of surgical intervention is:
(i) removal of dead bone;
(ii) elimination of dead space and cavities; and
(iii) removal of infected granulation tissue and sinuses.
Operative procedures:
a) Sequestrectomy: This means removal of the sequestrum. If it lies within the medullary cavity, a window is
made in the overlying involucrum and the sequestrum removed. One must wait for adequate involucrum
formation before performing sequestrectomy.
b) Saucerisation: A bone cavity is a ‘non-collapsing cavity’, so that there is always some pentup pus inside
it. This is responsible for the persistence of an infection. In saucerisation, the cavity is converted into a ‘saucer’
by removing its wall. This allows free drainage of the infected material.
c) Curettage: The wall of the cavity, lined by infected granulation tissue, is curetted until the underlying
normal-looking bone is seen. The cavity is sometimes obliterated by filling it with entamycin impregnated
cement beads or local muscle flap.
d) Excision of an infected bone: In a case where the affected bone can be excised en bloc without
compromising the functions of the limb, it is a good method e.g., osteomyelitis of a part of the fibula. With
the availability of Ilizarov’s technique, an aggressive approach, i.e., excising the infected bone segment and
building up the gap by transporting a segment of the bone from adjacent part has shown good results.
e) Amputation: It may, very rarely, be preferred in a case with a long standing discharging sinus, especially
if the sinus undergoes a malignant change.
COMPLICATIONS
1. An acute exacerbation or ‘flare up’ of the infection occurs commonly. It subsides with a period of rest,
and antibiotics, either broad-spectrum or based on the pus culture and sensitivity report.
2. Growth abnormalities: Osteomyelitis may cause growth disturbances at the adjacent growth plate, in one
of the following ways:
• Shortening, when the growth plate is damaged.
• Lengthening because of increased vascularity of the growth plate due to the nearby osteomyelitis.
• Deformities may appear if a part of the growth plate is damaged and the remaining keeps growing.
3. Pathological fracture may occur through a weakened area of the bone. Treatment is by conservative
methods.
4. Joint stiffness may occur because of scarring of soft tissues around the joint or due to the joint gettting
secondarily involved.
5. Sinus tract malignancy is a rare complication. It occurs many years after the onset of osteomyelitis.
It is usually a squamous cell carcinoma. The patient may need amputation.
6. Amyloidosis: As with all other long standing suppurations, this is a late complication of osteomyelitis.
PROGNOSIS
To cure a bone infection is very difficult. Operative intervention may be useful if there is an obvious factor
responsible for the persistence of the infection e.g., sequestrum, cavity etc.
2. BRODIES ABSCESS
It is a special type of osteomyelitis in which the body’s defense
mechanisms have been able to contain the infection so as to create a
chronic bone abscess containing pus or jelly-like granulation tissue
surrounded by a zone of sclerosis.
Clinical features: The patient is usually between 11 to 20 years of age.
Common sites are the upper end of the tibia and lower-end of the femur. It
is usually located at the metaphysis. A deep boring pain is the predominant
symptom. It may become worse at night. In some instances, it becomes
worse on walking and is relieved by rest. Occasionally, there may be a
transient effusion in the adjacent joint during exacerbation of symptoms. An examination may reveal
tenderness and thickening of the bone.
Radiological features: The radiological picture is diagnostic. It shows a circular or oval lucent area
surrounded by a zone of sclerosis. The rest of the bone is normal.
Treatment is by operation. Surgical evacuation and curettage is performed under antibiotic cover. If the
cavity is large, it is packed with cancellous bone chips.
3. TUBERCULOSIS
* TUBERCULOSIS OF THE SPINE (Pott's disease)
The spine is the commonest site of bone and joint tuberculosis; the dorso-lumbar region being the one
affected most frequently.
PATHOLOGY
Like tuberculosis of the bones and joints elsewhere in the body, TB of the spine is always secondary.
The bacteria reach the spine via the haematogenous route, from the lungs or lymph nodes. It spreads
via the para-vertebral plexus of veins i.e., Batson's plexus, which has free communication with the visceral
plexus of the abdomen, a common site of tuberculosis.
Types of vertebral tuberculosis: Lesions in the vertebrae may be of the following types:
a) Paradiscal: This is the commonest type. In this, the contiguous areas of two adjacent vertebrae along with
the intervening disc are affected.
b) Central: In this type, the body of a single vertebra is affected. This leads to early collapse of the
weakened vertebra. The nearby disc may be normal. The collapse may be a ‘wedging’ or
‘concertina’ collapse; wedging being commoner.
c) Anterior: In this type, infection is localised to the
anterior part of the vertebral body. The infection
spreads up and down under the anterior longitudinal
ligament.
d) Posterior: In this type, the posterior complex of
the vertebra i.e., the pedicle, lamina, spinous process
and transverse process are affected.
Pathology:
Basic pathology is the same as that in other bone and joint tuberculosis. In the commoner paradiscal
type, bacteria lodge in the contiguous areas of two adjacent vertebrae. Granulomatous inflammation results in
erosion of the margins of these vertebrae. Nutrition of the intervening disc, which comes from the end-plates
of the adjacent vertebrae is compromised. This results in disc degeneration, and as the process continues,
complete destruction.
Weakening of the trabeculae of the vertebral body results in collapse of the vertebra. Type of collapse
is generally a wedging, occurs early, and is severe in lesions of the dorsal spine. This is because, in the dorsal
spine the line of weight bearing passes anterior to the vertebra so that the anterior part of the weakened vertebra
is more compressed than resulting in wedging.
In the cervical and lumbar spines, because of their lordotic curvature (round forwards), wedging is less.
Destruction occurs early, and is severe in children.
Cold abscess: This is a collection of pus and tubercular debris from a diseased vertebra. It is called a cold
abscess because it is not associated with the usual signs of inflammation – heat, redness etc., found with a
pyogenic abscess.
The tubercular pus can track in any direction from the affected vertebra. If it travels backwards, it may
press upon the important neural structures in the spinal canal. Pus may come out anteriorly (pre-vertebral
abscess) or on the sides of the vertebral body (para-vertebral abscess). Once outside the vertebra the pus may
travel along the musculo-fascial planes or neurovascular bundles to appear superficially at places far away
from the site of lesion.
Healing: As healing occurs, the lytic areas in the bone are replaced by new bone. The adjacent vertebrae
undergo fusion by bony-bridges. Whatever changes have occurred in the shape of the vertebral body are,
however, permanent.
CLINICAL FEATURES
Presenting complaints: Clinical presentations of a case of TB of the spine is very variable – from a seemingly
non-specific pain in the back to complete paraplegia. Following are some of the common presenting
complaints:
• Pain: Back pain is the commonest presenting symptom. It may be diffuse; no more than a dull ache in the
early stages, but later becomes localised to the affected diseased segment. It may be a ‘radicular’ pain i.e., a
pain radiating along a nerve root. Depending upon the nerve root affected, it may present as pain in the arm
(cervical roots), girdle pain (dorsal roots), pain abdomen (dorso-lumbar roots), groin pain (lumbar roots) or
‘sciatic’ pain (lumbo-sacral roots).
• Stiffness: It is a very early symptom in TB of the spine. It is a protective mechanism of the body, wherein
the para-vertebral muscles go into spasm to prevent movement at the affected vertebra.
• Cold abscess: The patient may present the first time with a swelling (cold abscess) or problems secondary
to its compression effects on the nearby visceral structures, such as dysphagia in TB of the cervical spine. A
detailed examination in such cases reveals underlying TB of the spine.
• Paraplegia: If neglected, which is often the case in developing countries, a case of TB of the spine presents
with this serious complication.
• Deformity: Attention to TB of the spine may be attracted, especially in children, by a gradually increasing
prominence of the spine – a gibbus.
• Constitutional symptoms: Symptoms like fever, weight loss etc., are rarely the only presenting symptoms.
EXAMINATION
The aim of examination is:
(i) to pick up findings suggestive of tuberculosis of the spine;
(ii) to localise the site of lesion;
(iii) find skip lesions; and
(iv) to detect any associated complications like cold abscesses or paraplegia.
Following is the systematic way in which one should proceed to examine a case of suspected TB of the spine.
• Gait: A patient with TB of the spine walks with short steps in order to avoid jerking the spine. He may take
time and may be very cautious while attempting to lie on the examination couch. In TB of the cervical spine,
the patient often supports his head with both hands under the chin and twists his whole body in order to look
sideways.
• Attitude and deformity: A patient with TB of the cervical spine has a stiff, straight neck. In dorsal spine
TB, part of the spine becomes prominent (gibbus or kyphus*). Significant deformity is generally absent in
lumbar spine tuberculosis; there may just be loss of lumbar lordosis.
• Para-vertebral swelling: A superficial cold abscess may present as fullness or swelling on the back, along
the chest wall or anteriorly. It is easy to diagnose because of its fluctuant nature. Sometimes, an abscess may
be tense and it may not be possible to elicit fluctuation. A needle aspiration may be performed in such cases,
to confirm the diagnosis. It is important to look for cold abscesses in not so obvious locations, depending upon
the region of the spine affected
• Tenderness: It can be elicited by pressing upon the side of the spinous process in an attempt to rotate the
vertebra.
• Movement: There is no necessity to examine for spinal movement in a patient with obviously painful spine.
Spinal movement are limited in a case of TB of the spine, and can be tested, wherever considered suitable.
• Neurological examination: A thorough neurological examination of the limbs, upper or lower, depending
on the site of tuberculosis should be performed. In addition to motor, sensory and reflexes examination, an
assessment should be made of urinary or bowel functions. Aim of neurological examination is to find:
(i) whether or not there is any neurological compression;
(ii) level of neurological compression; and (iii) severity of neurological compression.
• General examination: A general physical examination should be performed to detect any active or healed
primary lesion. The patient may have some other systemic illness like diabetes, hypertension, jaundice etc.,
which may have a bearing on further treatment.
RADIOLOGICAL INVESTIGATIONS:
X – ray examination:
- Reduction of disc space
- Destruction of the vertebral body
- Evidence of cold abscess
* Para – vertebral abscess
* Widened mediastinum
* Retro – pharyngeal abscesstion
* Psoas abscess
- Rarefaction
- Unusual signs: aneurysmal sign
- Signs of healing
CT Scan
Biopsy
Other general investigations: ESR, Mantoux test, ELISA test for detecting anti-tubercular antibodies, chest
x – ray etc. to support the diagnosis of TB.
TREATMENT:
Principles of treatment: Aim of treatment is:
(i) to achieve healing of the disease; and
(ii) to prevent, detect early, and treat promptly any complication like paraplegia etc. Treatment consists
of anti-tubercular chemotherapy, general care, care of the spine, and treatment of the cold abscess.
Care of the spine: This consists of providing rest to the spine during the acute phase, followed by
guarded mobilization.
• Rest: A short period of bed rest for pain relief may be sufficient during early stages of treatment. In cases
with significant vertebral destruction, a longer period of bed rest is desirable to prevent further collapse and
pathological dislocation of the diseased vertebrae. In children, a body cast is sometimes given, basically to
force them to rest. Minerva jacket or a collar may be given for immobilising the cervical spine.
• Mobilisation: As the patient improves, he is allowed to sit and walk while the spine is supported in a collar
for the cervical spine, or an ASH brace for the dorso-lumbar spine. The patient is weaned off the brace once
bony fusion occurs. He is advised to avoid sports for 2 years.
Treatment of cold abscess: A small cold abscess may subside with anti-tubercular treatment. Abscesses
presenting superficially need treatment as discussed below;
• Aspiration: A thick needle is required because often there is thick caseous material. It should be an anti-
gravity insertion with the needle entering through a zig-zag tract.
• Evacuation: In this procedure, the cold abscess is drained, its walls curetted, and the wound closed without
a drain. This is unlike drainage of a pyogenic abscess, where a post-operative drain is always left. A psoas
abscess can be drained extra-peritoneally using a kidney incision.
COMPLICATIONS
1. Cold abscess: This is the commonest complication of TB of the spine. Treatment is as discussed above.
2. Neurological compression: At times the patient presents as a case of spinal tumour syndrome; the
first clinical symptom being a neurological deficit (discussed subsequently).
TUBERCULOSIS OF THE HIP
After spine, the hip is affected, most commonly. It usually occurs in children and
adolescents, but patients at any age can be affected.
PATHOLOGY
The usual initial lesion is in the bone adjacent to the joint i.e., either the acetabulum
or the head of the femur (osseous tuberculosis). In some cases, the lesion may begin
in the synovium (synovial tuberculosis), but quickly the articular cartilage and
the bones are affected. A purely synovial tuberculosis, as seen in the knee joint,
is uncommon in the hip.
Natural history: The infected granulation tissue harbouring the bacilli, from the
initial bony focus erodes the overlying cartilage or bone and reaches the joint. In
early stage, this results in synovial hypertrophy and effusion. The pannus of hypertrophied synovium around
the articular cartilage gradually extends over and under it. Cartilage is thus destroyed and the joint becomes
full of pus and granulation tissue. Synovium gets thickened, oedematous, grey and ulcerated. Denuded of their
protective cartilage, the bone ends become raw.
Multiple cavitation is typical of tuberculosis. Such cavities are formed in the femoral head and the
acetabulum. Eventually, the head or the acetabulum gets partially absorbed. By the constant pull of the muscles
acting on the hip, the remaining head of the femur may dislocate from the acetabulum onto the ilium, giving
rise to the so-called wandering acetabulum. In later stages, pus bursts through the capsule
and spreads in the line of least resistance. It may present as cold abscess in the groin or in the region of the
greater trochanter. Pus may perforate the acetabulum and appear as a pelvic abscess.
Healing: If left untreated, healing may take place by fibrosis, leading to ankylosis of the hip usually in a
deformed position (fibrous ankylosis).
CLINICAL FEATURES
Presenting complaints: The disease is insidious in onset and runs a chronic course. The child may be pathetic
and pale with loss of appetite before definite symptoms pertaining to the hip appear. One of the first symptoms
is stiffness of the hip, and it produces a limp. Initially, stiffness may occur only after rest, but later it persists
all the time. Pain may be absent in early stages, or if present, may be referred to the knee. The child may
complain of ‘night cries’, the so called ‘starting pain’, caused by the rubbing of the two diseased
surfaces, when movement occurs as a result of the muscle relaxation during sleep. Later, there may be
cold abscesses around the hip or these may burst, resulting in discharging sinuses.
EXAMINATION
It should be carried out with the patient undressed. Following physical findings may be present:
• Gait: Lameness is one of the first signs. In the early stage, it is because of stiffness and deformity of the hip.
Because of the flexion deformity at the hip, the child stands with compensatory exaggerated lumbar lordosis.
While walking the hip is kept stiff. Forward–backward movement at the lumbar spine is used for propulsion
of the lower limb. This is called the ‘stiff-hip gait’. Later the limp is exaggerated by pain so the child hastens
to take the weight off the affected side. This is called the ‘painful or antalgic gait’.
• Muscle wasting: The thigh muscles and gluteal muscles are wasted.
• Swelling: There may be swelling around the hip because of a cold abscess.
• Discharging sinuses: There may be discharging sinuses in the groin or around the greater trochanter. There
may be puckered scars from healed sinuses.
• Deformity: Gross deformities may be obvious on inspection. Minimal deformities are compensated for by
pelvic tilt and can be made obvious by tests. Commonly it is flexion, adduction and internal rotation deformity
of the hip.
• Shortening: There is generally a true shortening in TB of the hip, except in Stage I, in which an apparent
lengthening occurs. Limb length discrepancy can occur at this joint not only because of actual shortening of
the bones (true length) but also because of the adduction-abduction deformity, which results in pelvic tilt and
thus affects the length of the limb (apparent length).
• Movements: Both, active and passive movements are limited in all directions. An attempted movement is
associated with muscle spasm. There may be severe limitation of movements, both active and passive, in all
directions in late cases of tuberculosis. This is called ankylosis of the hip. If there is no movement at all, it is
bony ankylosis.
• Abnormal position of the head: In a dislocated hip, the head can be felt in the gluteal region.
• Telescopy: This test assesses the instability of the head if it is out of the acetabulum.
STAGES OF TB OF THE HIP

