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Clinical Medicine 1 > Thoracic Pathophysiology > Flashcards

Thoracic Pathophysiology Flashcards

1
Q

Thoracic disc conditions

A
  • 1% symptomatic disk herniations
  • asymptomatic disk protusion 37%
  • 2 yr follow up= little change in size of herniation
  • retrospective review 40 pts with symptomatic disk herniations, nonsurgical mgmt=77% return to premorbid level of function
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2
Q

incidence/prevalence of thoracic spine conditions

A
  • females generally experience a higher incidence of thoracic spine disorders
  • 12-month prevalence ranges from 15-34.8%
  • higher prevalence in adolescents (up to 41%)
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3
Q

scoliosis-pattern A=1degree prevention, B=impaired posture

A

general pathophysiology

  • type 1 dysfunction=lateral curvature spine
  • deformity rather than a disease process
  • named for convexity and region
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4
Q

nonstructural scoliosis (functional)

A
  • reversible lateral curvature

- corrected voluntarily or by underlying cause

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5
Q

structural scoliosis

A
  • irreversible lateral curvature
  • major curve=primary (1degree) curve
  • secondary curve (2degree)=compensatory curve
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6
Q

idiopathic curve pattern prognoses (incidence)

curve theyre born with

A
  • primary lumbar (23.6%): most benign and least deforming
  • thoracolumbar (16%): not severely deforming, between thoracic and lumbar
  • primary thoracic (22.1%):Worst, progresses rapidly and is severe. 5 years of active growth could INCREASE the curve
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7
Q

rib hump

A

curvature of spine causes rib hump posteriorly and and anteriorly on opposite sides, posterior hump is on side of concave deformity

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8
Q

scoliosis: etiology

A
  • nonstructural

- structural

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9
Q

nonstructural scoliosis etiology

A
  1. postural scoliosis
  2. pain and muscle spasm
    a. painful lesion of spinal nerve root
    b. painful lesion of spine
    c. painful lesion of abdomen
  3. limb length discrepency
    a. true vs apparent (rotation of sacro-iliac joint)
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10
Q

structural scoliosis etiology

A
  1. idiopathic scoliosis
  2. osteopathic scoliosis
  3. neuropathic scoliosis
  4. myopathic scoliosis
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11
Q

idiopathic scoliosis

A
  • 85% of all scoliosis
  • infantile: appears birth to 3yo
  • juvenile: appears 4 to 9 yo
  • adolescent: appears 10-end of growth period
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12
Q

osteopathic scoliosis

A

a. congenital: localized vs generalized (primary thoracic/lumbar)
b. acquired: fractures/dislocations/rickets

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13
Q

neuropathic scoliosis

A

a. congenital (spina bifida)

b. acquired (paralytic scoliosis), i.e cerebral palsy, paraplegia

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14
Q

myopathic scoliosis

A

a. congenital: hypotonia of neuromuscular origin-spinal muscular atrophy
b. acquired-muscular dystrophy

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15
Q

idiopathic scoliosis: incidence and etiology

A
  • present to some degree in .5% of the pop
  • familial incidence
    a. infantile: more common in boys
    b. juvenile and adolescent: more common in girls
  • pattern may be lumbar, thoracolumbar, thoracic or combined lumbar and thoracic (double major curve)
    a. most common is right thoracic in adolescent girls
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16
Q

idiopathic scoliosis: pathogenesis and pathology

A
  • characterized by rapid progression mostly in the adolescents, however, begins slowly, insidiously, and painlessly
  • as the curve progresses, wedge-shaped vertebrae form on the concave side
  • may be slow (1degree per year)
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17
Q

idiopathic scoliosis: diagnostic criteria

A
  • radiographic curve: 40 deg is severe
  • often not detected until~30 deg curve is present, after skeletal maturity, less than 30 deg does not generally progress
  • trunk forward flexion, radiographs (A-P and lateral full spine in standing), MRI (in presence of neurologic deficit, HA or neck stiffness)
  • cobb method (2 90deg angles drawn between vertebrae of curve, angle between diagnoses curve of spine)
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18
Q

idiopathic scoliosis: prognosis

A
  • dependent on the amount of growth that remains

- greater the degree of curvature at assessment=greater likelihood to increase

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19
Q

idiopathic scoliosis: intervention

A
  • goal: minimize progression of mild scoliosis and correct and stabilize a severe deformity
    1. nonoperative
    2. operative
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20
Q

nonoperative

A
  • exercises/body casts ineffective to prevent progression
  • 20-40deg curves with 2 or> years of skeletal growth, spinal braces can minimize increasing curvature and may provide some permanent correction
  • -milwaukee brace-primary thoracic
  • -boston brace: lumbar and T/L curves
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21
Q

