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Ortho Flashcards
Pelvic injury account
5 % of skeletal
injuries. 2/3 of pelvic injuries occur due to road traffic accident (RTA), 10 % of those are associated with visceral injuries with 10 % mortality rate.
Pelvic stability
The stability of pelvic ring depends on the rigidity
of the bony parts and the integrity of ligaments. These ligaments are the sacroiliac and iliolumber ligaments and supported by sacrotuberous and anterior and posterior sacrospinous ligaments and the ligaments of symphysis pubis.
Isolated pelvic fractures
Avulsion fractures
Direct fractures:
Ttt
bed rest and analgesia
Pelvic ring fractures
Classification
Young and Burgess classification: A. Anteroposteroir compression (open-book):
I- There is only slight (< 2 cm) diastasis of the symphysis, the pelvic ring is stable.
II- There is diastasis > 2 cm with tear of the anterior sacroiliac ligaments. The pelvic ring is stable.
III- There is diastasis of symphysis pubis and tear of both the anterior and posterior sacroiliac ligaments. The ring is unstable. Pelvic ring fractures
Classification: Young and Burgess classification: B. Lateral compression:
I- There is transverse fracture of pubic ramus, the ring is stable.
II- There is, in addition to the anterior fracture, a fracture of the iliac wing on the side of the impact, and the ring is stable.
III- There is fracture of pubic ramus (rami) with iliac wing and contralateral fracture of ilium. The ring is unstable. Pelvic ring fractures
Classification: Young and Burgess classification:
C. Vertical shear:
The hemipelvis is displaced in vertical direction.
The pelvic ring is unstable.
Pelvic ring fractures ix
CT-scan is essential in posterior pelvic ring disruptions and for complex acetabular fractures.
Intravenous urography is performed to exclude renal and ureteric injuries.
When urethral injury is suspected, urethrography should be done.
Cystography is done to exclude bladder injury.
Pelvic ring fracture mgx
- Early management:
Ensure that the airway is clear and ventilation is unimpaired, active bleeding is controlled. General examination is done.
The urethral meatus is inspected for signs of bleeding. The lower limbs are examined for signs of nerve injury. Pelvic ring fractures
Management:
- Management of severe bleeding:
Two i.v. lines should put, i.v. fluid and plasma expander given, cross-matched blood prepared and given to the patient.
Pelvic bleeding will be reduced rapidly by applying an external fixator.
Patients with suspicious abdominal signs should be further
investigated by peritoneal aspiration or lavage. If there is diagnostic tap, explorative laprotomy should be done.
Large retroperitoneal hemorrhage should not be open, because it produces a tamponade effect. Pelvic ring fractures
Management:
- Management of urethral and bladder injury:
Urological injuries occur in 10 % of patients with pelvic ring injury. There is no place for passing a diagnostic catheter (Foley’s catheter)
as this will convert any partial to complete tear.
For partial tear, the insertion of suprapubic catheter is required and
will be healed and little need further long term management. For complete tear, primary realignment of the urethra may be
achieved by performing suprapubic cystostomy, and then
threading a catheter across the injury to drain the bladder. Pelvic ring fractures
- Management of fracture:
— For isolated and minimally displaced fractures, bed rest and lower limb traction.
— Open-book injuries can be treated by bed rest and posterior sling to close the book (Homaxis traction).
— In more severe injuries, early application of external fixator is the most effective way for reducing hemorrhage and reverse shock.
— Fracture of iliac blade can be treated with bed rest.
— for type III fractures and vertical shear injuries, skeletal traction and external fixator can be used early and later on we do open reduction and internal fixation.
— Compound pelvic fractures are managed with external fixator and diversion colostomy.
Plevic ring fracture complications
- Sciatic nerve injury: it is essential to test the sciatic
nerve function both before and after treating pelvic fractures. The injury is usually neuropraxia and recovered after several weeks, rarely nerve exploration is needed.
- Urogenital problems: e.g. urethral stricture, incontinence, and impotence.
- Persistent sacroiliac pain: unstable pelvic fractures are often associated with partial or complete sacroiliac joint disruption, this can lead to persistent pain at the back of the pelvis.
Acetabular fractures
Classification
- Acetabular wall (roof) fractures: fractures of the anterior or posterior acetabular wall and affect the depth of the socket and lead to hip instability. Classification:
- Column fractures:
— Anterior column fractures: extends from symphysis pubis, along the superior pubic ramus, across the anterior acetabular column to the anterior part of ilium. These fractures are uncommon, and do not involve the weight-bearing area and have a good prognosis Classification:
- Column fractures:
— Posterior column fractures: extends from ischium across the posterior acetabular column to the sciatic notch and the posterior part of the ilium. It is usually breaking the weight-bearing part of acetabulum and usually associated with posterior hip dislocation and sciatic nerve injury.
- Transverse fractures: these fractures run transversely involving both the anterior and posterior columns, separating the iliac portion from pubic and ischeal portions. Sometimes a vertical split into the obturator foramen may coexist resulting in a T-fracture.
- Complex fractures: many acetabular fractures are complex injuries with damage to the anterior and posterior columns as well as the roof of acetabulum.
Acetabular fractures
Cf
Ix
Mgx
Complications
Clinical features:
The same clinical features of the pelvic fractures. The patient may be severely shocked, rectal examination is essential, there may be a bruising around the hip and the limb may lie in internal rotation (hip dislocation). Careful neurological examination is essential. Imaging:
AP, pelvic inlet and outlet views, and 45 degree right and left oblique views are essential.
CT-scan and 3-dimentional reformation scan are particularly helpful if surgical reconstruction is planned.
Management:
- Emergency treatment: counteract shock and reduce dislocation, then traction is applied to the lower limb (10 kg). Sometimes lateral traction through greater trochanter is needed for central dislocation, and the definitive treatment is delayed until the general condition of the patient is stable.
- Non-operative treatment: conservative treatment is indicated in:
a. Acetabular fracture with no or minimal displacement (< 3mm).
b. Displaced fractures that do not involve the superomedial weight-bearing acetabular roof .
c. Both column fractures that retain the ball and socket congruence of hip.
d. Fractures in elderly patients.
e. Patients with medical contraindications to surgery.
f. When the traction is released, the hip should remain congruent. The conservative treatments include closed reduction under general anesthesia (GA), skeletal traction supported with lateral traction is maintained for 6-8 weeks and hip movement and exercises are encouraged, then the patient is allowed up with crutches and partial weightbearing for another 6 weeks and then full weight-bearing.
- Operative treatment:
In recent years opinion has moved in favor of operative treatment for displaced acetabular fractures except the indications for conservative treatment. Prophylactic antibiotics are needed; post-operative hip movements are started as soon as possible. The patient starts partial weightbearing 7 days post-operatively, and exercises are continued for 3-6 months.
Complications:
- DVT is fairly common and serious.
- Sciatic nerve injury may occur either at the time of fracture or during the operation. The treatment is waiting for 6 weeks to see if there is any sign of recovery, if not, the nerve should be explored.
- Heterotopic bone formation is common, prophylactic indomethacin is useful.
- Avascular necrosis of the femoral head.
- Loss of joint movement and secondary osteoarthritis are common complications.
Sacrococcygeal injuries
Mechanism of injury:
A trauma from behind, or fall onto the tail, may fracture the sacrum or coccyx or sprain the joint between them. Clinically, there is tenderness when the sacrum or coccyx is palpated from behind or per rectum.
Clinical features: Imaging:
X-ray showed transverse fracture of the sacrum or fracture coccyx or a normal appearance if the joint was a sprain of the sacrococcygeal joint. Treatment:
If the fracture is displaced, reduction is done, the lower fragment may be pushed backwards by a finger in the rectum, the patient is advised to use a rubber-ring cushion when sitting. Rarely sacral fractures associated with urinary problems, necessitating sacral laminectomy.
Complaints of back pain begin around age
35 years and increase in prevalence up to age 50 years in men and age 60 years in women.
Mgx of scoliosis
Idiopathic :About 80% of scoliosis, may be seen as infantile ,juvenile and adolescent.
Adolescent idiopathic scoliosis : at age of 10 or more. 90% in females, Most of the curves are under 20 degree & resolves spontaneously .
But if the curve between 20-30 degrees needs close observation until puperty then if more than 30 degrees needs surgery to correct the angle & fix the curve to prevent more deterioration.
During the follow up we can use some pine braces to decrease the progression like (Milwaukee brace & Boston brace).
Instruments used in surgery like Harrington rods, with sub laminar wires.
Juvenile idiopathic scoliosis ( 4-9 years):
Rare but more severe , s.t. need surgical fusion even before puberty. but to use braces to let the pat. Reach the age of 10 years.
Infantile idiopathic scoliosis: ( age under 3 years)
Rare also but if the deformity is sever it needs serial elongation derotation flexion (EDF) casting under G.A.
Until pat grows enough to apply brace und treated as juvenile type.
Congenital (Osteopathic scoliosis) :
Due to anomalies of vertebrae (fusion or abnormal segmentation) .
Neuropathic and myopathic scoliosis :
Due to , poliomyelitis , C.P., syringomyelia , Mild curve (less than 20 degrees need no treatment , moderate curve (20-30 degrees) managed like idiopathic type, may needs surgery near or at puberty .
Scheuermann ds (adolescent kyphosis)
It is a growth disorder of the spine in which the vertebrae become slightly wedged shaped. If this occurs in thoracic spine will cause mild kyphosis.
The cause is unknown, but it might be a type of Osteochondritis* of the vertebral epiphyseal endplate, where they appear irregularly ossified.
Cl/F :
Condition start at puberty , in girls twice than occurs in boys, present as smooth thoracic kyphosis .
In X-Ray lateral view : the end plate of several vertebrae ( T6-T10 ) appear irregular or fragmented. In severe cases the vertebral body looked wedged anteriorly. Wedging of single vertebra of more than 5 degrees or the overall curve if more than 40 degrees are abnormal.
Treatment :
Curves up to 40 degrees needs no treatment except back strengthening exercises & postural training. While a curve of 60 degrees or more in older adolescent or young adults may need surgical correction.
Discitis
Blood borne infection, direct infection is possible after surgery, clinical features similar to spondylitis. Treatment depends on good diagnosis, by bed rest & antibiotics, some times needs surgical evacuation of the disc space.
Disc prolapse ttt
A- Rest & analgesia : keep the pat.in bed with hips & knees are flexed, good analgesics , local heat to sooth the pain.
B- Surgical removal of the prolapsed disc: indicated if there is 1-Cauda Equina Syndrome.
2- Failure of conservative treatment of three weeks.
C- Rehabilitation: physiotherapy & patient education.
Spondylolisthesis
Types
Cf
Ttt
It means forwards shift of the spine. The shift is nearly always between L4/L5. or L5 & sacrum.
Types:
1- Dysplastic (20%): the superior sacral facet is congenitally defective ,leads to forward displacemt of the L5 vertebra , s.t. associated with other anomalies like (Spina Bifida Occulta).
2- Lytic or Isthmic (50%) :there is defect in (pars interarticularis ) (spondylolysis), or repeated breaking &healing lead to elongation of the pars. The defect may present in early age (7years) but the symptoms not appear before teen ages.
3- Degenerative (25%) : degenerative changes of the facet joints & the discs permit forward slip despite intact laminae.
4- Post traumatic: fractures may be a cause.
5- Pathological: bone destruction due to T.B or tumours may be a cause .
6- Post operative: massive removal of the bone may cause instability.
Cl/F :
May be asymptomatic but accidentally discovered by routine X-Ray study. Otherwise may present in adulthood as low backache, or mild sciatica. According to the type, there might be a H/O trauma, lifting heavy thing or H/O degenerative spinal disease.
Treatment :
If the slip of up to 25 % , usually treated conservatively .
But for a slip of more than 50 % may need surgical fixation .
If more than 50 % slipping may needs reduction & surgical fixation to avoid nerve roots compression.
DDH
Insidence
Imagining
Ttt
At birth →10/1000; after 3 wks( hip become ˃ stable): 1/1000.
It is ˃ common in female with a ratio of ♀7:1♂; more on left.
side with ratio of Lt. 3:1 Rt.& bilateral 1 in every 5 cases.
Imaging: during first 6 mths, x-ray is not useful because both FH &acet. are cartilaginous, so U/S is the best.
After 6mths, X-ray become more useful:
Shenton’s line: normally, a line with inferior border of femoral neck is continuous with inferior border of upper pubic ramus, if broken→ dislocation or subluxation.
Perkin’s line: horizontal with triradiate cartilage &vertical with acetabular edge. Normal position of FH is medial to vertical & below horizontal; if not → dislocation or subluxation.
Management: according to the age
0-6 months → 90% of unstable hips will be stabilized spontaneously at 3 wks; So at 3 wks, if reduced & stable→ observe till 6 mths.
If reduced &unstable(dislocatable)→ abduction splint. If dislocated→ reduce & put in abduction splint. Splint: either Pavlik harness, Von Rosen splint or other hip abduction splint. The splint should be used until x-ray shows good acetabular roof.
6-18 months→ hip dislocation must be reduced either by closed or open method:
Closed reduction: this should be gradual. Apply traction to both legs using vertical frame (Gallows traction) with ↑ abduction gradually for 3 weeks (adductor tenotomy may be done if abduction is limited). Reduction is performed UGA &spica cast is applied for 2-3 months → abduction splint for 3-6 months. Open reduction: if closed reduction failed, do open reduction→ hip spica→ splint. Sometimes, for reduction to be stable, the leg should be internally rotated, if so, femoral derotation osteotomy in subtrochanteric region is done at the same time or later.
18mth- age limit→ is surgical by:open reduction± femoral derotation(± varus) osteotomy±pelvic osteotomy. Then hip spica for 3 mths → abduction splint for 3 mths.
Above age limit→ for unilateral dislocation, the age limit is 10 yrs. while for bilateral dislocation is 6 yrs. because with bilateral, the deformity is symmetrical &failure on one side will make it asymmetrical ¬iceable.
Persistent dislocation in adult→ THR.
Tv (W) position
The toes are directed inward during walking making the child trips over his feet during running.
Causes: below 3 yrs.→ forefoot adduction or tibial torsion.
