Table of Contents
- What is Osteomyelitis?
- Osteomyelitis Epidemiology
- Types of Osteomyelitis (Bone Infections)
- Routes of infection spread in Osteomyelitis (How it enters the bone)
- Etiology of Osteomyelitis (Causes of Bone Infections)
- Osteomyelitis Pathophysiology
- Differences between acute, subacute and chronic osteomyelitis
- Osteomyelitis Risk factors
- Clinical Signs and Symptoms of Osteomyelitis
- Special cases of Osteomyelitis
- Classification of Osteomyelitis
- Osteomyelitis Differential diagnosis
- Osteomyelitis Investigations to confirm Diagnosis and aid in management
- Osteomyelitis Treatment
- Osteomyelitis Complications
What is Osteomyelitis?
Infection of the bone and bone marrow is called Osteomyelitis. Bone infections are important because of their ability to cause serious complications and permanent disability. Infections of the bones are commoner in infants and toddlers than in children. The part of the bone commonly affected in Osteomyelitis is the metaphysis. The bones commonly affected are the femur and the tibia. In the femur, the lower part (distal) and in the Tibia, the upper part (proximal) is mostly affected; making osteomyelitis common around the knee which can spread the infection to the knee causing both osteomyelitis and septic arthritis of the knee. When the bone infection occurs early, it is called Acute Osteomyelitis, but when it persists or becomes recurrent, it is said to be chronic osteomyelitis. See more of Acute versus Chronic osteomyelitis below.
Acute Osteomyelitis has an incidence of 2 per 10,000 children while the incidence in Neonates is 1 per 1000 children. The annual incidence in people with sickle cell anemia is about 0.36%. The prevalence of osteomyelitis after foot puncture is about 16% and becomes increase to about 30 to 40 percent in people with diabetes.
Bones commonly affected in Osteomyelitis in descending order
- Tibia: affected in 50% of cases of bone infection
- Femur in 30%
- Fibula in 12%
- Humerus in 3%
- Ulna in 3%
- Radius in 2%
Sex: Male to female ratio is approximately 2:1, which shows that boys are more affected than girls.
Age: Generally, osteomyelitis has a bimodal age distribution; acute hematogenous osteomyelitis is mainly a disease in children whereas, direct trauma and spread by surrounding infections are commoner among adults and adolescents than in children. Spinal osteomyelitis is more common in persons older than 45 years than in younger persons.
Morbidity: Acute osteomyelitis starts as localized bone infection which then spreads to soft tissues or joints. When a bone infection is left to heal on its own, it progresses to chronic osteomyelitis with severe pain and disability that could lead to amputation of the involved extremity, generalized infection (sepsis). About 10 to 15% of patients with vertebral osteomyelitis will develop neurologic findings or have spinal cord compression. Death rates are low unless associated sepsis or an underlying serious medical condition is present.
Types of Osteomyelitis (Bone Infections)
Depends on the types of organism and therefore the type of host response; the result may be:
- Pyogenic bone infection such as pyogenic osteomyelitis or
- Granulomatous bone infection such as bone tuberculosis, yaws, syphilis and fungal infections.
- Acute Pyogenic Osteomyelitis
- Sub-acute Pyogenic Osteomyelitis
- Chronic Pyogenic Osteomyelitis
Acute Pyogenic Osteomyelitis
The organism usually reaches the bone through the blood stream hence its also called acute haematogenous osteomyelitis. Usually occurs in childhood. Adults only affected when there is low immunity as seen in generalized debility due to diseases or drugs. Casual Organisms that cause this type of Osteomyelitis include: staph aureus commonly, Gram positive organism like streptococcus pyogenes and strep pneumonia, and also Gram-negative organisms like Haemophilus influenza especially in the children less than 4 years. Other Gram-negative organisms include E. coli, pseudomonas aeruginosa, proteus mirabilis and anaerobic Bacteroides fragilis. Sickle cell patients are prone to infections by salmonella.
The blood stream is invaded usually from septic or contaminated sites such as a boil, septic tooth or ear and from skin punctures or abrasions. In the newborn it may come from infected umbilical cord. In adults the source may be a urethral catheter, an indwelling arterial line or a dirty needle and syringe. Organisms usually settle in the metaphysis commonly in the proximal tibia distal femur.
