Orthopaedic conditions

A written report about various orthopedic conditions.
source: handbook of orthopeadic surgery by;Brashear

1. ORTHOPAEDIC CONDITIONS
Congenital Talipes
 Talipes equinovarus (congenital club foot)

o Etiology
 Unknown; usually referred to as idiopathic club foot
 Isolated lesions may be result of a neurologic d/o that is not immediately evident at the
time of birth
 Most widely accepted pathogenesis:
 Arrested or anomalous development of this particular part of the embryo in the
first trimester of pregnancy.
 Inward rotation of the foot fails to occur at the 7
th
month of pregnancy.
 Muscle imbalance
o Incidence
 Occurs about once in every 1000 live births
 Twice as common in boys as in girls
 Slightly over half of the patients the disorder is bilateral
 In Unilateral cases right and left sides are affected with equal frequency
 Occasionally there is talipes equinivarus on one side with metatarsus varus or talipes
calcaneovalgus on the other.
o Pathology
 Achilles Tendon  shortened
 Ant. And post. Tibial tendons  cx in proportion to the degree of varus deformity
 Degenerative changes in fibers of certain ms. And anomalous insertion of tendons in the
foot
 At birth ligaments and joint capsules on the med. Side of the foot are cx.
 Consistent deformity neck of talus shortened & dev. Med.
 Most striking abnormality  talocalcaneonavicular jt.
 Navicular bone  displaced med. Around the head of the talus.
 Forepart of the foot follows the med. Displaced navicular
 Subtalar surfaces  tilted into varus & equinus & med. Rot.
 Calcaneous  slightly shortened & widened
 As the child grows  talus  wedge shape with its post. Surface apposed to the tibia,
calcaneous  points downward and rot. Med.
 Structural changes may be found in all other bones but in lesser degree
o Clinical picture
 Heel is drawn up, the entire foot below the talus is inverted, and the ant. Half of the foot
is adducted.
 Med. Border of the foot is concave, lat. Border is covex
 (+) transverse crease across the sole @ the level of the mediotarsal joint
 If not corrected before the infant starts to walk  suffers a serious handicap because of
inability to WB N°
 Ms.  Easily fatigued & (+) atrophy
 Pain is developed only by Adult Pt. (arthritic changes)
o Diagnosis
 Seen frequently in association with paralytic changes in the lower ex, in myelodysplasia,
CP & poliomyelitis
o Prognosis
 Range of severity and rigidity extends from a relatively flexible talipes equinvarus 
responds to non-operative Rx; tight resistant clubfoot  requires surgical correction.

2.  Foot  Cx med. & post. Tse. That make it resistant to gentle manual correction without
surgical release of the contracted soft tse  POOR prognosis
o Treatment
 Must start as the clubfoot is recognized
 Correcting thoroughly all elements of the deformity, maintaining the correction until N°
ms balance  developed; cont. until an over correction has been reached.
 Goal of every Rx: Position of DF & Ev of the foot & Abd of the forefoot.
 Functional result will be good if the final position can be obtained without the trauma of
forceful manipulation & without radical surgery  interference with bone growth and by
stiffness of the joints of the foot.
 Rx starts: first week or two after birth should consist of gently manipulating the foot to
improved position  holding the position by adhesive strapping or light plaster cast
repeated 1/week
 Key to success is reduction of the talonavicular joint  by gently stretching the med.
Border of the foot by longitudinal traction on the forefoot with a force directing the
navicular around the front of the head of talus; an everting and downward pull is exerted
on the tiny heel to roll the calcaneous lat. From its inverted position beneath the talus.
 When the full correction is achieved foot must be held in corrected position in a cast for
3-4 mo.; cast are changed 3-4 weeks, after child is fitted with clubfoot shoes attached to
denis browne splint  Worn day and night except during ex. And bathing. If infant is
ready to walk splints may be worn only at night & clubfoot shoes for day use.
 Simplest and most frequently used operation is lengthening of Achilles tendon to lessen
the equinus deformity; may be done early @ the age of 2/3 mo.
 The correction of clubfoot in a child more than 10years old or in an adult requires
operation on the tarsal bones.

