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Page 1 (row 1, column 1)

pelvic ring or ace- tabular fractures,

pelvis account for less than 5% of


all skeletal injuries,

important due to the potential risk of


severe blood loss.

pelvic ring is made up of the two


innominate bones and the sacrum,
articulating in front at the symphysis
pubis and posteriorly at the sacroiliac
joints.

transmits weight from the trunk to


the lower limbs

no inherent bony stability of


the pelvis.

three segments together

anteriorly

symphysis pubis

sacroiliac joints posteriorly.

stability of the pelvic ring depends


upon the integrity of the strong
ligaments

posterior stability by the posterior


anterior stability is provided by the anterior sacroiliac ligaments the sacrococcygeal
sacroiliac ligaments and the iliolumbar liga- ligaments, and the sacrotuberous and
ments sacrospinous ligaments
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Page 2 (row 2, column 1)

internal iliac vessels supply the


pelvic viscera,

external iliac vessels continue in their


journey to sup- ply the lower limbs

rich low-pressure venous plexus


posteriorly

It is bleeding from this plexus that


comprises the major blood loss in
pelvic haemorrhage.

lumbosacral plexus is at risk with


posterior pelvic injuries.

The L5 and S1 nerve roots

pelvic ring injuries

sciatic nerve

acetabular fractures.

urethra is much more mobile and


shorter in females, and it is less prone
to injury.
male urethra

commonest urogenital organ to


be damaged
severe pelvic injuries the
membranous urethra

pelvic colon, with its mesentery, is


a mobile

not readily injured

rectum and anal canal

more firmly tethered

therefore vulnerable

Nowadays, the application of a pel-


vic binder at the scene of the accident
is mandatory in any suspected pelvic
injury

Guarding or tenderness suggests the


possibil- ity of intraperitoneal bleeding
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Page 3 (row 3, column 1)

binder applied

X-rays should be taken following the


removal of the binder to ensure no
displacement of the pelvis has
binder removed. occurred

Neurological examination is very


important; there may be damage to
the lumbosacral plexus.

1 The sacroiliac joint area is


inspected for any dias- tasis or sacral
fracture.

2 The ilium is inspected for


any fracture.

a radiological feature which


correlates to the non-articular floor of
the acetabulum, and close inspection
in this area will reveal any acetabular
fracture.
Workspace for 'Apley_and_Solomon's_System_of orthopaedics'
a radiological feature which
correlates to the non-articular floor of
Page 4 (row 4, column 1) the acetabulum, and close inspection
in this area will reveal any acetabular
fracture.

systematically look at each line to


see which is broken.
4 The obturator foramen is inspected
for any fracture of the superior or helps to interpret the Letournel
inferior pubic ramus. classification

symphysis pubis is examined for


any fracture or diastasis.

Specialized radiographs

pelvic inlet and outlet views

30–40 degrees in a caudal and


cephalic angle and are used to assess
the pelvic ring.

(b) outlet view.
(a) Inlet view;

sacrum and sacroiliac joints, provides a true anteroposterior view


of the sacrum and pubic sym- physis
areas

Judet views (taken at


30 degrees obliquely)

obturator oblique iliac oblique view

anterior column of
the acetabulum posterior column and anterior wall
of the acetabulum.
CT scans can be reformatted to
provide Judet views,

a full ‘trauma CT scan’.

head, neck, chest, abdomen


and pelvis.

excluding a bladder rupture or


urethral injury
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Page 5 (row 5, column 1)

Avulsion fractures

most common avulsion injuries

anterior inferior iliac spine (rectus ischial tuberosity (hamstring origin)


femoris origin)

violent muscle con- traction;

adductor longus a piece of


the pubis
sartorius

anterior superior iliac spine

Stress fractures

common in osteoporotic bone


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Page 6 (row 2, column 2)

the most common cause of chronic


inflammatory joint disease.

most typical features

symmetrical polyarthritis

tenosynovitis,

morning stiffness,

elevation of the erythrocyte


sedimentation rate (ESR)

autoantibodies (rheumatoid factor


(RF) and anti-citrullinated peptide
antibodies (ACPAs))

Individuals with RA tend to


die younger

result of the effects of chronic


inflammation

early ischaemic heart disease

prevalence of RA in most popu-


lations is 1–2%,

peak incidence in the fourth or


fifth decades.

Women are affected three times

Important factors in the evolution


of RA

(1) genetic susceptibility


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Page 7 (row 3, column 2)

(2) an immunological reaction

focused on synovial tissue

(3) an inflammatory reaction in joints


and tendon sheaths

(4) the appearance of rheumatoid


factors (RF)

(anti-CCP or ACPA

(5) perpetuation of the


inflammatory process
(6) articular cartilage destruction

Genetic susceptibility

first-degree relatives of patients

(HLA) DR4

HLA-DR4 is encoded in the major


histocompatibility complex (MHC)
region on chromosome 6

HLA-DR4 binding groove called the


‘shared epitope’

HLA Class II molecules appear

(B lymphocytes, macrophages,
dendritic cells), which can act as anti-
gen-presenting cells (APCs)

T-cell immune reactions, the


process is initiated only when the anti-
genic peptide is presented

no such antigen has been


discovered.