This predilection for the metaphysis has been attributed to the peculiar arrangement of the blood vessels in this area where the non-anastomosing terminal branches of nutrient artery twist back in hair pin loops before entering the large network of sinusoidal veins. This arrangement causes relative vascular stasis which is thought to favor bacterial inoculation and colonization.
In young infants where there is still free anastomosis between metaphyseal and epiphyseal blood vessels, infection easily extends to the epiphysis.
The pathological process follows a characteristic pattern of inflammation, suppuration, necrosis, reactive new bone formation and resolution or progression to chronic stage.
Inflammatory Stage of Acute Pyogenic Osteomyelitis: This is the first pathological process. There is acute inflammatory reaction with vascular congestion, exudation of fluid and infiltration by White blood cells (WBCs).The intraosseous pressure rises rapidly causing intense pain, obstruction to blood flow and intravascular thrombosis leading to some degree of ischemia.
Suppuration Stage of Acute Pyogenic Osteomyelitis: About the 2nd or 3rd day, pus forms within the bone and forces its way along the volkmann canals to the surface where it produces a subperiosteal abscess. This pus spreads along the shaft and may re-enter the bone at another level or burst into the surrounding soft tissues forming soft tissue abscess. Pus also spreads through the medullary cavity.
In infants, infection usually spreads through the physis into the epiphysis and therefore into the adjoining joint because there is still anastomosis between the metaphyseal and epiphyseal vessels. In older children, the physis has formed a barrier between the metaphysis and epiphysis and direct spread is no longer possible; the joint is only affected when the metaphysis is partly intracapsular e.g. the hip, shoulder and elbow.
Stage of Necrosis in Acute Pyogenic Osteomyelitis: Increased intraosseous pressure, vascular stasis, infective intravascular thrombosis and periosteal stripping result in compromise of blood supply to the area of the bone involved leading to bone death. This occurs about end of 1st week of infection. In infants, the growth disc may be damaged and the epiphysis may undergo avascular necrosis leading to growth disturbance later. Granulation tissue grows from the living tissue into the boundary between it and the dead bone. Thus pieces of dead bone of various sizes separate as sequestra. Macrophages and lymphocytes then move in and slowly try to remove debris and the dead bones. However, large dead bones remain encased in the bone cavity surrounded by pus inaccessible to final destruction.
Stage of New Bone Formation in Acute Pyogenic Osteomyelitis: New bone starts forming from the inner layer of the stripped periosteum. This becomes visible from the x-ray by the end of 2nd week as a thin radio-opaque line next to the parent bone but separated by a radio lucent line referred to as periosteal new bone or visible periosteum or periosteal reaction. With time, this new bone thickens to form an involucrum, which encases the infected tissues and the dead bone. Perforations develop in the involucrum referred as cloacae through which pus discharges and tracks through the soft tissues to form subcutaneous abscess or through the skin surface as sinus. By the time dead bone and involucrum are formed the infection has progressed to osteomyelitis.
Resolution or Progression to Chronic Osteomyelitis: If infection is controlled and pressure released at the suppurative stage, progression to chronic stage can be aborted and resolution then sets in. The bone around the zone of infection is at first osteoporotic due hyperemia. With healing or resolution proceeding, there is appositional new bone formation. This together with earlier periosteal new bone results in bone sclerosis and thickening in the involved area. Sometimes, remodeling may restore the bone to its normal contour or it may be permanently deformed.
Routes of infection spread in Osteomyelitis (How it enters the bone)
- The majority of bone infections are hematogenous in origin.
- Direct inoculation from trauma penetrating skin
- Contiguous spread of infection e.g. septic arthritis or abscesses
- Iatrogenic-following surgery or internal fixation by plating or hip replacement
- Osteomyelitis associated with vascular insufficiency
Etiology of Osteomyelitis (Causes of Bone Infections)
(A.) Hematogenous osteomyelitis (mostly caused by single microbial infection):
- In Infants who are less one year of age, the common organisms involved include Group B Streptococcus, Staphylococcus aureus and Escherichia coli.
- In Children (aged 1 to16 years), the common organisms include Staphylococcus aureus, Streptococcus pyogenes and Haemophilus influenza.