Congenital Abnormalities of fingers and toes
 Syndactyly (webbed fingers/toes)

o Description
 A common anomaly occurs twice as often in boys as in girls & more often in the hand
than in the foot.
 Ulnar side is more affected, & thumb is seldom involved.
 Union between affected digits may consist only of skin and connective tissue  simple
syndactyly; if union includes bone  complex
o Treatment
 Separation of involved fingers  dividing soft tissues/bony structures; done bet. 18 mo
& 5 yrs., earlier when hand function is impaired.
 Macrodactyl

o Overdevelpment of one or more fingers/toes
o Rx: amputation but occasionaly a plastic operation to effect a reduction in size is preferable


 Polydactyl

o Supernumery digits; common & frequently inherited anomalies
o Often Bilateral; may be compined with syndactyly
o Amputation of the extra finger/ toe is indicated.

3. General Affectations of bones

 Osteitis Deformans
o Etiology
 Causative agent is unkown
o Pathology
 Active stages  blood flow to bone greatly ↑  high output cardiac failure
 Gross skeletal changes  developing thickening and bowing of the shafts of the long
bones (tibia and femur) & generalized thickening of the cranium
 Often affect only a single bone
 Bones lose their ability to withstand N° stresses & ↑ degree of curvature
 Spine (frequently involved)  partial collapse of one or more of the vertebral bodies 
kyphosis
 Later stage: bones matrix is laid down calcifies  thick, hard osseous structure
o Clinical picture
 Asymptomatic
 Affects man more frequently than women and occasionally it occurs in families
 40-60y.o when symptoms begin, may develop the ff:
 Severe intractable pain
 May complain of fatigue and aching in legs
 h/a & backache
 legs are becoming bowed, that the back is stooped or the head is becoming larger
 moderately advanced stage: head appears massive an too large for the body; face
is relatively small, head may droop forward, long dorsal kyphosis; chest is barrel
shaped & lumbar spine flexed, legs are bowed outward & forward
 no mental changes
 may develop deafness and tinnitus and an impairment of vision
o Treatment
 Required no treatment
 If with significant symptoms  drugs: Calcitonin. Bisphosphonates & mithramycin 
↓bone pain & control the activity of the dse.
 Bracing for long bones and spine
o Prognosis
 Cardiovascular complication  MC cause of death
 Length of life is good
 Pathologic Fx is the MC complication (femur)

 Ankylosing spondylitis (Strumpell –Marie Arthritis)
o Characterized by ossification of the ligaments of the spine and by involvement of the hips &
shoulders
o Sacroiliac joints are affected early
o Cause is unkown
o 10x < men
o Begins @ ages of 20-30 y.o
o Familial

o Pathology
 Progressive ossification  capsular & intervertebral ligaments fusing lower and later the
entire spine into a single mass.
 Vertebral bodies seemed to be osteoporotic

4.  (+) irregular spur formation & lipping of the vertebrae
o Clinical Picture
 Onset: maybe assoc. with acute pain
 Stiffness without pain may be the first symptom
 Malaise and fatigability accompanied with wgt loss
 Pain first appears @ hip, buttocks or lumbosacral region
 LBP while pt. is recumbent in early morning hours
 Pain & tenderness @ sacroiliac region when pelvic wings are pressed together /when hips
are stressed in extremes of rot.
 ↓spinal mobility & diminished chest expansion
 Associated with other conditions: Plantar fasciitis, tendinitis of Achilles tendon, heel
pain.
 Pain lessens as the stiffness ↑
 There is no involvement of the smaller joints
o Treatment
 General measures
 Rest & well- balanced diet
 Control of pain
o Regular dose of Aspirin
o Saliciylates and other NSAIDs
o Rare: steroid therapy
 Local non-surgical measures
 Bed rest (firm mattress/bed board should be use & rest without a pillow)
 Hyperextension ex. Should be done & position of extension should be maintained
 Wearing 3-point brace to prevent kyphosis
 Breathing ex.
 Surgical Rx
 Osteotomy of the spine
 Joint replacement  painful ankylosis of the hip

 TUMORS
 Osteochonndroma

o MC benign tumors of bone
o They are hamartomas rather than true tumors
o First Dx with persons ages 10 – 25 y.o. & typically situated near the ends of long bones
o Symptoms
 Swelling / lump is only pt’s complain
 Discomfort to adjacent bones
o MC location: near the adjacent ends of the femur & tibia / upper end of the humerus; flat bones,
scapula MC involved
o Treatment:
 Operation is not always necessary
 Any large osteochondroma in location that is prone to trauma must be removed
o Postpubertal enlargement and pain suggest malignant change.

