Core Topics

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Core topics in orthopaedics

AO Classification

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The AO group has developed a comprehensive classification of fractures. The classification is arranged in order of increasing severity according to the complexities of the fracture, difficulty of treatment and worsening prognosis.

More detailed information about the classification can be obtained from AO Foundation

 

Unicameral Bone Cyst (UBC)

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Unicameral Bone Cyst (UBC)

– solitary, fluid-filled cystic lesions located in metaphysis of long bones near physis in kids & adolescents
– predominantly proximal femur & proximal humerus

Signs & Symptoms:
– usu asymptomatic
– pathologic # associated with minimal trauma

Xrays:
– radiolucent, trabeculated lesion with well-defined borders surrounding by sclerotic margin
– ‘fallen leaf’ sign in pathologic #

Histology:
– lined with loose connective tissue membrane containing small numbers of fibroblasts, giant cells & hemosiderin-laden macrophages

Treatment:
– 15% will heal after # with observation alone
– treat # as you would for most #s of that region
– once # healed, aspiration & steroid injections (x 3)
– curettage & bone grafting improves healing rate & provides mechanical support

Adamantinoma

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Adamantinoma

– 1o bone tumor with predilection for tibial diaphysis presenting during early adulthood

Signs & Symptoms:
– painful masses with variable symptom duration ranging from few months to few years

Xrays:
– well-circumscribed, eccentric, lytic lesions of tibial diaphysis
– may be multicystic lesion with surrounding sclerosis
– expansion of bone +/- intact cortex but no periosteal reaction

Histology:
– wide variety of histologic appearances
– basaloid pattern composed of groups of cells which peripherally have palisading epithelial cells
– hypocellular, poorly organized, fibrous connective tissue between islands of epithelial cells

Treatment:
– wide excision (limb salvage vs amputation)
– 20-25% metastasize to lungs

Aneurysmal Bone Cyst (ABC)

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Aneurysmal Bone Cyst (ABC)

– solitary expansile lesion located in metaphysis of long bones, flat bones & vertebrae
– presents in 2nd decade
– cysts filled with blood

Signs & Symptoms:
– pain with tenderness & swelling at the site of the lesion

Xrays:
– expansile eccentric lesion surrounded by a thinned cortex with periosteal new bone formation
– CT/MRI – characteristic ‘fluid-fluid’ level
– beware of telangiectatic osteosarcoma – has fluid-fluid levels but far more aggressive looking

Histology:
– blood spaces separated by cellular septa lacking an endothelial cell lining & containing a variety of cells such as fibroblasts, multinucleated giant cells & histiocytes & metaplastic bone
– large solid cellular areas may be seen

Treatment:
– excision, curettage & bone grafting
– cryosurgery or chemical ablation may be used

Fibula – Approach

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Fibula – approach

* position – supine with sandbag under buttock or lateral

* incision – long. incision just post. to fibula beginning behin lat. malleolus & extending to level of fibular head

* internervous plane – peroneal muscles (SPN) & flexor muscles (tibial n.)

* dissection
– find post. border of BF as it sweeps down past knee before inserting on head of fibula
– incise fascia & ID CPN
– trace course of CPN as it winds around fibular neck
– mobilize CPN from groove on back of neck
– develop plane btw PL & soleus
– incise periosteum of fibula
– strip muscle off fibula
– strip interosseous membrane subperiosteally from prox. to distal

* dangers
– CPN – winds around neck of fibula
– dorsal cut. branch of SPN – ID at jxn of distal & middle 1/3 of fibula
– peroneal art. – terminal branches lie close to deep surface of lat. malleolus
– lesser saphenous vein

Clavicle Fractures

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Clavicle Fractures

3 Groups based on thirds
medial (5 %),middle (85%),distal (10 %)
*consider ORIF-open,n-v injury,skin compromise,ipsilateral scapula or flail chest

Distal Clavicle Classification
(Neer and Rockwood)
Type I-lateral to intact C-C ligaments (C/T)
Type II-complex injuries (30% non-union without surgery)
medial fragment separated from C-C ligaments by A-obligue # (ie. Iig attached to lateral fragment) or B-ligaments cause segmental avulsion from underside of clavicle
Type III-Intra-articular A-C joint fractures

Type I and III-Symptomatic treatment

12 – Humeral Diaphysis

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A-Simple fracture
12-A-1 spiral
12-A-2 oblique (>30 degrees)
12-A-3 transverse (<30)
B-Segmental\Wedge
12-B-1� spiral wedge
12-B-2 bending wedge
12-B-3 fragmented wedge
C-Complex Fracture
12-C-1 spiral
12-C-2 segmental
12-C-3 irregular

MCQs – Upper Extremity Peds

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MCQs-UE peds
– the most common reason for supracondylar osteotomy following malunion and gunstock deformity is cosmetic.

– the best treatment for Monteggia fracture is to do a closed reduction of ulna, closed reduction of radial head, then cast.

– lateral condyle fracture missed and seen at 3 weeks – probably fix it.

– a child with open growth plates who sustains an anterior shoulder dislocation has a nearly 90% chance of having recurrent dislocations.

– for a proximal humerus fracture with greater than 25 degrees of angulation near skeletal maturity -should probably do something.

– most common site of osteochondritis dessicans in the elbow is the capitellum. X-ray changes are confined to the capitellum until joint becomes arthritic. Rarefaction, fragmentation, irregular ossification, and a localized crater defect can be seen. The articular surface may look irregular. Occasionally, the radial head looks abit bigger than the other side.

– fixation of a medial epicondyle fracture is indicated if displaced > 1 cm, if ulnar nerve symptoms present, if trapped within the joint, or if valgus instability is present.

– the most important radiographic aid in determining what is broken in elbow fractures is to line up the capitellum with the radial head.

– for the posterior dislocation of the radial head with ulna fracture (Bado II) – treat with reduction and then immobilization in EXTENSION and PRONATION. Most (Bado I) are treated in flexion and supination.

– if you flex a supracondylar fracture without first applying traction – you’ll kink the neurovascular structures anteriorly

– for the posteromedially displaced supracondylar fracture – assume that the lateral structures are totally torn. So when immobilizing, you want to pronate them to hinge on the intact medial side.

– for posterolateral displaced supracondylar fracture – assume the medial side is torn – immobilize in supination

– immobilization of a supracondylar fracture for more than 4 weeks is probably too much – they might get stiff if left in for 6 weeks.

– failure to correct cubitus varus with supracondylar osteotomy is most often due to inadequate correction of the medial rotation.

– for post-traumatic radioulnar synostosis, they are more common with open reduction, more likely with proximal fractures, and can be resected but only after waiting 1-2 years.

– mallet deformities in a 5 year old are caused by salter I or II injuries. In older children, they end up being salter III injuries.

– in epiphyseal separations of the distal phalanx of the finger, it is important to know that the flexor tendons insert into the metaphysis, and the extensor tendons into the epiphysis (hence Mallet fingers are salter I or II injuries)

– camptylodactyly of 30 degrees of the hand that is correctable with MCP flexion (indicating abnormal lumbrical insertion) should be treated initially with dynamic splinting. ???

Peripheral Nerve 2

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Peripheral nerve2
Management – General Considerations

Which require surgery
For those that require surgery, when should you do it?
What surgery should you do?

Which injuries require surgery?

There are two scenarios – the closed injury with nerve dysfunction, and the open injury with nerve dysfunction. The mechanism of injury – compression, ischemia, traction, laceration – can be inferred from the trauma. The majority of acute traumatic nerve injuries are caused by blunt closed trauma, which often stretches and compresses a nerve but leaves it in continuity. Open injuries may be produced sharply or bluntly and may be associated with complete or partial nerve injury. Missile injuries often leave nerves in continuity but produce intraneural damage secondary to cavitation effects. First, a review of the types of nerve injuries:

Sunderland I – Neuropraxic Injuries
– conduction along the axon is physiologically interrupted at the site of the injury, but the axon is not actually disrupted and no wallerian degeneration occurs. The loss of function is variable, usually more profoundly affecting the motor function than sensory.

– Obviously, these injuries do not require surgery. They are detected clinically by fairly well preserved function, and by fairly early recovery.

Sunderland II – Axonotmetic Injuries
– disruption of the axon with wallerian degeneration distal to the point of injury and degeneration proximal for one or more nodal segments occurs. The integrity of the endoneurial tube is maintained, however, so that the anatomic course for regeneration is in place. Any permanent deficit is related to the number of neural cell bodies that die, with cell death occurring more commonly when the injury takes place proximally. Clinically, the neurological deficit is complete, with loss of motor, sensory, and sympathetic function. Motor reinnervation takes place in a progressive manner, and an advancing Tinel sign can usually be followed at the rate of 1 inch per month.

– Because the framework for axonal regeneration is already in place, these would not be improved upon by surgery either. Usually good function is achieved.

Sunderland III
– the axons and endoneurial tubes are disrupted, but the perineurium is preserved. The regenerative effort is impeded by the disruption of the endoneurial tubes and scar formation which obstructs tubes and diverts the sprouting axons. Clinically, the neurological loss is complete, and the duration prolonged. Complete return of neural function does not occur, distinguishing this from the Sunderland II injuries.

– Because it is unlikely that surgical repair could improve upon the intra-neural architecture, these injuries are better left managed non-surgically.

Sunderland IV
– the axons, endoneurium, and perineurium are disrupted, but not completely, so that complete severance of the entire trunk does not occur. Retrograde degeneration with axonal death is more common. Axonal sprouts exit through defects in the perineurium into the surrounding tissues. There will be no advancing Tinel sign.

– The recovery from these is uniformly poor without surgery.

Sunderland V (Neurotonmesis)
– complete transection of the nerve, resulting in a variable distance between the neural stumps. The likelihood of significant bridging by axonal sprouts is remote, as is the possibility of significant functional return.

– Obviously, these are better treated surgically

Type VI injuries (MacKinnon)
– mixed injures in which a nerve trunk is partially severed, and the remaining part sustains fourth, third, second, or even first degree injury.

– These require partial neurorrhaphy, possibly with internal neurolysis.

Unfortunately, patients arrive with neurologic deficits, and not with a Sunderland classification assigned to their injury. The trick is in clinically assessing the patient to determine which type of injury they have. For open wounds, exploration will usually demonstrate whether the nerve is in continuity or not.