- In Adults of age greater 16 years, Staphylococcus aureus, Coagulase-negative Staphylococcus species, Gram-negative bacilli such as Pseudomonas aeruginosa, Serratia marcescens and Escherichia coli
(B.) In sickle cell patients, osteomyelitis is mostly caused by salmonella but may still be caused staphylococcal aureus.
(C.) After surgery commonest organism is Pseudomonas aureginosa.
(D.) In IV drug users, commonest organism is staphylococcal aureus.
Acute hematogenous osteomyelitis is characterized by an acute infection of the bone caused by the seeding of the bacteria within the bone from a remote source. This condition occurs primarily in children. The most common site is the rapidly growing and highly vascular metaphysis of growing bones. The apparent slowing or sludging of blood flow as the vessels make sharp angles at the distal metaphysis predisposes the vessels to thrombosis and the bone itself to localized necrosis and bacterial seeding. The usual course of the disease, a septic embolus becomes lodged in a small blood vessel in the metaphysis of the long bone, usually on the venous side of the capillary loop, where the circulation is most sluggish.
The environment is ideal for bacterial proliferation, for it is richly nourished. Occlusion of the vein by thrombus prevents host defenses from reaching the bacteria. The inflammatory response is initiated with hyperemia, heat, and edema and combines with the bacteria to kill the bone; eventually an abscess cavity forms with bacteria, dead bone, and cellular debris, which at the center is inaccessible to host defenses. As the abscess expands, it penetrates the cortex, through harvesian system and lifts the periosteum. This deprives the underlying cortical bone of its blood supply because the abscess occludes the endosteal vessels and the pus strips the periosteum.
The disease process stimulates the periosteum to increase bone production. The old cortical bone, which has lost its blood supply, becomes an avascular sequestrum a large piece of debris in an abscess cavity. The new bone laid down by the periosteum becomes an involucrum. The involucrum may be mechanically inadequate and pathologic fracture can occur. The infection may penetrate the periosteum and involucrum to involve the soft tissues and the skin. In untreated disease, draining sinus tracts through the skin are common. Occasionally, the host processes themselves succeed in walling off the abscess in the metaphysis, leaving a Brodie abscess.
Pathological differences based on age
Basic differences exist in the pathology of osteomyelitis in infants, children, and adults.
In infants, small capillaries cross the epiphyseal growth plate and permit extension of infection into the epiphysis and joint space leading to septic arthritis. 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.
In adults, the growth plate has resorbed, and the infection may again extend to the joint spaces, as in infants. In addition, the periosteum is firmly attached to the underlying bone; as a result, subperiosteal abscess formation and intense periosteal proliferation are observed less frequently. The infection can erode through the periosteum, forming a draining sinus tract.
Differences between acute, subacute and chronic osteomyelitis
- Acute osteomyelitis is the first to occur before Chronic osteomyelitis
- Acute osteomyelitis cannot be seen on X-ray films within the first 5 days
- Chronic osteomyelitis can be seen with an X-ray only after 10 to 14 days after infection
- Chronic osteomyelitis may lead to sepsis but Acute does not except when it progresses to Chronic
- Osteomyelitis radiology shows presence of bone in bone appearance in Chronic osteomyelitis but only soft tissue swelling and periosteal reaction in acute osteomyelitis.
- Chronic osteomyelitis discharges pus and may form fistula or sinus
- Acute infection occurs less than 2 weeks, subacute infection occurs within weeks to months while chronic infection occurs after 3 months.
Osteomyelitis Risk factors
- Any causes of immune suppression-Protein energy malnutrition, HIV infection, steroids, Chronic organ failure
- Sickle cell disease and Other conditions which predispose to bone infarcts
- Intravenous Venous (IV) drug abusers
- Local trauma
- Open fractures
- Presence of prosthetic orthopedic implant
- Vascular insufficiency
- Diabetes mellitus
- Extremes of age
Clinical Signs and Symptoms of Osteomyelitis
The patient is usually a child who may presents with the following signs and symptoms of osteomyelitis:
- Severe pain
- Malaise (a feeling of being sick)
- In late presentation toxemia (poisoning of the blood) may be marked
- Inability to make use of the limb or to be touched
- There may be recent infection such as recent septic spot, sore throat or discharging ear
- The child will look ill and feverish
- There is increased pulse rate that is usually above 100 beats/min
- The limb is swollen and sometimes glossy
- In infants especially the newborn, the baby may just be only drowsy and irritable; so a high index of suspicion is needed especially where they are telltale history or sites of infection however mild. Metaphyseal tenderness and resistance to joint movement can signify either osteomyelitis or septic arthritis. Usually both coexist in infants, so the distinction hardly matters.