Above 3 yrs.: excessive femoral neck anteversion (hip internal rotation).
CF: clumsy gait. The child sits in(W-position) television position &when standing both patellae directed inward (squinting patellae).
Diagnosis is clinical; to assess the degree of anteversion→CT to measure the angle between the femoral neck & the transverse axis of femoral condyles.
Ŗ→ it usually will correct Spontaneously with time.
If it persists above the age of 8 yrs: femoral corrective osteotomy may needed.
Irritable hip syndrome (transient synovitis) :
transient synovitis characterized by transient hip pain &limping in an otherwise healthy child. It is the commonest cause of hip pain in children.
CF: usual age 6-12 yrs. Boys affected 3x than girls. The child presents with groin, thigh or even knee pain with limping.
O/E: only the extreme of hip movements are painful.
The symptoms last 1-2 weeks, then subsides spontaneously investigations are normal except U/S showing small joint effusion.
ÐḐ:1-Pyogenic arthritis: ill, toxic child with high fever &all hip ROM are more severely restricted & painful, ESR ↑, WBC ↑, blood culture 50% +ve, ASO titer ↑. 2-Tuberculous arthritis: can be similar to transient synovitis because the C.F. are subacute. ESR ↑. X-ray→ osteoporosis, lytic lesion &later joint destruction. In difficult cases, bone &synovial biopsy are needed.
3-Perthes’ disease: last ˃2 wks &x-ray: ↑ joint space.
4- Juvenile chronic arthritis: ESR ↑ with systemic features.
5- Slipped epiphysis: may presents as irritable hip, later x-ray is characteristic. Ŗ→ bed rest at home; in severe cases, admission for continuous traction. Weight bearing is allowed only when symptoms &joint effusion resolve.
Perthes ds
Is a painful disorder of childhood characterized by avascular necrosis of the femoral head. Incidence →1/10000. ♂:♀ ratio is 4:1; Age → 4-8years.. Cause: is unknown.
Pathogenesis: how the FH become ischemic?
Normally, the blood supply of the FH depends on the age:
Before 4 years→ it comes from 3 sources: 1-lig. teres(small amount) ; 2-lateral epiphyseal vessels; 3-metaphyseal vessels penetrating growth disc which ↓ gradually& disappear at 4 yrs. to reappear gradually &become full with epiphyseal closure.
By the age of 7 yrs the vessels in the lig. teres have developed, so there is a critical period between the age of 4-7 yrs. in which the FH depends entirely on lateral epiphyseal vessels. Any condition causing effusion (trauma or synovitis) will stretch the capsule → venous stasis →↑ intra osseous pressure → ischemia.
Pathology: the condition takes 2-4 years to complete healing passing through 3 stages: Ι-ischaemic &bone death: all or part of bony nucleus of FH is dead; on x-ray it looks smaller as it stops growing while the cartilage remains viable &becomes thicker causing ↑ joint space on x-ray.
ΙΙ-revascularization &repair: within weeks, revascularization begins gradually &new bone will form replacing the dead bone causing ↑bone density on x-ray. At the same time, dead bone is resorbed giving rise to fragmentation on x-ray. The metaphysis looks porous, wider & cystic. In severe cases, the acetabulum also involved.
ΙΙΙ-distortion &remodeling: if repair process is rapid, the head will restore its normal shape. If it is slow, the head will collapse &later growth will be distorted (flat, oval or mushroom) which gradually enlarge &displace laterally away from the acetabulum.
CF: a boy of 4-8 years complains of pain &start limping for weeks on end or recur intermittently.
O/E: the child looks otherwise well. The hip early is Irritable (extremes of all ROM are painful &limited). Later, limitation of abduction in flexion &internal rotation.
Ḑ: Early X-ray is normal except slight widening of j. space. Bone scan at this stage shows cold area.
Later: small dense FH → flattening of FH.
Still later: FH collapse→ fragmentation→ lateral displacement.
Metaphysis become wider, rarefied &cystic.
Note: the involvement of the FH is variable, sometime, only a small area is involved or 50% or 75% or 100% of FH.
After healing: large deformed FH, short F neck + subluxation.
Ŗ→ while the hip is irritable, the child should be in bed with
skin traction until pain subsides usually 3 wks. Then allowed restricted activities &checked regularly every month (symptomatic Ŗ).
If the condition get worse→ do containment of the FH within the acet. so it retains its normal shape during repair process. Either by holding the hip widely abducted by plaster or splint for 1-2 years; or by surgery (subtrochanteric varus osteotomy or innominate osteotomy).
Prognosis:
1- boys have better prognosis than girls.
2- the greater the degree of FH involvement the more worse the prognosis.
3- the older the age the worse the prognosis.
4- progressive FH subluxation→ bad prognosis.
Slipped capital femoral epiphysis
Displacement of proximal femoral epiphysis(epiphysiolysis) is uncommon. Usual age is 14 yrs.; ♂:♀ ratio 3:1. Left ˃ right; if one side slips, there is 30% risk for other side to slip.
Etiology: 1-hormonal imbalance (hypogonadism or hypothyroidism); 2-trauma in 50% of cases.
Pathology: the disruption occurs through hypertrophic zone of the physis. The femoral shaft rolls into external rotation with femoral neck displaces anteriorly while the epiphysis remains in the acet. This usually is associated with tear of anterior retinacular vessels.
CF: a child around puberty who is either fatty &sexually immature or tall &thin. The condition in 30% of cases is acute &in 70% is chronic or acute on chronic.
The presentation is painful limping which recurs with exercise. O/E: short limb &externally rotated with limited ROM.
X-ray: AP view→ pass a line(Klein) with upper border of femoral neck ,this normally should intersect part of epiphysis; if not→ slip.
Lat. view→ the angle between the growth plate & a line through the center of the neck should be 90ᵒ ; if less→ slip.
Ŗ→ is surgical stabilization of the physis &this depends on the degree of the slip:
1- Minor slip(˂1/3 slip): Ŗ→ fixation in situ by2-3 screws through the neck into the epiphysis.
2- Moderate slip( 1/3 - 2/3 slip):Ŗ→ again accept the deformity &
do fixation in situ; after 2 yrs., if deformity is severe, do corrective osteotomy below the neck.
3- Severe slip(˃ 2/3 slip): here the deformity is unacceptable &if untreated → OA. So the Ŗ→ is ORIF using 2-3 screws.
Complication: 1-Avascular necrosis of the FH due to forceful manipulation or operation which damage posterior retinacular vessels.
2-coxa vara; 3-other side slip, Ŗ→ prophylactic fixation in pre-slip stage. 4chondrolysis; 5-secondary OA.
Avn (on)
The FH is the commonest site of AVN. It is either post-traumatic or non-traumatic. Age is 20-50 yrs.
Non-traumatic ON: seen in:1-high dose steroid; 2-chemoŖ; 3-radiation; 4-alcohol abuse; 5-septic arthritis; 6-Perthes’ disease.
Staging(Ficat): Stage Ι-pain, limp &limited ROM; x-ray: normal; bone scan: FH ischemia. MRI:marrow ischemia.
Definite Ḑ: bone biopsy.
Stage ΙΙ-x-ray early changes: patchysclerosis, cystic lesion &fracture line.
Stage ΙΙΙ- x-ray shows collapse of the FH.
Stage ΙV- secondary OA changes.
Ŗ→ stage Ι & ΙΙ: osseous decompression to relief venous stasis &intraosseous compartment syndrome by removing a core (7mm) of bone from the neck. This may also improve the blood supply to FH by growth of new granulation tissue with new blood vessels.
Stage ΙΙΙ: if the collapse affects only small segment of FH &the patient is young(˂40 yrs.)→ realignment osteotomy to displace the necrotic segment away from the line of maximum stress of weight bearing.
Stage ΙV→ partial or THR.
Prognosis→ usually poor &most patient will need THR.
Knee angulation
Ttt
Bow legs in babies and knock knees in 4-year-olds are so common that they are considered to be normal stages of development
• these children are normal in all other respects; the parents should be reassured and the child should be seen at intervals of 6 months to record progress.
• • by the age of 10, If the deformity is still marked , operative correction should be advised.
• Stapling of the physes on one or other side of the knee can be done to restrict growth on that side and allow correction of the deformity • Hemi-epiphysodesis (fusion of onehalf of the growth plate) on the ‘convex’ side of the deformity
• Corrective osteotomy (supracondylar osteotomy for valgus knees and high tibial osteotomy for varus knees)
Patella pain $(patella over load $)
Ttt
CONSERVATIVE MANAGEMENT
• adjustment of stressful activities
• considered only if conservative treatment has lasted at least 6 months and there is a demonstrable abnormality that is correctable by operation
Causes of anterior knee pain
1 Referred from hip
• 2 Patellofemoral disorders
• • Patellar instability
• • Patellofemoral overload
• • Osteochondral injury
• • Patellofemoral osteoarthritis
CAUSES OF ANTERIOR KNEE PAIN
• 3 Knee joint disorders
• • Osteochondritis dissecans
• • Loose body in the joint
• • Synovial chondromatosis
• • Plica syndrome
• 4 Periarticular disorders
• • Patellar tendinitis
• • Patellar ligament strain
• • Bursitis
• • Osgood–Schlatter disease
OCD
Ttt
the lesion is ‘stable’, no treatment is needed but activities are curtailed for 6–12 months. Small lesions often heal spontaneously.
• treatment will depend on the size of the lesion and the age of the patient. A small fragment should be removed by arthroscopy and the base drilled; • A large fragment (say more than 1 cm in diameter) should be fixed in situ with pins or Herbert screws.
Acutely swelling of entire joint of knee
Septic arthritis (cf &ttt)
The joint is swollen, painful and inflamed. Blood tests reveal an elevated white cell count and ESR. Aspiration reveals pus in the joint;
• Treatment consists of systemic antibiotics and drainage of the joint – ideally by arthroscopy, with irrigation and complete synovectomy and weight-bearing is deferred for 4–6 weeks.
Keinbock ds
Is avascular necrosis of the lunate bone, it occurs in young adult (20-30 yrs), women are affected more than men.
Causes: 1- chronic stress or injury through the lunate may affect its blood supply leading ischaemia; 2- relative shortening of the ulna(‘negative ulnar variance’) may cause stress overload of the lunate between the radius &carpus.
Pathology & X-ray appearance: the disease is divided into: Stage I: wrist pain, x-ray is normal but bone scan is +ve. Stage II: ↑ lunate density on x-ray but shape is preserved. Stage III: collapse of the lunate.
Stage IV: secondary radio carpal osteoarthritis.
CF: pain &stiffness. O/E: tenderness over lunate & grip strength is diminished. Late: wrist mvt are painful &limited.
Ŗ: stage I &II→ splint the wrist for 2-3 months.
Early stage III→ shortening of the radius.
Stage 3&4 may require arthrodesis or excisional arthroplasty.
Ra of wrist
The wrist is the second most common site of RA after the MPJ. It is divided into 3 stages:
Stage I: synovitis of the wrist &tenosynovitis of the tendon sheath, clinically there is pain &swelling.
Ŗ→ by rest, splint, NSAID, local steroid injection.
Stage II: early destruction of the joint &tendon with beginning of the deformity (radial deviation of the wrist).
Ŗ→ synovectomy &tendon transfer to prevent deformity.
Stage III: severe joint destruction &deformity.
Ŗ→ arthrodesis or arthroplasty.
Cts
Define,causes,X-ray,cf,o/e,ttt
De quervain ds ( stenosing tenovaginitis)
Define,causes,cf,ttt
is the most common compressive or entrapment neuropathy of the upper extremity, in which there is compression of the median nerve at the wrist as it passes through the carpal tunnel which is a narrow fibroosseous tunnel formed by carpal bones &roofed by transverse carpal ligament( the flexor retinaculum).
The carpal tunnel is a narrow space containing median n. & 9 flexor tendons with their synovial sheaths, so any increase in the size of the of tendons or their sheaths or any space occupying lesion will lead to compression &ischemia of the median n.
Causes: it is often difficult to find a cause, however the condition is
common at menopause, in RA, in pregnancy & in myxoedema.
CF: usual age group is 40-50 yrs; more common in women than men(8x). The patient usually complains of pain &numbness in the thumb, index, middle fingers &lateral ½ of the ring finger. The night pain& numbness are typical for CTS which might awake the patient from sleep. Hanging the arm over bed side or shaking the hand may relieve the symptoms. Late, there is weakness in the hand during daily activities or even thenar wasting. The numbness can be reproduced by tapping over median n.(Tinel’s sign) or by holding the wrist fully flexed for 1-2 minutes(Phalen’s test).
Investigations: NCS &EMG will show slowing of the nerve conduction across the wrist.
Ŗ: mild to moderate CTS: conservative(3wk night splint, NSAID, diuretic, steroid injection). The same is used for pregnancy related CTS. Severe CTS: surgical division of the transverse carpal ligament.
De Quervian’s disease (stenosing tenovaginitis) Is a painful inflammatory thickening of the tendon sheath of extensor policis brevis &abductor policis longus.
Causes: it may occur spontaneously but usually initiated by over use &repetitive activity.
CF: a women 40-50 yrs, has pain &tenderness over the radial styloid with thickening of the tendons sheath, 2 clinical tests:
1-Extension of the thumb against resistant will produce pain. 2-Finkelstein’s test; by flexing the thumb then sharply adduct the wrist will produce pain.
Ŗ: Early→ wrist splint &steroid injection. Resistant cases need surgical release of the thickened tendons sheath.
Rotator cuffs $
Rotator cuff is a sheet of tendons of subscaularis, supraspinatus, infraspinatus& teres minor around the head of humerus, they pass under the coracoacromial arch.
Rotator Cuff Syndrome: a painful shoulder condition due to impingment of rotator cuff tendons (specially supraspinatus) under coraco-acromial arch.
1 Causes of impingement:
1.Osteophytes – on the antero-inferior ridge of acromion
2.Swelling of cuff or subacromial bursa due to inflammatory ds. as gout or R.A.
3.Osteoarthritic thickening of ACJ.
