Infection
دهشام القطان كسورAcute haematogenus osteomyelitis.
Subacute haematogenous osteomyelitis.
Chronic osteomyelitis.
Post-traumatic and post operative Osteomyelitis.
Acute suppurative arthritis.
Septic bursitis.
Tuberculosis.
Duration
acute (less than 2 weeks),
Subacute ( 2-6weeks)
chronic (>6 weeks)
acute haematogenus osteomyelitis
Inflammation of the bone and its content.
Acute pyogenic infections:
are characterized by formation of pus (concentration of dysfunction leukocytes, dead and dying bacteria and tissue debris.) which is often localized in an abscess.
A O M :
is almost invariably a disease of children.
When it is occurring in the adult there may be predisposing factor:
low resistance due to debility disease (diabetes).
Or drug(immunosupression ).
Causative organism
The causal organism is usually
Staphylococcus aureus.
streptococcus pyogenes ,strep.pnenmoniae.
In children > 4 years age:
Haemophilus influenza, E.Coli, pseudomonas aeruginosa proteus miribilis and anaerobic bacteriods fragilis.
salmonella in sickle cell infection.
Haemophilus influenza
E.Coli
Route of entry
Infection may reach the bones and joints via
1.The blood stream from the distant site (boil, tooth infection).
2.Or direct invasion from skin puncture.
SHAPE \* MERGEFORMAT
Pathology
The most common site is the metaphysis of the long bone particularly around the knee joint.
There are .peculiar arrangements of the blood vessels in that area :
the non anastomosing terminal branches of the nutrient artery twist back in hairpin loops arrangements of capillaries slow down the rate of blood flow before entering the large network of sinusoidal veins
The relative
2.vascular stasis favors bacterial colonization.
3. Presence of non organic material at the site of new bone formation from the epiphysis.
4.Low rate of phygocytosis.
5.Upper end of the long bones (metaphysis) liable for the direct trauma more frequently.
In infant
there is still a free anastomosis between metaphyseal and epiphyseal blood vessel.
In adult
haematogenous infection is more common in the vertebra than in long bones
The sequence of the pathological changes as follow
Inflammation.
Suppuration during (2,3 days).
Necrosis due to increasing (intraosseous pressure ).
vascular stasis .
infective thrombosis.
and periosteal stripping increasing compromise the blood supply, by the end of a week there is usually evidence of necrosis.
Pieces of bone may separate as SEQUESTRA which act as a foreign body causing Persistant discharge through a sinus until they removed.
Finally, it may through the skin to the surface and form a chronic sinus becoming a persistent sinus tract or cloacae.
reactive new bone formation
resolution, healing.
Location of infection
Children : primarily in the long bones
(femur, tibia, fibula, humerus).
Adults :(50-60s) - primarily vertebrae.
Neonates : have multiple bone infectious sites
Clinical feature history
The onset is rapid and attacks in short time.
The patient, usually a child or adolescent,.
complains a severe pain in a limb, and the pain is not relieved by rest.
A complete history and physical examination are required to search for possible primary foci of infection.
There may be some minor injury or insignificant infective lesion such as boil sore throat a few days earlier
The general symptoms of toxemia
①severe acute illness appear
②irritable and restless
③high fever, chill
④rapid pulse, nausea, vomiting etc
local signs
caloric, rubor, dolor, tumor.
Heat, red, pain or, swelling.
Initially, the lesion is within the meduallry cavity, there is no swelling, soft tissue is also normal.
The merely sign is deep tenderness.
Localized finger-tip tenderness is felt over or around the metaphysis.
it is necessary to palpate carefully all metaphysic areas to determine local tenderness.
pseudo paralysis .
Subperiosteal abscess formation
Edematous, red and fluctuation
indicating Subperiosteal abscess formation.
As the Subperiosteal abscess formed, signs of inflammation followed rapidly.
The extremity is held in semiflexion.
Surrounding muscles are in spasm .
Passive movement is resisted
An increase effusion in the adjacent joint proves in most cases to be a sympathetic synovitis with sterile clear fluid.
Hydroarthrosis should not be confused with septic arthritis.
It is important to remember that the metaphysis lie within the joint capsule of the hip, shoulder, ankle.
Therefore these joints can develop septic arthritis by extension of Osteomyelitis.
If the infection and septicemia proceeded the patient may have toxic shock syndrome.
Differential diagnosis
1. Cellulites
(wide spread superficial redness and lymphangitis).
2.Acute suppurative arthritis.
3.Acute rheumatism (flitting joint pain).
4.Sickle-cell crisis.
5.Gauchers disease.
Laboratory findings
The white blood cell count will show a marked leulocytosis as high as 20,000 or more.
The blood culture demonstrates the presence of bacteremia, the blood must be taken when the patient has a chill, especially when there is a spiking temperature.
Aspiration.
The point of maximal tenderness should be aspirated with a large-bore needle.
Any material aspirated should be gram stained and cultured to determine the sensitivity to antibiotics.