Stage I (stage of synovitis): There is effusion into the joint which demands the hip to be in a position of
maximum capacity. This is a position of flexion, abduction and external rotation. Since flexion and abduction
deformities are only slight and are compensated for by tilting of the pelvis, these do not become obvious. The
limb remains in external rotation. As the pelvis tilts downwards to compensate for the abduction deformity,
the affected limb appears longer (apparent lengthening), though on measuring true limb lengths, the two limbs
are found to be equal. This stage is also called the stage of apparent lengthening. It lasts for a very short
period. Very rarely does a patient present to the hospital in such an early stage of the disease.
Stage II (stage of the arthritis): In this stage, the articular cartilage is involved. This leads to spasm of the
powerful muscles around the hip. Since the flexors and adductors are stronger muscle groups than the
extensors and abductors, the hip takes the attitude of flexion, adduction and internal rotation. Flexion and
adduction may be concealed by compensatory tilt of the pelvis but internal rotation of the leg is obvious. As
the pelvis tilts upwards to compensate for the adduction, the affected limb appears shorter (apparent
shortening), although on comparing the limb lengths in similar positions, the two limbs are equal. This is also
called the stage of apparent shortening.
Stage III (stage of erosion): In this stage, the cartilage is destroyed and the head and/or the acetabulum is
eroded. There may be a pathological dislocation or subluxation of the hip. Attitude of the limb is the same as
that in Stage II i.e., flexion, adduction and internal rotation except for the fact that the deformities are
exaggerated. There is true shortening of the limb because of the actual destruction of the bone. In addition,
apparent length of the limb is further reduced because of the adduction deformity.
INVESTIGATIONS
Radiological examination:
Haziness, lytic lesion, reduction of joint space, irregular outline, acetabular changes, signs of healing.
Biopsy: It may be needed in some doubtful cases. This is done by exposing the hip by the posterior approach
and taking a piece of the synovium for histopathological examination. It is possible to do an arthroscopic
biopsy.
A) Other causes of monoarthritis of the hip
B) Inguinal lymphadenopathy or psoas abscess
C) Other diseases of the hip presenting at that age: Congenital dislocation of the hip, Congenital coxa vara,
Perthes’ disease
D) Osteoarthritis
TREATMENT:
Principles of treatment: It is to control the disease activity, and to preserve joint movement. In early stages
(Stages I and II), it is possible to achieve this by conservative treatment. In later stages (Stage II and after),
significant limitation of joint functions occur despite best treatment. Treatment may be conservative or
operative.
Conservative treatment:
It consists of antitubercular chemotherapy and care of the hip.
• Care of the hip: The affected hip is put to rest by immobilisation using below-knee skin traction.
In addition to providing pain relief, this also corrects any deformity by counteracting the muscle spasm.
Operative treatment: The following operative procedures may be indicated in TB of the hip.
• Joint debridement: The joint is opened using posterior approach. Pus, necrotic tissue, inflamed synovium
and dead cartilage are removed from the joint. Any cavities in the head of
the femur or acetabulum are curetted. The joint is washed thoroughly with
saline and the wound closed. Post-operatively the joint surfaces are kept apart
by traction to the leg. After the wound heals, the joint is mobilized.
• Girdlestone arthroplasty: The hip joint is exposed using the posterior
approach. Head and neck of
the femur is excised. Dead necrotic tissues and granulation tissues are
excised. Postoperatively,
bilateral skeletal traction is given for 4 weeks, followed by mobilization of the hip.
It is possible to regain reasonable movement of the hip by this procedure even in
severely damaged joints.
• Arthrodesis: In selected cases, where a stiff hip in a functional position is more suitable considering day-
to-day activities of the patient, it is produced surgically by knocking the joint out.
• Corrective osteotomy: Cases where bony ankylosis of the hip has occurred in an unacceptable position
from the functional viewpoint, a subtrochanteric corrective osteotomy of the femur may be required.
• Total hip replacement: There is enough evidence now, that a total hip replacement is a useful
operation in some patients with quiescent tuberculosis. But as of now in most Afro-Asian countries, where
most cannot afford a total hip replacement, and where most patients want to be able to squat even at the cost
of instability, an excision arthroplasty is a preferred option.
Deciding the plan of treatment: In early stages, ATT and skin traction is given. As the disease comes
under control, as is evident from the relief of symptoms; joint mobilisation is begun. By physiotherapy good
joint functions can be regained in most cases. In cases presenting in late stages, initial treatment is by ATT
and below-knee skin traction. The traction keeps the hip in a functional position with the joint surfaces apart
while healing occurs. As the disease activity comes under control and symptoms (pain etc.) subside, a
decision has to be made whether useful hip functions can be regained, depending upon the X-ray appearance
of the hip. In a case, where there is no or minimal destruction of the hip joint mobilisation is begun
with the hope of regaining as much movement as possible. In a case where the X-ray picture suggests
significant joint damage or subluxation, one expects that normal joint functions cannot be regained. In such
a situation, the options before the surgeon are essentially these:
a) To provide a painless, mobile but unstable joint by an excision arthroplasty (Girdlestone arthroplasty).
Though the hip becomes unstable and the limb short, one can expect that patient will be able to squat on the
floor.
b) To provide a painless, stable but fixed joint by surgically fusing the joint (arthrodesis) or by conservative
means. Though the hip is stable, lack of movement, and thus an inability to squat is the major problem. In
countries, where for most of day-to-day activities squatting is required, Girdlestone arthroplasty is still-
considered a suitable operation. In addition to providing a mobile hip, this operation enhances healing of the
disease as physical removal of the infected bone, synovium etc. is done. In selected patients, joint
debridement has resulted in a stable hip with reasonable mobility of the hip. A total hip replacement has also
been advocated in some cases of healed TB.
TUBERCULOSIS OF THE KNEE
The knee is a common site of tuberculosis. Being a superficial joint, early diagnosis is usually possible.
A delay in diagnosis can severely compromise joint functions.
PATHOLOGY
The disease may begin in the bone (osseous tuberculosis), usually in the femoral or tibial condyles, or more
rarely in the patella. More commonly, the disease begins in the synovial membrane (synovial tuberculosis),
leading to hypertrophy of the synovium. In early stages, the disease may be confined to the synovium without
significant damage to the joint.
Natural history: In later stages, the articular cartilage and bone are destroyed irrespective of the site of origin.
In all types, there occurs synovial hypertrophy, synovial effusion and pus formation in the joint. The
hypertrophied synovium spreads under and over the cartilage and destroys it. The cartilage may become
detached, leaving the bone exposed. Long standing distension of the joint and destruction of the ligaments
produces subluxation of the tibia. The tibia flexes, slips backwards and rotates externally on the femoral
condyles (triple subluxation). Pus may burst out of the capsule to present as a cold abscess, and subsequently
a sinus.
Healing: If untreated, nature's attempt at healing may result in fibrosis, and thereby stiffness of the joint in a
deformed position. Healing is by fibrosis (fibrous ankylosis).
CLINICAL FEATURES
Presenting complaints: The patient, usually in the age group of 10-25 years, presents with complaints of pain
and swelling in the knee. It is gradual in onset without any preceding history of trauma. Subsequently, pain
increases and the knee takes an attitude of flexion. The patient starts limping. There is severe stiffness of the
knee.
EXAMINATION
Following findings may be present on examination:
• Swelling: The joint is swollen, which may be due to synovial hypertrophy or effusion. The same can be
detected by tests.
• Muscle atrophy: Atrophy of the thigh muscles is more than what can be accounted for by disuse alone. This
is an unexplained feature of joint tuberculosis.
• Cold abscess: There may be swelling due to a cold abscess, either around the knee or in the calf.
• Sinus: There may be discharging or healed sinuses.
• Deformity: In early stages, there is a mild flexion deformity of the knee because of effusion in the knee, and
muscle spasm. Later, triple displacement (flexion, posterior subluxation and external rotation) occurs due to
ligament laxity.
• Movements: The movements at the joint are limited. There is pain and muscle spasm on attempting
movement.
INVESTIGATIONS
Radiological examination: X-ray is essentially normal in a case of synovial tuberculosis, except for a soft
tissue shadow corresponding to the distended knee. The joint space may be widened. There is diffuse
osteoporosis of the bones around the joint. In osseous tuberculosis, one may see juxta-articular lytic lesions.
The joint surfaces may be eroded. In later stages, joint space may be diminished or completely lost. In
advanced stages, triple subluxation with cavitatory bone lesions may be present.
DIFFERENTIAL DIAGNOSIS
Diagnosis is not difficult in a late case, but when the patient presents with synovitis, other causes of synovitis
should be excluded before arriving at a diagnosis of TB of the knee. These include subacute pyogenic
infection, monoarticular rheumatoid arthritis, chronic traumatic synovitis, rheumatic arthritis and hemophilic
arthritis.
TREATMENT
Principles of treatment: Aim of treatment is to achieve, wherever possible, a painless mobile joint. This is
possible if a patient has come early for treatment. In later stages, some amount of pain and stiffness persist in
spite of treatment.
Conservative treatment: This consists of antitubercular chemotherapy, general care and local care of the part
affected. It is started an all cases and decision for surgery taken if indicated.
• Care of the knee: The knee is rested by applying below-knee skin traction or an above-knee POP slab. This
helps in the healing process, and also takes care of the associated muscle spasm which keeps the knee in a
deformed position.
Operative treatment: Following operative procedures may be required in suitable cases:
• Synovectomy: It may be required in cases of purely synovial tuberculosis. Very often one
finds ‘melon seed’ bodies within the joint.
• Joint debridement: This may be required in cases where the articular cartilage is essentially preserved. The
pus is drained, the synovium excised, and all the cavities curetted.
• Arthrodesis: In advanced stages of the disease with triple subluxation and complete cartilage destruction, the
knee is arthrodesed in functional position, i.e., about 5-10o of flexion and neutral rotation. One popular method
of knee arthrodesis is Charnley's compression arthrodesis. With the current state of development of surgery,
all these operations can be performed by minimally invasive arthroscopic surgery.
Plan of treatment:
TUBERCULOSIS OF THE SHOULDER JOINT:

This TB I very rare, seen in adults, mostly with a history of pulmonary TB which is peculiarity; it is “dry”
without any joint effusion and hence known as “carrier sicca”. A common site is glenoid or head of the
humerus.
Clinical features: Pain and stiffness of the shoulder, Cold abscess may appear over deltoid region, biceps or
supraspinous fossa, Erosion of the joint occurs with osteoporotic appearance and osteolytic areas may be
present over the humeral head.
Differential diagnosis: Frozen Shoulder
Treatment:
Chemotherapy
Immobilization: immobilized shoulder joint in 90o abduction, 30o flexion and IR. After 3 months, a fabricated
abduction frame may be given till healing occurs. Arthrodesis: rarely undertaken in extreme cases of
continued pain, disease is uncontrolled or recurs.
ARTHRITIC CONDITIONS
1. PYOGENIC ARTHRITIS
Pyogenic arthritis of the joints is caused commonly by Staphylococcus and less commonly by
streptococci, pneumococci, gonococci, meningococci, etc. The invasion of the organisms into the joint may
occur through the following means:
1. Haematogenous: Spread through the blood stream from a focus of infection elsewhere in the body such as
tonsils, teeth, respiratory tract and intestines.
2. Secondary to osteomyelitis in the adjacent bones, e.g., septic arthritis of the hip following osteomyelitis of
the upper end of the femur.
3. Direct implantation of the bacteria into the joint through a punctured wound over the joint, infection from
a compound fracture.
4. Iatrogenic: Following surgical procedures on the joint such as aspiration, arthrotomy and arthroscopy.
Pathogenesis:
There is inflammation of the synovial membrane with excessive production of joint fluid/pus. The
fluid contains a large number of cells, bacteria and fibrin. There occurs destruction of the articular cartilage
and the underlying bone. When the joint is distended with pus, pathological dislocation of the joint may occur.
The capsule may get perforated and the pus may escape out forming sinuses. If untreated, the joint may get
disorganized and end up into fibrous or bony ankylosis.
Clinical Features:
High-grade fever, swelling and pain in the joint. Movements at the affected joint are not allowed by
the child due to pain and muscle spasm.
Investigations:
Radiographic Investigations:
• Early radiographs may be normal or may show increased joint space due to fluid or pus collection.
• Later radiographs show destruction of the cartilage, new bone formation, eventually bony ankylosis or
even pathological dislocation.
• Ultrasonography is required especially in children to detect collection of fluid.
Blood test:
• Marked elevation of ESR and leucocyte count
• Neutrophilic leukocytosis
• Blood culture shows growth of causative organism
• Aspiration of the joint fluid may show organisms on smear and culture.
Treatment:
1. Rest should be given to the joint by traction or splinting or by POP slab till the symptoms subside.
2. Appropriate broad-spectrum antibiotic drugs are started at the earliest.
3. Arthrotomy: Arthrotomy means opening of the joint. Open drainage of the pus is carried out as early
as possible to prevent permanent damage to the articular cartilage.
4. Gradual mobilization of the joint should be done.
5. If the disease is advanced with destruction of the articular cartilage, the joint is immobilized in the
optimal position and allowed to ankylose.
2. SEPTIC ARTHRITIS
This is an arthritis caused by pyogenic organisms. It presents as an acute painful arthritis, but it may present
as subacute or chronic arthritis. Other terms often used to describe this condition are pyogenic arthritis,
infective arthritis or suppurative arthritis.
AETIOPATHOGENESIS
It is more common in children, and males are more susceptible. Other predisposing factors are poor hygiene,
poor resistance, diabetes etc. Staphylococcus aureus is the commonest causative organism. Other organisms
are Streptococcus Pneumococcus and Gonococcus. The organisms reach the joint by one of the following
routes:
a) Haematogenous: This is the commonest route. There may be a primary focus of infection in the
form of pyoderma, throat infection, septicaemia etc.
b) Secondary to nearby osteomyelitis: This is a particularly common route in joints with intraarticular
metaphysis e.g., the hip, shoulder etc.
c) Penetrating wounds: The knee, being a superficial joint, is often affected via this route.
d) Iatrogenic: This may occur following intraarticular steroid injections in different arthritis, and during
femoral artery punctures for blood collection.
e) Umbilical cord sepsis in infants can travel to joints. As the organism reaches the joint by one of the
above routes, there begins an inflammatory response in the synovium resulting in the exudation of fluid within
the joint. Joint cartilage is destroyed by inflammatory granulation tissue and lysosomal enzymes in the joint
exudate. Outcome varies from complete healing to total destruction of the joint. The latter may result in a
complete loss of joint movement (ankylosis).
DIAGNOSIS
Diagnosis is mainly clinical. The patient is usually a child. The knee is the commonest joint affected. Other
joints commonly affected are the hip, shoulder, elbow etc. Presenting complaints: In its typical acute form, a
child with septic arthritis presents with a severe throbbing pain, swelling and redness of the affected joint.
This is associated with high grade fever and malaise. The child is unable to use the affected limb. In its
subacute form, the parents may notice that the child is not allowing anybody to touch the joint. He may not be
moving it properly. In the lower limbs, a painful limp may be the first thing to draw attention. It may be
associated with low grade fever.
On examination: The child is generally severely toxic with high temperature and tachycardia. The affected
joint is swollen and held in the position of ease (Table–22.2). Palpation reveals increased temperature,
tenderness and effusion. There is severe limitation in the joint movements in all directions. Any attempt at
either passive or active movements causes severe pain and muscle spasms. In subacute forms, some amount
of joint movement is possible.
INVESTIGATIONS
Radiological Examination: Diagnosis in early stage is crucial. X-rays are usually normal. A careful look at
the X-ray may reveal increased joint space and a soft tissue shadow corresponding to the distended capsule
due to swelling of the joint. Ultrasound examination is useful in detecting collection in deep joints such as the
hip and shoulder. If found, one could aspirate the fluid and send for culturing the organism responsible for
infection. In the later stage, the joint space is narrowed. There may be irregularity of the joint margins.
Occasionally, there may be a subluxation or dislocation of the joint.
Blood shows neutrophilic leukocytosis. ESR is markedly elevated. A blood culture may grow the causative
organism.
Joint aspiration is the quickest and the best method of diagnosing septic arthritis. The fluid may show
features of acute septic inflammation. Gram staining provides a clue to the type of organism, till one gets the
culture report.
A case with an acute septic arthritis should be differentiated from the following conditions:
a) Other acute inflammatory conditions:
b) Other causes of acute arthritis
• Rheumatic arthritis • Hemophilia: • Tubercular arthritis:
TREATMENT
In its early stage, before any signs of joint destruction appear on X-ray, a correct diagnosis and aggressive
treatment can save a joint from permanent damage. Whenever suspected, diagnosis of septic arthritis must be
confirmed or ruled out by joint aspiration. Broad-spectrum antibiotics should be started by parenteral route.
A combination of Ceftriaxone and Cloxacillin, in appropriate doses is usually given. These are subsequently
changed to specific antibiotics as per aspirate culture and sensitivity reports. The joint must be put to rest in a
splint or in traction.
Whenever pus is aspirated, the joint should be opened up (arthrotomy), washed and closed with a
suction drain. The same can be now done arthroscopically. As the inflammation is brought under control,
general condition of the patient improves, fever and local signs of inflammation subside, the joint is then
gradually mobilised. Antibiotics are continued for 6 weeks.
In late cases, with radiological destruction of the joint margins, subluxation or dislocation, it is not possible
to expect joint movement. In such cases, after an arthrotomy and extensive debridement of the joint.
It is immobilised in the position of optimum function, so that as the disease heals, ankylosis occurs in that
position.
COMPLICATIONS
These can be divided into general and local, as for osteomyelitis. Inadequate early treatment leads to the
following local complications.
1. Deformity and stiffness: The joint gets stiff due to intra-articular and peri-articular adhesions. In cases
with advanced disease, the articular cartilage may be completely damaged, resulting in ankylosis. Bony
ankylosis is the usual outcome of a neglected septic arthritis.
2. Pathological dislocation: As the joint gets filled with inflammatory exudate, the supporting ligaments and
joint capsule get stretched. Muscle spasm associated with the disease may result in pathological dislocation
of the joint. Posterior dislocation of the hip and triple displacement of the knee occur.
3. Osteoarthritis: Even if septic arthritis has been treated rather early, some permanent changes in the articular
cartilage occur, and give rise to early osteoarthritis a few years later.
SEPTIC ARTHRITIS IN INFANCY (Tom-Smith Arthritis)

This is a septic arthritis of the hip seen in infants. At this age, the head of the femur is cartilaginous and is
rapidly and completely destroyed by the pyogenic process. Onset is acute with rapid abscess formation, which
may burst out or be incised and heals rapidly. Usually it is mistaken as a superficial infection and the child
presents sometime later with complaint of a limp without any pain. On examination, it is found that the child
walks with an unstable gait. The affected leg is shorter and hip movements are increased in all directions.
Telescopy test is positive. On X-ray, one finds complete absence of the head and neck of the femur.
Clinically, this condition closely resembles a congenital dislocation of the hip (CDH) which also sometimes
presents at that age. Complete absence of the head and neck, and a normally developed round acetabulum
differentiate this condition from CDH. In the latter, acetabulum is shallow.
SYPHILYTIC INFECTION OF THE JOINTS

This is the rare condition caused by the microorganism Treponema pallidum. The Syphilytic infection may be
congenital or acquired. It mainly affects the elbow or the knee joint. The diagnosis is confirmed by a positive
test for syphilis.
CONGENITAL SYPHILIS
The joint may be affected early or late in congenital syphilis.
Early: During infancy, osteochondritis in the juxtaepiphyseal region results in breakdown of the bone and
cartilage.
Late: A manifestation of congenital syphilis, ‘Clutton’s joints’ is a painless synovitis occurring at puberty. It
most commonly affects the knee and elbow, mostly bilaterally.
ACQUIRED SYPHILIS
The joints may be affected in the secondary and tertiary stages of acquired syphilis. In the secondary stage,
transient polyarthritis and polyarthralgia involving the larger joints occur. In tertiary stage, gummatous
arthritis occurs where the larger joints are most often involved. Neuropathic (Charcot’s) joint is an indirect
consequence of syphilis.
BONE TUMORS
Bone tumor:
It is a neoplastic growth of tissue in bone. Abnormal growth found in the bone can be either benign or
malignant. Metastatic deposits in the bone are commoner than primary bone tumors.
1. OSTEOMA
This is a benign tumour composed of sclerotic, well-formed bone protruding from the cortical surface of a
bone. The bones involved most often are the skull and facial bones. The tumour is of no clinical significance
except that it may produce visible swelling.
▪ It is more prevalent in 40-50 years of age.
▪ Radiologic: dense ivory like appearance
Clinical features: Pain free bony lump near end of long bones, Bony deformities may occur (Diaphyseal
aclasis).
Treatment: No treatment is generally required except for cosmetic reasons, where a simple excision is
sufficient. It is not a pre-malignant lesion.
2. OSTEOSARCOMA
- It is the malignant tumor of connective tissue.
- Seen usually in 10 -25 years of age.
Origin:
- Bone tissue from multipotent mesenchymal cells.
- Tumor could be fibroblastic osteoblastic or chondroblastic
Common sites:
- Initiates at epiphysis but, after fusion of epiphysis occupies
metaphysis.
- Long bones
- Lower ends of femur
- Upper end of tibia or humerus or lower end of radius
Clinical features:
- Intermittent night pain, tenderness and swelling.
- Egg shell crackling may be present.
- Dilated veins
- Fatigue, anaemic metastasis to lungs or lymphatics through the blood or lymphatics.
Radiographic, laboratory investigations:
- Tumor site – sclerotic lesion
- Laying down of bone along the blood vessels gives an appearance of ‘sun rays’.
- Codman’s triangle is present.
- Pathological fractures may occur.
Differential diagnosis: Ewing’s Sarcoma
Treatment:
• Chemotherapy
• Radiotherapy – preoperative mega voltage therapy (4000-6000 rad)
• Immunotherapy – allogenic sarcoma tumor cell vaccine.
• BCG vaccine can be used.
• Early radical ablation
3. OSTEOCHONDROMA
• Benign cartilage forming lesions.
• Not a true neoplasm but regarded as disorder of growth and development.
• It may occur as solitary sporadic exostoses (EXT1) or multiple hereditary exostoses (mutation of gene
EXT1 and EXT2).
• Arise from metaphysis of long bone like lower femur, upper tibia, upper humerus, scapula, illium.
• Occur in adolescent and late childhood.
• Morphologic: Mushroom shaped cartilage capped lesions
Clinical features:
▪ Asymptomatic appearance of pain at early stage.
▪ Swelling
▪ May compress bursae, neurovascular structures and result in stiff joint.
Treatment:
It depends upon the behaviour of the tumor. Amputation is necessary for most tumors. Chemotherapy,
Radiotherapy is doubtful.
4. ENCHONDROMA
This is a benign cartilaginous tumor centrally located when it occurs in phalanges and humerus.
It causes destruction of the cancellous bone and has a potential for undergoing malignant change, especially
when it is situated in the long bones.
Age: 15 – 50 years
Origin: Cartilaginous
Site: Metaphysis of short long bones, e.g., Phalanges, Metacarpals and rarely humerus, pelvis.
Clinical features:
- Small sized slow progressing swelling with or without pain
- Lobulated enlargement at the tumor site
- Thin and expanded cortex
Radiographic, laboratory investigations:
- Cystic lobulated tumor could be contained in bone (enchondroma), or perforating the bony outline
(eccondroma).
- Stippling or calcification may be seen.
Treatment:
- Single small tumor – curettage
- Large tumor – excision with removal of capsule
- When the long bones are involved – radical resection with bone grafting.
5. EWING’S SARCOMA
▪ Ewing’s sarcoma is highly malignant and second most common tumour.
▪ It is small round cell occuring in age group of 5-20 years (more in females).
▪ Skeletal Ewing’s sarcoma arises in medullary canal of diaphysis and metaphysis.
▪ Common sites are shaft of femur, tibia, humerus, pelvis and scapula may also involved.
▪ Radiologic: onion peel like appearance.
Clinical features:
▪ Intermittent vague Pain worst at night
▪ Tenderness
▪ Swelling
▪ Redness of skin with dilated veins
▪ Periods of exacerbations and remissions
▪ Fever
▪ Leucocytosis and elevated ESR.
Differential diagnosis: Osteosarcoma, Osteomyelitis
Treatment: Radiotherapy and Chemotherapy
6. GAINT CELL TUMOR (OSTEOCLASTOMA)