4.excessive use of arm in impingment position(abd., flexion & internal rotation) Pathology
By repeated friction of cuff under coracoacromial arch leads to local inflammatory reaction —minute tears, vascular congestion—- which may lead to further impingement (acute tendenitis) which is common in young pt. in which wear, tear &repair is rapid &is more sever, while in old pt. repair is slow, less sever pain (subacute tendonitis)& may end with partial or complete tear of rotator cuff tendons.
C\F:
1- acute and subacute tendonitis: pt. usu. <40yrs,presented with shoulder pain after vigorous activity ,the site of attachment of supraspinatus tendon on greater tuberosity is acutely tender, more sever shoulder pain bet.60-120 degrees of abd. (painful arc) ,impingment test +ve (painful shoulder when we do flexion & internal rotation).
2- Chronic: pt. usu. >40yrs, Hx. of recurrent attacks of acute tendonitis, pain,stiffness, pain is less sever & more at night. O/E: shows features of subscute ten., rotator cuff disruption may occur after ch. ten. as partial or complete tear(tendon rupture) , it’s difficult to tell whether ch. ten. is
complicated by partial tear , & the Dx. Is only by MRI or arthroscopy. clinically to differentiate bet. partial &complete tear; by injection of the tendon by local anesthesia, if active abd.is possible = partial tear ,while in complete tear=no active abd., but passive abd., also pt. can keep abd. by action of deltoid(Abd. Paradox), & when he lowers it side way, it suddenly drops (Drop arm sign ). In long time of tear
secondary OA changes of shoulder joint.
Imaging:
- X-ray –early ;normal . In chronic erosion of greater tuberosity , thinning
of acromain process, OA changes of ACJ.
- Arthroscopy: 85% diagnostic for tear
- MRI :100% diagnostic.
Treatment of impingement syn.:
- Conservative Rx.: for
uncomplicated tendonitis by: a-NSAID,and physiotherapy as U/S waves, exercise,…etc.
b- local inj. of steroid. 2. Surgical Rx.: indications;
a- failure of conservative,
b- acute rupture of cuff in young patient surgery is; a-by decompression of arch, by excision of coraco-acromial lig. or excision of anteroinferior part of acromian(acromioplasty).
Surgery;. for cuff tear is by tendon transfer or proximal mobilization of rotator m. followed by protected arm in abd. Shoulder spica for 6-8 wks.,
it’s success rate is not so good!
Calcification of rotator cuff tendon:
Usu. in middle aged pt. after partial or complete tear of rotator cuff tendon. Pt. presented with painful shoulder, tenderness over rotator cuff ten. X-ray: fluff of calcification in supraspinatus tendon near its insertion to greater tuberosity.
Treatment: joint rest , analgesia, anti inflammatory drugs(NSAID).
if not improved—-surgical excision of calcified material.
Frozen shoulder
It’s progressive pain & stiffness of the shoulder which usu. resolve spontaneously after 18 months.
Pathology:
The process starts as chronic tendonitis in which the inflammation spreads to involve the entire cuff tendons & underlying joint capsules, as the inflammatory process subsides, the tissues contract, the capsule may stick on the humeral head. Its etiology is unknown, it is thought to be an autoimmune response to local tissue break down.
Pt. usu. aged 40-60y., may give a Hx. of trauma, often trivial, followed by pain in the shoulder & arm, pain is gradually increased in severity, often prevents sleeping on the affected side, after several mon. it subsides but stiffness become more & more, continuing for another 6-12m., after pain, gradually movement is regained, but it may return to normal.
O/E: slight m. wasting, tenderness, limitation of movements, severity of pain or LOM depends on the time of presentation.
X-ray: decrease bone density at the head of humerus.
Arthroscopy: contracted joint. DDx.:
- Post traumatic stiffness.
- Disuse stiffness.
- Reflex sympathetic dystrophy.
Rx.: aim of treatment is to relief pain & prevention of further stiffness usu. by NSAID + physiotherapy & reassurance of the pt. that recovery is certain once pain is subsided, manipulation of joint under GA, with local steroid injection, followed active exercise.
Hand infection
Are common, often caused by
staphylococci implanted by penetrating wound→acute inflam. With increasing edema→ suppuration & tissue tension→ decrease in the blood flow→ tissue necrosis & possible spread to nearby compartment or blood stream.
CF: swelling, redness, tenderness. In superficial infection, finger mvt is free; in deep infection, it is painful. Look for lymphangitis&lymphadenitis. X-ray: Early may show foreign body.
Later: OM, septic arthritis or bone necrosis.
Ŗ→1-AB: flucloxacillin or cephalosporin; for bone infection add fusidic acid; for plant prick add metranidazole.
2-Splint &elevation: rest the hand in a splint in the position
of safety &elevate it in an arm sling or if severe use overhead sling.
3-drainage: early, within 48 hrs, AB may be enough. If abscess develops it should be drained &left open for 2 nd look. 4-Exercise.
Nail-fold infection(paronychia): infection under nail fold is the commonest hand infection. The fold is swollen, red &tender then collects pus which may spread under the nail. Ŗ→ AB &pus drainage. Chronic paronychia may be due to fungal infection.
Pulp infection(felon): often caused by prick injury→swollen, red &tender finger tip pulp with throbbing pain. Ŗ→ AB, elevation &abscess drainage. If Ŗ is delayed, infection may spread to bone, joint or tendon sheath.
Other subcutaneous infections: anywhere in the hand.
Tendon sheath infection(suppurative tenosynovitis): is uncommon but dangerous. Often caused by penetrating injury-→ swollen, painful, very tender finger which is held in slightflexion &never allow mvt. If diagnosis is delayed→ risk of tendon necrosis or spread of infection proximally. Ŗ→ hand elevation &splint + i.v. AB; if no response within 24 hrs→ drainage by proximal &distal incisions with frequent saline irrigation by fine catheter.
Deep fascial space infection: infection of thenar & mid-palmar spaces from web space infection or may come from a wound or spread suppurative tenosynovitis.
CF: pain, tenderness, palm swelling is mild but extensive on the dorsum; the hand is held still refusing any mvt.
Ŗ→ i.v. AB, splint, elevation &drainage.
Septic arthritis: of MPJ or IPJ may come from penetrating wound or from blood stream. CF: the joint is painful, swollen, red with limited mvt. Ŗ→ i.v. AB, splint, drainage &leave wound open. Continue oral AB for 2-4 weeks.
Achilles tendon rupture
Rupture probably occurs only if the tendon is degenerate. Consequently most patients are over 40 years old. While pushing off (running or jumping), the calf muscle contracts; but the contraction is resisted by body weight and the tendon ruptures.
The patient feels as if he or she has been struck just above the heel, and is unable rise up on tiptoes. Soon after the tear occurs, a gap can be seen and felt about 5 cm above the insertion of the tendon. Plantarflexion of the foot is weak and is not accompanied by tautening of the tendon. Where doubt exists, Simmonds’ test is helpful: with the patient prone, the calf is squeezed; if the tendon is intact the foot is seen to plantarflex involuntarily; if the tendon is ruptured the foot remains still. Ultrasound scans can be used to confirm the diagnosis.
Treatment
If the patient is seen early, the ends of the tendon may approximate when the foot is passively plantarflexed. If so, a plaster cast or special boot is applied with the foot in equinus and is worn for 8 weeks; thereafter, a shoe with a raised heel is worn for a further 6 weeks. It is usually safe to commence physiotherapy at 4–6 weeks. Operative repair is probably more reliable, but immobilization in equinus for 8 weeks and a heel raise for a further 6 weeks are still needed.
Compare all types of OM
The micro-organisms may reach bones &joints either directly(skin wound, open # or operation) or indirectly via blood stream(from GIT, GUT, respiratory tract). Depending on type of micro-organism &body reaction, the result could be: pyogenic osteomyelitis or arthritis, chronic granulomatous reaction(TB), fungal
infection or hydatid(parasite) disease.
Pus, dead bacteria &tissue debris, it often localized in an abscess &when
pressure Ĺ it may spread through tissue plane, lymphatic (lymphangitis &adenitis) or via blood(septicemia). The associated fever &toxemia are due to release of bacterial enzymes &endotoxins &cellular breakdown products.
indirect (bectremia
*
Acute
hematogenous Osteomyelitis
Osteomyelitis
post-traumatic
=
Acute hematogenous osteomyelitis:
*
Children Adult
is a disease of children, if adults are affected, their resistance should be low by disease(DM, AIDS) or drugs.
Trauma may determine the site of infection by causing small hematoma or fluid collection in the bone.
> nidus
for
infection
> nidus for infection .
Micro-organism: the most common are: Staphylococcus aureus, Streptococcus species, Enterobacter species, Haemophilus influenzae. Depending on the age:
Above 4years→ 90% is G +ve: mostly S. aureus.
-
-
8nder years→ is *íve mostly +. influenzae.
-
~
Immune compromised patients may have unusual organism.
Patients with sickle-cell disease are prone to infection by Salmonella.
-
These may invade the blood from a skin abrasion, boil, septic tooth or urethral catheter. In children, they settle in the metaphysis(often tibia or femur), while in adults, in the vertebral body than in the long bones.
~ due to high vascularity Stasis and blood
Pathology: 5 stages * first 2 days 1-inflammation: it starts as acute inflammatory reaction with vascular of blood congestion, fluid exudation &P0 leucocytes infiltration→ Ĺintra-osseous symptom first pressure(intense pain)→ impending ischemia. Conservative , AB * S day rd 2-suppuration: by 3 6 day, pus forms within thining the bone &forces its way through from endostium to used Volkmann canals→ subperiosteal abscess &this either burst to surrounding soft or , Surgery reenter the bone at another level. In infant, infection spreads into the joint while in children this occurs only if the metaphysis is intracapsular(hip, elbow). In adults, the
↑ stasis
first
2
in
2
S
>
of
periosteum
-
-
spread is through medullary canal &in vertebral body, through the disc to adjacent vertebral body.
3-bone necrosis: occurs by 7 th 8 day due to bone ischemia secondary to Ĺ intra osseous pressure(↓blood flow), infective thrombosis & periosteal stripping; also bacterial toxins &leucocytes enzymes play a role in tissue destruction. The pieces of dead bone(sequesrtra) will m
nicus
of
infection
Eins be surrounded by granulation tissue which remove small but
not large sequestra which remain inside a cavity(involucrum).
4-new bone formation: by 14 th day, new bone forms under the stripped periosteum &with time this forms the involucrum enclosing the infected tissue &sequestra. Pus &small dead bone continue discharging through perforations into the skin by sinuses(now become chronic osteomyelitis).
5-resolution: if infection is controlled & intra osseous pressure released early, remodeling will restore the bone to normal shape; otherwise sclerosis &bone thickening will deform the bone permanently.
CF:child in severe pain, malaise,fever,toxemia with still limb. O/E: acute finger-tip tenderness near one of the large joints;
painful limitation of joint movement. Later, when pus escape from inside bone to soft tissue →local redness, swelling, warmth &edema. Infants: irritability &metaphyseal tenderness with resistance to joint mvt may be the whole picture.
Adults: the common site is thoracolumbar spine:
CF: mild fever with local tenderness.
*in elderly &those with immune deficiency, the systemic features are mild.
Diagnostic imaging:
X-ray: during first 10days→may be normal, only soft tissue swelling. After 2 weeks→ faint periosteal reaction.
/ater→ thick periosteal reaction + metaphyseal mottling.
Still later→ sequestrum &involucrum(chronic OM).
U/S: may detect subperiosteal abscess.
Radioactive bone scan: using 99m Tc→ very sensitive but less specific while 67 Ga-citrate &111 Ind-labeled leucocytes are more specific.
MRI: is very sensitive &can differentiate between OM &soft tissue infection.
Investigations:
Aspiration of pus from subpreiosteal abscess→ *ram
s stain and C&S. WBC count↑, CR3↑, ESR↑, HbĻ. Blood culture is ve in . Antistaphylococcus antibody ↑. In sickle cell disease→ Salmonella may be cultured from feces.
Differential diagnosis:
1-cellulitis: skin redness is more diffuse with lymphangitis &limb movements are free.
Look for distal wound. Often the child is not toxic.
2-rheumatic fever: pain is less severe &flit from one joint to another.
3-acute suppurative arthritis: the joint swelling is more severe; tenderness is diffuse &joint movements are completely restricted. In infants, OM will spread into the joint easily.
4-sickle-cell crisis:(causing osteonecrosis) is clinically similar to OM; so give AB until infection is excluded.
Treatment:
- if OM is suspected, start Ŗ before waiting for final diagnosis.
There are 4 aspects:
1-supportive Ŗ: pain needs analgesia; dehydration(fever &septicemia)→ I9). 2-splintage: of the affected part to Ļ pain &to prevent Moint contracture.
)or hip, use skin traction(also prevent ); for other site, use back-slab. 3-antibiotics: send blood &aspirate for examination &culture and start AB immediately.
The choice of AB depends on: direct exam of pus smear(later according to C&S), patient age &immunity, degree of toxemia, renal function, and AB allergy.
The route of administration: I9 for -wks or until clinical
improvement(pain, fever &toxemia) &CR3Ļ→ oral for 3-wks.
)or older children &adults(Staph)→ Flucloxacillin + fusidic acid If pus smear shows Streptococci→ benzylpenicillin.
)or children < 4yr(H. influenzae or smear show G-ve)→ cephalosporin (cefuroxime or cefotaxime)-act on Staph &G–ve; or amoxiclav(amoxicillin + clavulanic acid).
)or sickle-cell patients(Salmonella)→ chloramphenicol, cotri-moxazol or amoxiclav.
)or immune suppressed(unusual organisms)→ cephalosporin or (gentamicin + flucloxacillin).
4-drainage: is indicated if: -pus is aspirated; 2-signs of deep pus(fluctuation);
3-no improvement(fever &toxemia) after 3hr of starting AB.
Operation: incise skin &periosteum to drain pus, if no pus → drill multiple holes in the bone.
Complications:
-metastatic infection: to other organs(infants).
2-suppurative arthritis.