C - reactive protein :
is specific for the diagnosis with high reading.
x-ray findings
x-ray films are negative within 1-2 weeks,
Although carefully comparison with the opposite side may show abnormal soft tissue shadows.
It must be stressed that x-ray appearances are normal in the acute phase. There are little value in making the early diagnosis.
Radiography not appear till after 3 weeks.
decrease bone density
moth eaten.
Early diagnosis depends on followings:
1.severe acute illness, rapid onset and toxemia.
2.local severe pain and unwillingness to move limbs.
3.deep tenderness.
4.WBC count is as high as 20,000 or more .
5.Every effort must be made to obtain a bacterial culture and determinate the sensitivity to antibiotics.
Tc99m scanning.
CT or MRI.
Treatment
1.General treatment:
nutritional therapy or general supportive treatment by intaking enough caloric, protein, vitamin etc.
2. antibiotics therapy.
3.surgical treatment .
4.immobilization .
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Antibiotic therapy
The prompt administration of antibiotics is so vital that the result need not be waited, usually using wide-spectrum antibiotics, even by intravenous administration during the first 1-3 days.
The choice of antibiotics may subsequently be modified according to culture, sensitivity results, and clinical response.
The treatment should be continued for at least 2 weeks after the body temperature is down to the normal in order to minimize the possibly of reoccurrence.
Surgical treatment
As any infection in a closed space, immediate provision of drainage is of paramount importance.
This must be done at earliest possible opportunity even before signs of Subperiosteal abscess is evident.
To wait is to invite disaster.
Surgery is indicated when there has been no response to vigorous antibiotics treatment after 48-72 hours.
Surgery is achieved by making a window in the bone cortex to decompress rather than debridement.
Complication
Spread septicemia.
Persistant infection (chronic).Growth disturbance shortening or deformity.
. suppurative arthritis:
(in young children in intracapsular metaphysis.).
Chronic osteomyelitis
If any of sequestrum, abscess cavity, sinus tract or cloacae is present.
Hematogenous infection with an organism of low virulence may be present by chronic onset.
The imprisoned sequestra provoke a chronic seropurulant discharge which escapes through a sinus .
Bacteria may remain dormant for years.
Giving rise to recurrent flares of acute infection.M. O.
Stap.aureus.
E coli.
Stap .pyogenes.
Proteus and pseudomonas.
Stap epidermis.
Causes:
1.post acute infection.
2.post operative infection.
3.Compound fracture.
4.Chronic infection from the start as in T. B.
5.osteomyelitis of garea.
Pathology
1.Bone is destroyed or devitalized.
2.Cavities containing pus and pieces of dead bone (sequestrum).
3.Sinuses .
4.Involucrum.
5.Pathological fracture.
Clinical features
During the period of inactivity, no symptoms are present.
Only Skin-thin, dark, scarred, poor nourished, past sinus, an ulceration that is not easily to heal.
Muscles-wasting contracture, atrophy
Joint-stiffness
Bone-thick, sclerotic.
often contain abscess cavity
At intervals, a flare-up occurs.
The relapse is often the result of poor body condition and lower resistance.
A lighting up of infection is manifested by aching pain that is worse at night.
Examination
Locally there will be some heat.
Swelling.
Redness.
Tenderness.
Edema.
Because pus may build up in cavity, then a sinus may open and start to exudates purulent materials and small sequestrum.
The sinus closed and the infection subsided.
X-ray findings
Bone resorption=cavitation.
Sclerosis .
Sequestrum.
Pathological fracture may be present.
INVESTIGATIONS
E S R increased.
WBC may be increased.
culture from the sinus.
A sinogram may help to localize a particular focus of infection.
Bone scans are useful in revealing hidden foci and inflammatory activity.
Treatment
It is very difficult to provide a permanent cure for chronic Osteomyelitis.
most antibiotics fail to penetrate the barrier of fibrous tissue plus bone sclerosis.
Chronic osteomyelitis presents quite different problem from the acute form.
Its primary problem is surgical removal of all dead and poor vascularized tissues.
The operation must be carefully planed as it often means significant removal of bone and surrounding tissues.
Acute suppurative arthritis
local muscle flap procedures.
The most common - Staphylococcus aureus.
The hips and knees are the most frequently affected sites.
Route of infection
Hematogenous spread from an infective focus.
Spread from an adjacent focus (eruption of bone abscess).
Direct introduction by the wound.
Intra articular injection.
Arthroscopy.Causative organism:
Stap.
Haemo. Influ.
Less commonly
strep.
E-coli.
proteus.
Pathology
1. serous arthritis .
Synovium is congested, edematous and infiltrated with WBC. Synovial fluid increased in the amount with clear or slight opaque appearance and slight amount WBC
2.serofibrinous
arthritis-fibrin is excessive
3.Purulent arthritis:
Local necrosis occur.
Joint fluid full -WBC .
Opaque, thick gray or yellowish in colour.
The protolytic enzymes dissolve the articular cartilage, even erode the bone-fibrous ankylosis
Clinical features
In newborn infants:
Baby is irritable.
Refuse to eat.
Rapid pulse.
Fever.
