Mechanism

Hematogenous Direct spread

Adjacent infection of surrounding tissue

Exogenous
Penetrating trauma or bone is broken and is

protruding through the skin

Osteomyelitis

Acute Subacute Chronic

Acute osteomyelitis is an inflammation of bone marrow. It almost invariably occur in children. Adult are affected may be because of compromised host resistance due to debilitation, disease or drug.(e.g: immuno suppressive therapy). The causal organism is usually stayphylococcus aureus, less often streptococuss pyogenes or streptococcuss pneumoniae.

Clinical Features

The patient usually child, present with:

Pain Malaise Fever Toxaemie (in neglected cases) Sometimes a history of preceding skin lesion, an injury and sore throat.

The limb is held still and there is acute fingertip tenderness near one of the larger joint. Later signs and signify the presence of pus are:

Local redness Swelling Warmth Oedema

Clinical Features- In Infants

In infants, and especially in the newborn,

The constitutional disturbance can be

misleadingly mild. The baby simply fails to thrive and is drowsy but irritable.

Suspicion should be aroused by:

A history of birth difficulties Umbilical artery catheterization.

Metaphyseal tenderness Resistance to joint movement.

Clinical Features- In Adult

In adult, the commonest site of haematogenous infection is the spine. Suspicious features are:

Backache A mild fever

It takes weeks for x-ray signs to appear and the diagnosis needs to be confirmed by :
Fine-needle aspiration Bacteriological culture

Investigation
There is usually a leucocytosis and the blood culture may be positive. The clinical diagnosis can be confirm by :

Aspirate pus from the subperitoneal abscess of the

adjacent joint.
If no pus is found:
A smear of the aspirate is examined

immediately for cell and organism. A sample also send for:

Bacteriological examination Tests for sensitivity to antibiotic

Complication

Spread
Infection may spread to: joint (septic arthritis) Other bones (metastatic osteomyelitis)

Growth disturbance
If the physis is damage, there may later be: Shortening Deformity

Persistence infection
Treatment must be prompt and effective. If not may lead to chronic osteomyelitis.

Treatment
1)

Antibiotics
a) Older children and previously fit adults

who probably have a staphylococcal infection are started with:

intravenous flucloxacillin fusidic acid.

If there is clinical and laboratory evidence of improvement then followed by oral antibiotic. If methicilin-resistance staphylococcus aureus(MRSA) appears, vancomycin is used.

Treatment
1)

Antibiotics
b) Children under 4 years have higher incidence of heamophilus infection. If the Gram negative organism are seen in the smear, it is advisable to start with one of the 3rd generation cephalosporins. c) Heroin addict and immuno-compromised patients often have unusual infection and may need more specific antibiotic treatment.

Treatment
2) Analgesics Osteomyelitis is extremely painful Adequate and repeated analgesics must be given. 3) Splintage Complete bed-rest is essential. A splint is desirable but should not conceal the affected area.

Treatment
4) Drainage If antibiotic are given early, drainage may not be necessary. If a subperiosteal abscess detected, pyrexia and local tenderness persist for more than 24 hours after treatment with adequate antibiotic, the pus should be let out.
5)Follow-up Once the infection has subsided, movements are encouraged: however the patient has to use crutches for a few weeks. Out patient follow-up is important, to ensure that there is no recurrence of infection.

Osteomyelitis may present in a relatively mild form, presumably because the organism is less virulent or the patient more resistance. The distal femur and proximal and distal tibia are the common sites. The patient is usually a child or adolescent who had pain near one of the large joints for several weeks. The typical x-ray picture is small, oval cavity surrounding by sclerotic bone the classic Brodies abcess- but sometimes the lesion is more diffuse. A small abscess is easily mistaken for an osteoid osteoma and the diagnosis may be made only when the lesion is explored.

Chronic Osteomyelitis used to be common consequence to acute haematogenous osteomyelitis. Nowadays it more frequently follows an open fracture or operation. The common organism are Staph. aureus, Escherichia coli, Staph. Pyogenes, Proteus and Pseudomonas. In the presence of surgical implant, Staph. epidermidis is the commonest pathogen.

Clinical Features

Following acute bone infection, the patient returns with recurrent:

Pain Redness Tenderness at affected site.

Classic sign are healed and discharging sinuses. X-ray features:

A bone rarefaction surrounded by dense

sclerosis and cortical thickening :

Within this area of bone there may be an obvious

sequestrum.

Treatment

Treatment depends on frequency of relapsing flareups; if seldom, it can be conservative. A sinus may be painless and need a dressing simply to protect the clothing. Antibiotic are often use, though most fail to penetrate the barrier of fibrous tissue plus bone slerosis. Sequestrectomy should be performed only if the sequestrum is radiological visible and surgically accessible. In refractory or frequently recurring cases, it may be possible to excise the infected and/or devitalized segment of bone and then close the gap by the ilizarov method of transporting a viable segment from the remaining diaphysis.

1. Post-traumatic Osteomyelitis An infected open fracture is the usual cause of osteomyelitis. The most common organism responsible is Staphylococcus Aureus.

Clinical features: - fever - pain and swelling over fracture site - wound is inflamed - seropurulent discharge Investigations

- Blood tests showing leucocytosis and increased

sedimentation rate. - Culture

Treatment: - Debridement of open fractures - Drainage - Regular wound dressing

2. Post-operative Osteomyelitis 3-5% incidence rate Predisposing factors: - Debility - Chronic disease e.g. rheumatoid arthritis - Previous infection - Corticosteroid therapy - Hematoma formations - Tight wound dressings/plasters

The risk for post-operative osteomyelitis is increased with the presence of foreign material (metal, plastic, cement) Prevention: - Prophylactic antibiotics - Clean surgical environment Treatment is the same as post-traumatic infections.

Acute Septic Arthritis Route of Infection

direct invasion

penetrating wound intra articular injuries arthroscopy

eruption of bone abscess haematogenous

Acute Septic Arthritis Organism

staphylococus aureus haemophilus influenzae

streptococcus pyogenes
escherishae coli

Acute Septic Arthritis Pathology

acute synovitis with purulent joint effusion articular cartilage attacked by bacterial toxin and cellular enzyme complete destruction of the articular cartilage.

Acute Septic Arthritis Sequelae

complete recovery
partial loss of the articular cartilage fibrous or bony ankylosis

Sign and symptom

Fever Chills Swelling Redness Stiffness Warmth Diffuse tenderness

Acute Septic Arthritis Neonate

irritability resistant to movement

Acute Septic Arthritis Child

Acute pain in single large joint

reluctant to move the joint increase temp. and pulse increase tenderness

Acute Septic Arthritis Adult

often involves superficial joint (knee, ankle, wrist)

investigation

fbc, wbc, esr crp ,blood culture x ray ultrasound aspiration

Acute Septic Arthritis Differential Diagnosis

acute osteomyelitis trauma irritable joint hemophilia rheumatic fever gout

Acute Septic Arthritis Treatment

antibiotics - flucloxacillin, cephalosporin

Splintage rested the joint. Splint or split plaster surgical drainage

SEPTIC BURSITIS
Bursae are the satellite structures that form to protect tissues from bony prominences. The superficial bursae, including the: olecranon, prepatella, infrapatella, and bursae over the first metatarsophalangeal bunions, are more likely to become infected than are the deep bursae (subacromial, trochanteric, and iliopsoas bursae). The majority of cases occur in men, and antecedent trauma to the skin is frequent.

 Septic

bursitis of superficial bursae due to:

direct inoculation through the overlying skin (most common)

overlying cellulitis.

Deep

septic bursitis are due to contiguous spread from adjacent infected joints or hematogenous seeding. risk factors for septic bursitis include:

Predisposing

trauma to the skin, as may occur in plumbers, athletes, and

patients with chronic obstructive pulmonary disease (COPD) who frequently lean on the elbows; pre- or infrapatellar septic bursitis occurs in housecleaners, gardeners, and carpet layers.
At

least one third of patients with septic bursitis have an underlying comorbid illness such as diabetes mellitus, rheumatoid arthritis, gout, COPD, or alcoholism.

CLINICAL MANIFESTATION fever and erythema and warmth of the overlying skin; there may be swelling of the bursae. intact range of motion of the joints, which may be limited only at the extremes of flexion. Acute phase reactants such as C-reactive protein, the sedimentation rate, and the white blood cell count (WBC) may be elevated.

DIAGNOSIS AND DIFFERENTIAL DIAGNOSES Radiography Aspiration of bursal fluid. Ultrasound or computed tomography (CT) leukocyte count Bacterial culture and in vitro susceptibilities must be obtained; a Gram stain may be obtained, although its sensitivity may be as low as 15%. The presence of crystals does not exclude the possibility of septic bursitis.

 Staphylococcus aureus is the most common cause of septic bursitis, present in more than 80% of culture-proved cases, followed by -hemolytic streptococci. Chronic bursitis may be associated with systemic infections due to Brucella abortus, atypical mycobacteria, or Mycobacterium tuberculosis, as well as fungi

TREATMENT Treatment of septic bursitis depends on the underlying organism, in most cases, S. aureus. Most patients can be treated as outpatients Immunocompromised patients may require hospitalization for intravenous antibiotic therapy. Initial ambulatory treatment in patients without comorbidities may consist of an oral antistaphylococcal penicillin or first-generation cephalosporin.

 If

community-acquired methicillin-resistant S. aureus (MRSA) is suspected, co-trimoxazole or minocycline may be added to one of these agents. In patients who are allergic to penicillin, oral clindamycin or linezolid or vancomycin may be used. who have severe inflammation, are septic, or are immunocompromised may require hospitalization for initiation of treatment with intravenous nafcillin, oxacillin, or cefazolin; if MRSA is suspected, intravenous vancomycin, daptomycin, or linezolid should be used.

Patients

 The duration of antimicrobial therapy is guided by the clinical response and comorbid states. It should be continued until there is no longer bursal inflammation. This may require several weeks of intravenous or oral therapy and multiple aspirations.
Failure of the septic bursitis to respond to initial antibiotic therapy mandates a second course of therapy; recurrence thereafter or inability to adequately drain the bursa with needle aspiration is an indication for surgical intervention.

PREVENTION AND PROGNOSIS Use protective padding on elbow and knee Prognosis of superficial bursitis is generally excellent. The presence of comorbid conditions is associated with more intractable and difficult disease.

TUBERCULOSIS The skeletal manifestations of the disease are seen chiefly in the spine and the large joints, but the infection may appear in any bone or any synovial or bursal sheath. Predisposing conditions include: chronic debiltating disorders, diabetes, drug abuse, prolonged corticosteroid medication, AIDS and other disorders resulting in reduced defence mechanisms.

CLINICAL MANIFESTATION History of previous infection or recent contact with tuberculosis. Complains of pain and (in a superficial joint) swelling. Attacks of fever, night sweats, lassitude and loss of weight. Muscle wasting is characteristic and synovial thickening is often striking. Regional lymph nodes may be enlarged and tender. Movements are limited in all directions.

 As

articular erosion progresses the joint becomes stiff and deformed.

tuberculosis of the spine, pain may be deceptively slight patient may not present until there is a visible abscess (usually in the groin or the lumbar region to one side of the midline) or until collapse causes a localized kyphosis. the presenting feature is weakness or instability in the lower limbs. Multiple foci of infection are sometimes found, with bone and joint lesions at different stages of development. This is more likely in people with lowered resistance.

In

Occasionally

INVESTIGATION The ESR is usually increased and there may be a relative lymphocytosis.

The Mantoux or Heaf test will be positive: these are sensitive but not specific tests; i.e. a negative Mantoux virtually excludes the diagnosis, but a positive test merely indicates tuberculous infection, now or at some time in the past.
If synovial fluid is aspirated, it may be cloudy, the protein concentration is increased and the white cell count is elevated.

 Acid-fast

bacilli are identified in synovial fluid in 10 20 per cent of cases, and cultures are positive in over half. biopsy is more reliable: sections will show the characteristic histological features and acid-fast bacilli may be identified; cultures are positive in about 80 per cent of patients who have not received antimicrobial treatment.

A synovial

DIAGNOSIS A long history of pain or swelling Involvement of only one joint Marked synovial thickening Severe muscle wasting Enlarged and matted regional lymph nodes Periarticular osteoporosis on x-ray A positive Mantoux test.

TREATMENT Rest, which had to be prolonged, uninterrupted, rigid and enforced. Combination of anti-tuberculous drugs. (Isoniazid, Rifampicin, etc. ) Operative drainage especially if theres a cold abscess.