operative

A
  • curves>40deg or predicted to do so
  • internal spinal instrumentation and fusion
  • -harrington rodding 1962
  • -cotrel-dubousset system
  • -texas scottish rite hospital (TSRH) system
  • –post-op body cast at least 3 months for fusion to consolidate
  • wait till child is at least 10 y/o
  • very young with progressive->bracing inadequate, fusion contraindicated, 2deg to ceasing vertical growth
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22
Q

osteochondrosis

A
  • pattern F-..localized inflammation
  • pattern H-…fracture
  • pattern J-…surgical procedure
    1. scheuermann’s disease
    2. calve’s disease
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23
Q

scheuemermann’s disease

A

-osteochondrosis of secondary centers (pressure epiphysis) of ossification in the spine (end of long bones most often)

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24
Q

calve’s disease

A

-osteochondrosis of primary center of ossification in the spine

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25
Q

osteochondrosis

A
  • idiopathic avascular necrosis effecting the epiphyses
  • AN of subchondral bone that supports articular cartilage in synovial joints
  • loss of blood supply, death of bone (-Clastic), replacement of bone (blastic)
  • during pathological process, epiphysis may permanently deform with resultant OA
26
Q

osteochondrosis: general features

A
  • most common ages 3-10
  • boys>girls
  • lower limbs>upper limbs
  • idiopathic
  • self-limiting disorder-heals spontaneously
  • 4 phase pathological process
27
Q

osteochondrosis stage

1. early phase of necrosis

A
  1. early phase of necrosis (avascularity)
    - obliteration of blood vessels to epiphysis
    - death of marrow and osteocytes
    - A.C lives and grows in synovial fluid
    - symptomless and no deformity
28
Q

stage 2

A

phase of revascularization with bone deposition and resorption

  • vascular reaction of surrounding tissue to dead bone
  • revascularization of dead epiphysis
  • rim of epiphysis ossifies as well as within the ossific nucleus (ossification)
  • woven bone (fracture callus)
  • pathological fracture arises at site of greatest stress (often subchondral bone) (resorption)
29
Q

osteochondrosis phase 3

A

phase of bone healing

  • resorption ceases and deposition continues
  • biologic plasticity=with growth, can be molded into normal or abnormal shape depending on forces applied
  • when epiphysis reossification is complete the final contour can be determined
30
Q

phase 4 of osteochondrosis

A

phase of residual deformity

  • contour now unchanged, thus residual deformity persists
  • function can continue for some years satisfactory secondary to AC intact
  • however, residual deformity, joint incongruity, and motion limitation will lead to OA
31
Q

scheuermann’s disease

A
  • growth disturbance of epiphyseal plates anteriorly (sup and inf)
  • results in increased kyphosis
32
Q

scheuermanns disease: incidence and etiology

A
  • effects boys and girls
  • puberty to late teens (vertebral growth ceases)
  • some pt inherit with autosomal dominant pattern
  • often involves 3-4 adjoining vertebrae in the midthoracic region
33
Q

scheuemann’s disease: pathogenesis and pathology

A
  • schmorl’s nodes common
  • may interfere with epiphyseal growth
  • wedge shape vertebrae account for increased kyphosis
34
Q

scheuermann’s disease: clinical features and diagnosis

A
  • poor posture or rounded shoulders at puberty-symptomless often
  • moderate back pain in ensuing years, often at end of day
  • increased thoracic kyphosis awith compensatory increased lumbar lordosis
  • may have tenderness over SPs
  • when growth ceases symptoms subside spontaneously but deformity persists
35
Q

scheuermann’s disease: intervention

A
  • self-limiting, symptoms mild, often treatment not required
  • goal to minimize unsightly deformity if anticipated-may use milwaukee brace modified for approx one year
  • older adolescents or adults (growth ceased), severe pain or severe deformity requires spinal instrumentation and fusion
  • PT intervention?
36
Q

scheuermann’s disease: current diagnosis and treatment approach

A
  • brace treatment more effective if diagnosed prior to the curvature angle exceeding 50deg in patients continuing to grow. surgical treatment is rarely indicated for severe kyphosis (>75deg) with curve progression, refractory pain, or a neurologic deficit
  • clinical trials needed to evaluate the efficacy of conservative interventions, particularly different exercises and manual therapies in combination with bracing
37
Q

calve’s disease

A
  • less common than scheuermann’s disease
  • effects ages 2-8 most often
  • almost always limited to one vertebral body
  • avascular necrosis secondary to langerhans-cell histiocytosis (eosinophilic granuloma)-creates discrete but destructive lesions in bone (originates in epidermis)
38
Q