The inflammatory reaction

Once the APC/T-cell interaction


is initiated,

marked proliferation of

synovium,

appearance of new blood vessel


formation. Immune cells

action by the use of ‘short-range


hormones’ (cytokines)

activate inflammatory cells such as


macro- phages and B cells.

chemokines, attract other


inflammatory cells to the area.

cytokines are important in RA

tumour
necrosis factor
(IL-6) (TNF),
interleukin-1
(IL-1)

resulting synovitis, both in joints and in tendon


sheath linings, is the hallmark of early RA.

Rheumatoid factor

B-cell activation

production of anti-IgG
autoantibodies

detected

as ‘rheumatoid factor’ (RF)

Low levels of RF many ‘normal’ indi- viduals

high, an inflammatory disease


is likely

Other autoimmune conditions

(SLE) and Sjögren’s

associated with the presence


of RF.
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Page 8 (row 4, column 2)

Other autoimmune conditions

(SLE) and Sjögren’s

associated with the presence


of RF.

associated with RA

presence of anti-CCP is
very specific

Chronic synovitis and joint


destruction

Chronic rheumatoid synovitis

associated with

proteolytic enzymes, prostaglandins


and the cytokines TNF and IL-1

Immune complexes

in synovial joints

leads to depletion of the cartilage

Vascular proliferation and


osteoclastic activity

further to cartilage destruction and


periar- ticular bone erosion.

most characteristic lesions

the synovium or within rheumatoid


nodules. Th

four stages

In any one joint, features of different


stages can be occurring
simultaneously

Stage 1: Pre-clinical Stage 2: Synovitis


Stage 3: Destruction Stage 4: Deformity

RA becomes clinically apparent, new blood vessel formation,


causes joint and tendon articular destruction,
destruction
Raised ESR, C-reactive protein (CRP)
and RF proliferation of synoviocytes and capsular stretching
infiltration of the subsynovial layers
Articular cartilage is eroded
by polymorphs, lymphocytes and
detectable years before the plasma cells tendon rupture leads
first diagnosis.
direct invasion of the cartilage by a
thickening of the capsular structures pan- nus of granulation tissue creeping progressive instability
over the articular surface

villous formation of the synovium deformity of the joints.

bone is eroded by tissue invasion


cell-rich effusion into the joints and and osteoclastic resorption
tendon sheaths.

Similar changes occur in


reversible. tendon sheaths,

causing tenosynovi- tis,

partial or complete rupture


of tendons
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Page 9 (row 5, column 2)

EXTRA-ARTICULAR TISSUES LymphadenopathY Vasculitis Muscle weakness


Visceral disease

Rheumatoid nodules Not only the nodes draining life-threatening


generalized myopathy or
inflamed joints, Ischaemic heart disease and
neuropa- thy,
osteoporosis are common
small granulomatous lesion complications.
skin exclude spinal cord disease or cord
mediastinal nodes, can compression
cen- tral necrotic zone be affected
nailfold infarcts,
(atlantoaxial subluxation)
splenomegaly can also be
palisade of local histiocytes
associated with neutropaenia
Sensory changes
beyond that by inflammatory Felty’s syndrome.
granulation tissue.

a neuropathy
(especially over bony
prominences)

tendons result from nerve compression by


thickened synovium

sclera
3.2 Rheumatoid synovitis (a) The macroscopic
appearance of rheumatoid synovitis with fibrinoid mate- carpal tunnel syndrome
rial oozing through a rent in the capsule. (b) Histology
viscera.
shows proliferating synovium with round-cell infiltration
and fibrinoid particles in the joint cavity (×120).

usually insidious,

In the early stages In the later stages

polysynovitis, with soft-tissue


swelling and stiffness deformity becomes increas-
ingly apparent

Typically, a woman of 30–


40 years combination of joint instability and
tendon rupture produces the typical
‘rheumatoid’ deformities:
pain, swelling and loss of mobility in
the proximal joints of the fingers

ulnar deviation of the fingers


history of ‘muscle pain’, tiredness

radial and volar displacement of


the wrists
As time passes, the symptoms
‘spread’ to other joint
valgus knees

wrists, feet, knees and shoulders


valgus feet and clawed toes

order of frequency
stiffness in the cervical spine

generalized stiffness

early morning

stiffness typically lasts longer than


30 minutes.