3-physeal damage→ bone shortening. 4-chronic OM: in neglected or immune depressed patients. Subacute haematogenous OM: is more mild than acute HOM
possibly due to less virulent organism &/or the patient is more resistant. Site: distal femur, proximal/distal tibia(rarely cuboidal bone or epiphysis). Pathology: well-defined cavity in cancellous bone containing seropurulent fluid (not pus) & lined by granulation tissue with acute & chronic inflammatory cells; the cavity is surrounded by thick trabecular bone.
CF: an adolescent having pain for several weeks with slight swelling &tenderness near one of the larger joints. Temp &WBC are normal but ESR is often ↑.
X-ray: round or oval 1-2cm cavity in metaphyssis; it may be surrounded by a hallo of sclerosis(Brodie’s abscess).
Bone scan: shows ↑activity.
Differential diagnosis: osteoid osteoma &malignant bone tumor; if in doubt, take a biopsy &culture the fluid(+ve in 50%- usually Staph).
Treatment: flucloxacillin &fusidic acid for 6wks; if no response or the diagnosis is in doubt→ curettage.
Post-traumatic OM: open # is the commonest cause of OM in adults. Organism: often Staph. aureus. Sometimes E. coli, Proteus, Pseudo. Occasionally, anaerobic(Clostridia, anaerobic Strept or Bacteroides). CF: fever; pain &swelling of # site; wound inflammation with seropurulent discharge. WBC&ESR are↑; wound swab→ C&S. prophylaxis: 1-thorough cleaning &debridement of open #.2-leave the wound open until infection settled. 3-fracture fixation; 4-AB→ (cephalosporin)or(benzylpenicillin+flucloxacillin)
plus metronidazole *THE BEST “ANTIBIOTIC” IS A GOOD WOUND EXCISION Ŗ: 1-AB; 2-regular wound dressing &repeated excision of dead &infected tissues; 3-loose implant is replaced by external fixation.
Postoperative OM: the incidence is 5%.
Risk factors: local: open #, use of implant, multiple operation, hematoma formation, soft tissue damage &bone death.
General: elderly, obese, diabetic &immune suppressed patient. Types: early(within days) or late(months-years) &superficial or deep. Organism: mixed pathogenic &nonpathogenic.
Pathogenesis: both body &bacteria will compete to occupy implant surface; if body wins, it becomes inert biomaterial; if bacteria win the race, infection persists until implant is removed.
CF: superficial infection is mild; deep infection→ persistent pain, fever, inflamed discharging wound, ↑WBC&ESR; x-ray: bone resorption &periosteal reaction. MRI &scan: may help. Treatment: 1-AB, 2-abscess drainage &leave wound open, 3-excision of necrotic segment with AB beads or intermittent AB irrigation, 4-exchange the internal by external fixation.
Chronic OM: is a sequel of posttraumatic or postop. OM &less frequently following AHOM.
Organism: mixed &if there is implant(Staph epidermis).
Pathology: multiple areas of bone destruction forming cavities containing dead bone &pus, surrounded by reactive bone (sclerosis) & continue draining(sinus) until all sequestra are discharged or removed.
CF: discharging sinus or flare of acute infection.
X-ray: areas of bone resorption, sclerosis &thickening with dense sequestra. Sinogram: see connection of sinus to bone.
Bone scan, CT &MRI.
Treatment: 1-AB: to control flare & infection spread.
2-abscess drainage.
3-sequestrectomy with intermittent AB irrigation(3wks) or gentamicin beads(3wks).
4-bone graft &muscle flap.
5-Ilizarov bone transport(nonunion).
- What are the components of peripheral nerves?
- What are the types of nerve injury and their characteristics?
- How is nerve injury diagnosed?
- What are the principles of treatment for nerve injury?
- What are the types of nerve repair?
- What factors affect the prognosis of nerve injury?
- What are the types of brachial plexus injuries?
- What are the clinical features and treatment options for obstetrical palsy?
- What are the common types of median nerve injuries and their clinical features?
- What are the clinical features and treatment options for ulnar nerve injuries?
- What are the clinical features and treatment options for radial nerve injuries?
- What are the clinical features and treatment options for sciatic nerve injuries?
- What are the clinical features and treatment options for peroneal nerve injuries?
- What is cerebral palsy and its types?
- What are the clinical features and treatment options for cerebral palsy?
The peripheral nerves are composed of axons which carry motor, sensory &autonomic impulses. Many of these axons are surrounded by myelin sheath which is a lipoprotein membrane derived from Schwann cells. The axon is surrounded by connective tissue covering called endoneurium. The axons are arranged in bundles(fascicles) which are surrounded by perineurium, groups of these bundles are surrounded by epineurium to form the nerve trunk.
Types of nerve injury (pathology):
Transient ischaemia: acute nerve compression for 15 minutes causes numbness, for 30 minutes→ loss of sensation, for 45 minutes→ muscle weakness. these changes are due to transient anoxia &they leave no trace of nerve damage.
Neurapraxia: is transient physiological nerve conduction block result from segmental demyelination due to mechanical pressure(as in crutch palsy, tourniquet palsy &Saturday night palsy) leading to loss of some types of sensation & muscle power followed by spontaneous recovery after few days or weeks.
Axonotmesis: the axons are interrupted but their endoneurial tubes are intact, these injuries are seen in closed # and ≠. The distal parts of the
axons
will
disintegrate
&resorbed
by
phagocytes(Wallerian
degeneration).While the proximal parts, within hours, start regeneration inside their endoneurial tubes at a rate 1mm/day till they join their target organs(motor end-plate &sensory receptors) which must be in < 2years. Neurotmesis: the nerve trunk is divided (axons, endo-, peri- &epineurium) as in open injury; or the endoneurial tubes are destroyed as in severe crush or stretching injury. The regenerating proximal axons will form neuroma. Spontaneous recovery is unlikely.
Classification of nerve injury:
5
degrees
:
First degree injury This includes transient ischaemia and neurapraxia, the effects of which are reversible.
Second degree injury This corresponds to axonotmesis. Axonal degeneration takes place but, because the endoneurium is preserved, regeneration can lead to complete, or near complete, recovery without the need for intervention.
Third degree injury This is worse than axonotmesis. The endoneurium is disrupted but the perineurial sheaths are intact and internal damage is limited. The chances of the axons reaching their targets are good, but fibrosis and crossed connections will limit recovery. Fourth degree injury Only the epineurium is intact. The nerve trunk is still in continuity but internal damage is severe. Recovery is unlikely; the injured segment should be excised and the nerve repaired or grafted. Fifth degree injury The nerve is divided and will have to be repaired
Diagnosis of nerve injury:
Clinical features : Always look for nerve injury in any significant trauma because it is easily missed. Ask about numbness, parasthesia or muscle weakness in the related area. O/E: abnormal posture(e.g. foot or wrist drop), map of sensory disturbance(spinal or peripheral n.) &motor weakness (↓tone, power &reflexes). Anesthetic skin is dry(↓sweating).
Signs of chronic nerve injury The anesthetic skin may become smooth & shiny with evidence of ↓sensibility like cigarette burn in median n. palsy or foot ulcer in sciatic n. palsy. Muscle groups will be wasted &deformity may become fixed. Assessment of recovery: a low energy injury may cause neurapraxia while a high energy injury is likely to cause axonotmesis. An open injury or very high energy injury is likely to divide the nerve.
Tinel’s sign: is the feeling of peripheral tingling on nerve percussion, it is –ve in neurapraxia & +ve in axonotmesis or neurotmesis.
If Tinel’s sign is not progressing 1mm/day→ neurotmesis.
EMGand NCS shows denervation potentials on the 3 rd week if the injury was axonotmesis or neurotmesis. Motor recovery is slower than sensory recovery; the more proximal muscle will function first.
Principles of treatment of nerve injury
- Nerve exploration: is indicated:
(a) if the nerve was seen to be divided;(b) if the type of the injury
suggests that the nerve has been divided or severely damaged e.g. knife wound; (c) if recovery is delayed.
- Primary repair: at the time of wound toilet has a considerable
advantage because nerve ends have not retracted or rotated &there is no fibrosis. It is contraindicated in (a) dirty wound; (b) traction injury; (c) presence of other more urgent injury.
- Delayed repair: after weeks or months, is indicated in (a) missed injury( < 2 years); (b) failure of primary repair (c) delayed recovery of closed injury.
- Care of the paralyzed part: while recovery is awaited
(a) the skin must be protected from injury &burn; (b) joints should be moved through their full range to prevent stiffness.
types of repair:
1- epineuroraphy:by suturing the epineurium.
2-perineuroraphy: by microscopic surgical repair of each bundle .
3- endoneuroraphy:suturing of each axon microscopically. After any type of suturing ,we have to use splintage for 4-6 weeks followed by physiotherapy.
If we have a gap between the two ends of injuried nerve ,how we can close it:
1- proximal and distal release and mobilization.
2- nerve transposition.
3- joint flexion.
4-nerve graft(from where??)
5- bone shortening
Prognosis: of nerve injury depends on: 1- Type of injury:
neurapraxia the best, neurotmesis the worst.
2-Level of injury, the higher the worst.
3-Type of the nerve, pure motor or pure sensory better than mixed. 4-Size of the gap. 5-Age, children better prognosis. 6-Delay of the repair. 7-Associated injuries(vascular, tendon). 8- Surgical technique(skill, facilities).
Brachial plexus injuries
Birth injury (obstetrical palsy)
The diagnosis is obvious at birth, usually after a difficult delivery with excessive traction especially with the use of forceps; the baby has a floppy or flail arm. There are 3 types:
Erb’s palsy: is caused by injury of the upper roots (C5,C6& sometimes C7) leading to paralysis of shoulder abductors & external rotators, elbow flexors, forearm supinators &if C7 is involved, there is paralysis of finger extensors. therefore the arm is held adducted, internally rotated, elbow extended &pronated.
Klumpke’s palsy: is caused by injury of lower roots of the plexus (C8, T1) leading to paralysis of all hand muscles, it is rare but more severe than Erb’s palsy.There may be a unilateral Horner’s syndrome.
Complete palsy: caused by injury of all roots of the brachial plexus (C5—T1). It is a complete lesion result in paralysis of the entire limb.
Prognosis: after few weeks the paralysis may:
1- recover completely within 3 months especially for upper roots lesions(90%).
2- improve but residual weakness will persist.
3- remain unchanged as in lower or complete palsy. Treatment:
1-Conservative Ŗ by physiotherapy to keep joints mobile while waiting for recovery in early months.
2-Operative Ŗ is indicated in early stages if there is no improvement after 6 months → exploration & nerve grafting .
Late: shoulder internal rotation may need subscapularis release or rotation osteotomy of the humerus.
Adult lesions: are caused by severe traction injury as in fall on the side of the neck or by stab wound at the root of the neck.
CF: is either (1) upper roots similar to Erb’s palsy or (2) lower roots lesion with paralysis of hand intrinsic muscles forming a claw hand deformity, weakness of wrist &finger flexors, sensory loss on ulnar side of arm &forearm &Horner syndrome.
Radial nerve injury:
We have to know the anatomy(motor sensory and reflexes )related to radian nerve to understand the effects of its injury. The radial nerve may be injured at the elbow, in the upper arm or in the axilla;.
1- Low level injury:- are usually due to fractures or dislocations at the elbow, or to a local wound. Iatrogenic lesions of the posterior interosseous nerve.The patient cannot extend the metacarpophalangeal joints of the hand. In the thumb there is also weakness of extension. Wrist extension is preserved
2- High level injury:- occur with fractures of the humerus or after prolonged tourniquet pressure. There is an obvious wrist drop, due to weakness of the radial extensors of the wrist, as well as inability to extend the metacarpophalangeal joints or elevate the thumb. Sensory loss is limited to a small patch on the dorsum around the anatomical snuffbox. 3-Very high level injury:- may be caused by trauma or operations around the shoulder, or due to chronic compression in the axilla, e.g‘Saturday night palsy’) or in thin elderly patients using crutches (‘crutch palsy’). In addition to weakness of the wrist and hand, the triceps is paralyzed and the triceps reflex is absent.
Treatment: depend on type of injury
1- conservative: for neurapraxia,1 st and 2 nd degree nerve injury by physiotherapy
2- surgery: for open injury, and failure of conservative treatment of type 3 nerve injury, by surgical repair.
3- for late presentation: after 4-6 months surgical nerve repair is hopeless, tendon transfer may be helpful. ULNAR NERVE INJURY
Injuries of the ulnar nerve are usually either near the wrist or near the elbow, although open wounds may damage it at any level.
1-Low lesions:- are often caused by cuts on shattered glass. There is numbness of the ulnar one and a half fingers. The hand assumes a typical posture in repose – the claw hand deformity – with hyperextension of the metacarpophalangeal joints of the ring and little fingers, due to weakness of the intrinsic muscles.Hypothenar and interosseous wasting may be obvious by comparison with the normal hand. Finger abduction is weak and this, together with the loss of thumb adduction, makes pinch difficult. The patient is asked to grip a sheet of paper forcefully between thumb and index fingers while the examiner tries to pull it away; powerful flexion of the thumb interphalangeal joint signals weakness of adductor pollicis and first dorsal interosseous with overcompensation by the flexor pollicis longus (Froment’s sign).
2-High lesions:- occur with elbow fractures or dislocations.The hand is not markedly deformed because the ulnar half of flexor digitorum profundus is paralysed and the fingers are therefore less ‘clawed’ (the ‘high ulnar paradox’). Otherwise, motor and sensory loss are the same as in low lesions.‘Ulnar neuritis’ may be caused by compression or entrapment of the nerve in the medial epicondylar (cubital) tunnel, especially where there is severe valgus deformity of the elbow . Treatment Exploration and suture of a divided nerve are well worthwhile, and anterior transposition at the elbow permits closure of gaps up to 5 cm. Hand physiotherapy keeps the hand supple and useful. In case of late presentation, tendon transfer may indicated.
MEDIAN NERVE INJURY
The median nerve is most commonly injured near the wrist or high up in the forearm
1-Low lesions:- may be caused by cuts in front of the wrist or by carpal dislocations. The patient is unable to abduct the thumb, and sensation is lost over the radial three and a half digits. In longstanding cases the thenar eminence is wasted and trophic changes may be seen.