They are of 2 forms:
1. Benign Giant Cell Tumor
2. Malignant Giant Cell Tumor
a) Primary b) Secondary
BENIGN GIANT CELL TUMOR

- Benign giant cell tumor (GCT) is an osteolytic tumor arising from the epiphysis and is common in young
adults.
- Though it is benign, it is locally malignant. The presence of tumor giant cells is the hallmark of this tumor.
Sex: The male: female ratio is 1.5: 1.
Age: It is common between 15 and 35 years (80% occur in more than 20 years of age and the average age
group is 35 years).
Areas affected are asymmetric portions of the epiphysis of long bones. About 75 percent of GCT occurs in
lower end of femur, upper end of tibia, fibula and the distal end of radius.
Pathology
Gross
The tumor consists of ragged, friable, bleeding tissue filled with old or fresh blood clots with various sized
cysts and cavities. Colour varies from red to brown. Epiphyseal end of the bone is distorted. Tumor
extension into the joint cavity is usually not seen and there is no evidence of periosteal reaction.
Microscopy
The tumor is encompassed by a fibrous capsule at the periphery. Presence of abundant tumor giant cells is
quite characteristic. These cells are characterized by their larger size, multiple nuclei more than 150 in
number which are distributed throughout the cell. Appearance of spindle cells indicates malignant potential.
Clinical Features
The course of the tumor is chronic.
Pain is not the presenting feature but trauma is.
Swelling on one side of the bone.
Skin over the tumor is stretched, but there are no dilated veins.
Tenderness is mode rate or absent, eggshell-crackling sensation may be present or absent.
Limitation of joint movements is not seen until the late stages.
There is no increase in joint fluid and the joint and the joint is rarely invaded.
Pathological fracture is a late feature.
Radiographs
- An osteolytic area is seen near the epiphysis.
- The cortex is expanded and thin.
- There is no periosteal new bone formation.
- Thin septa of bone traverse the interior and produce a soap-bubble appearance.
-The cortex may be disrupted in late stages.
- Joint extension is rare.
MALIGNANT GIANT CELL TUMOR

Primary
This develops as a frank sarcomatous lesion. The swelling is quite gross and show other features of
malignancy. The X-rays show gross destruction of the epiphyseal region of the affected bone.
Secondary
This develops at the site of previously treated GCT
Treatment of GCT
Principles of tumor treatment:
- The tumor is invasive and aggressive.
- It commonly recurs, may become malignant after unsuccessful removal.
- Recurrence is treated with en bloc excision.
Treatment:
- En bloc excision is also indicated if the tumor has eroded the cortex and extended into the soft tissues.
- Irradiation therapy induces malignant change if it is given to the benign lesion.
- Megavoltage therapy is permissible only for inaccessible lesions located in the spine, sacrum, pelvis, etc.
- The recommended dosage is 1,500 – 5,000 rads for 5–6 weeks.
Surgical Methods:
- Curettage and bone grafting
- En bloc excision
- Curettage and acrylic bone cementation
- Curettage and cryosurgery
- Excision and reconstruction
- Turn-o-plasty technique:
- Arthrodesis is done by using the fibula from both the sides to bridge the excised gap.
- Arthroplasty: After tumor excision, arthroplasty is done either by using an autograft, allograft or prosthesis.
Other Methods
Marginal resection with curettage: This is done using power burrs with copious irrigation of 5 percent
phenol and 70 percent alcohol.
Resection of distal radius and using ipsilateral proximal fibula to reconstruct the wrist joint.
Amputation is done for widespread aggressive tumor as a last resort.
Treatment Facts of GCT:
Site Surgical option
* Upper limb
- Lower end of ulna Excision
- Lower end of radius Excision with reconstruction by ipsilateral fibula
* Lower limb
- Lower end of femur Excision with turn-o-graft
- Upper end of tibia Excision with turn-o-graft
7. MULTIPLE MYELOMA
▪ Multiple myeloma is a multifocal malignant proliferation of plasma cell derived from single clone of
cells(monoclonal).
▪ It can be osseous or extraosseous.
▪ Primarily affects elderly males than females above >65 yrs.
▪ Common sites are skull, ribs, lumbar spine, sacrum, pelvis.
▪ Radiologic: lytic punched out lesions
Clinical features:
▪ Early phase: asymptomatic
▪ Later stages: bouts of sharp pain
▪ Swelling at the site.
▪ backpain
▪ Anaemia, haemorrhages
▪ Late signs renal failure blockade by protein casts (kidney myeloma).
Investigations:
▪ Bone scan
▪ Computerized tomography (CT)
▪ Magnetic resonance imaging (MRI)
▪ Positron emission tomography (PET)
▪ X-ray
▪ Biopsy
Management:
Medical: Salicylates, NSAID’s, Analgesics, Antitumour antibiotics, Immunomodulators, Glucocorticoids
Surgical: Chemotherapy, Radiotherapy, chemotherapy and radiotherapy, Debulking of tumour surgery,
Irradiation followed by amputation or resection, Excision of tumour and Bone grafting.
8. METASTATIC TUMORS
- They are also called as “Secondary bone tumors.”
- These are metastatic deposits from primary tumors in some other tissues.
- The carcinoma of breast, kidney, lung, thyroid and prostate usually metastasize in the bone during or
after middle age.
- The common sites of metastatic deposits are vertebrae, pelvis, ribs, proximal humerus or proximal
femur.
Routes of Metastasis:
Through: a) Blood
b) Direct Spread
c) Lymphatic spread
Treatment:
Drugs: Analgesic drugs to control pain. Hormonal drugs in carcinoma of the breast and prostate.
Chemotherapy: To control primary focus and the spread
Radiotherapy: To obtain shrinkage of tumor
Surgery:
- It involves decompression when the tumor mass compresses upon the spinal cord.
- Division of the sensory nerves, nerve roots or nerve tracts may be necessary to control severe pain. If the
tumor fungates, its excision or amputation may be necessary.
- Pathological fractures due to secondary metastases of the long bones may need internal fixation.
PHYSIOTHERAPY MANAGEMENT FOR ALL TUMORS
Objective:
* The main objective is to use all the necessary physiotherapeutic measures to maintain and promote the
optimal function of the affected part in particular and the whole body in general.
* Definitive Physiotherapy measures cannot be specified due to the complexities of the disease and
remarkable individual variations in the disease process and the medical management.
General Principles of Physiotherapy

Early Stage
* Keep up the morale of Counselling, emphasizing moving unaffected body parts (ability) and
patients who are highly maximizing functional activities, Diversion procedures as per aptitude
depressed (e.g., reading and playing cards)
* Reduction of pain Pain-free relaxed rhythmic movements, Cryotherapy if accepted well,
Medications
* Reduction of Oedema Lymphoedema which persists longer and is difficult to control; it is
treated by:
- Relaxed full ROM free active movements to distal most joints
- Limb elevation
* Improvement in muscle Intermittent compression, Gentle effleurage, Simple full ROM or
function and joint flexibility maximum ROM exercise.
Late Stage
* Improving restoring Early initiation of assistive functional activities, to provide optimal
function in complicated functional independence.
cases involving limbs or Guidance and training in the use of orthosis or prosthesis for
major surgical procedures functional self-sufficiency.
CONTRA – INDICATIONS:
• Not to use any physiotherapeutic modality which results in increase in circulation (especially in early
stage).
• No thermotherapy should form part of therapy.
• Deep heating modalities close to the site of lesion are totally contraindicated.
PERTHES’ DISEASE (Coxa plana, Pseudocoxalgia)

This is an osteochondritis of the epiphysis of the femoral head. In this disease, the femoral head
becomes partly or wholly avascular and deformed. The cause is not definitely known, but it is supposed to be
due to recurrent episodes of ischaemia of the head in the susceptible age group, probably precipitated by
episodes of synovitis.
Pathologically, the disease progresses in three ill-defined stages:
(i) stage of synovitis;
(ii) stage of trabecular necrosis;
(iii) stage of healing.
The disease occurs commonly in boys in the age group of 5-10 years. The child presents with pain in
the hip, often radiating to the knee. There may be limping or hip stiffness. On examination, findings may be
minimal – sometimes the only findings being a limitation of abduction and internal rotation and shortening.
Radiological examination reveals collapse and sclerosis of the epiphysis of the femoral head. Hip joint
space is increased. In fact, the contrast between the paucity of symptoms and signs in the presence of gross
X-ray changes is striking. Bone scan may show a decreased uptake by the head of the femur. Four
groups have been described by Catterall (1972), depending upon the extent of involvement of the head. He
also describes the adverse prognostic signs (head at risk signs).
Treatment: Preventing the head from mis-shapening while the bone is in softening phase, is the primary aim
of the treatment. The head is required to be kept inside the acetabulum while the revascularization takes place
(head containment). This may be achieved by conservative methods (plaster, splint etc.) or by operation
(containment osteotomy).
AVASCULAR NECROSIS
Avascular necrosis (AVN) of the bone due to loss of a vascularity of a part of the bone occurs commonly
after a fracture or dislocation (e.g., AVN of head of the femur in a fracture of the femoral neck). A part of the
bone undergoes avascular necrosis spontaneously. The head of the femur is a common site of AVN. It occurs
in adults between the ages of 20-40 years. Some of the causes of avascular necrosis of the femoral head.
Causes of avascular necrosis of femoral head
• Idiopathic – commonest
• Alcoholism
• Steroid therapy
• Sickle cell disease
• Patient on renal dialysis
• Patient on anti-cancer drugs
• Post-partum necrosis
• Goucher's disease
• Caisson's disease
Diagnosis: The disease is often bilateral (75%). Patient complains of pain in the groin or in front of the thigh.
Pain is present at all times, but increases on exertion. X-rays may be normal in early stage; if suspicion is
strong, a bone scan may be done. In later stage, an osteolytic lesion can be seen in supero-lateral part of the
head. There may be diffuse osteosclerosis of the head, but the shape of the head may be maintained. In
advanced stage, the head collapses. Eventually, changes of secondary osteoarthritis become apparent. MRI
scan is the best modality for early diagnosis of avascular necrosis.
Treatment: In early stages, diagnosis is often missed as there are no X-ray findings. Core decompression and
fibular grafting is done if the head of the femur has not got deformed. In later stages, once the head gets
deformed, muscle-pedicle bone grafting using tensor facia lata has been shown to produce good results
(Baksi). In some cases, with involvement of a part of the head, an inter-trochantric osteotomy has be seen. In
cases with changes of advanced osteoarthritis, total hip replacement becomes necessary.
SLIPPED CAPITAL FEMORAL EPIPHYSIS

In this condition, the upper femoral epiphysis may get displaced at the growth plate, usually postero-medially,
resulting in coxa vara. The slip occurs gradually in majority of cases, but in some it occurs suddenly.
CAUSES
Aetiology is not known but it is thought to be a result of trauma in the presence of some not yet understood
underlying abnormality. It occurs more commonly in unduly fat and sexually underdeveloped; or tall, thin
sexually normal children.
CLINICAL FEATURES
Following are the salient clinical features:
• Age: It occurs at puberty (between 12-14 years).
• Sex: It is commoner in boys.
• Side: It occurs on both sides in 30 per cent of cases.
• There is a definite history of trauma in some cases.
• It is commoner in patients with endocrine abnormalities.
Presenting symptoms: Pain in the groin, often radiating to the thigh and the knee is the
common
presenting complaint. Often in the initial stages, the symptoms are considered due to a
‘sprain’, and are disregarded. They soon disappear only to recur. Limp occurs early and
is more constant.
Examination: The leg is found to be externally rotated and 1-2 cm short.
Limitation of hip movements is characteristic – there is limited abduction and
internal rotation, with a corresponding increase in adduction and external rotation.
When the hip is flexed, the knee goes towards the ipsilateral axilla. Muscle bulk may be reduced.
Trendelenburg's sign may be positive.
RADIOLOGICAL FEATURES
X-ray changes are best seen on a lateral view of the hip. The
following signs may be present:
On AP view: The growth plate is displaced towards the
metaphyseal side. A line drawn along the superior surface of the
neck remains superior to the head unlike in a normal hip where it
passes bisecting the head –Trethowan's sign
On lateral view: The head is angulated on the neck. This can be
detected early.
TREATMENT
It is based on the following considerations:
a) Treatment of an acute slip: This is by closed reduction and pinning, as for a fracture of the neck of the
femur.
b) Treatment of a gradual slip: This depends upon the severity of the slip present. If it is less than 1/3 the
diameter of the femoral neck, the epiphysis is fixed internally in situ. If the slip is more than 1/3, a corrective
osteotomy is performed at the inter-trochanteric region.
c) Treatment of the unaffected side in unilateral cases: Since the incidence of bilateral involvement is 30
per cent, prophylactic pinning of the unaffected side in a case with unilateral slip is justified.
METABOLIC BONE DISEASES

