Metabolic bone diseases, and infection

Question 1

what is Paget’s disease (osteitis deformans)?

Answer 1

disorder of bone turnover characterised by enlargement and thickening of bone but internal architecture of bone abnormal and bone unusually brittle.
alternating phases of rapid bone resorption (vascular stage) and formation, so cortices thickened but irregular and may appear more porous than usual or more sclerotic.
in the late stage, bone is increasingly sclerotic and brittle

Question 2

characteristic cellular change in paget’s disease?

Answer 2

marked increase in osteoclastic and osteoblastic activity

Question 3

in which people does paget’s disease of bone present?

Answer 3

those over 50 years

men and women equally affected

Question 4

common sites affected by paget’s disease?

Answer 4

pelvis
tibia
femur
skull
spine
clavicle

Question 5

presentation of paget’s disease?

Answer 5

often asymptomatic and incidental finding on X-ray or isolated rasied ALP on bloods
if pain, it is dull and constant
lower limb deformities-limb looks bent and feels thick, skin warm
appearance of short neck due to skull base flattening
considerable kyphosis
cranial nerve compression-impaired vision, facial palsy, trigeminal neuralgia or deafness
vertebral thickening may cause spinal cord or nerve root compression

Question 6

x-ray appearance of paget’s disease?

Answer 6

localised areas of osteolysis in resoprtive phase
later, bone thick and sclerotic with coarse trabeculation
diagnosis may only be made when pt presents with a pathological fracture

Question 7

results of investigations in paget’s disease?

Answer 7

bloods: bone profile-raised ALP, Ca2+ and PO43- levels usually normal, ALP correlates with activity and extent of disease
24hr urinary excretion of pyridinoline cross-links good indicator of disease activity and bone resorption

Question 8

complications of paget’s disease of bone?

Answer 8

pathological fractures
nerve compression and spinal stenosis
bone sarcoma-around 1% frequency of malignant transformation to osteosarcoma which presents in the elderly, always suspect if known affected site becomes more painful, swollen or tender
high output cardiac failure-due to prolonged, increased bone blood flow
hypercalcaemia-in pts immobilised for long periods

Question 9

symptoms of hypercalcaemia?

Answer 9

abdominal pain
depression
renal stones-renal colic
nausea
anorexia
fatigue
muscle weakness
polyuria
joint symptoms-due to chondrocalcinosis

Question 10

tment of paget’s disease?

Answer 10

calcitonin (normally secreted by parafollicular cells of thyroid), reduces bone resorption by decreasing activity and number of osteoclasts, maintenance injections once or twice wkly

bisphosphonates-osteoclast apoptosis, bind to hydroxyapatite crystals inhibiting their rate of growth and dissolution
operative tment for pathological fracture

Question 11

usual causative organism in acute haematogenous osteomyelitis?

Answer 11

S.aureus
less often strep pyogenes or strep pneumoniae
H.influenzae prev common in children but now much less due to type B vaccination
sickle cell anaemia pts prone to salmonella typhi infection-*sickle cell crisis may present similarly to acute osteomyelitis, espec. where salmonella typhi endemic should treat pts with Abx until infection excluded-3rd gen cephalosporin e.g. ceftriaxone, or fluroquinolone e.g. ciprofloxacin

Question 12

where do bacterial organisms causing acute osteomyelitis in children ususally settle?

Answer 12

vascular metaphysis of a long bone, usually proximal or distal end of femur
or proximal end of tibia
=area of lowered oxygen tension
in infants where still anastamoses between metaphyseal and epiphyseal vessels, infection can reach epiphysis

Question 13

pathological processes in acute osteomyelitis?

Answer 13

classical changes are those seen in children: inflammation to suppuration to necrosis to new bone growth to resolution or intractable chronicity
inflam: intraosseous pressure rises causing pain and b.flow obstruction
by 2nd day, pus in medulla, travels to surface via volkmann canals to form subperiosteal abscess, thens preads along shaft to renter bone at another level or burst out onto surface, often travels into epiphysis in infants, then into joint, pus may also discharge into joint in older children where metaphysis is intracapsualr e.g. hip, shoulder or elbow
necrosis by end of 1st wk due to rising intraosseous pressure, vasc stasis, infective thrombosis and periosteal stripping
new bone forms from deep layer of periosteum, thickens to form casing (involucrum) enclosing infected tissue and sequestra, if persisting infection with pus discharge in this casing and track by sinuses to skin surface then established as chronic osteomyelitis
progress halted with release of intraosseus pressure early on and infection controlled, bone can thicken with increase bone density around infection and periosteal reaction

Question 14

presentation of acute osteomyelitis in children?

Answer 14

most commonly children over 4 yrs affected
present with severe pain, malaise and fever
sometimes hx of preceding skin lesion, injury or sore throat
limb held still, acute fingertip tenderness near one of larger joints, restricted joint movement (pseudoparalysis)
local erythema, swelling, warmth=later signs indicating pus

infants and newborn: baby failing to thrive, drowsy but irritable
hx of birth difficulties or umbilical artery catheterisation, note can be infection from infected umbilical cord
metaphyseal tenderness, resistance to joint movement, multiple infection sites common

Question 15

acute osteomyelitis presentation in adults?

Answer 15

spine=commonest site of haematogenous infection
backache and mild fever, possible following urological procedure e.g. urethral catheter
often diagnosis needs to be confirmed with fine-needle aspiration and bacteriological culture

Question 16

investigation results in acute osteomyelitis?