2-High lesions:- are generally due to forearm fractures or elbow dislocation, but stabs and gunshot wounds may damage the nerve at any level. The signs are the same as those of low lesions but, in addition, the long flexors to the thumb, index and middle fingers, the radial wrist flexors and the forearm pronator muscles are all paralysed. Typically the hand is held with the ulnar fingers flexed and the index straight (the ‘pointing sign’). Also, because the thumb and index flexors are deficient, there is a characteristic pinch defect: instead of pinching with the thumb and index fingertips flexed, the patient pinches with the distal joints in full extension.
Treatment If the nerve is divided, suture or nerve grafting should always be attempted. Postoperatively the wrist is splinted in flexion to avoid tension; when movements are commenced, wrist extension should be prevented. In case of late presentation, tendon transfer may indicated.
SCIATIC NERVE INJURY
Division of the main sciatic nerve is rare except in gunshot wounds. Traction lesions may occur with traumatic hip dislocations and with pelvic fracture.
Clinical features In a complete lesion the hamstrings and all muscles below the knee are paralysed; the ankle jerk is absent.Sensation is lost below the knee, except on the medial side of the leg which is supplied by the saphenous branch of the femoral nerve. The patient walks with a drop foot and a high-stepping gait.
Electrodiagnostic studies will help to establish the level of the injury. Treatment If the nerve is known to be divided, suture or nerve grafting should be attempted even though it may take more than a year for leg muscles to be re-innervated. While recovery is awaited, a below-knee drop-foot splint is fitted. Great care is taken to avoid damaging the insensitive skin and to prevent trophic ulcers.The chances of recovery are generally poor and, at best, will be long delayed and incomplete. Partial lesions.
PERONEAL NERVES INJURY
Injuries may affect either the common peroneal (lateral popliteal) nerve or one of its branches, the deep or superficial peroneal nerves.
Clinical features The common peroneal nerve is often damaged at the level of the fibular neck by severe traction when the knee is forced into varus (e.g. in lateral ligament injuries and fractures around the knee, or by pressure from a splint or a plaster cast. The patient has a drop foot and can neither dorsiflex nor evert the foot. He or she walks with a high-stepping gait to avoid catching the toes. Sensation is lost over the front and outer half of the leg and the dorsum of the foot. Pain may be significant.
Treatment Direct injuries of the common peroneal nerve and its branches should be explored and repaired or grafted wherever possible. As usual, the earlier the repair, the better the result. While recovery is awaited a splint may be worn to control ankle weakness. Pain may be relieved and drop foot is improved in almost 50% CEREBRAL PALSY
Is a group of disorders that results from non-progressive brain damage during early development , characterized by neuromuscular incardination ,dystonia,weakness and spasticity.
Incidence: is about 2/1000 of life birth Causes: brain damage causes by maternal toxaemia, prematurity,perinatal anoxia,kernicterus,post natal infection or injury.
Types:
1- spastic(60%) as hemiplegia,paraplegia,tetraplagia and rarely monoplagia 2-athetotic: rare
3- ataxic. 4- rigid. 5- mixed.
Clinical features: history of risk factors, difficulty in sucking and
swallowing and stiff baby, with obvious delay in mile stone.
Treatment: they need special center with team of pediatrician, orthopedic surgeon,neurologist, psychiatrist …ect.
1- physiotherapy: passive and active exercise.
2-splintage; to prevent fixed or progressive deformity. 3-surgery: ideal age of surgery between 4-8 years.
Types of operations a- release or lengthening of tight muscles.
b- tendon transfer.
c- bone surgery for fixed deformity by corrective osteotomy or arthrodesis.
- What are some common causes of cervical spine injuries?
- How should a fractured cervical spine be treated in an unconscious patient with a head injury?
- What imaging techniques are used to evaluate cervical spine injuries?
- What are the characteristics of a C1 ring fracture?
- How are C2 pars interarticularis fractures classified?
- What are the treatment options for odontoid fractures?
- What are the different types of fractures in the lower cervical spine?
- What are the mechanisms of injury for thoracolumbar spine injuries?
- How are thoracolumbar spine injuries diagnosed and treated?
- What are the types of neural injuries that can occur in spinal injuries?
- What are the signs and symptoms of a cervical spine injury?
- How should plain x-rays be inspected to evaluate cervical spine injuries?
- What is the significance of the distance between the odontoid peg and the back of the anterior arch of the atlas in adults and children?
- How are upper cervical spine injuries, such as C1 ring fractures, diagnosed and treated?
- What are the different types of C2 pars interarticularis fractures and their mechanisms of injury?
- How are odontoid fractures classified and what are the treatment options?
- What are the characteristic features and diagnostic imaging techniques for lower cervical spine fractures?
- What are the treatment options for flexion, axial compression, and flexion-rotation fractures in the thoracolumbar spine?
- How are spinal cord and nerve root injuries diagnosed in spinal injuries?
- What is the overall management strategy for patients with traumatic paraplegia and quadriplegia?
- What is the difference between stable and unstable cervical spine fractures?
- How are wedge compression fractures in the cervical spine treated?
- What are the characteristics and potential complications of burst and compression-flexion fractures?
- What imaging techniques are recommended for evaluating burst and compression-flexion fractures?
- How are fracture-dislocations in the cervical spine managed?
- What is an avulsion injury of the spinous process in the cervical spine?
- What is a sprained neck or whiplash injury, and what are its common causes?
- What are the typical fracture patterns in thoracolumbar spine injuries?
- How do low-energy insufficiency fractures differ from high-energy fractures in the thoracolumbar spine?
- What are the three varieties of neural injuries that can occur in spinal injuries?
- What are some common causes of cervical spine injuries?
- How should a fractured cervical spine be treated in an unconscious patient with a head injury?
- What imaging techniques are used to evaluate cervical spine injuries?
- What are the characteristics of a C1 ring fracture?
- How are C2 pars interarticularis fractures classified?
- What are the treatment options for odontoid fractures?
- What are the different types of fractures in the lower cervical spine?
- What are the mechanisms of injury for thoracolumbar spine injuries?
- How are thoracolumbar spine injuries diagnosed and treated?
- What are the types of neural injuries that can occur in spinal injuries?
- What are the signs and symptoms of a cervical spine injury?
- How should plain x-rays be inspected to evaluate cervical spine injuries?
- What is the significance of the distance between the odontoid peg and the back of the anterior arch of the atlas in adults and children?
- How are upper cervical spine injuries, such as C1 ring fractures, diagnosed and treated?
- What are the different types of C2 pars interarticularis fractures and their mechanisms of injury?
- How are odontoid fractures classified and what are the treatment options?
- What are the characteristic features and diagnostic imaging techniques for lower cervical spine fractures?
- What are the treatment options for flexion, axial compression, and flexion-rotation fractures in the thoracolumbar spine?
- How are spinal cord and nerve root injuries diagnosed in spinal injuries?
- What is the overall management strategy for patients with traumatic paraplegia and quadriplegia?
- What is the difference between stable and unstable cervical spine fractures?
- How are wedge compression fractures in the cervical spine treated?
- What are the characteristics and potential complications of burst and compression-flexion fractures?
- What imaging techniques are recommended for evaluating burst and compression-flexion fractures?
- How are fracture-dislocations in the cervical spine managed?
- What is an avulsion injury of the spinous process in the cervical spine?
- What is a sprained neck or whiplash injury, and what are its common causes?
- What are the typical fracture patterns in thoracolumbar spine injuries?
- How do low-energy insufficiency fractures differ from high-energy fractures in the thoracolumbar spine?
- What are the three varieties of neural injuries that can occur in spinal injuries?
- What is the treatment approach for transverse process fractures in the cervical spine?
- How are flexion-compression injuries in the cervical spine managed?
- What are the treatment options for flexion-distraction injuries in the cervical spine?
- How are lateral compression injuries in the cervical spine treated?
- What are the potential complications of burst fractures in the thoracolumbar spine?
- How are flexion-rotation injuries in the thoracolumbar spine managed?
- What is the management strategy for avulsion injuries of the spinous process in the cervical spine?
- How are sprained neck or whiplash injuries diagnosed and treated?
- What are the treatment options for minor thoracolumbar spine injuries?
- How are major thoracolumbar spine injuries with neurological involvement treated?
CERVICAL SPINE INJURIES The patient will usually give a history of a fall from a height, a diving accident or a vehicle accident in which the neck is forcibly moved.
In a patient unconscious from a head injury, a fractured cervical spine should be assumed (and acted upon) until proved otherwise.
An abnormal position of the neck is suggestive, and careful palpation may elicit
tenderness. Movement is best postponed until the neck has been x-rayed. Pain or paraesthesia in the limbs is significant, and the patient should be examined for evidence of spinal cord or nerve root damage.
Imaging Plain x-rays must be of high quality and should be inspected methodically.
• In the anteroposterior view the lateral outlines should be intact, and the spinous processes and tracheal shadow in the midline.
An open-mouth view is necessary to show C1 and C2 (for
odontoid and lateral mass fractures).
In the lateral view the smooth lordotic curve should be followed, tracing four parallel lines formed by the front of the vertebral bodies, the back of the bodies, the posterior borders of the lateral masses and the bases of the spinous processes; any irregularity suggests a fracture or displacement. If the cervico-thoracic junction cannot be seen, then the lateral view should be repeated while the patient’s shoulders are pulled down.
The distance between the odontoid peg and the back of the anterior arch of the atlas should be no more than 3 mm in adults and 4.5 mm in children.
• Compare the shape of each vertebral body with that of the others; note particularly any loss of height, fragmentation or backward displacement of the posterior border of the vertebral body.
• Examine the soft-tissue shadows. The retropharyngeal space may contain a haematoma; the prevertebral soft-tissue shadow should be less than 5 mm in thickness above the level of the trachea and less than one vertebral body’s width in thickness below.
UPPER CERVICAL SPINE
C1 ring fracture
Stable,
associated may
with
dysphagia
+
pain
Sudden severe load on the top of the head may cause a ‘bursting’ force which fractures the ring of the atlas(Jefferson’s fracture). => fall tip of the head There is no encroachment on the neural canal and, usually, no neurological damage. The fracture is seen on the open-mouth view (if the lateral masses are spread away from the odontoid peg) and the lateral view.
on
.
-
-
A CT scan is particularly helpful in defining the fracture.
If it is undisplaced, the injury is stable and the patient wears a semi-rigid collar or halo-vest until the fracture unites. (4 6W) If there is sideways spreading of the lateral masses (more than 7 mm on the open-mouth view), the transverse ligament has ruptured; this injury is unstable and should be treated by a halo-vest for several weeks.
-
If there is persisting instability on x-ray, a posterior C1/2 fixation and fusion is needed.
Jefferson’s fracture – bursting apart of the lateral masses of C1.
C2 pars interarticularis fractures In the true judicial ‘hangman’s fracture’ there are bilateral fractures of the pars interarticularis of C2 and the C2/3 disc is torn; the mechanism is extension with distraction.
–
In civilian injuries, the mechanism is more complex, with varying degrees of extension, compression and flexion. This is one cause of death in motor vehicle accidents when the forehead strikes the dashboard. Neurological damage, however, is unusual because the fracture of the posterior arch tends to decompress the spinal cord. Nevertheless the fracture is potentially unstable.
‘Hangman’s fracture’ – fracture of
the pars interarticularis of C2. C2 Odontoid process fracture Odontoid fractures are uncommon. They usually occur as flexion injuries in young adults after high velocity accidents or severe falls. However, they also occur in elderly, osteoporotic people as a result of low-energy trauma in which the neck is forced into hyperextension, e.g. a fall onto the face or forehead.
A displaced fracture is really a fracture-dislocation of the atlanto-axial joint in which the atlas is shifted forwards or backwards, taking the odontoid process with it.
Classification Odontoid fractures have been classified by Anderson and D’Alonzo (1974) as follows:
• Type I – An avulsion fracture of the tip of the odontoid process due to traction by the alar ligaments.
The fracture is stable (above the transverse ligament) and unites without difficulty.
• Type II – A fracture at the junction of the odontoid process and the body of the axis. This is the most common (and potentially the most dangerous) type.
The fracture is unstable and prone to non-union.
• Type III – A fracture through the body of the axis.
The fracture is stable and almost always unites with immobilization.
I II III Clinical features The history is usually that of a severe neck strain followed by pain and stiffness due to muscle spasm.
The diagnosis is confirmed by high quality x-ray examination; In some cases the clinical features are mild and continue to be overlooked for weeks on end. Neurological symptoms occur in a significant number of cases.
Imaging Plain x-rays usually show the fracture, although the extent of the injury is not always obvious – e.g. there may be an associated fracture of the atlas or displacement at the occipito-atlanto level.
Tomography is helpful but MRI has the advantage that it may reveal rupture of the transverse ligament; this can cause instability in the absence of a fracture. Treatment Type I fractures Isolated fractures of the odontoid tip are uncommon. They need no more than immobilization in a rigid collar until discomfort subsides.
Type II fractures These are often unstable and prone to non-union, especially if displaced more than 5 mm.
Undisplaced fractures can be held by fitting a halo-vest or – in elderly patients – a rigid collar.
Displaced fractures should be reduced by traction and can then be held by operative posterior C1/2 fusion; a drawback is that neck rotation will be restricted.
Type III fractures If undisplaced, these are treated in a halo-vest for 8–12 weeks. If displaced, attempts should be made at reducing the fracture by halo traction,then 12 weeks immobilization by halo_vest.
LOWER CERVICAL SPINE Fractures of the cervical spine from C3 to C7 tend to produce characteristic fracture patterns, depending on the mechanism of injury: flexion, axial compression, flexionrotation or hyperextension.
Wedge compression fracture A pure flexion injury results in a wedge compression fracture of the vertebral body. The middle and posterior elements remain intact and the injury is stable. All that is needed is a comfortable collar for 6–12 weeks.
A note of warning: The x-ray should be carefully examined to exclude damage to the middle column and posterior displacement of the vertebral bodyfragment, i.e. features of a burst fracture (see below) which is potentially dangerous. If there is the least doubt, an axial CT or MRI should be obtained.
wedge compression fracture
Burst and compression-flexion (‘teardrop’) fractures These severe injuries are due to axial compression of the cervical spine, usually in diving or athletic accidents. If the vertebral body is crushed in neutral position of the neck the result is a ‘burst fracture’. With combined axial compression and flexion, an antero-inferior fragment of the vertebral body is sheared off, producing the eponymous ‘tear-drop’ on the lateral x-ray. In both types of fracture there is a risk of posterior displacement of the vertebral body fragment and spinal cord injury.