RICKETS AND OSTEOMALACIA
Rickets and Osteomalacia are the diseases where the organic matrix of the bone fails to calcify properly,
leaving large osteoid seams. Manifestations of the two diseases are different only with respect to the stage in
life at which they occur. Rickets occurs in the growing bones of children; osteomalacia in the bones of adults.
Both conditions are primarily due to a deficiency of vitamin D or a disturbance in its
metabolism secondary to renal disease.
Vitamin D and its metabolism: The endogenous form of vitamin D i.e., cholecalciferol, is found in the skin
as a product of cholesterol metabolism in a process requiring ultraviolet radiation. The exogenous form of the
vitamin is usually D3. The two most important nutritionally useful forms of vitamin D are D2 (ergocalciferol)
and D3 (cholecalciferol).
Steps in activation: The basic forms, vitamin D2 and D3 are inactive until hydroxylated. The first step of
hydroxylation (25 hydroxylation) occurs in the liver and the second step (1 hydroxylation) occurs in the
kidney. 1,25 dihydroxylated form is the active form and stimulates the intestinal absorption of calcium and
also acts on the bone.
Control: The most sensitive of the physiological actions of 1-25 dihydroxy vitamin D is to increase intestinal
absorption of calcium. The action of vitamin D metabolites in bone tissue is controversial. To calcify the bone
matrix properly, small amounts of the metabolites are necessary along with sufficient calcium.
1. RICKETS
Rickets is a disease of the growing skeleton. It is characterized by failure of normal mineralization, seen
prominently at the growth plates, resulting in softening of the bones and development of deformities.
CAUSES:
• There are two types of rickets i.e., Type I and Type I
• In Type I, there is either a deficiency of vitamin D or a defect
in its metabolism.
• In Type II, the rickets occurs due to a deficiency of
phosphates in the extra-cellular fluid because of defective
tubular resorption or diminished phosphate intake.
• Nutritional deficiency continues to be the commonest cause
of rickets in developing countries because of poor socio-
economic conditions.
Types of rickets
Type I
a) Due to a deficiency of vitamin D
• Diminished intake e.g., malnutrition
• Diminished absorption e.g.,
– mal-absorption syndrome
– gastric abnormalities
– biliary diseases
• Lack of exposure to sunlight
b) Due to disturbance in vitamin D metabolism
• Hepatic factor e.g.,
– lack of 25 hydroxylation of vitamin D
– increased degradation of vitamin D in patients on prolonged anti-convulsant therapy
• Renal factor e.g.,
– lack of 1 hydroxylation (autosomal recessive)
• Unresponsiveness of target cells to 1-25 dihydroxy vitamin D
• Renal osteodystrophy
Type II
a) Defective absorption of phosphates through renal tubules
• Hypophosphataemic rickets (x-linked dominant)
• Fanconi syndrome
• Renal tubular acidosis
• Oncogenic rickets
b) Diminished intake or absorption of phosphates
CLINICAL FEATURES:
Nutritional rickets occurs in children about 1 year old. It may occur in older children with mal-absorption
syndrome.
Following are the clinical features:
• Craniotabes: This is the manifestation of rickets seen in young infants. Pressure over the soft membranous
bones of the skull gives the feeling of a ping pong ball being compressed and released.
• Bossing of the skull: Bossing of the frontal and parietal bones becomes evident after the age of 6 months.
Broadening of the ends of long bones, most prominently around wrists and knees. It is seen around 6-9
months of age.
• Delayed teeth eruption is noticed in infants.
• Harrison's sulcus: A horizontal depression, along the lower part of the chest, corresponding to the insertion
of diaphragm.
• Pigeon chest: The sternum is prominent.
• Rachitic rosary: The costo-chondral junctions on the anterior chest wall become prominent, giving rise to
appearance of a rosary.
• Muscular hypotonia: The child's abdomen becomes protruberant (pot belly) because of marked muscular
hypotonia. Visceroptosis and lumbar lordosis occurs.
• Deformities: Deformities of the long bones resulting in knock knees or bow legs is a common presentation
of rickets, once the child starts walking.
RADIOLOGICAL FEATURES:
Early radiological changes are observed in the lower
ends of the radius and ulna. X-rays of both wrists and
knees – antero-posterior views are used for screening
a patient suspected of rickets.
Following radiological signs may be seen:
• Delayed appearance of epiphyses.
• Widening of the epiphyseal plates: Normal width
of the epiphyseal plate is 2-4 mm. In rickets it is
increased because of excessive accumulation of uncalcified osteoid at the growth plate.
• Cupping of the metaphysis: Normally, the metaphysis meets the epiphyseal plate as a smooth line of
sclerosis (zone of provisional calcification). In rachitic bones, this line is absent and the metaphyseal end
appears irregular. The cartilage cells accumulating at the growth plate create a depression in the soft
metaphyseal end, giving rise to a cup shaped appearance.
▪ Splaying of the metaphysis: The end of the metaphysis is splayed because of the pressure by the cartilage
cells accumulating at the growth plate.
• Rarefaction of the diaphyseal cortex occurs late.
• Bone deformities: Knock knees, bow legs and coxa vara are common deformities in older children.
OTHER INVESTIGATIONS:
Serum calcium is usually normal or low, serum phosphate is low, but serum alkaline phosphatase is high.
TREATMENT:
It consists of medical and orthopaedic treatment.
Medical treatment: Administration of vitamin D 6,00,000 units as a single oral dose induces rapid healing.
If the line of healing (a line of sclerosis on the metaphyseal side of the growth plate) is not seen on X-rays
within 3-4 weeks of therapy, same dose may be repeated. In cases where the child responds to vitamin D
therapy, a maintenance dose of 400 I.U. of vitamin D is given per day. If there is no response even after the
second dose, a diagnosis of refractory rickets is made. Such patients are evaluated in detail by multi speciality
team of nephrologist, endocrinologist and physician.
Orthopaedic treatment:
It is required for the correction of deformities by conservative or operative methods.
a) Conservative methods:
Mild deformities correct spontaneously, as rickets heals. Some surgeons use specially designed splints
(mermaid splints) or orthopaedic shoes for correction of knee deformities.
b) Operative methods:
Moderate or severe deformities often require surgery. This can be performed any time after 6 months of
starting the medical treatment. Corrective osteotomies, depending upon the nature of deformities, are
performed.
2. OSTEOMALACIA
Osteomalacia, which means softening of bones, is the adult counterpart of rickets. It is primarily due to
deficiency of vitamin D. This results in failure to replace the turnover of calcium and phosphorus in the organic
matrix of bone. Hence, the bone content is demineralised and the bony substance is replaced by soft osteoid
tissue.
Aetiology:
It is common in women who live in ‘purdah,’ and lack exposure to sunlight. Other causes are: dietary
deficiency of vitamin D, under-nutrition during pregnancy, mal-absorption syndrome, after partial
gastrectomy, etc.
Clinical Features: In its early stages, symptoms and signs are nonspecific and the diagnosis is often missed.
Following presentations may be seen:
• Bone pains: Skeletal discomfort ranging from backache to diffuse bone pains may occur. Bone tenderness
is common.
• Muscular weakness: The patient feels very weak. He may have difficulty in climbing up and down the
stairs. A waddling gait is not unusual. Tetany may manifest as carpopedal spasm and facial twitching.
• Spontaneous fractures occur usually in spine, and may result in kyphosis.
Investigations: Following investigations may be carried out:
• Radiological examination: Plain X-rays appear to be of ‘poor quality’ i.e., not sharp and well-defined.
Following findings may be present:
• Diffuse rarefaction of bones.
• Looser's zone (pseudo-fractures): These are radiolucent zones occurring at sites of stress.
Common sites are the pubic rami, axillary border of scapula, ribs and the medial cortex of the neck of the
femur. These are caused by rapid resorption and slow mineralization and may be surrounded by a collar of
of callus.
• Triradiate pelvis in females.
• Protrusio-acetabuli i.e., the acetabulum protruding into the pelvis.
• Bone biopsy: A bone biopsy from the iliac crest usually confirms the diagnosis. The characteristic
histological finding is excessive uncalcified osteoid.
• Serum: The serum calcium level is low; the phosphates are low and alkaline phosphatase high.
Treatment
When osteomalacia is due to defective intake, vitamin D supplementation therapy, as for rickets, brings
dramatic results. Vitamin D in daily maintenance doses of 400 I.U. is sufficient. If there is mal-absorption,
higher dose or intramuscular dose may be needed. In patients with renal disease, alfa-calcidol (an activated
form of vitamin D) may be used. Calcium supplementation should also be given. In addition, the underlying
cause is treated.
3. OSTEOPOROSIS
Osteoporosis is by far the commonest metabolic bone disease. It is characterised by a diffuse reduction in the
bone density due to a decrease in the bone mass. It occurs when the rate of bone resorption exceeds the rate
of bone formation.
Causes: Several aetiological factors may be operative in a given patient. Commonest factor in males is senility
and in females is menopause.
Causes of generalised osteoporosis
• Senility
• Post-immobilisation e.g. a bed-ridden patient
• Post-menopausal
• Protein deficiency: Inadequate intake – old age, illness, Malnutrition, Mal-absorption, Excess protein loss
(3rd degree burns, CRF etc.)
• Endocrinal: Cushing's disease, Cushing's syndrome, Hyperthyroid state
• Drug induced: Long term steroid therapy, Phenobarbitone therapy
Clinical Features
Osteoporosis is an asymptomatic disorder unless complications (predominantly fractures) occur. Loss of bone
mass leads to loss of strength so that a trivial trauma is sufficient to cause a fracture. Dorso-lumbar spine is
the most frequent site. Pain from these fractures is usually the reason for a person to consult a physician. Other
fractures whose aetiology has been linked to underlying osteoporosis are Colles' fracture and fracture of the
neck of femur.
On examination, the findings are subtle and can be missed. A slight loss of height and increased kyphosis
due to compression of the anterior part of the vertebral bodies is seen in most cases.
Radiological Features
Radiological evidence of decreased bone mass is more reliable, but about 30 per cent of the bone mass must
be lost before it becomes apparent on X-rays. Following features may be noticed on X-rays:
• Loss of vertical height of a vertebra due to collapse.
• Cod fish appearance: The disc bulges into the adjacent vertebral bodies so that the disc becomes biconvex.
• Ground glass appearance of the bones, conspicuous in bones like the pelvis.
• Singh's index: Singh et al. graded osteoporosis into 6 grades based on the trabecular pattern of the femoral
neck trabeculae. Details are outside the scope of this book.
• Metacarpal index and vertebral index are other methods of quantification of osteoporosis.
Other Investigations
These include the following, some of them more recent:
• Biochemistry: Serum calcium, phosphates and alkaline phosphatase are within normal limits. Total plasma
proteins and plasma albumin may be low.
• Densitometry: This is a method to quantify osteoporosis. In this method absorption of photons (emitted
from gamma emitting isotopes) by the bone calcium is measured.
Two types of bone densitometry are available
– ultrasound based and X-ray based. DEXA scan is an X-ray based bone densitometry, and is the gold standard
in the quantification of bone mass.
• Neutron activation analysis: In this method, calcium in the bone is activated by neutron bombing, and its
activity measured.
• Bone biopsy.
Treatment
Since the aetiology of osteoporosis is multifactorial and the diagnosis usually delayed, treatment becomes
difficult. There are no set treatment methods as yet. The principle objectives of treatment are alleviation of
pain and prevention of fractures. Treatment can be divided into medical and orthopaedic.
Medical treatment: This consists of the following:
• High protein diet: Many elderly patients suffer from malnutrition. Increasing their protein intake may
increase the formation of organic matrix of the bone.
• Calcium supplementation: Its role is doubtful, but may be helpful in cases with deficiency of calcium in their
diet.
• Androgens: These hormones have an anabolic effect on the protein matrix of bone, and in some instances
ameliorate symptoms.
• Estrogens: Estrogens have been shown to halt the progressive loss of bone mass in postmenopausal
osteoporosis.
• Vitamin D: This is given, in addition to the above, to increase calcium absorption from the gut.
• Fluoride: The use of fluoride is still under study. It is supposed to make the crystallinity of the bone greater;
thereby making bone resorption slower.
• Alandronate: These are used in once a day dose, empty stomach. Oesophagitis is a troubling complication.
• Calcitonin: Parenteral administration of calcitonin helps in building up the bone mass and also acts as an
analgesic.
• Teriparatide: Anabolic agent increasing osteoblastic new bone formation.
• Denosumab, Strontium: Antiresorptive agents.
Orthopaedic treatment: This consists of the following:
• Exercises: Weight bearing is a major stimulus to bone formation. Increased guarded activity would therefore
be of benefit to the patient.
• Bracing: Prophylactic bracing of the spine by using an ASH brace or Taylor brace may be useful in
prevention of pathological fractures in a severely osteoporotic spine.
4. OSTEOPENIA
Definition:
• Osteopenia is a condition characterised by the loss of bone mineral density (BMD).
• This loss of BMD is not as severe as it is in the case of osteoporosis.
• Osteopenia is a term to define bone density that is not normal but also not as low as osteoporosis. By
definition from the World Health Organization osteopenia is defined by bone densitometry as a T
score -1 to -2.5. By deduction osteopenia is often called a severe precursor for the development of
osteoporosis. A person can be diagnosed with osteopenia but will not always develop osteoporosis.
Etiology
• Throughout a patient’s lifetime BMD is constantly lowering. But the rate at w hich this happens is
about 0.7%/year, this means that even at old age the loss of BMD is not critical.
• However, when a patient has low BMD to begin with the process of BMD-loss can create a great
risk of fractures
• The process of bone maintenance is called “re-modeling”, this process takes about 8 months and is
quite slow. Osteoblast develop into new bone cells and thus compensate for the breakdown of old
and worn cells.
• At the same time osteoblasts secrete a hormone which keeps osteoclast activity under control, thus
preventing excessive bone breakdown.
• Peak BMD is achieved around the age of 21, after this point it starts to lower.
• This means it is extremely important to develop a high BMD at young age, this can be achieved by
having a healthy and active lifestyle. Sports like running are recommended because they put stress
on the bones and increase the activity of osteoblasts.
• In the case of women extra risk comes with aging. Post-menopausal women have a significant
change in their hormone balance, this influences the function of osteoblasts and thus the balance
between bone remodeling and re-uptake.
Differential diagnosis
The only way to differentiate between different degrees of BMD loss is by interpreting the t-score
provided by a DEXA scan.
Diagnostic procedures
Diagnostic procedure usually consists of a DEXA (dual emission x-ray absorptiometry) scan of the
lumbar spine and hip.
during this process 2 x-rays with different energy levels are aimed at the patient.
Depending on how much of the energy of each beam is absorbed by the patient’s bones, the test results
in a t-score: international classifications determine that:
T-score between +1 and -1 indicates normal bone density.
T-score between -1 and -2.5 indicates low bone density or osteopenia.
T-score of -2.5 or lower is proof of osteoporosis.
Outcome Measures
Examination: Add text here related to physical examination and assessment.
Medical management: Medical treatment is generally not given to people with early stage osteopenia.
This type of treatment is reserved for patients diagnosed with high risk of developing actual
osteoporosis and people who actually have osteoporosis.
Physiotherapy management: The purpose of the therapy is the same in every case: trying to enhance
BMD and slowing/preventing loss of BMD.
Pre-menopausal:
In this group of patients the effects of exercise therapy are more significant and almost always result in
an increase of BMD. Evidence was found that lower extremity exercise can result in an increase of
BMD at the hip and great trochanter but does not have increasing effects on the spine.
However when combined with upper body exercises significant increase of BMD was measured in th e
lumbar spine.
Post-menopausal:
Exercise therapy has proven to be a valuable therapy resource in the slowing down or preventing of
BMD loss, there is however contradictory evidence when it comes to the increase of BMD effects.
Some studies mention an actual increase while others do not.
The exercise therapy consisted of specific high impact exercises and there was report of an increase in
Bone mineral content.
CHAPTER 15: CERVICAL AND LUMBAR PATHOLOGY
1. PROLAPSED INTERVERTEBRAL DISC
The term 'prolapsed disc' means the protrusion or extrusion of the nucleus pulposus through a rent in the
annulus fibrosus. It is not a one-time phenomenon; rather it is a sequence of changes in the disc, which
ultimately lead to it prolapse.
Pathology:
These changes consist of the following:
a) Nucleus degeneration: Degenerative changes occur in the disc before displacement of the nuclear material.
These changes are:
(i) softening of the nucleus and its fragmentation; and (ii) weakening and disintegration of the posterior part
of the annulus.
b) Nucleus displacement: The nucleus is under positive pressure at all times. When the annulus becomes
weak because a small area of its entire thickness has disintegrated spontaneously or because of injury, the
nucleus tends to bulge through the defect. This is called disc protrusion. The nucleus comes out of the annulus
and lies under the posterior longitudinal ligament; though it has not lost contact with the parent disc. This is
called disc extrusion. The disc does not go back. The posterior longitudinal ligament is not strong enough to
prevent the nucleus from protruding further. The extruded disc may lose its contact with the parent disc, when
it is called sequestrated disc. The sequestrated disc may come to lie behind the posterior longitudinal ligament
or may become free fragment in the canal.
c) Stage of fibrosis: This is the stage of repair. This begins alongside of degeneration. The residual nucleus
pulposus becomes fibrosed. The extruded nucleus pulposus becomes flattened, fibrosed and finally undergoes
calcification. At the same time, new bone formation occurs at the points where the posterior longitudinal
ligament has been stripped from the vertebral body and spur formation occurs. The site of exit of the nucleus
is usually posterolateral on one or the other side. Occasionally, it can be central (posterior-midline) disc
prolapse. The type of nuclear protrusion may be: a protrusion, an extrusion or a sequestration. A dissecting
extrusion, (an extrusion with disc material between the body of the vertebra and posterior longitudinal
ligament, stripping the latter off the body), may occur. The commonest level of disc prolapse is between L4-
L5 in the lumbar spine and C5-C6 in the cervical spine. In the lumbar spine, it is uncommon above L3 – L4
level.
Secondary changes associated with disc prolapse: As a consequence of disc prolapse, changes occur in the
structures occupying the spinal canal and in the intervertebral joints. These are as follows:
a) Changes in structures occupying spinal canal:
• Commonly, the unilateral protrusion is in contact with the spinal theca and compresses one or more roots in
their extra-thecal course.
Usually, a single root is affected. Sometimes, two roots on the same or opposite sides are affected. The nerve
root affected is usually the one which leaves the spinal canal below the next vertebra. This is because the root
at the level of the prolapsed disc leaves the canal in the upper-half of the foramen. Thus, the nerve root affected
in a disc prolapse between L4-L5 vertebrae is L5, although it is the L4 root which exits the canal at this level.
• Pressure effects on the intra-thecal roots of the cauda equina may occur by a sudden large disc protrusion in
the spinal canal and may present as cauda equina syndrome. This is uncommon.
b) Changes in the intervertebral joints: With the loss of a part of the nucleus pulposus and its subsequent
fibrosis, the height of the disc is reduced. This affects the articulation of the posterior facet joints. The
incongruity of the facet articulation leads to degenerative arthritis.
DIAGNOSIS: The diagnosis is mainly clinical. Investigations like CT scan and MRI scan may be done to
confirm the diagnosis, especially if surgery is being considered.
CLINICAL FEATURES
The patient is usually an adult between 20-40 years of age, with a sedentary lifestyle. The commonest
presenting symptom is low back pain with or without the pain radiating down the back of the leg (sciatica). A
preceding history of trauma is present in some cases. In a few cases, there is a history of exertion such as
having lifted something heavy or pushed something immediately preceding a sudden onset backache. The
following symptoms are common:
• Low backache: The onset of backache may be acute or chronic. An acute backache is severe with the spine
held rigid by muscle spasm, and any movement at the spine painful. The patient may be able to go about with
difficulty. In extreme cases, he is completely incapacitated, any attempted movement producing severe pain
and spasm. In chronic backache, the pain is dull and diffuse, usually made worse by exertion, forward bending,
sitting or standing in one position for a long time. It is relieved by rest.
• Sciatic pain: This is usually associated with low back pain, but may be the sole presenting symptom. The
pain radiates to the gluteal region, the back of the thigh and leg. The pattern of radiation depends upon the
root compressed. In S1 root compression, the pain radiates to the postero-lateral calf and heel. In L5 root
compression the pain radiates to the anterolateral aspect of the leg and ankle. In a disc prolapse at a higher
level (L2-L3 etc.), the pain sideways tilt tends to exaggerate on attempted bending forwards.
• Movements: The patient is unable to bend forwards; any such attempt initiates severe muscle spasm in the
paraspinal muscles.
• Tenderness: There is diffuse tenderness in the lumbo-sacral region. A localised tenderness in the midline or
lateral to the spinous process is found in some cases. May radiate to the front of the thigh. Often the radiation
may begin on walking, and is relieved on rest (neurological claudication).
• Neurological symptoms: Sometimes, the patient complains of paraesthesias, most often described as ‘pins
and needles’ corresponding to the dermatome of the affected nerve root. There may be numbness in the leg or
foot and weakness of the muscles. In cases with large disc material compressing the theca and roots, a cauda
equina syndrome results, where the patient has irregular LMN type paralysis in the lower limbs, bilateral
absent ankle jerks, with hypoaesthesia in the region of L5 to S4 dermatomes and urinary and bowel
incontinence.
EXAMINATION
The back and limbs are examined with the patient undressed. The following observations are made:
• Posture: The patient stands with a rigid, flattened lumbar spine. The whole trunk is shifted forwards on the
hips. The trunk is tilted to one side (sciatic tilt or scoliosis). The sideways tilt tends to exaggerate on attempted
bending forwards.
• Movements: The patient is unable to bend forwards; any such attempt initiates severe muscle spasm in the
paraspinal muscles.
• Tenderness: There is diffuse tenderness in the lumbo-sacral region. A localised tenderness in the midline or
lateral to the spinous process is found in some cases.
• Straight leg raising test (SLRT): This test indicates nerve root compression. A positive SLRT at 40° or
less is suggestive of root compression. More important is a positive contralateral SLRT.
• Lasegue test: This is a modification of SLRT where first the hip is lifted to 90° with the knee bent. The knee
is then gradually extended by the examiner. If nerve stretch is present, it will not be possible to do so and the
patient will experience pain in the back of the thigh or leg.
• Neurological examination: A careful neurological examination would reveal a motor weakness, sensory
loss or loss of reflex corresponding to the affected nerve root. Of special importance is the examination of the
muscles of the foot supplied by L4, L5 and S1 roots, as these are the roots affected more commonly. The
extensor hallucis longus muscle is exclusively supplied by L5 root and its weakness is easily detected by asking
the patient to dorsiflex the big toe against resistance. Sensory loss may merely be the blunting of sensation or
hypoesthesia in the dermatome of the affected root.
INVESTIGATIONS
Plain X-ray: It does not show any positive signs in a case of acute disc prolapse. X-rays are done basically to
rule out bony pathology such as infection etc. In a case of chronic disc prolapse, the affected disc space may
be narrowed and there may be lipping of the vertebral margins posteriorly.
Myelography: With the availability of non-invasive imaging techniques like the CT scan, the usefulness of
myelography has become limited.
It is performed in cases where precise localization of the neurological signs is not possible. It is also used in
cases where facilities for a CT scan are not available. Following myelographic features suggest disc prolapse:
• Complete or incomplete block to the flow of dye at the level of a disc
• An indentation of the dye column
• Root cut off sign: Normally, the dye fills up the nerve root sheath. In cases where a lateral disc prolapse is
pressing on the nerve root, the sheath may not be filled. It appears on the X-ray, as an abrupt blunting of the
dye column filling the root sheath.
CT scan: Normally, in an axial cut section, the posterior border of a disc appears concave. In a case where
there is disc prolapse, it will appear flat or convex. There will be loss of pre-thecal fat shadow normally seen
between the posterior margin of the disc and theca. The herniated disc material can be seen within the spinal
canal, pressing on the nerve roots or theca.
MRI Scan: This is the investigation of choice. It shows the prolapsed disc, theca, nerve roots etc. very clearly.
Electromyography (EMG): Findings of denervation, Localised to the distribution of a particular nerve root,
helps in localising the offending disc in cases with multiple disc prolapse. This test is rarely required.
A prolapsed disc is a common cause of low backache, especially the backache associated with sciatic pain.
One must be extremely cautious and avoid misdiagnosing other diseases that may mimic a disc prolapse.
These include ankylosing spondylitis, vascular insufficiency, extra-dural tumour, spinal tuberculosis etc.
TREATMENT
PRINCIPLES OF TREATMENT
Aim of treatment is to achieve remission of symptoms, mostly possible by conservative means. Cases who do
not respond to conservative treatment for 3-6 weeks, and those presenting with cauda equina syndrome may
require operative intervention.
CONSERVATIVE TREATMENT
This consists of the following:
• Rest: It is most important in the treatment of a prolapsed disc. Rest on a hard bed is necessary for not more
than 2–4 days.
• Drugs: These consist mainly of analgesics and muscle relaxants.
• Physiotherapy: This consists of hot fomentation, gentle arching exercises, etc.
• Others: These consist of lumbar traction, transcutaneous electrical nerve stimulation (TENS) etc.
OPERATIVE TREATMENT
Indications for operative treatment are:
(i) failure of conservative treatment;
(ii) cauda equina syndrome; and
(iii) severe sciatic tilt. The disc is removed by the following techniques:
• Fenestration: The ligamentum flavum bridging the two adjacent laminae is excised and the spinal canal at
the affected level exposed.
• Laminotomy: In addition to fenestration, a hole is made in the lamina for wider exposure.
• Hemi-laminectomy: The whole of the lamina on one side is removed.
• Laminectomy: The laminae on both sides, with the spinous process, are removed. Such a wide exposure is
required for a big, central disc producing cauda equina syndrome.
2. SPINAL CANAL STENOSIS