Answer 16

FBC: rasied WCC
CRP-good for monitoring tment response and ESR raised
+ve blood cultures
pus aspiration from subperisoteal abscess or adjacent joint
aspirate smear examined for cells and organisms, and sent for bacteriological examination-microscopy and culture, and Abx sensitvity
plain X-rays-no abnormality for 1st 10 days, by ne dof 2nd wk may be signs of rarefraction of metaphysis and periosteal new bone formation, bone may become increasingly ragged later on, sclerosis and thickening of cortex with healing
radio-isotope scan-increased activity-non-specific sign f inflamamtion
MRI-early changes, distinguish bone from soft tissue infection, and can detect focus of infection in axial skeletion

Question 17

how can cellulitis be distinguished from acute osteomyelitis?

Answer 17

cellulitis-widespread erythema and lymphangitis

MRI will help distinguish bone infection from soft tissue infection

Question 18

acute osteomyelitis tment in children?

Answer 18

empirical Abx must be given, don’t await results of blood cultures
neonates and infants up to 6 mnths: flucloxacillin plus 3rd gen cephalosporin e.. cefotaxime, targeting pen resistant s.aureus, group b strep and gram -ve
6mnths to 6 yrs: must cover h.influenzae, IV flucloxacillin and cefotaxime/cefuroxime-also used in elderly and prev. unfit adults where gram -ve infection risk greater
older children and prev. fit adults: IV fluclox and fusidic acid, against s.aureus, 2nd or 3rd gen ceph if allergic to penicillin e.g. cefuroxime (2nd), ceftriaxone (3rd)

can adjust choice after results of blood cultures
give IV, CRP usually normalised after 2-4 wks, then continue Abx PO for at least another 3-6 wks, should track serum Abx levels now

continuous bed rest
splint affected limb
adequate analgesia
if clinical features do not improve within 36hrs of starting tment, or even earlier if signs of deep pus-swelling, fluctuation, oedema, and if pus aspirated, abscess needs drainage by open surgery with GA
encourage movement once infection signs gone, aloow walking with aid of crutches, full WB usually possible after 3-4wks
OP F/U to ensure no infection recurrence

Question 19

complications of acute osteomyelitis in children?

Answer 19

spread-septic arthritis, or other bones-metastatic osteomyelitis
pathological fracture
growth disturbance if physis damaged
persistent infection-chronic osteomyelitis

Question 20

presentation of subacute osteomyelitis?

Answer 20

relatively mild form e.g. less virulent organism
pt usually child or adolescent with pain near 1 of large joints for several weeks
commonly affects distal femur, or prox or distal tibia
x-ray: small oval cavity surrounded by sclerotic bone (Brodie’s abscess)
radio-isotope scan-increased activity

open biopsy may be required if diagnosis in doubt as small abscess can easily be mistaken for osteoid osteoma, and larger lesion for a bone tumour

Question 21

tment subacute osteomyelitis?

Answer 21

immobilisation
Abx-IV flucloxacillin and fusidic acid 4 or 5 days, then PO for another 6wks
open curettage followed by further Abx if x-ray shows no healing

Question 22

most common cause of osteomyelitis in adults?

Answer 22

post-traumatic e.g. open fracture

usually S.aureus

Question 23

clinical features of chronic osteomyelitis?

Answer 23

following acute bone infection, pt presents with recurrent bouts of pain, erythema and tenderness ata ffected site
healed and discharging sinuses
x-ray: densely sclerotic bone, cortical thickening and bone rarefaction
sinogram-localise focus of active infection
bone scans-hidden foci of inflammatory activity
CT and MRI for planning operative tment, show reactive oedema and extent of bone destruction, hidden abscesses and sequestra

Question 24

tment of chronic osteomyelitis?

Answer 24

rest
sinus dressing
incision and drainage of acute abscess
Abx e.g. fusidic acid and cephalosporins, for 4-6wks, before considering operative tment, most Abx fail to penetrate barrier of fibrous tissue and sclerotic bone
operative tment: external fixation so that internal fixation devices can be removed e.g. if post-traumatic infection
rpt debridement
Abx impregnanted beads, bone grafts, muscle flaps with split skin grafts to deal with resulting ‘dead space’

Question 25

presentation of acute suppurative arthritis (pyogenic arthritis/septic arthritis)?

Answer 25

usually S.aureus infection
acute single large joint pain and swelling, commonly hip in children and knee in adults
erythema, swelling, joint held flexed
all movements grossly restricted and often completely abolished by pain and spasm
tachycardia and swinging pyrexia
WBC raised, and blood cultures may be positivie

infants=septicaemia emphasis-irritable baby refusing to feed, rapid pulse, fever.

X-rays: soft-tissue swelling, joint space widening due to effusion, periarticular osteoporosis, joint space narrowing later in cartilage attack

Question 26

confirmation of pyogenic arthritis diagnosis?

Answer 26

joint aspiration and microbiological fluid investigation
+ve blood cultures
bloods: raised WCC, CRP and ESR

Question 27

pyogenic arthritis complications?

Answer 27

dislocation
epiphyseal destruction, espec. in infants where largely cartilaginous
growth disturbance with physeal damage
ankylosis (stiffness) if articular cartilage eroded

Question 28

tment of pyogenic arthritis?

Answer 28

aspirate joint and examine fluid
IV flucloxacillin if gram positive, cephalosporin can cover both gram positive and negative, start as soon as aspiration has been done, IV for several wks, then PO for further 2 or 3 weeks
rest joint on a splint or in a widely split plaster, if hip, hold abducted and 30 degrees flexed
under anaesthesia, pus drained and joint washed out
gentle and gradually increasing movements encouraged once general condition good and joint no longer inflamed
but if articular cartilage been destroyed, keep joint immobile in optimum position while ankylosis awaited.