There may be an evidence of umbilical cord infection.
In children:
acute pain in single large joint like hip.
reluctance to use the limb.
ill.
rapid pulse.
swinging fever.
skin look red.
joint swelling.
local warmth.
marked tenderness.
all movement is limited
In adults:
Often that the superficial joint is painful.
Swollen.
Inflamed.
Local warmth .
Tenderness.
Movement is restricted.
Investigations
X-ray in early cases is normal.
Ultrasound shows joint effusion.
In E-coli there may be an evidence of gas in the joint.
WBC ,E S R is increased.
Blood culture positive.
Examination of the joint aspirate. with gram stain.
Diferential diagnosis
Acute osteomyelitis.
Trauma.
Irritable joint (the child not ill, no sign of infection).
Rheumatic fever.
Haemophilic bleed.
Gout and pseudogout.
Gauchers disease.
Treatment
Essential principles in the management
The joint must be adequately drained.
Antibiotics must be given to diminish the systemic effects of sepsis.
The joint must be rested in a stable position.
Antibiotics.
The initial choice of antibiotics is based on the judgment of the most likely pathogen's.
Then according the culture and sensitivity.
Drainage.
If the diagnosis is made early and the involved joint is superficial, such as the elbow or ankle.
Aspiration should be performed .
Repeated if necessary.
The joint should be
splinted in a position of function.
Patient should be observed.
For a decrease in.
Pain.
Swelling.
Temperature.
And for improved joint mobility.
Although some infections clear up within days, antibiotic regimens often
should be continued
for 4 to 6 weeks, depending on the clinical course.
After care.
If the articular cartilage is preserved so gently and gradually increasing movement.
If the cartilage is destroyed. So the aim to keep the joint immobile while ankylosis is awaited.
Complications
Epiphyseal destruction (in neglected infants).
Growth disturbance.
( shortening or deformity).
Ankylosis (due to cartilage damage).
tuberculosis
Tuberculosis causes a granulomatous reaction which is associated with tissue necrosis and caesation.
Mycobacterium tuberculosis (human, less commonly bovine ).enter via the lung or gut or rarely through the skin.
Pathology
1.Primary complex:
the initial lesion in lung, pharynx or gut, with lymphatic spread to regional lymph node.
2.Secondary spread:
If the resistance to the original infection is low, wide spread dissemination via the blood stream, giving rise to miliary TB ,or meningitis.
3.Tertiary lesion:
Bone or joint is affected in about 5%.
there is predilection to vertebral bodies, and the large synovial joints.
In endemic area skeletal t. b. is seen mainly in children.
In non endemic area is seen in chronic debilitating disease (AIDS).
Once the bacilli have gained afoot hold, so chronic inflammatory reaction.
Then granulomatous lesion started (giant cell surrounded with necrosis and round cell at the periphery).
Spread to soft tissue lead to cold abscess.
Followed with sinus and end with secondary pyogenic infection.
These changes affected either the synovium or the bone is affected and then spread to the near by structure.
Large joint usually involved( hip ,knee, less often shoulder or ankle.
If the disease is arrested at an early stage, healing may be by resolution to normality.
If the cartilage is destroyed healing by fibrosis and incomplete ankylosis.
Clinical feature
In monoarticular atrthritis
History of previous infection.
The patient usually a child ,or young adult
Pain .
Swelling.
Fever .
Lassitude .
Loss of weight.
Night cries
(the joint splinted by muscle spasm during the day, relaxes with sleep and damage tissues are stretched).
Muscle wasting.
Movement in all direction limited.
In T B spine:
Pain may be slight.
Kyphosis (gibbus).
Occasionally the presenting feature is weakness or loss of sensibility in the lower limb.
In neglected cases patient presented with paralysis (potts paraplegia).
Radiography
Early changes:
Soft tissue swelling, Periarticular osteoporosis
Bone ends washed out.
Narrowing the articular ends.
Later on :
Erosions of the subarticular cartilage.
cystic changes appeared.
T B spondylitis may appear as localized bone erosion and collapse across an intervertebral disc space.
There may be soft tissue traces of paravertebral abscess.
E S R increased.
Relative lymphocytosis.
Mantoux test positive.
Synovial fluid aspirate (high protein).
Acid fast bacilli ,cultures is positive.
Synovial biopsy is more reliable.
Diferential diagnosis
Transient synovitis.
Monoarticular rheumatoid arthritis.
Subacute arthritis.
Heamorrhagic arthritis.
Pyogenic arthritis.
Metastatic bone disease.
Multiple myeloma.
Sarcoidosis.
Diagnosis
Long history.
Involvement only one joint.
Marked synovial thickening.
Marked muscle wasting.
Periarticular osteoporosis.
Treatment
Main stay in RX
Chemotherapy
(Rifampicin, INH for 6 months) .
in resistance to INH may call for
pyrazinamide and streptomycin, or ethambutol.
Rest.
(splintage for several months , traction).
Operation for drainage or clearance of Tuberculous abscess .
In severe deformity
Osteotomy.
Arthrodesis.
Joint replacement.