Definition:
Spinal stenosis is a condition in which the spinal canal narrows and the nerve roots and spinal
cord become compressed. Because not all patients with spinal narrowing develop symptoms, the term
"spinal stenosis" actually refers to the symptoms of pain and not to the narrowing itself.
Aetiology:
Spinal stenosis can be subdivided in a congenital, acquired or mixed form . Congenital spinal
stenosis is present at birth and occurs mostly in the lumbar tract. It can be part of a skeletal syndrome
such as Morquio syndrome, achondroplasia or Down syndrome, but it can also be idiopathic. The latter
condition is characterized by shortness and thickness of the pedicles, shortness of the laminae or sagittal
orientation of the facet joints. Shorter pedicles and laminae reduce the size of the foramen vertebrate and
thus also a smaller spinal canal. The acquired spinal stenosis onsets at another point in life and occur
more frequently both in the cervical and lumbar tract. Several possible causes are known: spondylosis
(Cervical Spondylosis and Lumbar Spondylosis), disk bulging or disc herniation (this is not lasting, the
herniated part of the disc dystrophies), ligamentous degeneration (hypertrophy/ossification of the
ligamentum flavum), spondylolisthesis or a combination of these disorders. It may also be the result of
systematic illneses, such as endocrinopathies (Cushing disease or acromegaly), calcium metabolism
disorders (hypoparathyroidism and Paget disease), inflammatory diseases (rheumathoid
arthritis and ankylosing spondylitis) and infectious diseases. A mixed form is a combination of
congenital abnormalities with superimposed degenerative changes. This applies to patients who already
have a narrow spinal canal and undergo degenerative changes.
Characteristics/Clinical Presentation:
Spinal stenosis can be congenital/primary or, as in most cases, developed/secondary and can have
several possible causes. In most cases it concerns a chronic degeneration. Other causes can be rheumatoid
arthritis, spine trauma, bone tumors or calcification of the ligamentum flavum. Spinal stenosis can occur
at cervical, lumbar and less commonly at thoracic level. Lumbar spinal stenosis occurs more frequently,
but is less dangerous than cervical spinal stenosis. The narrowing can be asymptomatic, but during the
aging process most patients will notice radiating pain, weakness and/or numbness. These are secondary
complaints caused by compression of the spinal nerves.
Symptoms and clinical presentation of cervical and lumbar stenosis:
Cervical Spinal Stenosis Lumbar Spinal Stenosis
Pain in neck Low back pain
Pain and weakness in upper extremity Pain and/or weakness in legs and buttocks
Pain intensifies during neck flexion Pain intensifies during prolonged standing, back
extension and (downhill) walking. Pain decreases during
sitting, stooping, lying and back flexion.
Deterioration in fine motor skills (clumsiness) Associated numbness or weakness (symptoms of sciatic)
Inability to walk at a brisk pace Neurogenic intermittent claudication
Heavy feeling in the legs Heavy feeling in the legs
In neck, shoulder, arms and hands: Low back, buttocks and legs:
- Burning, tingling, numbness, pins& needles - Burning, tingling, numbness, pins & needles
- Bladder & bowel dysfunction (in severe - Bladder and bowel dysfunction (in severe cases)
cases) - Loss of function or paraplegia (rare)
- Loss of function or paraplegia (rare)
Differential Diagnosis:
Hip Osteoarthritis, peripheral vascular disease, trochanteric bursitis, ankylosing spondylitis, spinal
compression fracture, metastatic disease of the spine, vertebral osteomyelitis or discitis, primary spinal.
Diabetic Neuropathy, peripheral neuropathy and radiculopathy due to a herniated disc are others disease that
could be confused with spinal stenosis.
Diagnostic Procedures: X-rays are useful in searching for fractures due to trauma. It is also helpful in the
evaluation of the alignment, loss of disc height and osteophyte formation. With oblique views a defect of the
pars interarticular is detectable while instability is detectable with dynamic views. Instability is confirmed
when the view shows a translation of more than 5 mm or a rotation of more than 10-15 degrees.
MRI (Magnetic Resonance Imaging) is used most frequently and gives the best results. MRI is very sensitive
to degeneration and is used for the evaluation of lateral recess stenosis.
CAT-scan (Computerized Axial Tomography)
A myelogram, which requires an injection of liquid dye into the spinal canal, is useful when followed by a
CT-scan. The combination of both displays a good image of the center lateral canal and defines any extradural
cause of compression.
Bone scan (shows where bone is breaking down or being formed).
Examination
Possible symptoms that occur during the examination are neurogenic claudication, which includes pain in the
buttocks, thigh or leg during ambulation that improves during rest, or radicular leg symptoms with associated
neurological deficits.
Following tests should be conducted:
Bicycle Stress Test: During this test the patient first pedals on a cycle ergometer in upright position with
preservation of neutral lumbar lordosis. The distance the patient has pedaled in a certain amount of time is
recorded. The patient has to pedal a second time in a slumped position with lumbar delordosing. The distance
the patient has pedaled in the same time is recorded again. If the patient can pedal further in slumped position
than in upright position, lumbar spinal stenosis is indicated.
Two-Stage Treadmill Test: This test is evaluated on a treadmill. When the patient walks on the flat (0°)
treadmill their back is in an extended position. The walking distance in a certain amount of time is recorded.
The patient walks on the treadmill a second time with an uphill slope, which means they walk in a flexed
position. The walking distance in the same amount of time is recorded again. If the patient walks further on
an uphill slope than on the flat treadmill, lumbar spinal stenosis is indicated.
Exercise stress testing on a treadmill:
- Grade 1 = patients who were able to walk symptom-free
- Grade 2 = patients who were able to complete the test with some neurologic symptoms
- Grade 3 = patients who were able to walk 5 – 15 minutes
- Grade 4 = patients who were able to walk less than 5 minutes
Medical Management
Spinal stenosis rarely leads to progressive neurological injury. Therefor non-operative modalities should be
attempted first. These modalities are symptomatic, which means they help improve pain symptoms, but do
not alter the underlying narrowing.
Medication and epidural injections are non-operative treatment modalities for spinal stenosis[14].
Medications
Medication includes anti-inflammatory medication, muscle relaxers, desensitizing medication and in some
cases anti-depressant medication. Opioids and antidepressants are prone to increase the risk of falls and
therefore in the senior age group this should be highlighted to client and preventative falls training be sourced.
Epidural steroid injection may relieve symptoms of spinal stenosis temporarily
Decompression surgery
Types of decompression surgery:
Laminectomy: removal of the entire lamina, a portion of the enlarged facet joints and the thickened ligaments
overlying the spinal cord
Laminotomy: removal of a portion of the lamina and ligaments → decreased risk of postoperative spinal
instability
Foraminotomy: removal of bone around the neural foramen when disc degeneration has caused the height of
the foramen to collapse (possibly performed with a laminectomy or laminotomy)
Laminaplasty: expansion of the spinal canal by cutting the lamina on one side (only used in case of cervical
spinal stenosis)
Spinal fusion surgery
Physiotherapy Management
Conservative treatment: Physical therapy includes a combination of different interventions: Bed rest
Flexion-based exercise programs:
-Lumbar flexion exercises are done to reduce the lumbar lordosis. This position for the patient because the
symptoms reduces in combination with a decrease of the epidural pressure in the lumbar spinal canal.
-Single and double leg knees to chest in supine position. This position should be held maintained for 30
seconds. In the single leg exercise the patient should alternate the legs. Double knee is a progressive exercise.
-This exercise program should have a stepwise logistic regression during the first 6 weeks.
-Treadmill walking is the final step in this program.
Manual therapy
Lumbar isometric and stretching exercises, Static and dynamic postural exercises, Individualized muscle
strengthening, Endurance exercises, Stabilization of abdominal and back muscles to avoid excessive lumbar
extension. Postural and ergonomic advice, Aerobic fitness, Cycling exercises, Home exercises.
3. SPONDYLOSIS
A) CERVICAL SPONDYLOSIS
This is a degenerative condition of the cervical spine found almost universally in persons over 50 years of age.
It occurs early in persons pursuing 'white collar jobs' or those susceptible to neck strain because of keeping
the neck constantly in one position while reading, writing etc.
PATHOLOGY
The pathology begins in the intervertebral discs. Degeneration of disc results in reduction of disc space and
peripheral osteophyte formation. The posterior intervertebral joints get secondarily involved and generate pain
in the neck. The osteophytes impinging on the nerve roots give rise to radicular pain in the upper limb.
Exceptionally, the osteophytes may press on the spinal cord, giving rise to signs of cord compression. Cervical
spondylosis occurs most commonly in the lowest three cervical intervertebral joints (the commonest is at C5-
C6).
CLINICAL FEATURES
Complaints are often vague. Following are the common presentations:
• Pain and stiffness: This are the commonest presenting symptom, initially intermittent but later persistent.
Occipital headache may occur if the upper-half of the cervical spine is affected.
• Radiating pain: Patient may present with pain radiating to the shoulder or downwards on the outer aspect
of the forearm and hand. There may be paraesthesia in the region of a nerve root, commonly over the base of
the thumb (along the C6 nerve root). Muscle weakness is uncommon.
• Giddiness: Patient may present with an episode of giddiness because of vertebro-basilar syndrome.
EXAMINATION
There is loss of normal cervical lordosis and limitation in neck movements. There may
be tenderness over the lower cervical spine or in the muscles of the para-vertebral
region (myalgia). The upper limb may have signs suggestive of nerve root compression
– usually that of C6 root involvement. Motor weakness is uncommon. The lower limbs
must be examined for signs of early cord compression (e.g. a positive Babinski reflex
etc.).
RADIOLOGICAL FINDINGS
X-rays of the cervical spine (AP and lateral) are sufficient in most cases. Following
radiological features may be present:
• Narrowing of intervertebral disc spaces (most commonly between C5-C6).
• Osteophytes at the vertebral margins, anteriorly and posteriorly.
• Narrowing of the intervertebral foramen in cases presenting with radicular symptoms,
may be best seen on oblique views.
The diseases to be considered in differential diagnosis of cervical spondylosis are:
(i) other causes of neck pain such as infection, tumours and cervical disc prolapse; and
(ii) other causes of upper limb pain like Pancoast tumour, cervical rib, spinal cord tumours, carpal tunnel
syndrome etc.
TREATMENT
Principles of treatment: The symptoms of cervical spondylosis undergo spontaneous remissions and
exacerbations. Treatment is aimed at assisting the natural resolution of the temporarily inflamed soft tissues.
During the period of remission, the prevention of any further attacks is of utmost importance, and is done by
advising the patient regarding the following:
a) Proper neck posture: Patient must avoid situations where he has to keep his neck in one position for a
long time. Only a thin pillow should be used at night.
b) Neck muscle exercises: These help in improving the neck posture.
During an episode of acute exacerbation, the following treatment is required:

Analgesics, Hot fomentation, Rest to the neck in a cervical collar, Traction to the neck if there is stiffness,
Anti-emetics, if there is giddiness.
In an exceptional case, where the spinal cord is compressed by osteophytes, surgical decompression may be
necessary.
B) LUMBAR SPONDYLOSIS
This is a degenerative disorder of the lumbar spine characterised clinically by an insidious onset of pain and
stiffness and radiologically by osteophyte formation.
CAUSE
Bad posture and chronic back strain are the commonest cause. Other causes are, previous injury to the spine,
previous disease of the spine, birth defects and old intervertebral disc prolapse.
PATHOLOGY
Primarily, degeneration begins in the intervertebral joints. This is followed by a reduction in the disc space
and marginal osteophyte formation. Degenerative changes develop in the posterior facet joints. Osteophytes
around the intervertebral foramen may encroach upon the nerve root canal, and thus interfere with the
functioning of the emerging nerve.
DIAGNOSIS
Clinical features: Symptoms begin as low backache, initially worst during
activity, but later present almost all the time. There may be a feeling of ‘a
catch’ while getting up from a sitting position, which improves as one walks
a few steps. Pain may radiate down the limb up to the calf (sciatica) because
of irritation of one of the nerve root. There may be complaints of transient
numbness and paraesthesia in the dermatome of a nerve root, commonly on
the lateral side of leg or foot (L5, S1 roots) respectively.
EXAMINATION
The spinal movements are limited terminally, but there is little muscle
spasm. The straight leg raising test (SLRT) may be positive if the nerve root
compression is present.
RADIOLOGICAL FINDINGS
Good AP and lateral views of the lumbo-sacral spine should be done after preparing the bowel with a mild
laxative and gas adsorbent like charcoal tablets. It is particularly difficult in obese patients, the ones usually
suffering from this disease.
Following signs may be present:
• Reduction of disc space
• Osteophyte formation
• Narrowing of joint space of the facet joints
• Subluxation of one vertebra over another
TREATMENT
Principles of treatment: Like cervical spondylosis, lumbar spondylosis also undergoes spontaneous
remissions and exacerbations. Treatment is essentially similar to cervical spondylosis. In the acute stage, bed
rest, hot fomentation and analgesics are advised. As the symptoms subside, spinal exercises are advised. In
some resistant cases, a lumbar corset may have to be used at all times. Spinal fusion may occasionally be
necessary.
4. SPONDYLOLYSIS
Definition: Spondylolysis is a unilateral or bilateral bony defect in the pars interarticularis or isthmus of the
vertebra. It can cause a slipping of the vertebra.
Epidemiology /Etiology
This condition appears in the first or second decade of life; the
frequency of spondylolysis increases with age until 20 years. Men
are affected twice as often as women. There is a possible genetic
tendency for people with lower cortical bone density at the pars
interarticularis. There is increased prevalence in specific ethnic, sports and
family groups. Spondylolysis occurs more frequently in the young
athletic population. There is an increased risk in gymnasts, football
players, cricketers, swimmers, divers, weight lifters and wrestlers.
Spondylolysis is considered to be a stress fracture that results from mechanical stress at the pars
interarticularis. These stress fractures occur due to repetitive load and stress, rather than being caused by a
single traumatic event. The stress distribution at the pars interarticularis is the highest in extension and rotation
movements. Spondylolysis occurs mostly at L5 (80-95%) due to repetitive hyperextension, which increases
the contact between the caudal edge of the inferior articular facet of L4 and the pars interarticularis of L5.
• Onset of pain is gradual or acute (after intense athletic activity)
• Possible history of local trauma (recent or historical)
• Intense pain restricts activities of daily living or sporting performance
• Symptoms become aggravated after a stressful event
• Rest usually relieves the symptoms
• Specific symptoms depend on the region of the spine that is affected. Lumbar spondylolysis will
show other symptoms than thoracic or cervical spondylolysis.
Symptoms for lumbar spondylolysis are:
• Focal low back pain with radiation into the buttock or proximal lower limb
• Symptoms can increase with movement specifically lumbar extension or rotation
• Children under 13 years old show tenderness or pain on extension
• Children can present a postural deformity or abnormal gait pattern
• Pain throughout lumbar range of movement.
• Disc Injuries: Disc Herniation
• Lumbosacral Discogenic Pain Syndrome
• Facet Joint Syndrome
• Acute Bony Injuries
• Sprain/Strain Injuries
• Spondylolisthesis
• Myofascial Pain in Athletes
• Sacroiliac Joint Injury
• Lumbar radiculopathy
• Osteoid osteoma
• Osteomyelitis
• Spinal stenosis
Diagnostic Procedures
The golden standard for the diagnosis of spondylolysis is the combination of SPECT and computed
tomography (CT). MRI shows promising results in detecting spondylolysis but can also be used to determine
the state of the disc above and below the affected vertebra.
Examination
The most common findings for lumbar spondylolysis are hyperlordotic posture and low back pain during
lumbar extension. The Michelis' test or unilateral extension test can be performed to confirm diagnosis. The
patient performs hyperextension of the lumbar spine while standing on one leg. In a positive test, pain is
reproduced. Unilateral lesions often produce pain when standing on the ipsilateral leg. Neurologic exam is
usually normal but neurogenic symptoms can arise if the condition progresses to spondylolisthesis.
Medical Management
• Conservative treatment is usually sufficient to treat symptomatic spondylolysis and aims to reduce
pain and facilitate healing processes.
• Possible features of conservative treatment are:
• NSAIDs to provide pain relief
• Cessation of aggravating (sporting) activities
• The use of a spinal brace to prevent motion at the injured pars and allow bony repair.
• Physical therapy
• When severe pain is persistent, progression to spondylolisthesis needs to be prevented: surgical
treatment may be required. This only occurs in some patients and evidence of long-term benefit is still
uncertain. Latest procedures attempt a repair of the affected pars with preservation of the segmental
mobility whereas earlier methods sometimes included a spinal fusion procedure.
Physical Therapy Management
Physiotherapy in spondylolysis has multiple goals:
• Facilitating the healing processes by promoting additional blood flow and thus healing of the affected
pars. This can be accomplished by isometric contractions of the surrounding muscles.
• Avoiding aggravation or turning into a chronic state by handling underlying causes (e.g.
hypermobility, hyperextension in specific sports such as wrestling or skating)
• Optimization of physical function
• Global and specific strengthening exercises
• Reduce pain
• Promoting normal movement patterns
A rehabilitation program should progress in four stages:
Control pain and inflammation: Taking stress off the injured area allows physiological healing processes to
take place. Therefore, it may be necessary to avoid rotational shearing forces and extension movements by a
temporary cessation of sporting activities and/or wearing a brace. It reduces the pain intensity and functional
disability levels.
Strength and flexibility: As paraspinal muscle spasms and hamstrings tightness are often seen in patients
with spondylolysis, stretching exercises can be added to the rehabilitation program. Flexibility training is
useful in patients with hypomobility of the spine. A global strengthening program should be started which can
include specific back strengthening exercises.
Stabilization: Neuromuscular stabilization techniques, including activation of transversus abdominis and
other core stabilizer muscles have been shown to decrease pain in some older research. This section includes
education and postural training. There is evidence suggesting that specific trunk stabilizing exercises to
spondylolysis.
Functional movement: The main goal of physiotherapy is to increase functional abilities through a home
exercise program. As soon as primary pain decreases, patients have to be encouraged to resume activities as
tolerated.
5. SPONDYLOLISTHESIS
Spondylolisthesis is forward displacement of a vertebra over the one below
it. It commonly occurs between L5-S1, and between L4-L5. Occasionally, the
displacement is backwards (retrolisthesis).
PATHOLOGY
Forward displacement of a vertebral body is prevented primarily by the
engagement of its articular processes with that of the vertebra below it. The
attachments of the intervertebral disc and ligaments between vertebrae
also check this displacement, but to a small extent. Any defect in this
‘check’ mechanism leads to has been divided into the following types:
a) Isthmic: This is the commonest type overall. The lesion is in the pars
interarticularis*.
Three sub-types are recognized:
• Lytic: Fatigue fracture of the pars inter articularis
• Intact but elongated pars interarticularis
• Acute fracture of the pars interarticularis.
The defect allows the separation of the two halves of the vertebra.
The anterior half (i.e., the body with the pedicles and superior articular
facet) along with the whole of the spinal column above it, slips forwards
over the vertebra below. The posterior half of the affected vertebra (i.e., laminae and inferior articular facets),
remain with the lower vertebrae.
b) Dysplastic: In this, the least common type, there is a congenital abnormality in the development of the
vertebrae, so that one vertebra slips over the other.
c) Degenerative: This is seen fairly commonly in elderly people. The posterior facet joints becomes unstable
because of osteoarthritis, and subluxate. Vertebral displacement is occasionally backwards rather than
forwards (retrolisthesis). Displacement is usually not severe, and neurological disturbance is unusual.
d) Pathological: This type results from a generalized or localised bone disease weakening the articulation
between the vertebrae.
e) Traumatic: This is a very rare type, where one vertebra slips over other following an injury.
DIAGNOSIS
Clinical features: The isthmic type of spondylolisthesis presents in adolescents and young adults. The
degenerative type occurs in old age. The presenting symptom is usually backache, with or without sciatica.
Symptoms become worse on standing or walking. Sometimes, there may be neurological symptoms in the
lower limbs. In a large number of cases, the abnormality is symptomless, and is detected on a routine X-ray
taken during screening for a health checkup.
On examination, there is often a visible or palpable 'step' above the sacral crest due to the forward
displacement of the spinal column. There may be increased lumbar lordosis. There may be evidence of
stretching of the sciatic nerve, as found by the straight leg raising test (SLRT).
X-ray examination: Anterior displacement of one vertebra over other can be
seen on a lateral view of the spine. The displacement can be graded into four
categories depending upon the severity of slip. Grade I spondylolisthesis
means vertebral displacement up to 25 per cent of the antero-posterior width
of the lower vertebral body, whereas grade IV means the complete forward
displacement of the affected vertebra. An oblique view of the spine may show
defect in the pars interarticularis. In this view, in a normal vertebra, the pars
interarticularis looks like a 'scottish dog'. If the appearance is that of a scottish
dog ‘wearing a collar’, the defect is in the isthmus (pars interarticularis), and
the patient has a spondylolysis (a defect without slipping of the vertebra). If the
head of the ‘scottish dog’ is separated from the neck, the patient has
spondylolisthesis (a defect with slip of the vertebra).
TREATMENT
Principles of treatment: For a mild symptomless spondylolisthesis, no treatment is required. When
symptoms are mild, they are adequately relieved by conservative methods, such as a brace and spinal
exercises. When symptoms are moderately severe or more, especially if these hamper the activity of the
patient, an operation may be required.
Methods of treatment:
These consist of conservative and operative methods.
Conservative methods consist of rest and external support to
the affected segment followed by flexion exercises. The
patient is advised to change his job to a physically less
demanding one.
Operative methods consist of decompression of the
compressed nerves if any, followed by fusion of the affected
segments of the spine. This is commonly achieved by fusion
between the transverse processes of adjacent vertebrae
(intertransverse fusion). Use of internal fixation devices like
pedicular screws and rods has helped in early
mobilisation of the patient.
6. LUMBAGO/LUMBOSACRAL STRAIN
Definition/Description
Lumbar strain is a commonly wielded diagnosis for mechanical low back pain but is without
anatomical or histologic evidence. Much of the knowledge of lumbar strain is extrapolated from peripheral
muscle strains. In strains, the muscle is subjected to an excessive tensile force leading to the overstraining of
the myofibers and, consequently, to their rupture near the myotendinous junction.
The classification of muscle injuries identifies mild, moderate and severe injuries based on the
clinical impairment they bring about.
The lumbar spine is designed to be incredibly strong, protecting the highly sensitive spinal cord and
spinal nerve roots. At the same time, it is highly flexible, providing for mobility in many different planes
including flexion, extension, side bending, and rotation.Lumbar strain can origine in the following muscles:
M. erector spinae (M. iliocostales, M longissimus, M. spinalis) M semispinales, Mm multifidi, Mm rotatores
M. quadratus lumborum M. serratus posterior.
Epidemiology /Etiology
Strains are defined as tears (partial or complete) of the muscle-tendon unit. Muscle strains and tears
most frequently result from a violent muscular contraction during an excessively forceful muscular stretch.
Any posterior spinal muscle and its associated tendon can be involved, although the most susceptible
muscles are those that span several joints. Acute and chronic lumbar strain. Acute pain is most intense 24 to
48 hours after injury. Chronic strains are characterized by continued pain attributable to muscle injury.
Low back pain is the second most common symptom that causes patients to seek medical attention in
the outpatient setting. Approximately 70% of adults have an episode of LBP as a result of work or play.
Common symptoms include pain: This pain is a diffuse pain in the lumbar muscles, with some radiation to
the buttocks. The pain could be exacerbated during standing and twisting motions. With active contractions
and passive stretching of the involved muscle the pain will increase. Other symptoms are point tenderness,
muscle spasm, possible swelling in and around the involved musculature, a possible lateral deviation in the
spine with severe spasm, and a decreased range of motion.
Degenerative disk or facet process: Localized lumbar pain, Diffuse pain in lumber muscles
Herniated disk: Osteoporotic compression fracture, spine tenderness
Spinal stenosis or osteoarthritis: may have weak/asymmetric reflexes, decreased in extension
Spondylolisthesis: exaggerating lumbar lordosis, palpable ‘step-off’, tight hamstrings
Ankylosing spondylitis: tenderness over sacro-iliacal joints, decreased back motion.
Diagnostic Procedures
Laboratory tests: No abnormalities.
Radiographs: Imaging is not indicates unless there are: any red flag signs, any radicular or abnormal
neurological clinical features or if the symptoms have persisted for more than a month.
In these cases, it is important to exclude other differential diagnosis, by using X-rays or MRI.
Examination
The physical examination contents:
• Inspection: Inspect the spine for abnormal curvatures (i.e. scoliosis), Erythema, Observe the gait (posture
and movement) let the patient walk across the room, turn around and let him come back, Observe the seated
position of the patient abnormal posture caused by pain and muscle spasm.
• Palpation - Point tenderness, Bony tissue, Soft tissue
• ROM: Flexion of the back, Signs of limited range of motion or a decreased lumbar lordosis are important
but most of the low back pain patients show this symptoms.
• Special tests: Neurovascular assessment (L4-S1).
° Test heel and toe walking
° Positive test: marked asymmetry
• SLR± ankle dorsiflexion: Positive test: radiated pain into calf
• Crossed SLR: Pain in the affected limb, when testing the unaffected limb
• SLR + Lasègue
• Bowstring sign: SLR until pain, then flex the knee.
Positive test: reduces pain when nerve is irritated
• FABER Test
Flexion Abduction External Rotation of the hip
Pain when SI-pathology
• One leg extension test: standing on 1 leg with the back in extension, pain can indicate spondylolysis
• Hamstring flexibility
• Leg length evaluation: Measure from ASIS to medial malleolus (cm)
Medical Therapy
Non-steroidal anti-inflammatory drugs (NSAIDs) are recommended in the acute phase to help reduce the
swelling and inflammation.
- Diclofenac (voltaren)
- Ibuprofen(ibuprin,advil,motrin).
- Cox-2 selective NSAID’s (less effects on the gastrointestinal tract)
Muscle relaxants can also be prescribed to treat muscle spasms and facilitate light physical therapy. No
studies support the use of oral steroids in patients with acute low back pain.
Physical Therapy Management
In the acute phase of a lumbar strain Cold therapy should be applied (for a short period up to 48 h) to the
affected area to limit the localized tissue inflammation and edema. TENS and ultrasound are often used to
help control pain and decrease muscle spasm. The resulting pain and muscle spasm from acute strains must
first be resolved with modalities (ice, TENS, ultrasound), mild stretching exercises along with limited activity.
A few stretching exercises:
1. Single en double knee to chest: Lie down on your back with your knees bent and your heels on the floor.
Pull your knee or knees as close as you can to your chest, and hold the pose for 10 seconds. Repeat these 3 to
5 times.
2. Back stretch: Lie on your back, hands above your head. Bend your knees and, keeping your feet on the
floor, roll your knees to one side, slowly. Stay at one side for 10 seconds repeat 3 to 5 times.
3. Press up: Begin by lying flat on the ground (face down). When doing this exercise, it is important to keep
the hips and legs relaxed and in contact with the floor. Keep your hands in line with your shoulders. Inhale,
then exhale and press up using the hands keeping the lower half of your body relaxed. Hold until you need to
inhale, then move down, lay flat on the ground to rest, and repeat ten times.
Kneeling lung (stretching iliopsoas), stretching piriformis, stretching quadratus lumborum
Prognosis
A Lumbar strain improves within 2 weeks. Normal functions are restored after 4 – 6 weeks.
7. SACRALISATION
Sacralization is a common irregularity of the spine, where the fifth vertebra is fused to the sacrum bone at the
bottom of the spine. The fifth lumbar vertebra, known as L5, may fuse fully or partially on either side of the
sacrum, or on both sides. Sacralization is a congenital anomaly that occurs in the embryo.
Sacralization often has no symptoms. It’s sometimes is associated with lower back pain or problems with
posture and movement. It's also called lumbosacral transitional vertebrae or LSTV.
Symptoms: The extent and type of sacralization varies widely from individual to individual. Some people
with sacralization have lower back pain. It’s not clear whether sacralization causes the back pain.
Other symptoms associated with sacralization may include: Arthritis at the fusion site, bursitis, disc
degeneration, biomechanical difficulties in movement, limits to range of motion, posture control problems,
scoliosis, leg pain, buttock pain
Types: Sacralization has several forms, classified according to whether the fusion seen on an X-ray is partial
or total, and whether the fusion is on only one side (unilateral) or both (bilateral). The commonly used Castellvi
classification is:
Type 1: a fusion at least 19 mm in width on one (1a) or both sides (1b)
Type 2: incomplete fusion with a pseudo joint created on one side (2a) or both sides (2b)
Type 3: complete fusion of the L5 to the sacrum on one side (3a) or the other (3b)
Type 4: combination of Type 2 and Type 3
Causes: The cause of sacralization isn’t yet known. It occurs during embryonic development, when the
vertebrae begin to ossify, in about the eighth week. There may be a genetic predisposition involved.
Diagnosis: A sacralization diagnosis also requires X-rays of the lumbar spine, MRI imaging.
Treatment: Treatment depends on the type and degree of sacralization and what your symptoms are. Each
individual is different, and there’s no set treatment. The conservative treatment given for pain associated
with sacralization is the same as for other lower back pain.
Pain relief: This may include the standard treatments for lower back pain: anti-inflammatory drugs, muscle
relaxants, steroid injections.
Physical therapy: Physical therapy can help to strengthen and stabilize the muscles involved and improve
movement. Chiropractic provide relief, by spinal manipulation, soft tissue work, stretching, and exercise.
Surgery may be recommended to correct specific disc or other abnormalities that result from the sacralization.
For example, sacralization may cause strain on the disc between the fourth and fifth vertebrae, leading to disc
slippage or degeneration. It can also cause compression of the spinal nerve and pain in your spine or legs,
scoliosis, or sciatica.
8. LUMBARISATION
Lumbarization of S1 or lumbarization of first sacral vertebra is a condition in which the first sacral vertebra
is not completely attached to its fused sacral components but instead this first sacral vertebra appears like the
other lumbar vertebrae.
It is also called as an extra vertebra, additional lumbar vertebra or transitional vertebra. It occurs due to
non-fusion of first and second sacral segments.
This lumbarized S1 vertebra may also have a disc like the other lumbar segments or may have a disc space
that remains underdeveloped.
Signs and Symptom:
This lumbarized S1 vertebra is not completely a fused sacral segment nor does it become a normal lumbar
segment.
This makes it difficult to accommodate the additional vertebral joint while performing daily tasks and may
make this vertebra more vulnerable to injury and joint irritation.
With advancing age and activities, the lumbarized first sacral vertebra can find it difficult to cope and may
become an area that triggers pain, discomfort or may remain prone to injury.
In some cases complaints like
1. Back pain
2. Inflammation
3. Swelling
4. Stiffness of back
5. Muscle spasms
6. Increased risk of injury
7. Inter-vertebral disc problems with radiculopathy.
Cause:
Due to the semi fused or bilaterally fused L5 vertebrae to S1, the first thing to get compromised is mobility
unlike lumbarization.
All the efforts are upon L4 now which will not be able to cope up with the stresses of load bearing like L5.
More wear and tear of intervertebral joints can take place at L4-L5 and L5-S1 level due to reduced disc
space.
Can lead to IVDP which may further require surgical intervention.
Diagnosis: Mainly X – rays, CT Scan, MRI
Treatment:
Medications: NSAID’S, SMR, Steroid injection forever pain and discomfort.
Surgical: Surgical excision surgeries are opted where the symptoms are severe.
Rehabilitation: Electrical modalities.
Symptomatic treatment: Spinal traction, IFT, TENS, US therapy, SWD, Laser, MWD, Spinal Corset, Rest.
Specific treatment: Exercise regimen: Muscle strengthening, Muscle stretching, Core strengthening
exercises.
Manual therapy
9. COCCYDYNIA
Inflammation of the coccyx bone and cartilage is called as “coccyniditis” or “coccyditis” or “Coccydynia”.
Causes: Prolonged sitting on hard surface, prolonged bike riding, sudden fall on your gluteus, any injury
(direct force leading to injury).
Signs and Symptoms: Severe pain at tail bone, tenderness, swelling (sometimes), sitting or riding bike –
aggravating factor; Standing – relieving factor.
Radiological factors: Sometimes normal (within 4 – 5 days), After 1 or 2 months, then calcified tail bone and
color changes are observed, Sometimes fractures.
Medical and Physiotherapy treatment:
- Rest
- McKenzie coccydynia brace/cushion
- Icing: Icepack/Ice cube should be used – 15 minutes for 2 – 3 times per day.
- NSAID’s X 2 days with antacid
Physiotherapy Management:
- Ultrasound (Small ultrasound head).
- IFT → 4 poles vector → gluteus muscle relaxation.
10. HEMIVERTEBRA
Hemivertebra is a type of vertebral anomaly and results from a lack of formation of one half of a vertebral
body. It is a common cause of congenital scoliosis.
Epidemiology: The estimated incidence is at ~0.3 per 1000 live births 2.
Pathology: It falls under the spectrum of segmentation anomalies and can involve one or multiple levels.
A hemivertebra acts as a wedge within the vertebral column, resulting in curvature away from the side on
which it is present.
Classification
A hemivertebra can be classified according to many types which include:
1. Fully segmental (free)
- Not attached to either vertebra above or below
- Most concerning
2. Semi segmental: Half segment is fused with
vertebra above or below with no intervening
intervertebral disc
3. Non-Segmental
- Not separated from (i.e. connected to) either level
above or below
- Causes less of a concern
4. Incarcerated
- Joined by pedicles to levels above and below
- Causes less of a concern
Orientation
• Dorsal Hemivertebra: classically results in kyphosis
• Lateral Hemivertebra: classically results in scoliosis
• Ventral Hemivertebra (extremely rare): results in lordosis
Radiographic features
Antenatal ultrasound
A hemivertebra may be seen as an asymmetrical vertebral body on sagittal or coronal scanning, while on axial
scanning, a focal defect may be seen on either side of the vertebral column.
Plain radiograph / CT
Usually directly outlines the bony anomaly and is often seen as a wedge-shaped vertebral body.
Differential diagnosis: Block Vertebrae, Bullet Shaped Vertebrae and butterfly vertebrae.
Treatment and prognosis
The prognosis can be variable dependent on the type of segmentation anomaly, from being a progressive to a
non-progressive deformity. The strongest negative impact is when a hemivertebra occurs at the lumbosacral
level.
CHAPTER 12: INFLAMMATORY AND DEGENERATIVE CONDITIONS
1. OSTEOARTHIRITIS
It is a non – inflammatory degenerative disorder of the joints characterised by progressive deterioration of the
articular cartilage and formation of new bone (osteophytes) at the joint surface.
• Mainly occur due to wear and tear of joints
TYPES: Primary and Secondary
Primary OA:
• Occur in old age mainly in WB Joints like hip and knee
• Trapeziometacarpal joint of thumb and DIPJ of fingers
Secondary OA
• Due to an underlying primary disease of joint which cause degeneration and OA
• Like in adolescence in hip joint due to AVN, Coxa Vara, CDH, Malunited fractures.
Predisposing factors for Secondary OA
• Congenital maldevelopment of joint
• Irregularity of joint surfaces from any previous trauma
• Internal derangement of knee
• Mal Alignment
• Obesity
Pathology of OA
• Mainly affects the articular cartilage
• First increased water content and depletion of proteoglycans from cartilage matrix.
• And repeated WB on such cartilage leads to fibrillation
• Cartilage get abraded by grinding mechanism at point of contact between the surfaces till the bone is
exposed
• And later with further rubbing the bone become hard and glossy called as “Ebrunated”.
• Now the bone and joint margins form spurs also called as “Osteophytes” and leads to subchondral cyst.
Clinical Features:
• More in elderly people
• More in WB extremity
• More in western population and they have OA hip
• Asian population have OA knee
• Pain
• Crepitus
• Swelling due to inflammation of synovial tissues
• Stiffness due to pan and muscle spasm
• Loose bodies
On Examination
• Tenderness on joint line
• Crepitus on moving the joints
• Irregular and large looking joint
• Varus knee and Flexion, adduction and ER of hip can be seen
• Effusion
• Terminal limitation of joint movement
• Wasting of quadriceps
Investigations
On X - ray:
• Narrowing of joint space
• Subchondral sclerosis
• Subchondral cyst
• Osteophyte formation
• Loose bodies
TREATMENT
Principles of treatment:
• To delay the occurrence
• To stall the progress of the disease
• To rehabilitee the Patient without surgery
• Methods of treatment:
• Drugs: Analgesics
• Chondroprotective agents like glucosamine
• Viscos supplementation like sodium hylarium
• Supportive therapy:
• Weight reduction if obese patient
• Avoid stress and strains on affected joints in ADL
• Local heat for pain relief
• Local counter irritants
• Surgical treatment
• Osteotomy: Mainly in cases with arthititic joints like high tibial osteotomy like high tibial osteotomy
• Joint replacement
• Joint debridement: Affected joint deepened, degenerated cartilage smoothened and osteophytes are excised
• Arthroscopic: Remove loose bodies, meniscal tears
2. RHEUMATOID ARTHRITIS
Rheumatoid arthritis is a systemic disease which results in chronic inflammation and destruction of synovial
joints. It is an autoimmune disease that involves system/organs other than the bones and joints alone.
RA is a chronic non suppurative inflammation of synovial joints by American Rheumatism Association
Diagnostic criteria for RA
• Morning stiffness
• Swelling of 3 or more specified joints
• Swelling of joint in hand and wrist
• Symmetrical swelling
• Rheumatic nodule
• RF positive
• X ray shows erosion
AETIOLOGY
1.Genetic predisposition: HLA –drw4/HLA-DR
2.Agents like mycoplasma and clostridium
3.Inflammatory reactions in synovial joints and tendon sheath leads to destruction of joint
4.Rheumatic factor in blood
Pathology:
Synovial become odematous have exudates and increased synovial fluid → Inflammation persists and
synovium get hypertrophied and surrounds articular cartilage to form PANNUS → Pannus extends over
cartilage from periphery and go in subchondral bone → Leads to cartilage worn off and bone surface become
raw → Leads to joint deformities due to spasm and later fibrosis of capsule.
•There may be adhesions present between opposing layers of pannus leading to fibrosis ankylosis and later
bony
•Later stages subluxation of joints can happen
•Adjacent to diseased joints osteoporosis can occur