 Osteogenic sarcoma (Osteosarcoma)

o MC malignant primary bone tumor

5. o Typically develops in the metaphysis of a long bone in late childhood or early adult life (bet. 10
& 20 y.o.)
o Aggressive tumor  rapid growth, early pulmonary metastases,
o No definite cause
o Pathology
 MC sites  Upper tibia, lower femur, & upper humerus
 Hallmark: Osteoid matrix produced by the tumor cells
o Clinical Picture
 MC in children & young adults
 Males>females
 Occasionally occurs In later adult years, but usually 2° to a pre-existing lesions such as
paget’s dse.
 Dull, constant, aching pain first symptom
 Hard bony enlargement that is slightly tender and typically located above/below the knee
or near the sho.
 Discomfort  limping
 Rapidly growing tumors  distention of the superficial veins and ↑ of skin temp.
o Treatment and prognosis
 Classical methods of amputation or disarticulation well above the lesion
 Chemotherapy

 FRACTURE
o Any break in the continuity of the bone.
 Open Fx
 A fx where there is a communication bet. The bone and outside
 Complicated by infection. Osteomyelitis, delayed union & even nonunion
 Close Fx – there is no such communication
 Pathologic Fx- occurs in bones weakened by pre-existing dse such as tumor, cysts,
osteomyelitis or osteoporosis.
 Stress Fx – result of bone fatigue from repeated unaccostumed loading & inadequate
muscular support.
o Described as;
 Transverse – caused by simple angulatory forces
 Oblique – unstable
 Spiral- result from torsion ; unstable
 Comminuted - the bone is broken into 3/more fragments; unstable
o FX Rx 3 basic objectives:
 Reduction / replacement of the bone fragments to as near anatomic position as possible.
 Manipulation
 Traction
 Open surgery
 Maintenance of reduction until healing is sufficient to & tendonsprevent displacement
 External fixation (cast/splint)
 Traction
o Skin traction
 Buck’s extension
 Russell’s traction
o Skeletal traction
 Steinmann pin
 Kirschner wire

6.  Internal Fixation
o Transfixion screw
o Bone plate
o Intramedullary rod or nail
 Preservation and restoration of function of ms. Joints
o Fx in children
 Greenstick Fx - An incomplete Fx in which the angulating force bends the cortex on the
compression side and breaks it on the distraction side
 Torus Fx- Frequently seen in the distal fourth of the radius, where mild angulation casues
buckling or buldging of the cortex on the compression side.
o Fx healing
 Fx heal by physiologic process similar to the repair of wounds of soft tissues, conditioned
by factors such as:
 Rigidity of bone
 Tendency of the Fx fragments to displace
o Spiral fx heals more rapidly than transverse fx.
 Length of time required for newly formed bone to restore strong union of
fragments.
o Humerus & FA – 3 mo
o Femur & tibia – 4-6 mo.
 3 late bony complications of Fx
 Delayed union – fx healing is abnormally slow
o (+) if tibia close fx does not become clinically firm in 20 weeks, humerus
in 10 weeks 7 femur in 20 weeks
 Causes of delay
 Inaccurate reduction
 Inadequate/ interrupted immobilization
 Severe local traumatization
 Impairment of bone circulation
 Infection
 Loss of bone substance
 Distraction or separation of fragmentd
o Rx
 Early, accurate and gentle reduction and immobilization
 Maintenance of function
 Abstention from repeated trauma
 Sound judgement and technique in the us of Internal Fixation
 Non-union – healing stops short of firm union
o NO Fx should be considerd ununited until @ least 6 mo. After the date of
injury
 Factors
 Malnutrition
 Generalized illness
 Extensive tissue damage
 Impairment of bone blood supply
 Infection
o Rx
 Acceptance of the defect
 Use of simple brace
 Electrical stimulation