The x-ray images should be carefully examined for evidence of middle column damage and posterior displacement (even very slight displacement) of the main body fragment.
Traction must be applied immediately and CT or MRI should be performed to look for
retropulsion of bone fragments into the spinal canal. TREATMENT If there is no neurological deficit, the patient can be treated surgically or by confinement to bed and traction for 2–4 weeks, followed by a further period of immobilization in a halo-vest for 6–8 weeks.
If there is any deterioration of neurological status while the fracture is believed to be unstable, and the MRI shows that there is a threat of cord compression, then urgent anterior decompression is considered – anterior corpectomy, bone grafting and plate fixation, and sometimes also posterior stabilization.
Fracture-dislocations Bilateral facet joint dislocations are caused by severe flexion or flexion–rotation injuries. The inferior articular facets of one vertebra ride forward over the superior facets of the vertebra below. One or both of the articular masses may be fractured or there may be a pure dislocation – ‘jumped facets’. The posterior ligaments are
ruptured and the spine is unstable; often there is cord damage.
Management
The lateral x-ray shows forward displacement of a vertebra on the one below of greater than half the vertebra’s antero-posterior width.
The displacement must be reduced as a matter of urgency. Skull traction is used, starting with 5 kg and increasing it step-wise by similar amounts up to about30kg; When x-rays show that the dislocation has been reduced, traction is diminished to about 5 kg and then maintained for 6 weeks. During this time MRI can be performed to rule out the presence of an associated disc disruption.
Another alternative is to carry out a posterior fusion as soon as reduction has been achieved; the patient is then allowed up in a cervical brace which is worn for6–8 weeks. Posterior open reduction and fusion is also indicated if closed reduction fails.
a
b
c
d
Cervical fracture-dislocation (a) Fracture-dislocation in the lower cervical spine. (b,c) Stages in the reduction of this fracture-dislocation by skull traction; (d) subsequent posterior wiring to ensure stability.
Avulsion injury of the spinous process Fracture of the C7 spinous process may occur with severe voluntary contraction of the muscles at the back of the neck; it is known as the clay-shoveller’s fracture. The injury is painful but harmless. No treatment is required; as soon as symptoms permit,
neck exercises are encouraged. SPRAINED NECK (WHIPLASH INJURY) Soft-tissue sprains of the neck are so common after motor vehicle accidents that they now constitute a veritable epidemic. There is usually a history of a low-velocity rearend collision in which the occupant’s body is forced against the car seat while his or her head flips backwards and then recoils in flexion. This mechanism has generated the imaginative term whiplash injury, which has served effectively to enhance public apprehension at its occurrence. However, similar symptoms are often reported with flexion and rotation injuries. Women are affected more often than men, perhaps because their neck muscles are more gracile.
THORACOLUMBAR INJURIES Most injuries of the thoracolumbar spine occur in the transitional area – T11 to L2 between the somewhat rigid upper and middle thoracic column and the flexible lumbar spine.
The upper three-quarters of the thoracic segments are also protected to some extent by the rib-cage and fractures in this region tend to be mechanically stable. However, the spinal canal in that area is relatively narrow so cord damage is not uncommon and when it does occur it is usually complete (Bohlman, 1985). The spinal cord actually ends at L1 and below that level it is the lower nerve roots that are at risk.
Pathogenesis Pathogenetic mechanisms fall into three main groups:
low-energy insufficiency fractures arising from comparatively mild compressive stress in osteoporotic bone; minor fractures of the vertebral processes due to compressive, tensile or tortional strains; and high-energy fractures or fracture-dislocations due to major injuries sustained in motor vehicle collisions, falls or diving from heights, sporting events, horse-riding and collapsed buildings. It is mainly in the third group that one encounters neurological complications, but lesser fractures also sometimes cause nerve damage. The common mechanisms of injury are:
• Flexion–compression – failure of the anterior column and wedge-compression of the vertebral body. Usually stable, but greater than 50 per cent loss of anterior height suggests some disruption of the posterior ligamentous structures.
• Lateral compression – lateral wedging of the vertebral body resulting in a localized ‘scoliotic’ deformity.
• Axial compression – failure of anterior and middle columns causing a ‘burst’ fracture and the danger of retropulsion of a posterior fragment into the spinal canal. Often unstable.
• Flexion–rotation – failure of all three columns and a risk of displacement or dislocation. Usually unstable.
• Flexion–distraction – the so-called ‘jack-knife’ injury causing failure of the posterior and middle columns and sometimes also anterior compression.
• Extension – tensile failure of the anterior column and compression failure of the posterior column. Unstable. Examination Patients complaining of back pain following an injury or showing signs of bruising and tenderness over the spine, as well as those suffering head or neck injuries, chest injuries, pelvic fractures or multiple injuries elsewhere, should undergo a careful examination of the spine and a full neurological examination, including rectal examination to assess sphincter tone.
Imaging X-rays The anteroposterior x-ray may show loss of height or splaying of the vertebral body with a crush fracture. Widening of the distance between the pedicles at one level, or an increased distance between two adjacent spinous processes, is associated with posterior column damage.
The lateral view is examined for alignment, bone outline, structural integrity, disc space defects and soft-tissue shadow abnormalities. Always look carefully for evidence of fragment retropulsion towards the spinal canal.
CT and MRI Rapid screening CT scans are now routine in many accident units. Not only are they more reliable than x-rays in showing bone injuries throughout the spine, and indispensable if axial views are necessary, but they also eliminate the delay, discomfort and anxiety so often associated with multiple attempts at ‘getting the right views’ with plain x-rays. In some cases MRI also may be needed to evaluate neurological or other soft-tissue injuries.
Treatment Treatment depends on: (a) the type of anatomical disruption;
(b) whether the injury is stable or unstable;
(c) whether there is neurological involvement or not;
(d) the presence or absence of concomitant injuries.
MINOR INJURIES Fractures of the transverse processes The transverse processes can be avulsed with sudden muscular activity. Isolated injuries need no more than symptomatic treatment.
MAJOR INJURIES Flexion–compression injury This is by far the most common vertebral fracture and is due to severe spinal flexion, though in osteoporotic individuals fracture may occur with minimal trauma.
The posterior ligaments usually remain intact, although if anterior collapse is marked they may be damaged by distraction. CT shows that the posterior part of the vertebral body (middle column) is unbroken.
Pain may be quite severe but the fracture is usually stable. Neurological injury is extremely rare.
Management Patients with minimal wedging and a stable fracture pattern are kept in bed for a week or two until pain subsides and are then mobilized; no support is needed.
Those with moderate wedging (loss of 20–40 per cent of anterior vertebral height) and a stable injury can be allowed up after a week, wearing a thoracolumbar brace or a body cast applied with the back in extension.
If loss of anterior vertebral height is greater than 40 per cent, it is likely that the posterior ligaments have been damaged by distraction and will be unable to resist further collapse and deformity. If the patient is neurologically intact, surgical correction and internal fixation is the preferred treatment.
A
b
c
d
f
e
Wedge-compression fractures (a) Central compression fracture of the vertebral body and (b) anterior wedge-compression fracture with less than 20 per cent loss of vertebral body height. In both cases the middle and posterior columns are intact; further collapse can be prevented by immobilization for 8–12 weeks in (c) a plaster ‘jacket’ or (d) a lightweight removable orthosis. (e,f) More severe and potentially unstable compression fractures may need posterior internal fixation.
If there is complete paraplegia with no improvement after 48 hours, conservative management is adequate; the patient can be rested in bed for 5–6 weeks, then gradually mobilized in a brace.
Axial compression or burst injury Severe axial compression may ‘explode’ the vertebral body, causing failure of both the anterior and the middle columns. The posterior column is usually, but not always, undamaged. The posterior part of the vertebral body is shattered and fragments of bone and disc may be displaced into the spinal canal. The injury is usually unstable. Anteroposterior x-rays may show spreading of the vertebral body with an increase of the interpedicular distance. Posterior displacement of bone into the spinal canal (retropulsion) is difficult to see on the plain lateral radiograph; a CT is essential. Treatment If there is minimal anterior wedging and the fracture is stable with no neurological damage, the patient is kept in bed until the acute symptoms settle (usually under a week) and is then mobilized in a thoracolumbar brace or body cast which is worn for about 12 weeks.
Any neurological symptoms such as tingling, weakness or alteration of bladder or bowel function must be reported immediately and should call for further imaging by MRI; anterior decompression and stabilization may then be needed if there are signs of present or impending neurological compromise
a
b
(a) Burst fracture in a 44-year-old man who fell from his horse; 3 months later he developed paraesthesia in both legs. (b–) Internal fixation and grafting through a transthoracic transdiaphragmatic approach provided total stability (the Kaneda method).
Chance fracture, in which the split runs through the
spinous process, the transverse processes, pedicles and the vertebral body. Neurological damage is uncommon, though the injury is (by definition) unstable. Xrays may show horizontal fractures in the pedicles or transverse processes, and in the anteroposterior view the apparent height of the vertebral body may be increased. The Chance fracture (being an ‘all bone’ injury) heals rapidly and requires 3 months in a body cast or well-fitting brace.
NEURAL INJURIES In spinal injuries the displaced structures may damage the cord or the nerve roots, or both; cervical lesions may cause quadriplegia, thoracolumbar lesions paraplegia. The damage may be partial or complete. Three varieties of lesion occur: neurapraxia, cord transection and root transection.
o 3
/16
Spinal injury
Cord 5 -chic
-
& paraplagic
To
Conus
-L2
medullaris
&
below
Canda
equina Neurapraxia Motor paralysis (flaccid), burning paraesthesia, sensory loss and visceral paralysis below the level of the cord lesion may be complete, but within minutes or a few hours recovery begins and soon becomes full.
Cord transection Motor paralysis, sensory loss and visceral paralysis occur below the level of the cord lesion; as with cordconcussion, the motor paralysis is at first flaccid. This is a temporary condition known as cord shock, but the injury is anatomical and irreparable.
After a time the cord below the level of transection recovers from the shock and acts as an independent structure; that is, it manifests reflex activity. Within 48 hours the primitive anal wink and bulbocavernosus reflexes return. Within 4 weeks of injury tendon reflexes return and the flaccid paralysis becomes spastic, with increased tone, increased tendon reflexes and clonus; flexor spasms and contractures may develop with inadequate management.
Root transection Motor paralysis, sensory loss and visceral paralysis occur in the distribution of the damaged roots. Root transection, however, differs from cord transection in two ways: recovery may occur and residual motor paralysis remains permanently flaccid.
ANATOMICAL LEVELS Cervical spine With cervical spine injuries the segmental level of cord transection nearly corresponds to the level of bony damage.
High cervical cord transection is fatal because all the respiratory muscles are paralysed.
Between T1 and T10 vertebrae The first lumbar cord segment in the adult is at the level of the T10 vertebra.
Consequently, cord transection at that level spares the thoracic cord but isolates the entire lumbar and sacral cord, with paralysis of the lower limbs and viscera.
Below T10 vertebra The cord forms a slight bulge (the conus medullaris) between the T10 and L1 vertebrae, and tapers to an end at the interspace between the L1 and L2 vertebrae. The L2 to S4 nerve roots arise from the conus medullaris and stream downwards in a bunch (the cauda equina) to emerge at successive levels of the lumbosacral spine. Therefore, spinal injuries above the T10 vertebra cause cord transection, those between the T10 and L1 vertebrae cause cord and nerve root lesions, and those below the L1 vertebra only root lesions.
The sacral roots innervate:
• sensation in the ‘saddle’ area (S3, S4), a strip down the back of the thigh and leg (S2) and the outer two-thirds of the sole (S1);
• motor power to the muscles controlling the ankle and foot;
• the anal and penile reflexes, plantar responses and ankle jerks;
• bladder and bowel continence.
The lumbar roots innervate:
• sensation to the groins and entire lower limb other than that portion supplied by the sacral segment;
• motor power to the muscles controlling the hip and knee;
• the cremasteric reflexes and knee jerks. DIAGNOSIS Clinical examination of the back nearly always shows the signs of an unstable fracture; Neurological examination should be painstaking. Without detailed information, accurate diagnosis and prognosis are impossible; rectal examination is mandatory. Complete cord lesions Complete paralysis and anaesthesia below the level of injury suggest cord transection. During the stage of spinal shock when the anal reflex is absent (seldom longer than the first 24 hours) the diagnosis cannot be absolutely certain; if the anal reflex returns and the neural deficit (sensory and motor) persists, the cord lesion is complete. Complete lesions lasting more than 72 hours have only a small chance of neurological recovery.
Incomplete cord lesions Persistence of any sensation distal to the injury (peri-anal pinprick is most important) suggests an incomplete lesion.
The commonest is the central cord syndrome where the initial flaccid weakness is followed by lower motor neuron paralysis of the upper limbs with upper motor neuron (spastic) paralysis of the lower limbs, and intact peri-anal sensation (sacral sparing). Bladder control may or may not be preserved from an early stage.
With the less common anterior cord syndrome there is complete paralysis and
anaesthesia but deep pressure and position sense are retained in the lower limbs(dorsal column sparing).
The posterior cord syndrome is rare; only deep pressure and proprioception are lost. The Brown-Séquard syndrome (due to cord hemisection) is usually associated with
penetrating thoracic injuries. There is loss of motor power on the side of the injury
and loss of pain and temperature sensation on the opposite side. Most of these patients improve and regain bowel and bladder function and some walking ability.
MANAGEMENT OF TRAUMATIC PARAPLEGIA AND QUADRIPLEGIA
With both complete and incomplete paralysis it is the overall management of the patient that is most important– from the early stages onwards.
The patient must be transported with great care to prevent further damage, and preferably taken to a spinal centre. The strategy is outlined below.
Skin Within a few hours anaesthetic skin may develop large pressure sores; this can be prevented by meticulous nursing. Creases in the sheets and crumbs in bed are not permitted. Every 2 hours the patient is gently rolled onto his or her side and the back is carefully washed (without rubbing), dried and powdered.
Bladder and bowel For the first 24 hours the bladder distends only slowly, but, if the distension is allowed to progress, overflow incontinence occurs and infection is probable. In special centres it is usual to manage the patient from the outset by intermittent catheterization under sterile conditions.
Bladder training is begun as early as possible.
The bowel is more easily trained, with the help of enemas, aperients and abdominal
exercises.
Muscles and joints The paralysed muscles, if not treated, may develop severe flexion contractures. These are usually preventable by moving the joints passively through their full range twice daily. Later, splints may be necessary.
Tendon transfers Some function can be regained in the upper limb by the use of tendon transfers.
- Why are tumors, tumor-like lesions, and cysts considered together?
- What is the basis for classifying tumors?
- What are the clues in history and examination that can help in diagnosing bone tumors?
- What imaging techniques are used to assess bone tumors?
- What are the treatment options for benign bone lesions?
- What are the characteristics of osteosarcoma?
- How is Ewing’s sarcoma diagnosed and treated?
- What is the age group most commonly affected by chondrosarcoma?
- What are the signs and symptoms of multiple myeloma?
- What are the common sites for secondary malignant bone tumors?
- How are soft-tissue tumors differentiated between benign and malignant?
1. Why are tumors, tumor-like lesions, and cysts considered together and what similarities do they share in terms of presentation and management?
2. How is the classification of bone lesions determined and what role does the recognition of the dominant tissue in the lesion play?
3. In terms of history and examination, what are some important factors to consider when diagnosing bone tumors? How can age be a useful clue in the diagnosis?
4. What are the different symptoms associated with bone tumors and how should they be interpreted? How does pain, swelling, and lump characteristics differ between benign and malignant tumors?
5. When it comes to the examination of bone tumors, what aspects should be assessed in terms of the lump, swelling, and tenderness? How can the presence of neurological symptoms or pathological fractures indicate the presence of a tumor?
6. What imaging techniques are commonly used to evaluate bone tumors and what information can they provide? How does x-ray, computed tomography (CT), magnetic resonance imaging (MRI), and bone scans contribute to the diagnosis and staging?
7. When it comes to laboratory tests, what are some important markers to consider in the diagnosis of bone tumors? How can the levels of ESR, HB, S. alkaline phosphatase, and other specific markers help differentiate between different types of tumors?
8. What is the role of biopsy in the diagnosis of bone tumors and what are the different types of biopsy procedures available? How reliable are needle biopsies compared to open biopsies?
9. What are some common differential diagnoses to consider when evaluating bone tumors? How can soft tissue hematoma, myositis ossificans, stress fractures, tendon avulsion, bone infections, gout, and non-neoplastic lesions mimic tumor presentations?
10. What factors are considered in the staging of bone tumors and why is it important to determine the aggressiveness and spread of the tumor? How does intracompartmental and extracompartmental tumor spread differ?
11. In terms of surgical staging, how is sarcoma divided and what are the different subtypes and stages? How does the surgical approach differ based on the stage and type of sarcoma?
12. What are the different management options for bone lesions, including benign and suspected malignant tumors? When is surgical excision or curettage recommended? What are the considerations for amputation, limb-sparing operation, chemotherapy, and radiotherapy?
13. What are some characteristics and treatment options for specific benign bone lesions such as non-ossifying fibroma, fibrous dysplasia, osteoid osteoma, chondroma, periosteal chondroma, chondroblastoma, chondromyxoid fibroma, osteochondroma, simple bone cyst, aneurysmal bone cyst, giant-cell tumor, and multiple myeloma?
14. What are the distinguishing features and treatment approaches for primary malignant bone tumors like osteosarcoma, Ewing’s sarcoma, chondrosarcoma, fibrosarcoma, and multiple myeloma?
15. How do secondary malignant bone tumors differ from primary tumors and what are their common sites of origin? How do they spread and what are the treatment options for metastatic bone disease?
16. How can differentiation between benign and malignant soft tissue tumors be made and what are the key factors to consider in their diagnosis?
Tumors, tumor-like lesions &cysts are considered together because . their presentation &management are similar &some may change to another ,Classification: is based on recognition of the dominant tissue in the lesion .though this is not necessarily the tissue of origin
:Diagnosis
History &examination: the history is often prolonged. A useful clue is the-1 Age:Children &adolescent→ osteosarcoma, Ewing’s sarcoma &many benign lesions.Older people(4th -6 th decades)→ chondrosarcoma, fibrosarcoma
.&myeloma .Over 70 years→ metastasis Symptoms: the condition may be asymptomatic &discovered accidentally(benign &slowly growing malignant tumor). pain especially progressive &continuous should not be taken lightly. Swelling or lump especially painful &enlarging are more alarming. History of trauma is frequent(often patients link their conditions to previous injury). Neurological symptoms caused by nerve compression or invasion by tumor. pathological fracture especially after minor injury or an elderly get mid.shaft fracture Examination: lump→ site, well / ill-defined, soft or hard or pulsatile &tenderness. swelling→ if overlying skin is warm &inflamed, may be mistaken for infection. A nearby joint may get effusion &limitation of movements. Spine lesion may cause back stiffness or scoliosis. Don’t forget→ lymphatic drainage, chest, abdomen, .spine &pelvis Imaging: x-ray→ site of the lesion/cyst(diaphysis, metaphysis or bone end),-2 central or eccentric or cortical, size, single or multiple, margins(well-defined &sharp or sclerotic =benign or ill-defined &hazy=malignant), contents(calcified =cartilage tumor). Cortical destruction leading to spread of tumor outside the .bone with periosteal new bone formation is suggestive of malignant tumor Computed tomography(CT): is excellent to show cortical erosion, #, tumor .extension in &outside the bone, spine &pelvic tumors &pulmonary metastasis MRI: to assess tumor spread &it’s relation to neurovascular structures. It is the .best for soft tissue tumor assessment .99m Tc-bone scan: useful in detecting small tumor, skip lesion &’silent’ secondaries Laboratory tests: help to exclude infection &metabolic disorder. Malignant-3 tumor may have ↑ESR, ↓HB, ↑S. alkaline phosphatase. In prostate carcinoma, .serum acid phosphatase is↑. In myeloma, test Bence-Jones protein in urine . Biopsy: is essential for definite diagnosis-4 Needle biopsy(large-bore needle) is less reliable, though useful in inaccessible sites. Open biopsy is better: Incisional biopsy: expose part of tumor, take several tissue blocks from tumor boundary (normal tissue, capsule &abnormal tissue), ensure hemostasis &close without drain. Excisional biopsy: used for benign tumor
.(remove the entire lesion). For cyst, tissue is taken by careful curettage
:Differential diagnosis
soft tissue hematoma: painful lump with irregular bone surface on x-ray may be-1 .mistaken for tumor but history & rapid onset may help myositis ossificans: tender swelling after injury with x-ray opacity near the bone-2 .will arise suspicion, but soon pain will↓& opacity become well-defined new bone stress fracture: pain followed by x-ray signs of bone ‘destruction’ &periosteal-3 .reaction(even biopsy may be similar to osteosarcoma), is an avoidable error tendon avulsion: like an adolescent engaged in sports, may get pain &x-ray-4 .opacity(callus) at site of muscle insertion like ischial tuberosity or pubic body bone infection: a child with painful swelling near a large joint with x-ray-5 showing metaphyseal bone destruction &periosteal reaction is easy mistaken for .malignancy especially if systemic features are mild because of AB treatment .gout: a large tophus causes painful swelling with bone excavation on x-ray-6 non-neoplastic lesion e.g. fibrous cortical defect &bone infarct-7 .may mimic tumor
Staging: any tumor must be removed as wide as necessary, but
:damage must be kept to a minimum. This require knowing .how tumor usually behaves(how aggressive it is)-1 .how far it has spread-2 Aggressiveness: depends on cell character &clinical behavior(likelihood of recurrence &spread). Benign lesion(from spontaneous recovery to possible malignant change). Sarcoma is either low-grade: metastasize .late(25% risk) or high-grade: metastasize early Spread: means the anatomic extent of the tumor→ intracompartmental tumor: is confined to an enclosed tissue space like bone, joint cavity or .muscle group in its fascial envelope extracompartmental tumor: is extending into interafascial or extrafascial plane .with no natural barrier to spread like perivascular sheath, pelvis or axilla
:Surgical staging: sarcoma is divided into І- low-grade sarcoma; П-high-grade sarcoma; Ш-metastasized sarcoma & of any grade. Each one is subdivided into type A(intracompartmental) type B(extracompartmental). So an osteosarcoma confined to bone is ІІA; if .it has spread into soft tissue=ПB; if there are pulmonary metastasis=stage Ш
:Management
Benign lesions→ may need no Ŗ but if painful or enlarging or diagnosis is in .doubt→ local excision or curettage Suspected malignant tumor→ admission for firm diagnosis &staging(blood tests, CXR, CT, MRI, pulmonary CT &tumor biopsy).Then discuss with the patient the .Ŗ options: amputation, limb sparing operation, chemotherapy &radiotherapy
:Methods: 1-Tumor excision Intracapsular excision/curettage: is incomplete tumor removal, so used .only for benign lesions with low risk of recurrence Marginal excision: goes just beyond the tumor(in the reactive zone) .suitable for benign lesions Wide excision: remove the tumor passing through normal tissue, used .for ІA tumor; also for ІІA if combined with chemotherapy
Radical resection: remove the entire compartment en block without exposing the tumor(if limb sparing facilities are avialable) or amputation .above the involved compartment. Used for stage ІІ B
Limb-sparing surgery: sometimes, in stage ІІ sarcoma, amputation can be avoided by wide excision +pre-&post-operative chemotherapy. The defect is replaced by bone graft(vascularized or non-vascularized), allograft, custom.made implant or prosthesis
.Amputation: for stage ІІ sarcoma if the limb can’t be saved
Chemotherapy: for sensetive tumors, they can: reduce the size of-2 primary lesion, prevent metastatic seeding &improve the chance of survival. Start 2-3months preoperatively→ check their effects on resected tumor, if no .necrosis change the drugs; otherwise continue for 6-12 months
Radiotherapy: used only for highly sensitive tumors(like Ewing’s sarcoma),-3 sometimes without amputation if combined with chemotherapy. Radio-&chemo therapy also used for: inoperable tumor(large size or local spread), metastatic .deposits, myeloma &malignant lymphoma
:Benign bone lesions
Non-ossifying fibroma(fibrous cortical defect): is the commonest. It is a
.developmental defect(a nest of fibrous tissue in bone ossifying within years) .CF: asymptomatic &discovered accidentally .Age: children .Site: long bone metaphysis; sometimes, multiple lesions .X-ray: eccentric(within cortex) oval lytic lesion surrounded by thin sclerosis Pathology: it is a solid lesion(not a cyst)of fibrous tissue with scattered giant cells. With growth it heals spontaneously, but it may enlarge leading to .pathological #. There is no risk of malignant change Treatment: is unnecessary; if the defect is large or causing .repeated #→ curettage &bone graft
Fibrous dysplasia: is also developmental disorder in which areas .of trabecular bone are replaced by fibrous tissue containing osteoid &woven bone .# ,CF: small lesion is asymptomatic while large one may cause pain, deformity .Age: appears in childhood &persists through adult life ,Site: metaphysis or diaphysis. If one bone is affected(monostotic) .one limb(monomelic), many bones(polyostotic) .X-ray: lytic lesions with ‘ground glass’ appearance .’A classic deformity is the ‘Shepherd’s crook Pathology: cellular fibrous tissue with patches of woven bone &scattered giant .cells Treatment: small lesions need no Ŗ. Large, painful lesions about to #→ curettage .&grafting .Recurrence: is high .Malignant transformation: is 10% in polyostotic but rare in monostotic lesions .Osteoid osteoma: is a tiny bone tumor CF: male <30 years, having persistent pain typically relieved .by aspirin. Spinal lesions may cause backache &scoliosis .Site: any bone except the skull; 50% affecting tibia &femur X-ray: lytic nidus(<1.5cm) surrounded by dense sclerosis in metaphysis; while in the diaphysis, there may also be .marked cortical thickening(nidus seen only by tomogram) .Tc 99m bone scan: shows intense localized activity .Pathology: the nidus consists of unorganized sheets of osteoid &bone cells Treatment: is complete removal of the nidus: localize the lesion by x-ray or CT &excise it with a block of bone which should be x-rayed to be sure it .contain the nidus. No risk of malignant change
Osteoblastoma(giant osteoid osteoma): is similar
.to osteoid osteoma but more larger &more cellular .CF: young male with pain &muscle spasm .Site: spine &flat bones X-ray: well-defined lytic lesion surrounded by thin sclerosis, sometimes contain .flecks of ossification
Pathology: is similar to osteoid osteoma but more cellular that may resemble .low grade osteosarcoma .Treatment: excision &bone grafting
.Recurrence: is common &malignant transformation has been reported
Chondroma(enchondroma): is arising from islands of cartilage that .persist in bone metaphysis; they grow to form benign cartilage tumor .Age: young people. There may be multiple lesions .Site: any bone but often the tubular bones of hands &feet
.# CF: asymptomatic &discovered incidentally or after pathological
X-ray: well-defined central lytic lesion at the junction of metaphysis &diaphysis with pathognomonic central calcification(mature lesion). The .bone may be expanded .Pathology: simple hyaline cartilage
.Treatment: is unnecessary; pathological #→ curettage &grafting .Recurrence: is common .Malignant transformation: is about 2% &never in children →Signs of malignant changes: in patients >30years are
onset of pain. 2-enlargement of the lesion. 3-cortical erosion. Biopsy-1
.often can’t differentiate benign lesion from low-grade chondrosarcoma
Periosteal chondroma(ecchondroma): arising from cartilage cells under the periosteum &bulging into surrounding soft tissue as a lump which is .not seen on x-ray(only cortical irregularity due to pressure effect)
.MRI: will show the whole lesion .Pathology: highly cellular cartilage. Recurrence: is common .Treatment: marginal excision to avoid recurrence .Malignant changes: not occur
.Chondroblastoma: arises from immature cartilage cells
.CF: adolescent male with constant joint pain .Site: epiphysis of humerus, femur or tibia X-ray: rounded, well-defined epiphyseal lytic .lesion, sometimes extending into the joint or through physeal line .Pathology: chondroblast, immature fibrous tissue &giant cells Recurrence: is common; though it does not undergo .malignant changes, but it is locally aggressive Treatment: marginal excision is better but in children, to avoid .physeal damage, curettage &bone grafting could be satisfactory
:Chondromyxoid fibroma
.Age: adolescents &young adults .Site: any bone, often in the lower limbs .# CF: discovered accidentally or after pathological X-ray: metaphyseal eccentric round or oval lytic lesion surrounded by .dense sclerosis ±central calcification Pathology: fibrous tissue, islands of hyaline cartilage &myxomatous .tissue .Recurrence: is common .Treatment: excision(better) or curettage &bone grafting .Malignant changes: extremely rare
Osteochondroma(cartilage-capped exostosis): is
a common developmental lesion. It start as cartilage overgrowth at edge of physeal plate which continue growing with its parent bone &stops when parent bone stop growing. Any further growth is suggestive of .malignant transformation .CF: a teenage or young adult discovers a painless lump
.Site: any bone but often around knee, proximal humerus &ilium
X-ray: well-defined metaphyseal exostosis with its base continuous .with the parent bone. The cartilaginous cap is invisible unless calcified
.Multiple lesions are seen in hereditary multiple exostosis
Pathology: a narrow base or pedicle of bone &a cap of hyaline
.cartilage, sometimes containing central degeneration &calcification .Malignant transformation: 1% for solitary lesions & 6% for multiple
Treatment: excision→ 1- if it causes symptoms: painful overlying bursa, .pressure on nearby nerve or vessel or soft tissue impingement if, in adult, it has become bigger or painful(suggests malignancy), then -2 .operation is urgent(treat it as a chondrosarcoma even if biopsy is ‘benign’)
.Simple bone cyst: is not a tumor (solitary cyst or unicameral bone cyst)
.Age: appears in children &heals spontaneously .Site: proximal metaphysis of humerus &femur .# CF: discovered accidentally or after pathological
X-ray: well-defined, central, metaphyseal, uni-or multi-locular lytic lesion extending up to the physis; the cortex may be thinned &the bone .expanded Pathology: the lesion is a cavity containing straw-colored fluid, lined by .membrane of fibrous tissue with giant cells
.Recurrence is considerable &malignant change does not occur
Treatment: is not necessary in older children with asymptomatic inactive cyst. A cyst is active if enlarging, reaching the physis, in a young child→ .aspirate the cyst fluid &inject 80-160mg of methylprednisolone .# Curettage &bone grafting is indicated in: 1-pathological .enlarging cyst in spite of steroid injection-2 .atypical cyst to confirm the diagnosis-3 :Aneurysmal bone cyst
may affect any age &any bone but often long bone metaphysis of young
.adults .CF: large lesions cause pain or even bony swelling X-ray: well-defined, eccentric, trabeculated, expansible, meta physeal\ lytic lesion. Occasionally, affects vertebrae or flat bones. In children, it resemble SBC &other benign cartilage tumors; in adult, GCT but never .reach joint surface
Pathology: the cyst is filled with blood; the lining membrane
.consists of fibrous tissue with vascular spaces &giant cells .Recurrence is high &malignant change dose not occur
.Treatment: thorough curettage &bone graft or bone cement
:Giant-cell tumor
.is a tumor of uncertain origin .Age: never seen in children; affects adults only .Site: around knee, proximal humerus &distal radius .# CF: young adult with pain, swelling or pathological
X-ray: eccentric subchondral lytic lesion with thin cortex &bone
expansion. The endosteal margin is well-defined in benign tumor &illdefined in aggressive tumor which may extend into the soft tissue or joint .cavity
.CT, MRI &biopsy: for staging as tumor is potentially aggressive Pathology: giant cells &stromal cells. In aggressive .lesion, there is more cellular atypia &mitotic figures Treatment: Benign GCT(well-defined edges, slow-growing with benign .histology)→ thorough curettage, hydrogen peroxide swab &bone grafting
Aggressive or recurrent GCT→ excision &bone grafting or prosthetic
.replacement. If complete excision is difficult(spine)→ radiotherapy
Giant-cell sarcoma: is a malignant tumor with features like that of highly .aggressive GCT; metastasis is high. Ŗ→ wide or radical excision
:Primary malignant bone tumors
:Osteosarcoma is a highly malignant bone producing sarcoma, arising within bone .&spreads rapidly to surrounding soft tissues .Age: children &adolescent .Site: often around knee &proximal humerus CF: early is constant pain, more at night &increasing in severity. Lump
.or pathological # are late. ESR &serum alkaline phosphatase are high
X-ray: a poorly defined metaphyseal lesion containing hazy osteolytic :&osteoblastic areas. If it breaches the cortex, there often be
& Sunburst effect: bone streaks radiating out from the cortex .Codman’s triangle: reactive new bone at angles of periosteal elevation .Staging: CT &MRI to show extent of tumor. Bone scan for skip lesions .CXR &pulmonary CT for lung metastasis .Biopsy: malignant spindle cells with osteoid matrix Treatment: most cases are ІІA or ІІB so Ŗ→ radical surgery: wide excision + bone graft(or custom-made implant)or radical amputation through or above , joint proximal to tumor. Chemotherapy is helpful
.Long term survival is 50% following wide resection &chemotherapy :Ewing’s sarcoma
arise from endothelial cells in bone marrow. Age: 10-20 yrs
.Site: diaphysis of long bone(tibia, fibula or clavicle) CF: throbbing pain, warm &tender swelling, fever, ill-health &↑ESR,
.↑WBC; all suggest osteomyelitis
X-ray: mid-diaphysis area of bone destruction with Codman’s ∆, sunray .Onion-peel effect: fusiform layers of new bone around the lesion& .CT &MRI: for extra-osseous extension .Bone scan: show multiple lesions(25%) .Biopsy: irregular sheets of small, dark, round cells with no matrix Treatment: preop. chemotherapy→ wide excision(or amputation) .radiotherapy→ chemotherapy for one year ± .The 5 year survival is 50%
:Chondrosarcoma
.is a slow growing tumor with late metastasis. Age: male in his 4th -5 th decade .# CF: dull ache or slowly enlarging lump or pathological .Site: proximal &distal femur, proximal humerus, pelvis &scapula
=Primary chondrosarcoma(90%): either: intramedullary ,Central(99%)→ osteolytic lesion with central calcification .or peripheral(juxtacortical)→ as a mass on bone surface
Secondary chondrosarcoma(10%): arising from previous cartilage lesion: usually the cap of osteochondroma→ enlarging cap with .ill-defined calcification; or arising from enchondroma Staging: CT, MRI &biopsy→ malignant chondrocytes in chondroid .matrix: low-grade or high-grade or dedifferentiated chondrosarcoma Treatment: wide excision(if all tumor can be removed without tumor exposure &without unacceptable loss of function) or .amputation. It is resistant to chemotherapy &radiotherapy
:Fibrosarcoma of bone
.is rare, arising from fibrous dysplasia, bone infarct or after irradiation .# CF: adult having pain, swelling or path .X-ray: ill-defined area of bone destruction .CT &MRI: soft tissue extension .Biopsy: fibroblastic tissue with collagen(low or high-grade)
;Treatment: ІA→ wide excision
.ІІA or ІІB→ radical excision or amputation + radiotherapy
:Multiple myeloma
.is a plasma cell tumor(B-lymphocytes) ,Age: 45-65 yr. X-ray: generalized osteoporosis, crushed vertebra multiple punched-out defects(without sclerosis) in the skull, pelvis .&proximal femur or single lytic lesion(plasmacytoma) Lab tests: ↓Hb, ↑ESR, ↑s. creatinine, ↑s. calcium, urine Bence-Jones .protein(in 50%), serum protein electrophoresis→ characteristic band .marrow puncture→ myeloma cell(eccentric nuclei with spoke-chromatin) Treatment: ORIF of #(with bone cement); cord decompression, .chemotherapy; radiotherapy for plasmacytoma
Secondary malignant bone tumors
the skeleton is a common site for :(or metastatic bone disease ) .secondary cancer. Age: >50 yrs .Site: spine, pelvis, proximal humerus, proximal femur
.Source: breast, prostate, kidney, lung, thyroid, bladder, &GIT .In 10%, no primary is found
.Spread: via blood stream; occasionally, direct spread(pelvis &rib) .# CF: asymptomatic, pain, pathological .# X-ray: osteolytic lesion or moth-eaten or pathological .Osteoblastic lesion suggest prostate cancer
.Tc-bone scan: is very sensitive for detecting ‘silent’ metastasis Lab tests: low Hb, ↑ESR, ↑S.alkaline phosphatase;In prostate cancer, the .S.acid phosphatase is high
.Treatment: pain control(drugs, radiotherapy, hormone therapy) Pathological #→ ORIF± bone cement(nail, plating, prosthesis)→radiotherapy. .Impending #→ prophylactic fixation ,Spine #→ brace, posterior or anterior fusion .decompression or radiotherapy
:Soft-tissue tumors
.benign ST tumors are common, malig. ones rare ,Features suggestive of malignancy: pain in previously painless lump .rapid ↑in size &attachment to surrounding structures .U/S: may differentiate malig from benign tumors Biopsy: excisional if possible(with margin of .normal tissue). Staging: CT, MRI, CXR &lab tests
:Fatty tumors .Lipoma: lobules of fat in(often)subcut. layer surrounded by capsule .It is the commonest of all tumors. Site: anywhere &may be multiple .CF: patient over 50 with painless lump .O/E: lobulated, soft, fluctuant, with well-defined edge .X-ray: radiolucent. Ŗ→ marginal excision if troublesome
Liposarcoma: is rare, suspected it if a lipoma(especially in buttock or thigh) .get bigger, firm &painful. CT &MRI: for staging .Ŗ: low-grade→ wide excision; high-grade→ radical resection .If inaccessible→ radiotherapy is often effective
:Fibrous tumors
.Fibroma: is a benign tumor of fibrous tissue .CF: small, painless nodule or lump .Ŗ→ not necessary or marginal excision
.Fibromatosis: is a benign aggressive FT tumor .CF: subcut. thick cord or plaque in a limb or trunk of young adult .Pathology: difficult to differentiate from low-grade fibrosarcoma Treatment: wide excision to ↓ the rate of recurrence which is .more aggressive &more proximal but with No metastasis :Fibrosarcoma .Site: anywhere but more in the extremities .CF: ill-defined, painless mass .Biopsy: atypical spindle cells .Staging: CT, MRI. CXR→ lung metastasis .Treatment: low-grade→ wide excision .High-grade→ wide excision + Radiotherapy
:Synovial tumors
.Pigmented villonodular synovitis: is a benign synovial disorder .Site: any synovial membrane, often hip, knee &ankle .CF: young adult with boggy swelling of a joint .X-ray: juxta-articular excavation on both joint sides Pathology: hypertrophied synovium consisting .of fibroblastic tissue with histiocytes &giant cells Treatment: complete synovectomy to avoid .recurrence, otherwise followed by radiotherapy Giant cell tumor of tendon sheath(xanthoma of tendon sheath): is the
same disorder but affecting synovial membrane of hands or feet tendons
.causing nodular thickening with pressure erosion of adjacent bone(x-ray) Synovial sarcoma causes rapid swelling :(malignant synovoma) .of a joint(hip, knee, shoulder, hand or foot) .X-ray: calcified soft tissue mass near a joint Biopsy: atypical synovial cells &fibroblastic .tissue in an acinar arrangement .Treatment: low-grade→ wide excision + High-grade→ radical excision .chemo &radiotherapy
:Blood vessel tumors
.Haemangioma: is a benign lesion(hamartoma) .Age: child or at birth .’Types: capillary hemangioma→ cutaneous red patch like ‘birth mark :Cavernous hemangioma→ is a collection of blood spaces, either Superficial: blue skin patch or .Deep: in muscle or involve the whole limb .X-ray: may show calcified phleboliths .Treatment: not necessary .No malignant change .Recurrence: is common .Glomus tumor: is rare, arises from neuromyoarterial glomus body .Site: nail bed .CF: young adult with episodes of intense pain .O/E: tender, small, blue nodule under nail .X-ray: erosion of underlying phalanx. Ŗ: excision
:nerve tumors
Neuroma: is not a tumor but an overgrowth of .fibrous tissue &nerve fibrils following nerve injury CF: tender; local percussion may induce distal .paraesthesia(Tinel’s sign) Neurilemmoma or neurinoma or .Schwannoma: benign tumor of peripheral or spinal nerve sheath .CF: pain, paraesthesia &sometimes, palpable swelling ;Involvement of spinal nerve may cause sciatica .x-ray: erosion of intervertebral foramen .Ŗ: excision without nerve damage .Neurofibroma: is a benign tumor of neural &fibrous tissues It can be solitary(90%) or multiple; may be associated with .scoliosis or pseudoarthrosis(tibia, radius, ulna) .CF: peripheral nerve lump; paraesthesia &muscle weakness If spinal nerve is involved→ similar to disc prolapse .with pedicle erosion or enlarged neuroforamen :Multiple neurofibromatosis1(von Recklinghausen’s disease) is an autosomal dominant disease; the child presented with skin .nodules &café-au-lait patches. Malignant changes is about 5-10% .Ŗ: if tumor is troublesome→ excision Neurosarcoma(malignant schwannoma): may arise from nerve .sheath or from pre-existing neurofibroma. Ŗ: usually amputation
:Muscle tumors
Rhabdomyoma: is a rare cause of muscle lump; a common cause & is muscle rupture(both can be moved only from side to side harden with contraction) which appears suddenly, with proximal .or distal depression & not enlarging with time .Ŗ: excision. Malignant change may occur Rhabdomyosarcoma: Site: around hip or shoulder. CF: young adult with .painful ill-defined lump moving with the affected muscle .Biopsy: high-grade malignant muscle cells .Ŗ: radical resection or amputation ± radiotherapy