symmetrically distributed swelling


and tenderness of the
metacarpophalangeal joints

Tenosynovitis

extensor compartments of
the wrist

flexor sheaths of the fingers;

thickening,

crepitation over the back of the


wrist or the palm while passively mov-
ing the fingers

If the larger joints are involved,

local warmth, synovial hypertrophy

appearance of nodules Less specific features include

small subcutaneous lumps muscle wasting

rubbery in consistency, lymph- adenopathy

elbows, scleritis,

ten- dons (where they may cause nerve entrapment syndromes,


‘triggering’ or rupture
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skin atrophy

vasculitis

peripheral sensory neuropathy

X-rays

Early later stages

soft-tissue swelling and periarticular marginal bony erosions


oste- oporosis and narrowing

especially in the proximal joints

hands and feet

Flexion and extension views of the cervical spine often show subluxation at the atlan- toaxial or mid-cervical levels;

Ultrasound scanning and MRI

Ultrasound

synovitis and early erosions.

Blood investigations

Normocytic, hypochromic
anaemia

aggravated by

non-steroidal anti-
inflammatory drugs

In active phases the ESR and CRP


concentration are usually raised

anti-CCP antibodies have added


much greater specificity

Synovial biopsy

needle biopsy

non-specific

persisting for at least 6 weeks.

subcutaneous nodules or X-ray signs


of periarticular erosions, the diagnosis
is certain

chief value of the RF tests

prognosis:

Atypical forms of presentation

rapid appearance of severe joint pain


and stiffness

disease starts with chronic pain and


swelling of a single large joint

presence of

all metacarpophalangeal
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Page 11 (row 7, column 2)

all metacarpophalangeal

early morning stiffness

at least 30 minutes

raised ESR

diagnosis of rheumatoid arthritis.

Calcium pyrophosphate
differential diagnosis deposition disease

older people
Seronegative inflammatory Ankylosing spondylitis
polyarthritis

psoriatic arthritis affects large joints


sacroiliac and intervertebral joints

Still’s disease, X-ray signs


causing back pain

systemic lupus erythematosus characteristic

Polyarticular gout
Reiter’s disease/reactive arthritis

Tophaceous gout
conjunctivitis.
erosions are quite different from
urethritis or colitis
those of rheumatoid arthritis

lumbosacral spine are the


the diag- nosis is clinched by
main targets
identifying typical birefringent urate
crystals

Sarcoid disease

symmetrical small-joint
polyarthritis

large joint s

knee or ankle

Erythema nodo- sum and hilar


lymphadenopathy on chest X-ray are
clues to the diagnosis.

Sarcoid disease

Acute sarcoidosi Chronic sarcoidosis

subsides spontaneously within


granulomatous infiltration of lungs,
6 months
bone, synovium

X-ray features

punched-out ‘cysts’ and cortical


erosions in the bones of the hands
and feet

ESR and serum angiotensin


converting enzyme (SACE) RAISED

typical noncaseating granulo- mas.

(NSAIDs)

Treatment

corticosteroids

Lyme disease Viral arthritis

flu-like symp- toms


transient polyarthralgia

Treatment with doxycycline


typically parvovirus B19

spreads to multiple organs

flu-like illness
asymmetrical inflammatory
polyarthritis
early morning stiffness,

larger joints

absence of ‘rheumatoid’ X-ray


features and subcutaneous nodules

Polyarticular osteoarthritis (OA)

involves the finger joints,

whereas RA affects the proximal


OA always involves the distal joints of the hand and predominantly
interphalangeal joints erosive features

causes a nodular arthritis

radiologically obvious
osteophytes,
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Polyarticular osteoarthritis (OA)
Page 12 (row 8, column 2)
involves the finger joints,

whereas RA affects the proximal


OA always involves the distal joints of the hand and predominantly
interphalangeal joints erosive features

causes a nodular arthritis

radiologically obvious
osteophytes,

confusion may arise

later stages, is associated with loss


of articular cartilage and secondary
OA.

Rheumatoid arthritis –
differential diagnosis

mainly the proximal joints were affected


(rheumatoid arthritis); the distal joints were the worst (Heberden’s were asymmetrical nodular swellings around the
osteoarthritis) joints (gouty tophi).

Treatment

no cure for rheumatoid arthritis

multidisciplinary approach

include a rheumatologist, orthopae-


dic surgeon, physiotherapist,
occupational therapist,

Poor prognosis

female sex,

multiple joint involvement

high ESR

CRP,

positive RF

anti-CCP,

younger age,

high BMI

the presence of erosions


at diagnosis.

smoking

aimed at controlling inflamma- tion


as rapidly as possible.

corticosteroids for their rapid onset


(initially oral doses of 30 mg of
prednisolone o

Steroids should be rapidly tapered


to prevent significant side effects.

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