7.  Bone grafts
 Autogenous bone – taken from the patient
 Homogenous bone – taken from other person
 Malunion- healing takes place in unsatisfactory alignments

 AMPUTATION
o May be a result of congenital limb deficiencies or may be acquired
o Indications/ common reason
 Vascular disease/accident
 Trauma
 Tumor
 Infection
 Thermal, chemical or electrical injury
 Congenital anomaly
o Types of surgical amputation
 Disarticulation – amputation preforemed through a joint
 Open amputation – surface of the wound is left unclosed
 Closed amputation – a final or definitive amputation  stump
 Minor amputations amputations through th or distal to the metacarpus or the metatarsus
 Major amputations – all amputations proximal to the metacarpal or metatarsal bones.
o amputation levels

8.  SCOLIOSIS
o Scoliosis is a lateral deviation of the vertebral column.
o MC found in the thoracic region and may be caused by muscular or vertebral defects.
o Scoliosis is a deformity rather than a disease, and its causes are many often, scoliosis is
compensatory and may be caused by a short leg or hip disease.
o Classification and Etiology
 Non-structural Scoliosis (Functional)
 Not accompanied by rotational or asymmetric changes in the individual
structures of the spine.
 The curve is not fixed, in that in the bending in the opposite direction is not
restricted, and the patient can actively and completely correct the deformity by
sitting erect.
 It may result from poor posture or leg length discrepancies and usually poses no
major therapeutic problem.
 It may also be caused by nerve root irritation such as sciatic scoliosis seen in
acute lumbar disk herniation.
 Functional scoliosis can become structural if untreated.
 Structural Scoliosis
 A fixed curvature of the spine associated with vertebral rotation and asymmetry
of the ligamentous supporting structures.
 It can be caused by deformity of the vertebral bodies and may be:
o Congenital – defect in embryologic development of the vertebrae or ribs
(e.g., wedge vertebrae, fused ribs or vertebrae, hemivertebrae)
o Musculoskeletal (e.g., osteoporosis, spinal tuberculosis, rheumatoid
arthritis)
o Neuromuscular – associated with a great variety of paralytic disorders
that causeasymmetric paralysis of the trunk muscles. (e.g., cerebral palsy,
polio, myelomeningocele, muscular dystrophy)
o Idiopathic (MC) – Scoliosis with unknown pathogenesis
o Pathology
 All the structures of the concave side are compressed or shortened; those in the convex
side may remain normal or become lengthened.
 The apical vertebrae, situated at the middle of the curve, shows the greatest curve, shows
the greatest change, being wedge shaped and most rotated.
 The vertebrae above and below it undergo similar but less pronounced changes. It always
turns toward the convex side of the curve, and spinous process toward the concavity.
 The IVD are compressed on the opposite side as a result of the pressure; nucleus
pulposus migrates toward the convex side.
 The anterior longitudinal ligament is thickened on the concave side and thinned on the
convex side.
o Age of onset: from birth onward
 infantile (0 to 3 years)
 juvenile (ages 3 to 10)
 adolescent (age 10 until bone maturity at between 18 and 20 years of age)
 adult (after skeletal maturation)
o Clinical manifestations

9.  Curvatures of < 20 degrees rarely cause significant problems.
 Back most prominent features:
 Spinal curvature
 Asymmetric flank folds
 unLevel pelvis
 Prominence of the scapula and shoulder 
 Severe untreated scoliosis (> 60 degrees) may produce
 pulmonary insufficiency
 reduced lung capacity
 back pain
 degenerative spinal arthritis
 disk disease
 vertebral subluxation
 sciatica
 The adult with scoliosis  back pain d/t:
 muscle fatigue
 trunk imbalance
 facet arthropathy
 spinal stenosis
 degenerative disk disease
 Curves are designated as right or left depending on the convexity
 Two primary curvatures may exist
 rib hump (gibbus)
o tests and Measures
 Diagnosis by clinical examination:
 Forward bend
 Scoliometer
 Plumb line test
 Leg length discrepancy
 neurologic examination to rule out an underlying neurologic disorder
 Cobb method
 Risser-Ferguson method
 Nash-moe scale
o Treatment
 Conservative care
 Exercise
o Cotrel
o Klapp’s
 electrical stimulation
 Observation and monitoring
 spinal orthoses
 Milwaukee
 Boston
 Wilmington
 Charleston Bending brace
 Surgeries for curvatures greater than 45 degrees have been recommended.
 adult with scoliosis:
 conservative nonoperative course of physical therapy
 Non-narcotic analgesics