STAGES OF RA
STAGE 1: SYNOVITIS
• Potentially reversible soft tissue proliferation is also called as synovitis
• Disease limited to synovium
• Synovial hypertrophy and effusion
• No destruction of cartilage on x-ray seen.
STAGE 2: DESTRUCTION
• Controllable but irreversible soft tissue destruction
• Early cartilage erosion
• X ray show reduction in joint space
• Outline of articular surface is maintained
STAGE 3: DEFORMITY
• Irreversible soft tissue and bony changes leading to formation of deformity
• Pannus destroy cartilage and erode subchondral bone
• Joint become ankylosed
• Subluxation or dislocation can also occur.
DIAGNOSIS
• Occur between age of 20 to 50 years
• Women affected 3 times more than men
1.Acute symmetrical polyarthritis
1.Pain and stiffness in at least 4 joints and main in morning
2.Articular inflammation present
3.Mainly affects MCPJ of Index Finger
4.Joint unstable
5.No deformity at this stage
6.Fever can be present in children
ON EXAMINATION
• Swollen boggy joint
• Late stages leads to deformities
1.Hand: Ulnar drift, Boutonniere and Swan neck deformity

2.Elbow: flexion deformity
3. Knee early: flexion deformity,
Late: Triple subluxation (Flexion, post-subluxation and ER of knee)
4. Ankle: Equinus deformity
5. Foot: Hallux valgus and Hammer toes
TREATMENT
Principle of treatment:
1.Induction of remission and maintenance
2.Preservation of joint function and prevention of deformities
3.Repair of joint damage
MEDICAL TREATMENT
•Anti rheumatic drugs: NSAIDS, DMARDS, Steriods
OPERATIVE TREATMENT
• Synovectomy of wrist, knee
• Tendon lengthening
• Tendon transfer.
3. HAEMOPHILICARTHRITIS
• Occurs due to a number of bleeding disorders
• Occurs in males
• Joints affected commonly are knee, elbow and ankle
• May present as acute or chronic haemarthrosis. There are other manifestations of bleeding disorders
• X-ray –non-specific signs including bone resorption, cyst formation, osteoporosis, widening of intercondylar
notch in the knee.
• Treatment –rest during acute stage along with factor VIII supplementation or other deficient factor
replacement.
• In the chronic stage, physiotherapy, bracing are required. Deformities may be corrected by conservative or
operative methods.
4. CHARCOT'S JOINT
• These are changes seen in a neuropathic joint, where repeated strain on a joint due to loss of sensations leads
to severe degeneration
• Clinically, the joint manifests as painless effusion, deformity or instability
• The X-ray changes are those of severe osteoarthritis but without much clinical findings like pain, muscle
spasm etc.
• Treatment is difficult.
• Bracing is usually advised for some joints. Fusion of the joint may be required.
5. ANKYLOSING SPONDYLITIS (Marie strumpell disease)

Ankylosing spondylitis is a chronic disease characterised by a progressive inflammatory. This will cause pain
at the affected sacroiliac joint.
• Pump-handle test: With the patient lying supine, the examiner flexes his hip and knee completely, and forces
the affected knee across the chest, so as to bring it close to the opposite shoulder. This will cause pain on the
affected side.
• Tests for cervical spine involvement: In advanced stages, the cervical spine gets completely stiff. The Fle'che
test may detect an early involvement of the cervical spine.
• Fle'che test: The patient stands with his heel and back against the wall and tries to touch the wall with the
back of his head without raising the chin. Inability to touch the head to the wall suggests cervical spine -
involvement.
• Thoracic spine involvement: Maximum chest expansion, from full expiration to full inspiration is measured
at the level of the nipples. A chest expansion less than 5 cm indicates involvement of the costo-vertebral joints.

Extra-articular manifestations: In addition to articular symptoms, a patient with ankylosing spondylitis may
have the following extra-articular manifestations:
a) Ocular: About 25 per cent patients with ankylosing spondylitis develop at least one attack of acute iritis
sometimes during the natural history of the disease. Many patients suffer from recurrent episodes, which may
result in scarring and depigmentation of the iris.
b) Cardiovascular: Patients with ankylosing spondylitis, especially those with a long-standing illness, develop
cardiovascular manifestations in the form of aortic incompetence, cardiomegaly, conduction defects,
pericarditis etc.
c) Neurological: Patients may develop spontaneous dislocation and subluxation of the atlanto-axial joint or
fractures of the cervical spine with trivial trauma, and may present with signs and symptoms of spinal cord
compression.
d) Pulmonary: Involvement of the costo-vertebral joints lead to painless restriction of the thoracic cage. This
can be detected clinically by diminished chest expansion, or by performing pulmonary function tests (PFT).
There may also occur bilateral apical lobe fibrosis with cavitation, which remarkably simulates tuberculosis
on X-ray.
e) Systemic: Generalised osteoporosis occurs commonly. Occasionally, a patient may develop amyloidosis.
INVESTIGATIONS
Radiological examination: In a suspected case, X-rays of the pelvis (AP), and dorso-lumbar spine (AP and
lateral) are required. Oblique views of sacro-iliac joints may be required in early stages to appreciate their
involvement. Following changes may be seen on X-ray of the pelvis:
• Haziness of the sacro-iliac joints
• Irregular subchondral erosions in SI joints
• Sclerosis of the articulating surfaces of SI joints
• Widening of the sacro-iliac joint space
• Bony ankylosis of the sacro-iliac joints
• Calcification of the sacro-iliac ligament and sacro-tuberous ligaments
• Evidence of enthesopathy – calcification at the attachment of the muscles, tendons and ligaments, particularly
around the pelvis and around the heel. X-ray of the lumbar spine may show the following:
• Squaring of vertebrae: The normal anterior concavity of the vertebral body is lost because ligament.
• Loss of the lumbar lordosis.
• Bridging ‘osteophytes’ (syndesmophytes).
• Bamboo spine appearance.
In the peripheral joints, X-ray changes are similar to those seen in rheumatoid arthritis, except that there is
formation of large osteophytes and peri-articular calcification. Bony ankylosis occurs commonly.
Other investigations: These are the following:
• ESR: elevated
• Hb: mild anaemia
• HLA-B27: positive (to be tested in doubtful cases)
In early stages, ankylosing spondylitis may be confused with other disorders,
Differential diagnosis of Ankylosing spondylitis
1. Stiffness
a) TB Spine
b) Fluorosis
2. Back pain
a) Lumbo – sacral strain
b) Disc prolapse
c) Osteoarthritis
3. SI joint diseases
a) TB of SI joint
b) Osteitis condensans iliac

TREATMENT
No specific therapy is available. Aim is to control the pain and maintain maximum degree of joint mobility.
This can readily be achieved by lifelong pursuit of a structured exercise programme. In some cases, surgical
intervention is required.
Conservative methods: These consist of: (i) drugs—NSAIDs are given for pain relief; Indomethacin is
effective in most cases; long acting preparations are preferred; (ii) physiotherapy– this consists of proper
posture guidance, heat therapy and mobilisation exercises; (iii) radiotherapy – in some resistant cases; and
(iv) yoga therapy.
Operative methods: Role of operative treatment is in correction of kyphotic deformities of the spine by
spinal osteotomy, and joint replacement for cases with hip or knee joint ankylosis.
6. GOUTY ARTHRITIS
• Disturbed purine metabolism leading to excessive accumulation of uric acid in the blood
• The result is accumulation of sodium biurate crystals in some soft tissues.
• Tissues of predilection are cartilage, tendon, bursa
• Patient, usually beyond 40 years of age,
• Presents as
(i) arthritis –MP joint of the big toe being a favouritesite, onset is acute, pain is severe;
(ii) bursitis –commonly of the olecranon bursa; or (iii) tophi formation deposit of uric acid salt in the soft
tissue
• Confirmation of diagnosis –urate crystals in the aspirate from a joint or bursa, high serum uric acid levels
• Treatment –NSAIDs, uricosuric drugs, uric acid inhibitors.
7. PSORIATIC ARTHROPATHY
• Presentation is like rheumatoid arthritis –a polyarthritis, distal IP joints of hands involved (unlike rheumatoid
arthritis, where these are spared)
• Classic skin lesions help in diagnosis
• Treatment is by steroids
8. STILL’s DISEASE (JUVENILE RHEUMATOID ARTHRITIS)

This is a juvenile chronic polyarthritis, which could be nay of the following: systemic, polyarticular,
oligoarticular.
In Systemic disease: malaise, weight loss and evening rise of temperature are present with enlargement of
spleen and lymph glands. Rashes appear with fever of following the use of external heat.
Polyarticular involvement develops into chronic arthritis. The disease has a better prognosis when it affects
fewer joints (oligoarticular). An accompanying eye disease (iridocyclitis) may lead to blindness, especially if
there are positive antinuclear antibodies (ANAs).
Treatment: It is the same as the adult RA except that corticosteroids are used with precision.
JUVENILE RHEUMATOID ARTHRITIS
A seropositive autoimmune connective tissue disease commonly affects female adolescents, mainly affecting
connective tissues. It follows the course of RA mostly affecting small joints of the hand and feet.
1. Systemic onset (Still disease): ashes, high fever, lymphadenopathy, splenomegaly, carditis and arthritis.
2. Pauciarticular onset: Involving less than four joints.
3. Polyarticular onset: Involving four or more joints.
4. Iridocyclitis: Leading to blindness.
CONNECTIVE TISSUE DISORDERS

1. SYSTEMIC LUPUS ERYTHEMATOSIS
• Is an autoimmune disease. In this disease, the immune system of the body mistakenly attacks healthy tissue
• It can affect the skin, joints, kidneys, brain, and other organs.
Causes
• The cause of SLE is not clearly known. It may be linked to the following factors:
• Genetic
• Environmental

• Hormonal
• Certain medicines
SLE has joint pain and swelling arthritis.
• SLE often affects the joints of the fingers, hands, wrists, and knees.
• Fatigue.
• Fever with no other cause.
• General discomfort, uneasiness, or ill feeling (malaise).
• Hair loss.
• Weight loss.
• Mouth sores.
• Sensitivity to sunlight.
• Skin rash: A "butterfly" rash
• Swollen lymph nodes.
• Brain & nervous system: Headaches, numbness, tingling, seizures, vision problems, and personality changes
• Digestive tract: Abdominal pain, nausea, and vomiting
• Heart: Valve problems, inflammation of heart muscle
• Lung: Buildup of fluid in the pleural space, difficulty breathing
• Skin: Patchy skin color and fingers that change color when cold (Raynaud phenomenon)
• Kidney: Swelling in the legs
2. SCLERODERMA
• Refers to a range of disorders in which the skin and connective tissues tighten and harden. It is a long-term,
progressive disease
• It is considered a rheumatic disease and a connective tissue disorder.
• Results in an overproduction of collagen
• Scleroderma means "hard skin."
• Early symptoms of scleroderma include changes in the fingers and hands, for example, stiffness, tightness,
and puffiness because of sensitivity to cold or emotional stress.
• There may be swelling in the hands and feet, especially in the morning.
Overall symptoms of scleroderma include:
• Calcium deposits in connective tissues
• A narrowing of the blood vessels to the hands and feet, known as Raynaud's disease
• Problems of the esophagus, which links the throat and stomach
• Tight, thickened skin on the fingers
• Red spots on the face and hands
TYPES
• The two main types of scleroderma are localized and systemic.
• Localized scleroderma mainly affects the skin, but it may have an impact on the muscles and bones.
• Systemic scleroderma affects the whole body, including the blood and internal organs, and especially the
kidneys, esophagus, heart, and lungs.
• It is sometimes known as CREST syndrome:
C: Calcinosis, or calcium deposits in tissues and under the skin
R: Raynaud's disease
E: Esophageal problems, including GERD
S: Sclerodactyly, or thick skin on the fingers
T: Telangiectasias, or enlarged blood vessels, manifesting as red spots
3. DERMATOMYOSITIS
• Dermatomyositis is an inflammatory disease marked by muscle weakness and a distinctive skin rash
• In adults, dermatomyositis usually occurs from the late 40s to early 60s.
• In children, it most often appears between 5 and 15 years of age
• Dermatomyositis affects more females than males.
SYMPTOMS
• Skin changes: A violet-colored or dusky red rash develops
• The rash, which can be itchy and painful
• Muscle weakness: Progressive muscle weakness involves the muscles closest to the trunk, such as those in
your hips, thighs, shoulders, upper arms and neck. The weakness affects both the left and right sides of your
body, and tends to gradually worsen.
Complications
• Difficulty swallowing: Problems swallowing (dysphagia), which can cause weight loss and malnutrition.
• Aspiration pneumonia: Difficulty swallowing can also cause you to breathe food or liquids, including
saliva, into your lungs (aspiration).
• Breathing problems: If the condition affects your chest muscles, you might have breathing problems, such
as shortness of breath.
• Calcium deposits: These can occur in your muscles, skin and connective tissues (calcinosis) as the disease
progresses. These deposits are more common in children with dermatomyositis and develop earlier in the
course of the disease
4. POLIOMYELITIS
• Commonly called polio, is an acute infectious disease caused
by the poliovirus
• The poliovirus enters the body either through the faeco-oral
route or by inhalation of droplets.
• The infection occurs commonly in summer.
Stages of poliomyelitis.
(a) Incubation period (b) Pre-paralysis stage (c) Stage of maximum
paralysis (d) Stage of recovery (e) Post-polio residual paralysis
• The virus multiplies in the intestine.

• From here it travels to the regional lymph nodes and reticulo-endothelial structures and enters blood
circulation.
• If the defense mechanism of the body is poor, the virus reaches the nervous system (mainly the anterior horn
cells) via the blood or peripheral nerves
• The neurons undergo varying degree of damage
• Lead to permanent paralysis; while the others may regenerate, so that partial recovery of the paralysis may
occur
• It is this residual paralysis (called post-polio residual paralysis –PPRP) which is responsible for the host of
problems associated with a paralytic limb (deformities, weakness etc.).
Clinical Features:
• Child around the age of 9 months
• The mother gives a history that the child developed mild pyrexia associated with diarrhea, followed by
inability to move a part or whole of the limb.
• The lower limbs are affected most commonly
• Paralysis is of varying severity and asymmetrical in distribution.
• In extreme cases, the respiratory muscles may also be paralyzed
• Recovery of power, if it occurs, may continue for a period of 2 years
• Most of the recovery occurs within the first 6 months
EXAMINATION
• In early stage: It is asymmetric i.e., the involvement of the affected muscles is haphazard.
• It occurs commonly in the lower limbs because the anterior horn cells of the lumbar enlargement of the
spinal cord are affected most often. The muscle affected most commonly is the quadriceps. The muscle which
most often undergoes complete paralysis is the tibialis anterior. The muscle in the hand affected most
commonly is the opponenspollicis. The motor paralysis is not associated with any sensory loss.
• Bulbar or bulbo-spinal polio: This is a rare but life-threatening polio, where the motor neurons of the medulla
are affected. This results in involvement of respiratory and cardiovascular centres, and may cause death.
• In late stage (PPRP), the paralysis may result in wasting, weakness, and deformities of the limbs.
• The deformities result from imbalance between muscles of opposite groups at a joint, or due to the action of
the gravity on the paralysed limb.
• The common deformity at the hip is flexion-abduction-external rotation.
• At the knee, flexion deformity is common; in severe cases triple deformity comprising of flexion, posterior
subluxation and external rotation occurs
• At the foot, equino-varus deformity is the commonest; others being equino-valgus, calcaneo-valgus and
calcaneocarus,
• In the upper limbs, polio affects shoulder and elbow muscles. The limb may become short.
Poliomyelitis Asymmetrical, lower motor neurone type, no sensory loss, improves with time
or is static
Myopathy Usually symmetrical follows a pattern, lower motor neurone type, no sensory
loss, deteriorates with time.
Spina bifida and Usually symmetrical, motor and sensory loss, deteriorates with growth.
other spinal disorders
Neuropathy Usually bilateral ‘Glove and stocking’ pattern, motor and sensory loss, may
improve with treatment.
The treatment appropriate to each stage of the disease is best considered stage by stage.
1 - Stage of onset:
• It is generally not possible to diagnose polio at this stage.
• In an endemic rea, if a child is suspected of having polio, intramuscular injections and excessive physical
activity should be avoided.
2 - Stage of maximum paralysis: In this stage, the child needs mainly supportive treatment.
• A close watch is kept for signs suggestive of bulbar polio.
• Signs of paralysis of the vagus nerve, causing weakness of the soft palate, pharynx and the vocal cords –
hence problem in deglutition, and speech
• Respiratory muscles are paralyzed
• Paralytic limbs may have to be supported by splints to prevent the development of contractures
• Full range of motion several times a day.
• Muscle pain may be eased by applying hot packs.
3. Stage of recovery:
Principles of treatment are
• Prevention of deformity by proper splintage, and joint mobilizing exercises.
• Correction of the deformity
• Retraining of muscles that are recovering by exercises
• Encourage walking with the help of appliances
4.Stage of residual paralysis:
• It is the stage where more active orthopaedic treatment is required
• Detailed evaluation of the patient
• Prevention or correction of deformities
• Tendon transfers
• Stabilization of flail joints
• Leg length equalization
5. MIXED CONNECTIVE TISSUE DISEASE (MCTD)
The symptoms of all three varieties of connective tissue disease are present in MCTD.
Polyarteritis nodosum (PAN): Inflammation occurs in the arteries. This results in ischaemia of the end organ.
Skin lesions (vasculitis) and renal complications may be present.
Polymyalgia rheumatica: Pain and stiffness of the neck and shoulder in the morning with tenderness are
common. Synovitis may occur in hands and knees. Arteritis involving temporal arteries may be present.
Corticosteroids are effective in combating the disease.
Erythema nodusum: In this disease, erythematous raised lesions are present on the anterior aspect of the
skin. The symptoms of arthritis may occur. Corticosteroid therapy is effective.
Sjogren syndrome: Dryness of eyes and mouth with peripheral arthropathy are present. RA, thyroid, hepatic
or renal diseases may accompany.
SOFT TISSUE INJURY AND HEALING
• Sports injury prevention can be characterized as being 'primary: 'secondary' or 'tertiary'.
• Examples of primary prevention include health promotion and injury prevention (e.g. ankle braces being
worn by an entire team, even those without previous ankle sprain).
• Secondary prevention can be defined as early diagnosis and intervention to limit the development of
disability or reduce the risk of reinjury. e.g. early RICE treatment of an ankle sprain.
• Tertiary prevention is the focus on rehabilitation to reduce and/or correct an existing disability attributed to
an underlying disease.
• Important factors that may assist in the prevention of injury:
• Warm-up • Stretching taping and bracing • Protective equipment
• Suitable equipment • Appropriate surfaces • Appropriate training
• Adequate recovery • Psychology • Nutrition.
SEQUENCE FOR PREVENTION OF SPORTS INJURIES
RISK FACTORS FOR SPORTS

INJURIES
• The internal risk factors - factors that may
predispose to or protect the athlete from
injury.
• includes athlete characteristics as age,
maturation, gender, body composition and
fitness level.
• Internal risk factors can be modifiable and
non-modifiable.
• Modifiable risk factors may be targeted by
specific training methods.
• Non-modifiable factors (such as gender)
can be used to target intervention measures
to those athletes who are at an increased risk.
• The second group of risk factors is the external factors the athletes are exposed to, for example, floor friction
in indoor team sports, snow conditions in alpine skiing, a slippery surface (running track), very cold weather,
or inappropriate footwear.
INJURY CAUSATION MODEL
WARM UP
It prepares the body for exercise.
• The type of exercise to be performed
determines the type of warm up.
• Most effective warm-up consists of
both general and specific exercises.
• General exercises may jogging,
general stretching and resistance
exercise.
• Specific exercises include stretches
and movements that are
appropriate for the particular about to
be undertaken.
Warm-Up Conditions
• Make sure your warm-up does the following:
• Increases heart rate and breathing rate
• Elevates body temperature
• Utilizes muscles you will use in the upcoming activity
• Takes your joints through a full range of motion needed for the upcoming activity.