Hematogenous osteomyelitis usually presents with a slow insidious progression of symptoms. Direct osteomyelitis generally is more localized, with prominent signs and symptoms continue along the entire length of the bone.
Hematogenous osteomyelitis symptoms
- Sudden fever that is high (fever is present in only 50% of neonates with osteomyelitis)
- Restriction of movement (pseudoparalysis of limb in neonates)
- Limb swelling
- Painful limb
- Recent history of infection – a septic toe, a boil, a sore throat or a discharge from the ear
Hematogenous vertebral osteomyelitis symptoms
- Insidious onset
- History of an acute bacteremic episode
- May be associated with contiguous vascular insufficiency
- Swelling and pain
Chronic osteomyelitis Symptoms
- Non healing ulcer
- Sinus tract drainage
- Chronic fatigue
- History of predisposing factors to osteomyelitis such as remote infections as Upper Respiratory Tract Infections (URTI),abscesses, trauma to the limb with open wound or bruise, Previous surgery and prosthetic implants, DM, HIV, Malnutrition, Steroids, Vascular diseases, sickle cell, IV drug use and Hemodialysis
- Fever (present in only 50% of neonates)
- Limb swelling with shiny, stretched skin
- Reduction in the use of the extremity (such as reluctance to move around if the lower extremity is involved or pseudoparalysis of limb in neonates)
- Chronic -Sinus tract drainage, hyperpigmented skin, swelling, chronic ulcer , fever on and off
- Local redness, swelling, warmth and oedema are later signs and signify that pus has escaped from the interior of the bone
Special cases of Osteomyelitis
Chronic Recurrent Multifocal Osteomyelitis
Chronic recurrent multifocal osteomyelitis (CRMO) is an inflammatory disease of children and young adults that is characterized by recurrence of episodes of low-grade fever, pain and swelling over the bones affected and in which there is yet no known infectious agent that causes it; the radiologic abnormalities are suggestive of osteomyelitis. In this type, Females are more frequently affected than males. The median age of onset of this disease is about 10 years. Chronic recurrent multifocal osteomyelitis sometimes is associated with sacroiliitis, palmoplantar pustulosis, arthritis, psoriasis inflammatory bowel disease and Sweet syndrome.
Radiographic abnormalities occur most commonly in the metaphysis of long bones and are characterized by radiolucent bone lesions with reactive sclerosis and soft-tissue swelling. Other parts often affected include the vertebral bodies, the sternal end of the clavicle, and the smaller bones of the hands and feet. Radiographic changes are similar to those seen in acute osteomyelitis, but multiple, often symmetrical lesions are present in Chronic recurrent multifocal osteomyelitis. Bone scanning and MRI are useful in determining the extent and evolution of disease. An infectious cause of Chronic recurrent multifocal osteomyelitis has not been determined.
The course of Chronic recurrent multifocal osteomyelitis consists of prolonged bone pain with remissions and relapses over several years; the average duration of disease is about 6 years. In a long-term follow-up study of 23 patients with Chronic recurrent multifocal osteomyelitis, 26% had active disease at a median of 13 years after diagnosis. Although the clinical outcome in most patients is good, approximately 20% of patients have a prolonged and severe course.
Young age at onset and multiple sites of involvement shows bad prognosis. Treatment of Chronic recurrent multifocal osteomyelitis with a variety of antibiotics has no apparent effect on the course or prognosis. Some experts have advocated the use of corticosteroids or nonsteroidal anti-inflammatory agents for relief of symptoms. Other therapies utilized in small numbers of patients have included colchicine, Interferon-, IFN-, and infliximab. Due to the fact that multifocal bone lesions in childhood can occur with leukemia, neuroblastoma, staphylococcal osteomyelitis, and histiocytosis X, histologic examination and culture of bone specimens should be performed. Histologic findings in Chronic recurrent multifocal osteomyelitis are non-specific acute and chronic inflammatory changes; in the chronic phase of the disease, granulomatous changes can be seen
Fungal osteomyelitis is unusual in healthy children, occurring occasionally in neonates, immunocompromised patients, and intravenous drug users. Osteomyelitis caused by Candida species is reported in intravenous drug users and in premature babies. Aspergillus species cause osteomyelitis in children with chronic granulomatous disease, often resulting from direct spread of infection from the lungs. Histoplasma capsulatum, Coccidioides immitis, Cryptococcus neoformans and Blastomyces dermatitidis cause osteomyelitis in indigenous geographic regions and in immunosuppressed hosts.
Classification of Osteomyelitis
- Based on Duration: Acute and Chronic Osteomyelitis
- Based on Site affected: bone infection of the big toe, jaw or hip.
- Based on organism involved: Methicillin-resistant Staphylococcus aureus (MRSA) osteomyelitis
- Based on anatomic extent: the Cierny and Mader classification. See below.
Cierny and Mader Classification of Chronic Osteomyelitis
The Cierny and Mader staging system for chronic osteomyelitis is classified according to the anatomic extent of the bone infection and also by the physiologic status of the host rather than by chronicity or etiology. The four stages are characterized by the pattern of bony involvement of the infection in order of increasing complexity
- Stage 1: bone infection involves the medullary area only
- Stage 2 involves the superficial cortex of the bone only
- Stage 3: bone infections involves the localized medullary and cortical areas
- Stage 4 is a diffuse medullary and cortical bone involvement
Osteomyelitis Differential diagnosis
- Cellulitis: in this, there is wide-spread superficial redness and lymphangitis
- Pyomyosistis: There is board-like swelling of the limb and pain is more diffuse, MRI will differentiate it from osteomyelitis
- Acute Septic arthritis: Tenderness is diffuse and all movement at the joint is abolished by muscle spasm
- Vasoocclusive crisis of Sickle cell disease
- Trauma-Soft tissue injury or fracture
- Neoplasms-Osteogenic sarcoma (may present similar picture including radiological features as in Osteomyelitis. Biopsy should be done for histological clarification), Squamous Cell Carcinoma of skin, Rhabdomyosarcoma or Ewings sarcoma (cancer cells found in bone or in soft tissue).
- Gauchers disease
- Acute Rheumatic Fever: pain is less severe and it tends to flirt than it is in osteomyelitis
- Hemarthrosis in hemophiliacs.
Osteomyelitis Investigations to confirm Diagnosis and aid in management
1. Osteomyelitis radiology
X-rays findings in Osteomyelitis
- Appear normal in the first 10 days except for evidence of soft tissue swelling which appear within 3 to 5 days following bone infection.
- At about 2 weeks following infection with acute osteomyelitis, Initially manifest as periosteal elevation then periosteal new bone (periosteal reaction or visible periosteal) appears. This is a classic sign of acute osteomyelitis.
- Patchy metaphyseal rarefaction, which appears radiologically as lucent mottling in the metaphysis about the level of periosteal reaction. When this is marked, it gives an appearance of ragged irregular area of bone destruction.
- There is cortical sclerosis and thickening
- Loss of corticomedullary junction
- At this time, sequestrum may be seen as discrete piece of bone separated from the parent bone but more radiopaque.
- With time the periosteal new bone enlarges and becomes continuous with the parent bone and now becomes the involucrum. Of course, at this stage chronic state has set in.
Ultrasonography findings in Osteomyelitis
- May detect sub periosteal and other soft tissue collection of fluid
- But cannot distinguish between pus and hematoma.
- 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.
Radionuclide Scan with 99mm Tc HDP (Scintigraphy)
It is non-specific as other inflammatory conditions will present likewise. The 3-phase bone scan Uses technetium (Tc) 99m bound to phosphorus as the tracer, which accumulates in areas of increased osteoblast activity (reactive new bone formation and increased blood flow). The images obtained are immediate (flow), 15 minute (blood pooling), and 4 hour (bone imaging).
The scan findings are different in cellulitis and osteomyelitis. Cellulitis results in increased activity in the first 2 phases and normal or diffusely increased activity in the third phase. Osteomyelitis will show increased activity (hot spots), that is, there is an in intense uptake in all 3 phases.