10.  nutritional counselling
 smoking (or tobacco-use) cessation
 and nerve root blocks
 facet injections
 epidural steroid injections before surgery is considered
o Prognosis
 Postural curvatures resolve as the primary problem is treated.
 Structural curvatures are not eliminated but rather increase during periods of rapid
skeletal growth.
 If the curvature is <40 degrees at skeletal maturity, the risk of progression is small.
 In curvatures >50 degrees, the spine is biomechanically unstable, and the curvature will
likely continue to progress at a rate of 1 degree/yr throughout life.
 Poor seating can contribute to this progression.
 In severe kyphoscoliosis, pain and comfortable positioning can complicate care, and
pulmonary compromise can lead to death.

 AFFECTATIONS OF THE HIP
 Coxa vara and coxa valga
o Coxa vara
 Abnormality of the upper end of the femur, consisting of a decrease in the neck-shaft
angle (angle of inclination)  shortening of the limb Limits abduction of the hips.
 May be congenital or acquired (MC)
o Coxa valga
 Increase of the neck – shaft angle  N° in infants before WB, persist in children who
are unable to stand because of chronic disability & seen as a secondary deformity in
congenital dislocation of the hip.

 AFFECTATIONS OF THE KNEE
 Cruciate ligaments injuries
o ALC tear (MC)- hyper / force pushing the femur backward on the tibia
o PCL tear – force applied to the front of the tibia push the tibia backward on the femur.
o MCL tear – a valgus / abduction force sometimes associated with rotation or hyper /
o LCL tear – a varus / Adduction force
o LL< common than ML
o Clinical picture
 Usually accompanied by hemarthrosis
 @ time of injury pt. will often note a definite “pop”
 ACL  associated with abnormal forward movement of the tibia on the femur; (+)
Lachman test
 PCL  Abnormal forward or backward displacement of tibia on femur; (+) posterior
drawer sign
 MCL pain & swelling, tenderness on med. Side which may be localized just above or
below the joint line; (+) valgus stress test; <5mm min., 5-10 mm mod., >10mm severe
injury
 LCL  swelling 7 tenderness on lat. Side; (+) Varus stress test
o Classification of ligamentous injury
 Mild/grade I – (-) instability & tear is only partial/interstitial
 Mod./ grade II – mild instability, secondary supporting structures are intact
 Severe/grade III – complete rupture of the ligaments and gross instability of the joint.
o Rx

11.  Grade I
 Short period of immobilization in soft splint
 Early movement of the knee (pain and swelling subsides)
 Grade II
 Immobilization in plaster cast for 6-8 weeks
 Early movement
 Exercises for the quads & hamstrings
 Ex. Involving Terminal ext. of knee should be avoided in ACL injuries
 Grade III
 Require surgical repair
 Close Rx with cast immobilization
 Brace that allow limited ROM
 Exercises
 Patellar tendinitis (Jumper’s knee)
o A common affectation of athletes
o Characterized by pain & tenderness over the patellar tendon & pain on forceful / of the knee
o Rx
 Rest & restriction of forceful knee /
 Use of splints/cast
 Surgical debridement (rare)