How to do warm up
• General warm up
• Stretching warm up
• Sports specific warm up
The general warm-up is divided into two
• Joint rotations
• Fingers and knuckles, wrists, elbows,
shoulders, neck, trunk/waist, hips, legs,
knees, ankles and toes).
• Aerobic activity
• Running, jogging, games, etc.
Stretching
• Light stretching should be done after the
warm-up
• Deep stretching after the entire workout
• Remember to breathe when you stretch!
• Benefits of stretching, include:
• Improving and maintaining joint
range of motion
• Helps reduce risk of injury
• Helps reduce soreness
• Promotes better posture
• Improves circulation
• Relieves stress
Warm-Up Stretching
• After the warm-up, stretch the muscles that you will be using during your workout.
• Each stretch should last 10-30 seconds.
• Going on a Walk? : Concentrate on stretching your…
• Quadriceps, hamstrings, gluteal, adductors, hip flexors, calves, and lower back.
HOW LONG TO WARM UP:

• Should be relative to particular sports or activity
• A minimum of 10 min
• Warming up should at least consist of the following:
1. 5 to 10 minutes jogging - to increase body temperature
2. 10 to 15 minutes static and dynamic stretching exercises – reduce muscle stiffness
3. 10 to 15 minutes general and event specific drills - preparation for the session or competition.
STRETCHING
Principles of stretching
The basic principles of stretching are:
• Warm-up prior to stretching
• Stretch before and after exercise
• Stretch gently and slowly
• Stretch to the point of tension but never pain.
TAPING AND BRACING

• Taping (or strapping) and bracing are used to restrict undesired, potentially harmful motion and allow desired
motion.
Indication of taping or bracing:
1. Prevention - taping is used as a preventive measure in high-risk activities, for example, basketball players'
ankles
2. Rehabilitation - taping is used as a protective mechanism during the healing and rehabilitation.

Suitable equipment
• Running shoes, football boots, ski boots and tennis racquets are important elements that contribute to, or
prevent, sports injuries.
• Forefoot flexibility must be adequate to allow easy motion of the foot flexing at toe-off.
• With a rigid sole, the calf muscles need to perform extra work in order to plantar flex the foot during
propulsion.
• A shoe with a lack of flexibility leads to metatarsalgia. The midsole of the shoe is probably the most
important feature
• Midsoles are usually made of EVA, which is light and a good shock absorber
• The midsole houses the more complex shock-absorbing materials such as gel pads and air bladders.
• The most important feature of the midsole is its density (durometer). It should be appropriately firm or soft
depending on the mechanics and weight of the individual.
APPROPRIATE SURFACES
• Surface on which sports person plays is the major cause of sports injury
• Playing surface hardness its association with overuse injuries such as stress fractures, shin pain and
tendinopathy.
• A hard surface such as concrete generates greater force through the musculoskeletal system than a forgiving
surface such as grass.
• Sporting activities can generate extremely high loads that may, or may not, be modulated by the surface.
APPROPRIATE TRAINING
▪ Training' is the pursuit of activity that will ultimately lead to an increase in performance in a given sport.
Basic Principles of training
1. Principle of individuality 2. Principle of specificity. 3. Principle of disuse.
4. Principle of progressive overload.
5. Principle of hard/easy.
6. Principle of periodization.
Principle of individuality
• Except identical twins, no two people have identical genetic characteristics
• So different individuals will show different levels of adaptation to a given exercise training program
•Variations in cellular growth rates, metabolism, endocrine and neural regulation will also cause these
individual variations.
Eg: some individuals shows great improvement after participating in a given exercise program and others
shows little or no change following the same training program
•People vary in initial fitness state at the start of a conditioning program and thus respond differently to the
same training stimulus.
• For this reason, any training program
• Specific needs and abilities of individuals to whom it is designed- principle of individuality
• Coaches and trainers should recognize how athletes and trainees respond to a given exercise stimulus and
adjust the exercise prescription based on that response.
Principle of specificity
• Training adaptations are highly specific to the type of activity intensity volume of exercise performed.
•Eg: for shot-putter would not emphasize on distance running or slow, low intensity resistance training.
Similarly, distance runner would not concentrate the sprint type interval training.
• According to principle of specificity the training program must stress
• The physiological system that are critical for the optimum performance in the given sport in order to achieve
the specific training adaptations.
• Aerobic fitness for swimming, bicycling, running, or rowing improves most effectively when the exerciser
trains the specific muscle required for the activity. In essence, specific exercise elicits specific adaptation
creating specific training effects referred to as the SAID principle—specific adaptations to imposed demands.
Principle of disuse/ Reversibility principle

• Regular exercise will improve the muscle capacity to generate more energy and to resist fatigue

• Principle of training says that if you stop the training then the status of fitness will comes down to a level
that meets only the demands of daily use.
• In other words, whatever gains you achieved with training will be lost
• The reversibility of training effects, referred to as detraining, occurs relatively rapidly when a person quits
his or her exercise training regimen.
• After only a week or two of detraining, measurable reductions occur in physiologic function and exercise
capacity, with a total loss of training improvements occurring within several months.
• In one experiment, VO2max decreased 25% in five subjects confined to bed for 20 consecutive days; a
similar decrease in maximal stroke volume and cardiac output accompanied the loss of aerobic capacity (1%
per day). Capillary number within trained muscle also decreased 14% to 25% over the detraining period.
• Thus, it is important that all types of training program should have some maintenance plan.
Principle of progressive overload

• Progressive training and overload components are the foundations of all types of training program
• Eg: To gain strength muscles must be overloaded, which means they must be loaded beyond the point to
which they are normally loaded.
• Progressive resistance training means as the muscle become stronger followed by training proportionately
greater resistance is required to further stimulate the muscle.
• So as the training progress the intensity and Volume (duration and repetition) of exercise should increase
in order to get an optimum effect.
• In other words, in order to achieve the appropriate overload requires manipulating combinations of training
frequency, intensity, and duration, with focus on exercise mode.
• The concept of overload applies to the athlete, sedentary, disabled, and even cardiac patient.
Principle of hard/easy
• Continuous hard training or long duration training will cause maladaptation of body to the exercise due to
less time of recovery.
• Thus, this principle suggest that followed by a hard training there should be an easy training session which
will allow the body to recover actively.
• In other words, after a high intensity training session (hard training) you can include an low intensity exercise
session(easy).
Principle of periodization
• This principle mainly popular in the area of resistance training
• It refers changes or variation in the exercise training program over a period of time such as a year
• It helps to keep the individual away from the overtraining.
• It consists of 5 phases in each training cycle
• The first phase characterized by high volume (repetition and sets) and low intensity
• During the next 3 phases volume is decreased and intensity is increased.
• Followed by this there will be an active recovery phase in which either light resistance activity or an
unrelated activity is used to allow the body to recover both physically and mentally
• Once the active cycle recovery phase completed the entire cycle will be repeated
• It can vary from one cycle per year to 2 or 3 cycles per year.
• The main idea is gradually decreasing the volume while gradually increasing the intensity
• The number of repetition and sets can be varied to accommodate the particular sport.
Variable Phase 1 Phase 2 Phase 3 Phase 4 Phase 5
Sets 3–5 3–5 3–5 1–3 General activity or light resistance
training
Repetition 8 -20 2–6 2–3 1–3
Intensity Low High High Very
High
Duration (weeks) 6 6 6 6 2
Phase 1: Muscle Hypertrophy Phase 2: Strength
Phase 3: Power Phase 4: Peak strength
Phase 5: Active recovery

Other topics:
1. Introduction: [3 Hours]
a) Clinical examination in an Orthopedic patient PAGE NO: 36 (M)
b) Common investigative procedures: Radiological and Imaging techniques in Orthopeadics.
PAGE NO: 38 (M)
c) Inflammation and repair PAGE NO: 10 (M)
d) Soft tissue healing PAGE NO: 108 (NOTES)
2. Traumatology [3 Hours]
a) Fracture: Definition, types, signs and symptoms. PAGE NO: 1 (M)
b) Fracture healing. PAGE NO: 10 (M)
c) Complications of fractures. PAGE NO: 42 (M)
d) Conservative and surgical approaches. PAGE NO: 13 (M)
e) Principles of management – reduction (open/closed, immobilization etc.) PAGE NO: 13 (M)
f) Subluxation/ dislocations – definition, signs and symptoms, management (conservative and
operative). PAGE NO: 54 (M)
3. Fractures and Dislocations of Upper Limb [6 Hours]

Fractures of Upper Limb - causes, clinical features, mechanism of injury, complications,
conservative and surgical management of the following fractures:
a) Fractures of clavicle and scapula. PAGE NO: 88 (M) AND 89
b) Fractures of greater tuberosity and neck of humerus. PAGE NO: 92 (M)
c) Fracture shaft of humerus. PAGE NO: 93 (M)
d) Supracondylar fracture of humerus. PAGE NO: 97 (M)
e) Fractures of capitulum, radial head, olecranon, coronoid, and epicondyles. PAGE NO: 103 – 107 (M)
f) Side swipe injury of elbow. PAGE NO: 3 (M)
g) Both bone fractures of ulna and radius. PAGE NO: 109 (M)
h) Fracture of forearm – monteggia, galaezzi fracture –dislocation. PAGE NO: 110 - 111 (M)
i) Chauffer’s fracture. PAGE NO: 3 (M)
j) Colle’s fracture. PAGE NO: 111 (M)
k) Smith’s fracture. PAGE NO: 114 (M)
l) Scaphoid fracture. PAGE NO: 115 (M)
m) Fracture of the metacarpals. PAGE NO: 118 (M)
n) Bennett’s fracture. PAGE NO: 117 (M)
o) Fracture of the phalanges. (Proximal and middle.) PAGE NO: 118 (M)
Dislocations of Upper Limb –
p) Anterior dislocation of shoulder – mechanism of injury, clinical feature, complications, conservative
management (Kocher’s and Hippocrates maneuver), surgical management (putti plat, bankart’s) etc.
Recurrent dislocation of shoulder. PAGE NO: 89 (M)
q) Posterior dislocation of shoulder – mechanism of injury, clinical features and management. PAGE NO:
89 (M)
r) Posterior dislocation of elbow – mechanism of injury, clinical feature, complications & management.
PAGE NO: 105 (M)
4. Fracture of Spine [4 Hours]

a) Fracture of Cervical Spine - Mechanism of injury, clinical feature, complications (quadriplegia);
Management- immobilization (collar, cast, brace, traction); PAGE NO: 148 (J)
b) Management for stabilization, management of complication (bladder and bowel, quadriplegia).
PAGE NO: 277 (M)
c) Clay shoveller’s fracture. PAGE NO: 273 (M)
d) Hangman’s fracture.
e) Fracture odontoid.
f) Fracture of atlas. PAGE NO: 272 (M)
g) Fracture of Thoracic & Lumbar Regions - MOI, clinical features, management —conservative and
surgical of common fractures around thoracic lumbar regions. PAGE NO: 164 (J)

h) Fracture of coccyx.
i) Fracture of Rib Cage - Mechanism of injury, clinical features, management for Fracture Ribs. PAGE
NO: 164 (J)
j) Fracture of sternum.
5. Fractures and Dislocations of Lower Limb [5 Hours]

Fracture of Pelvis and Lower Limb - causes, clinical features, mechanism of injury, complications,
conservative and surgical management of the following fractures:
a) Fracture of pelvis. PAGE NO: 123 (M)
b) Fracture neck of femur – classification, clinical features, complications, management - conservative
and surgical. PAGE NO: 132 (M)
c) Fractures of trochanters. PAGE NO: 138 (M)
d) Fracture shaft femur—clinical features, mechanism of injury, complications, management-
conservative and surgical. PAGE NO: 141 (M)
e) Supracondylar fracture of femur. PAGE NO: 145 (M)
f) Fractures of the condyles of femur. PAGE NO: 145 (M)
g) Fracture patella. PAGE NO: 147 (M)
h) Fractures of tibial condyles. PAGE NO: 146 (M)
i) Both bones fracture of tibia and fibula. PAGE NO: 155 (M)
j) Dupuytren’s fracture
k) Maisonneuve’s fracture.
l) Pott’s fracture – mechanism of injury, management.
m) Bimalleolar fracture
n) Trimalleolar fracture.
o) Fracture calcaneum – mechanism of injury, complications and management. PAGE NO: 164 (M)
p) Fracture of talus. PAGE NO: 165 (M)
q) Fracture of metatarsals—stress fractures jone’s fracture. PAGE NO: 166 (M)
r) Fracture of phalanges. PAGE NO: 167 (M)
s) Dislocations of Lower Limb - mechanism of injury, clinical features, complications,
management of the following dislocations of lower limb.
t) Anterior dislocation of hip. PAGE NO: 131 (M)
u) Posterior dislocation of hip. PAGE NO: 130 (M)
v) Central dislocation of hip. PAGE NO: 131 (M)
w) Dislocation of patella. PAGE NO: 152 (M)
x) Recurrent dislocation of patella. PAGE NO: 153 (M)
8. Amputations [2 Hours]
A) Definition, levels of amputation of both lower & upper limbs, indications, complications. PAGE NO:
328 (M)
9. Traumatic Spinal Cord Injuries [2 Hours]

A) Clinical features, complications, medical and surgical management of Paraplegia and Quadriplegia.
PAGE NO: 276 (M)
16. Orthopedic Surgeries [3 Hours]

Indications, Classification, Types, Principles of management of the following Surgeries:
a) Arthrodesis. PAGE NO: 83 (M)
b) Arthroplasty (partial and total replacement). PAGE NO: 84 (M)
c) Osteotomy PAGE NO: 83, 136 (M)
d) External fixators. PAGE NO: 371 (M)
e) Spinal stabilization surgeries (Harrington’s, Luque’s, Steffi plating) etc.,
f) Limb re-attachments.
10. Deformities: Refer written notes

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ORTHOPAEDICS

SL.NO TITLE PAGE NO.

2 Soft tissue injuries 7 – 19

6 Diseases of bone and joints 55 – 82

7 Cervical and lumbar pathology 83 – 97

8 Inflammatory and degenerative conditions 98 – 107

9 Soft Tissue injury and healing 108 - 111

1|Page Viresh – Orthopaedics

1. THORACIC OUTLET SYNDROME

2|Page Viresh – Orthopaedics

NON - OPERATIVE MANAGEMENT

3|Page Viresh – Orthopaedics

The brachial nerve plexus, subclavian artery and subclavian

4|Page Viresh – Orthopaedics

5. LEVATOR SCAPULE SYNDROME

5|Page Viresh – Orthopaedics

6|Page Viresh – Orthopaedics

7|Page Viresh – Orthopaedics

8|Page Viresh – Orthopaedics

CRUCIATE INJURIES IN KNEE

MEDIAL AND LATERAL COLLATERAL INJURIES OF KNEE

Test: Valgus Stress test (Abduction) positive.

Treatment: Same as ACL.

2. LATERAL COLLATERAL LIGAMENT:

Test: Varus Stress (Adduction) test

Treatment: Same as ACL.

Indications for Surgery

Mild > 90° Normal Capillary rupture: Blood into 6 days

Moderate 45 - 90° Antalgic Crushing of the muscle fibres with 56 days

Return to sports criteria

Causes of a calf contusion

Symptoms of a Deltoid Contusion

2. ROTATOR CUFF MUSCLES (for detail – refer chapter 17 )

• Localised tenderness in bicipital grove

Biceps load test

Management: Goal: to return to sports

2. ROTATOR CUFF TENDINITIS

So, position of Abduction, Flexion and IR is called as

1. Subacute tendinitis (Painful arc syndrome)

Biceps load test

2. GOLFER’S ELBOW/ MEDIAL EPICONDYLITIS

3. STUDENT’S ELBOW/OLECRANON BURSITIS/MINERS ELBOW/DRAUGHTSMAN ELBOW

3. TRIGGER FINGER/THUMB/ STENOSING TENOSYNOVITIS

4. MALLET FINGER/HAMMER FINGER/BASEBALL FINGER

5. CARPAL TUNNEL SYNDROME

Differential diagnosis that mimic CTS:

6. DUPUYTREN’S CONTRACTURE/SUPERFICIAL PALMAR FASCITIS

PELVIS AND HIP

2. A) PREPATELLAR BURSITIS/HOUSEMAIDS KNEE

C) INFRAPATELLAR BURSITIS/CLERGYMANS KNEE

7. FAT PAD SYNDROME (HOFFA’S SYNDROME)

ANKLE AND FOOT

Medial portion: Thinner

Risk factors of plantar fasciitis:

Diagnosis of plantar fasciitis:

4. TARSAL TUNNEL SYNDROME

Lesions in the Brain

PRE – SCHOOL PERIOD

SCHOOL AGE AND ADOLESCENCE

Stages and their corresponding features:

POST POLIO SYNDROME:

Lipomeningocele refers to the fatty contents of a spina bifida lesion.

Post – operative Care: