Osteomyelitis

OSTEOMYELITIS Zameer Ali PG orthopaedics St stephens hospital

The term osteomyelitis literally means inflammation of bone and its marrow regardless of whether it is due to pyogenic organisms ,tuberculosis ,syphylis ,virus, fungus,or presence of foreign body

However universal acceptance of term is applied only to infection by pyogenic organisms organisms less commonly due to granulamatous inflammation of tuberculosis

Osteomyelitis is an acute or chronic inflammatory process of the bone and its structures secondary to infection with pyogenic organisms.

General Principles Bone and joint infections remain a formidable challenge to the orthopaedic surgeon The high success rate obtained with antibiotics in other bacterial disease has not been obtained in bone and joint infection

Osteomyelitis occurs when an adequate number of a sufficient virulent organisms overcome the hosts natural defenses

Etiology Multifactorial Patient dependant factors Surgeon dependant factors

Patient dependant factors Nutritional Status Malnourishment adversely affects Humoral and cell mediated immunity

Patient dependant factors Impairs neutrophil chemotaxis Diminishes bacterial clearance Depresses neutrophil bactricidal function and delivey of inflammatory components to foci

Patient dependant factors Malnourishment identified as Albumin level <3.4mg/dl ALC (absolute lymphocyte count) <1500 Basal energy requirements increase by 30% to 55% in infected patients Fever of 1 degree increases BMR by 13%

Patient dependant factors Jensen et al ( JBJS 64 A:1263,1982) Recommended nutritional support before elective surgery in Patients with weight losses >10 pounds Serum albumin<3.4mg/dl ALC<1500

Immunological status Body's main defense mechanism are Neutrophillic response Humoral immunity Cell mediated immunity Reticuloendothelial cells

A defeciency in production or function of these predispose to infection

Deficiencies in immune system can be Congenital Acquired

Congenital Chronic granulamatous disease Hemophilia Hypogammaglobbulinemia Sickle Cell haemoglobinopathy Terminal Complement Deficiency Leukocyte adhesion Deficiency

Acquired Diabetes Mellitus Haematological Malignancy HIV Pharmacological immunosuppresion Organ transplantation Collagen vascular disease Uraemia Malnutrition Radiation therapy

Abnormal Neutrophils and cell mediated immunity implicated in infections caused by Encapsulated bacteria. Increased incidence of pseudomonas infection in heroin addicts

Increased incidence of Salmonella and Pneumococccus infections in patients with sickle cell anemia Neutrophillic count<5500 predispose to Staph , Candida,Aspergillus,gram neg Bacilli

Patients with hypogammaglobbulinemia are at a risk of infection with Streptoccus Haemophillus Neisseria

Secondary cell mediated defeciency can cause infection due to Fungal and mycobacterial infections Herpes virus Pneumocystis carnii

Surgeon dependant factors Skin preparation Operating room environment Prophylatic antibiotic therapy

Diagnosis May be obvious or obscure Characteristic features may or may not be present Pain is probably the most common symptom Fever, chills , nausea ,vomiting may also be present

Laboratory studies CBC: The WBC count is usually elevated A leftward shift is common with increased polymorphonuclear leukocyte counts The C-reactive protein level usually is elevated and nonspecific; it may be more useful than the erythrocyte sedimentation rate.

It will show elevation earlier than the erythrocyte sedimentation rate (ESR). The erythrocyte sedimentation rate usually is elevated (90%); this finding is clinically nonspecific.

With osteomyelitis, culture or aspiration findings in samples of the infected site in osteomyelitis are normal in 25% of cases. Blood culture results are positive in only 50% of patients with hematogenous osteomyelitis

Imaging studies Radiography Negative Films are ususally negative within first 10 days thereafter a localized area of bone destruction is observed in metaphysis surrounded by wide area of decalcified bone

Later within next few weeks the periosteal shadow is elevated a t same level and multiple laminations of bone deposition parellel with shaft are seen Eventually more spongy trabeculae are destroyed given moth eaten appearance that extend for a variable distance in medulla towards diaphysis

The external and internal surface of cortex may display multiple scalloped erosions If a segment of necrotic bone is present it retains its original architecture and appears denser than surrounding decalcified bone

te Radiographic evidence of acute osteomyelitis first is suggested by overlying soft-tissue edema at 3-5 days after infection. Bony changes are not evident for 14-21 days and initially manifest as periosteal elevation followed by cortical or medullary lucencies. By 28 days, 90% of patients demonstrate some abnormality.

Approximately 40-50% focal bone loss is necessary to cause detectable lucency on plain films

Radiograph reveals a lytic lesion and periosteal reaction of the posterior cortex.

MRI The MRI is effective in the early detection and surgical localization of osteomyelitis. Studies have shown its superiority compared with plain radiography, CT, and radionuclide scanning in selected anatomic locations. Sensitivity ranges from 90-100%.

MRI of the lateral aspect of distal femur.

Radionuclide bone scanning Bone scan with technetium 99m is probably the initial imaging modality of choice. In special circumstances, additional information can be obtained from further scanning with leukocytes labeled with gallium 67 and/or indium 111.

Fig. 16-6 Bone scan showing increased uptake in area of osteomyelitis.

CT scanning CT scans can depict abnormal calcification, ossification, and intracortical abnormalities. It probably is most useful in the evaluation of spinal vertebral lesions. It may also be superior in areas with complex anatomy: pelvis, sternum, and calcaneus.

Ultrasonography This simple and inexpensive technique has shown promise, particularly in children with acute osteomyelitis. Ultrasonography may demonstrate changes as early as 1-2 days after onset of symptoms.

Abnormalities include soft tissue abscess or fluid collection and periosteal elevation. Ultrasonography allows for ultrasound-guided aspiration. It does not allow for evaluation of bone cortex.

Culture Studies Every effort to be made to take culture before antibiotic therapy is started Deep culture is more reliable

Classification of Osteomyelitis Duration of infection Acute ( <2 WEEKS) Subacute (2-3 WEEKS) Chronic ( >3 WEEKS)

However, the time limits defining these classes are somewhat arbitrary.

Mechanism of infection Exogenous Haematogenous

The mechanism of infection can be exogenous or hematogenous . Exogenous osteomyelitis is caused by open fractures, surgery (iatrogenic), or contiguous spread from infected local tissue. The hematogenous form results from bacteremia.

Acute Haematogenous osteomyelitis Acute hematogenous osteomyelitis is the most common type of bone infection and usually is seen in children. It is more common in males in all age groups affected. Acute hematogenous osteomyelitis is caused by a bacteremia, which is a common occurrence in childhood.

The causes of bacteremia are many. Bacteriological seeding of bone generally is associated with other factors such as localized trauma, chronic illness, malnutrition, or an inadequate immune system. In many cases the exact cause of the disease cannot be identified

Acute Haematogenous osteomyelitis Most common type of bone infection Usually seen in children More common in males in all groups 85% of patients with hematogenous osteomyelitis are younger than 17 years, accounting for 20% percent of the total cases of osteomyelitis

pathophysiology In children the infection generally involves the metaphyses of rapidly growing long bones. Bacterial seeding of nutrient artery> inflammatory reaction >>>>cause local ischemic necrosis of bone >>>> subsequent abscess formation.

As the abscess enlarges>> intramedullary pressure increases >>> cortical ischemia, which may allow purulent material to escape through the cortex into the subperiosteal space. >>subperiosteal abscess then develops

Metaphysis of long bone is the most common site of infection

Acute haemategenous osteomyelitis is caused by a bacteraemia , which is a common occurrence in childhood

Bacteriological seeding of bone is associates with other factors such as localized trauma chronic illness malnutrition inadequate immune response

Bacterial seeding leads to inflammotory reaction which can cause Ischaemia Necrosis of bone Subsequent abscess formation

Age distribution bimodal Children under 2 years Children between 8-12 years of age

Pathological differences based on age In infants , Small capillaries cross the epiphyseal growth plate and permit extension of infection into the epiphysis and joint space The cortical bone of neonates and infants is thin and loose, consisting predominantly of woven bone, which permits escape of the pressure caused by infection but promotes rapid spread of the infection directly into the subperiosteal region.

A large sequestrum is not produced because extensive infarction of the cortex does not occur; however, a large subperiosteal abscess can form.

In children older than 1 year infection presumably starts in the metaphyseal sinusoidal veins and is contained by the growth plate. The joint is spared unless the metaphysis is intracapsular.

The infection spreads laterally where it breaks through the cortex and lifts the loose periosteum to form a subperiosteal abscess

If infection spreads to diaphysis the endostesl blood supply may be jeopardised and can result in extensive sequetrum and chronic osteomyelitis if not treated properly

In adults The growth plate has resorbed, and the infection may again extend to the joint spaces

adults The periosteum is firmly attached to the underlying bone; as a result, subperiosteal abscess formation and intense periosteal proliferation are observed less frequently. Vertebral bodies are affected commonly.

Commonly isolated organisms Infants (<1 y ) Group B Streptococcus Staphylococcus aureus Escherichia coli

Children (aged 1-16 y ) S aureus Streptococcus pyogenes Haemophilus influenzae

Adults (>16 y) S aureus Coagulase-negative Staphylococcus species Gram-negative bacilli (vert body infections) P aeruginosa ( iv drug abusers ) Serratia marcescens

Diagnosis In hematogenous osteomyelitis, local symptoms referable to bones are more frequently absent in neonates than in children. In adults, soft tissue findings may be more prominent than bony involvement.

in infants local findings can include decreased motion of a limb and edema Infact child may lie still without moving limb (pseudoparalysis) joint effusion adjacent to the bone infection (present in 60-70% of cases).

Children with hematogenous osteomyelitis typically have the following systemic symptoms Abrupt fever Irritability Lethargy Refusal to use the affected limb

Local signs of inflammation present for 2 weeks or less Signs of systemic toxicity other than minimal temperature elevation are absent in 50% of children with osteomyelitis.

In adults Acute clinical presentations include of fever, chills, swelling, and erythema over the involved bones Vertebral osteomyelitis is usually hematogenous in origin but may be secondary to trauma

A preceding history of urinary tract infection or injection drug use often is present. Other sources of infection include skin and soft tissue, respiratory tract, infected intravascular device site, endocarditis, dental infection, or unknown sources

Evaluation of acute haemategenous osteomyelitis History and physical examination WBC,ESR,CRP Blood cultures(+50% cases) Plain roentgenograms Technetium 99m bone scan +/- MRI Aspiration of suspected abscess

Treatment Surgery and antibiotic treatment are complimentary to each other Choice of antibiotic is based on highest Bacteriocidal activity Least toxicity Lowest cost

General measures IV fluids Appropriate analgesia Comfortable positioning of limb

treatment Nades principles (JBJS 65B :109,1983) Nades proposed 5 principles for treatment of acute hematogenous osteomyeliyis 1. Apppriate antibiotic will be effective before pus formation 2. Antibiotics will not sterilize avascular tissues or abscesses and such area require surgical removal

3. If such removal is effective , antibiotics should prevent their reformation therefore primary closure should be safe

4. Surgery should not damage already ischaemic bone and soft tissue 5. . Antibiotics should be continued after surgery

If no appreciable clinical improvement is noted with antiobiotic within 24 to 48 hours occult abscess must be sought and surgical drainage considered

Two main indications of surgery in acute hematogenous osteomyelitis are 1The presence of abscess requiring drainage 2 And failure of patient to improve despite appropraite intavenous antiobiotics

The patient should be treated for 4-6 weeks with appropriate antimicrobial therapy, dating from the initiation of therapy or following the last major debridement surgery

With hematogenous osteomyelitis (newborn to adult), Primary treatment is a combination of penicillinase-resistant synthetic penicillin and a third-generation cephalosporin. Alternate therapy is vancomycin or clindamycin and a third-generation cephalosporin.

In addition to these above-mentioned antibacterials, ciprofloxacin and rifampin may be an appropriate combination therapy for adult patients. If there is evidence of infection with gram-negative bacilli, include a third-generation cephalosporin.

In patients with sickle cell anemia and osteomyelitis, the primary bacterial causes are S aureus and Salmonellae species the primary choice for treatment is a fluoroquinolone antibiotic (not in children). A third-generation cephalosporin (eg, ceftriaxone) is an alternative choice

Salmonella osteomyelitis is relatively rare 1 several bones are involved 2 symmetrical involvement of bones

3 severe osteomyelitis 4 spine may be involved 5 sickle cell anaemia present 6 Stool culture positive

Salmonella osteomyelitis tends to be diaphyseal rather than metaphyseal

Objectives of surgery- Drain any abscess cavity Remove all non viable tissue

When a sub periosteal abscess is found in children several holes should be drilled through the cortex to the medullary canal If pus is found a small cortical window is removed The intramedullary pus is evacutated and necrotic tissue debrided

Skin is closed over drains Limb is splinted Once wound is healed protected weight bearing is begun

Limb protected for many weeks to prevent pathological fracture Patient is followed for one year with periodic roentgenograms

Differential diagnosis 1 Acute septic arthritis joint movements are more painfull and severely restricted 2 scurvy features of pseudoparalysis ,bleeding gums are features 3 cellulitis it is difficult to differentiate however it has no limits ,no pus ,no fluctuation , no edge

r 4 ewings sarcoma destruction is diffuse Constitutinal symptoma are less severe and tumor responds to radiotherapy 5 rheumatic fever pain is confined to joints and responds to ACTH AND STEROIDS

Erethema nodosum ,, sickle cell anaemia

Complications Seen in 5 % of cases 1 septicaemia 2 pyaemia 3 septic arthritis 4 chronic osteomyelitis 5 pathologic fracture

Pathologic fracture after destruction of cortical bone

6 Recurrence rate 7 mortality rate is less than 2 percent

Osteomyelitis

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