 AFFECTATIONS OF ANKLE AND FOOT
 Foot strain
o Common overuse condition characterized by pain & tenderness  Longitudinal arch d/t
excessive & unaccustomed standing & walking.
o Clinical Picture
 Acute foot strain
 Manifested by pain & tenderness  longitudinal arch  antalgic gait
 Chronic foot strain
 Complains of fatigue & aching in the feet
 Discomfort  longitudinal arch  calves
 Symptoms is worst @ the end of the day, by evening feet may feel tight and swollen
 M.I. finding  localized tenderness under the NAVICULAR bone @ the apex of long.
Arch.
o Rx
 Local Rx  Hot soaks/contrast baths = relieve discomfort
 Chronic strain
 felt / sponge rubber arch pad
 shoe with a long counter & firm shank will give inc. support
 Thomas heel  give support to navicular bone
 Weight reduction.
 Hallux Valgus
o Lat. Angulation of the great toe @ its MTP joint.
o Etiology & Pathology
 Frequently familial
 Women>men
 Med. Deviation of the 1
st
metatarsal is accompanied by lat. Deviation of the great toe
 Ant part of foot is widened & metatarsal arch depressed
 Cx of FHL &EHL is associated with a lat. Displacement of extensor tendons

12. o Rx & prognosis
 Mild cases  properly fitting shoes & repeated overcorrection by stretching
 If accompanied by diabling pain  surgery  removal of exostosis & bursa
 Silver operation  EHL tendon is sectioned/ lengthened
 Keller/ Schanz operation  resection of the proximal half of the first phalanx (for severe
deformity)
 Arthodesis of MTP joints
 Osteotomy of Proximal or distal portions of 1
st
metatarsals / proximal phalanx
 After operation:
 Splint/cast/soft cushion pad placed bet. 1
st
& 2
nd
toe
 Warm soaks & corrective foot ex.

 Hallux Varus
o Medial angulation of the great toe @ the MTP joint
o May be congenital in origin
o Casuse: Trauma, infection, ms. Imbalance, paralysis of Add Hallucis & bunion operation
o Rx:
 Mild cases corrected by surgically relaeasing Cx structures on the med. Side of the toe
& placating the lat. Part of the joint capsule
 Severe  osteotomy of the metatarsal head & use of sectioned EHB in a tenodesis to
maintain the corrected alignment.

 AFFECTATION OF NECK & SHOULDER
 TORTICOLLIS (WYRNECK)
o A deformity of the neck  rotation & flexion
o 1 SCM is shortened  tilting of the head towards the affected side & rot. Of chin to the opposite
side; shoulder of affected side is elevated
o Congenital torticollis (muscular torticollis)
 Cause: unknown
 Seen with relative frequency after difficult deliveries, with breech presentation &
primiparas
o Clinical picture:
 Girls>boys
 facial asymmetry develop within the first 3 months (affected: on the side which the head
is tilted)
o Prognosis
 Proper Rx = complete cure
 Incomplete surgical correction  recurrence
 Corrected before 3 / 4 y.o.  facial asymmetry msy completely disappear
o Rx
 Non-surgical
 Passive stretching of the neck in overcorrected position
 Proper positioning of the head during sleep
 If old enough  active exercises to strtch the short SCM
 Surgical
 Section of SCM
 Maintenance of overcorrection of the deformity  plaster cast, brace/ traction
 Program of ex. For securing ms. Balance to maintain the correction permanently

13.  Operation MC used  open resection of 1 cm segmentof SCM near its origin
from sternum & clavicle; platysma miss also included
 After operation: corrective ex for 6 mo.
o Acquired torticollis
 Accompanied by pain & stiffness as well as bizarre deformities of the neck
 Types
 Acute traumatic/inflammatory  caused by cervical injuries, atlantoaxial rotary
subluxation or inflammation of the ms/lymph nodes
 Chronic infectious/ neoplastic caused by osteomyelitis, tuberculosis, or tumors
of the spine.spinal cord
 Arthritic  caused by RA, ankylosing spondylitis or OA
 Cicatricial  Cx of scar tse after burn
 Paralytic  assymetric flaccid/spastic paralysis of neck ms.
 Hysterical  Psychogenic inability of the pt. to control neck ms.
 Spasmodic  CNS/ cervical root lesion & manifested by involuntary rhythmic
Contraction of the neck ms.
 Rx
 Is that of its 1° cause
 Helps treating the symptoms
o Hot application
o Gentle massage
o Horizontal/vertical neck traction
o Cervical orthoses