clinical features and diagnosis

A
  • mild back pain but otherwise healthy
  • slight kyphosis and m. spasm
  • wafer thin vertebrae on x-ray
39
Q

prognosis and intervention

A
  • within 2-3 years reossification of bone and continued growth of secondary centers results in almost complete restoration of the vertebra
  • self-limiting, palliative treatment indicated, sometimes short term spinal brace
40
Q

postural syndrome-pattern B

A
  • defined as prolonged endrange stress placed on normal tissues (no pathology)
  • can lead to dysfunction
  • generally ages 20-35, sedentary lifestyle
  • females>males
  • all special tests are negative, static positioning symptomatic
  • no surgical intervention
  • correct posture
  • local or referred pain, no radicular pain, intermittent
41
Q

thoracic outlet syndrome

A
  • Signs and symptoms that result from compression of the neurovascular bundle as it emerges from the thorax and enters the upper limb
  • thoracic outlet (inlet)-space b/w clavicle and the first rib, compartmentalized by the scalenes
  • subclavian vein enters from arm and exits b/w clavicle, first rib and anterior scalenes
  • brachial plexus and subclavian artery exit b/w ant. and middle scalenes and first rib
42
Q

scalene triangle composed of

A

anterior and middle scalenes

first rib

43
Q

scalene triangle narrowing

A

scalenes:
-shortening
-tightening
-hypertrophy
-spasm
First Rib:
-inhalation
These may cause thoracic outlet syndrome

44
Q

clavicular space made of

A

clavicle
first rib
space has nerves and vascular structures that may be compressed by above

45
Q

clavicular space narrowing

A 
cervical rib:
-present in 0.2% of pop
clavicle fracture:
-malunion
normal mechanics
cervical rib and clavicle fracture can compress structures
46
Q

pectoralis minor

A
  • pectoralis minor attaches to coracoid process
  • crosses nerve space, tightness may impact thoracic outlet syndrome
  • shortening or tightening
  • hyperabduction crompresses strucutres
  • coracoid process
  • -tethered
  • -compression
47
Q

thoracic outlet syndrome: signs and symptoms

A
  • numbness and/or paresthegias
  • weakness of hand, muscle wasting
  • pallor or cyanosis
  • cold to touch
  • heaviness, fatigue
  • intermittent
48
Q

thoracic outlet syndrome: intervention

A
  1. conservative (PT)
  2. surgical
    - cervical rib resection (congenital deformity where rib on 7th vertebrae and not 1st)
    - first rib resection
    - scalenectomy
49
Q

fractures of thoracic spine and ribs

A
  • most common are compression type (either wedge compression or bursting compression)
  • most often are stable injuries
  • caused by fall from height most often onto buttocks
  • less common but more serious are fracture dislocations-most often are unstable
50
Q

wedge compression fractures: signs and symptoms

A
  • often mild local tenderness

- lateral radiographs most beneficial

51
Q

intervention

A

-stable injury, therefore, apply body cast or bed rest a few weeks then AROM exercises

52
Q

burst compression fracture

A
  • often fall from height and land on feet
  • ligaments intact and spinal cord relatively stable
  • spinal cord or cauda equina injury may result from fragment of comminuted fracture
53
Q

signs and symptoms

A
  • as with wedge fracture but heightened intensity

- lateral radiographs and MRI for retropulsion of fragments into spinal canal

54
Q

intervention

A
  • often no reduction needed
  • if retropulsion of fragments occurred, surgery indicated for excision, decompression
  • post-op bed rest first few weeks then plaster body cast for 8 weeks
55
Q

fracture dislocations

A
  • occurs with high velocity injuries (i.e. MVA)

- post. long. ligament torn, facet joints fractured, vertebral fracture, spinal column dislocated and entirely unstable

56
Q

signs and symptoms

A
  • shock form severity of injury

- neurological deficit evident

57
Q

intervention

A
  • treat neurologic compromise first

- ORIF with bone grafting

58
Q

rib fractures

A
  • MOI-stricken by hard or blunt object, MVA, sports injury, etc
  • rarely displaced secondary to intercostal muscles
  • heal readily, nonunion practically unknown
  • rib subluxations/dislocations
  • -more common with traumatic events
59
Q

signs and symptoms

A
  • local pain, aggravated by breathing, coughing, sneezing
  • “through the chest pain”
  • plain radiographs detect well
60
Q

intervention

A
  • immobilize chest

- PT

Clinical Medicine 1 (7 decks)

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