 AFFECTATIONS OF THE SHOULDER
 Adhesive Capsulitis (frozen shoulder)
o A chronic affectation characterized by pain and LOM (sho) that becomes worse over a period of
3-12 mo.
o Frequently seen in pt.’s over 40y/o
o Women> men
o A.k.a. Periarthritis, obliterative bursitis & diffuse rotator cuff tendinitis
o Pathology
 Changes in jt. Capsule  Edema, Fibrosis, round cell infiltration (indicating low-grade
inflammatory process)
 Synovial recesses  adherent  LOM
 Periarticular tse  lose elasticity, become shortened & fibrotic  fixing the head in the
glenoid cavity
 (+) ms. Atrophy
 Cx CHL & subscapularis tendon  prevent ER of humerus
 Articular surface  uninvolved
o Clinical picture
 May have an insidious onset
 Frequently follows supraspinatus tendinitis, subacromial bursitis & tenosynovitis of the
long head of biceps
 May result from AC arthritis . play a part in shoulder-hand syndrome  Arm is kept in
AdIr
 (+) pain  ExAbEr
 Night time pain  loss of sleep  emotionally upset

14.  ↓ Active & passive mobility in SH joint  restriction: ExAb
o Rx
 Conservative tx
 HMP
 Gravity free ex. Within painless arcs of motion
 Analgesic & anti-inflammatory drugs
 Antigravity ex. (later part) e.g. finger ladder
 Procaine blocks of the suprascapular nn.  relieve pain temporarily
 Adhesive Tx
 Late stage: Acromioplasty or resection of the acromioclavicular jt.

 AFFECTATIONS OF THE ELBOW
 Pulled elbow
o Common in children bet. 2-5 y/o
o Locking of FA in pronation / neutral rot. When a segment of annular ligament is pilled over the
edge of the radial head
o A.k.a nursemaid’s elbow
o MOI: sudden direct pull on the elevated limb with the elbow / and FA pronated
o Clinical Picture
 Child refuses to use the arm & the elbow is held slightly flexed
 All N° ROM except supination
 Attempts to supinate causes pain & a sensation of mechanical blocking
o Rx
 Brief manipulation without anesthesia  elbow flex to a right angle  FA supinated
quickly while pressure is everted to the radial head.  a click is felt, if not carried out 
spontaneous reduction.

 AFFECTAIONS OF THE WRIST AND HAND
 Rupture of the central extensor slip
o Rupture: near the insertion into the base of the mid phalanx  flexion deformity of the PIP jt.
o A.k.a boutonniere (buttonhole)
o Rx: suturing the central slip if possible, repositioning the lat. Bands & releasing them distally
 Avulsion of the Flexor Profundus Tendon
o MOI: d/t forced / of firmly flexed fingers
o MC in young athletes, usually involved the ring finger
o (+) loss of active flexion of the distal joint & tenderness & swelling on the volar aspect of the
finger
o Rx: surgical reattachment of the avulsed tendon
 Mallet Finger (baseball/dropped finger)
o MOI: sudden forcible flexion of the distal phalanx may cause an avulsion of the extensor tendon
@ its insertion
o Common: athletes
o (+) inability to / actively the distal phalanx
o (+) swelling and tenderness
o Rx: DIP is held constantly in hyper / for 6 weeks done with a plaster splint/ small metal/plastic
splint
o Late cases: suture of the tendon/ bone fragment to the phalanx = unsatisfactory
o Disability : very slight
 Dupuytren’s Cx
o A slow progressive Cx of the palmar fascia

15. o Men > women
o Between ages 55 -75 y/o
o When it occurs in women  younger group
o Changes involves:Ring finger, Little finger or both
o Usually Bilat. ; when unilat.  right MC
o Pathology
 Chronic inflammation of the palmar fascia  progressive fibrosis  Cx of Palamar
aponeurosis
 Advance cases: skin is involved
o Etiology: unkown
o Clinical picture
 (+) small nodular painless thickening in the palmar fascia overlying a flexor tendon in the
region of MCP jt. often associated with dimpling of the skin.
 Thickened longitudinal band is formed  flexion Cx of finger ↑
 MCP & adjacent IP joints become flexed
 DIP jt.  remains N°
o Rx
 Earliest cases  frequent passive stretching
 Limited/Partial Fasciectomy
 Post-op:/ splint + ex.
 Active and passive motion must begin as the healing of the skin permits