In special circumstances, additional information can be obtained from further scanning with leukocytes labeled with gallium 67 and/or indium 111. In this situation, it has an estimated sensitivity and specificity of almost 95% and findings generally are positive in 2-3 days of infection.
False-positive findings can occur with posttraumatic injury, following surgery, diabetic feet, septic arthritis, noninfectious inflammatory bone disease, cancer, healed osteomyelitis, and Paget disease
Magnetic Resonance Imaging (MRI)
The MRI is effective in the early detection and surgical localization of osteomyelitis. Is very sensitive and more specific and can differentiate between soft tissue infection and osteomyelitis even in the very early stage; it can also be able to differentiate pus and blood collection; MRI is also used to delineate epidural involvement and spinal cord impingement. It provides useful anatomic detail in planning for surgical debridement, since it may show abscesses that need drainage.
Computed Tomographic (CT) scanning
CT scans can detect abnormal calcification, ossification, and intracortical abnormalities. It very useful in the evaluation of spinal vertebral lesions and is superior in areas with complex anatomy such as the pelvis, sternum, and calcaneus.
2. Blood Tests in Osteomyelitis
- Full blood count will show: increased WBC count, decreased Hemoglobin level, raised ESR.
- C-reactive protein level usually is elevated; it will show elevation earlier than (ESR)
- Blood Culture: Is positive in 50% of cases
- Anti-staphylococcal antibody titer may be raised
- Genotype is done to exclude Sickle Cell Disease
- Aspirate Tests: Aspirate is drawn from the point of maximum tenderness for Microscopy, Culture and Sensitivity
- Gram Stain: Gram positive or negative organisms
Osteomyelitis treatment is both supportive and definitive.
Supportive measures in treating a bone infection
- Gentle handling of the patient and the limb to avoid unnecessary pain
- Analgesics at repeated appropriate intervals
- Intravenous fluid for hydration and for giving of drugs
- Patient should be admitted for bed rest
- The affected limb is splinted with appropriate splint, to rest the limb and to avoid causing joint contractures (the splint should not obscure the affected area)
- Antibiotics should be started immediately after taking the blood and aspirate sample. The choice of antibiotic should be a broad-spectrum agent which should be based on the knowledge of prevalent organisms causing acute osteomyelitis in the area and also the type of medical condition the patient has such as Sickle cell anemia patients or IV drug use in those who abuse it; Appropriate antibiotic based on sensitivity should be used as soon as culture and sensitivity result becomes ready. The Antibiotic should be given parenteral preferably until patients condition starts to improve before it can be changed to oral.
- Antibiotics should be continued for another 3 to 6 weeks. Sicklers with acute osteomyelitis should be started initially on Chloramphenicol or co-trimoxazole or combined amoxicillin and clavulanic acid.
- Drainage of Pus: This may not be necessary if antibiotics are started early, but if there are signs of deep pus such as swelling, edema and fluctuation or if clinical features do not improve within 36 hours of starting antibiotic treatment, then drainage of pus should be done. It is by an open surgical operation under general anesthesia. The wound is closed without a drain. Once the signs of infection subside, movements are encouraged; subsequently walking with or without aid depending on the integrity of the diseased bone are encouraged.
Definitive bone infections treatment
Medical therapy in Osteomyelitis
The primary treatment for osteomyelitis is parenteral antibiotics that penetrate bone and joint cavities. Treatment is required for at least 4-6 weeks. After intravenous antibiotics are initiated until the systemic manifestations of the disease are over then oral antibiotics may be continued for the rest of the time. Empirical antibiotic therapy should cover the most common organism – Staphylococcus aureus. The Most common gram-negative organism is P aeruginosa, and the most common anaerobe is Peptostreptococcus species; however, in immunocompromised patients, other organisms must also be considered, including fungi and mycobacteria.
Empirical antibiotics include Flucloxacillin or Vancomycin or Clindamycin (Dalacin C). Change antibiotics appropriately as the results of culture of aspirate or biopsy result in chronic osteomyelitis.
If there is evidence of infection with gram-negative bacilli, include a third-generation cephalosporin in the above regimen.
In special circumstances such as in patients with sickle cell anemia and osteomyelitis, the primary bacterial causes are Staphylococcus aureus and Salmonella species. The primary choice for treatment is a fluoroquinolone antibiotic such as ciprofloxacin. Since this cannot be used in children, a third-generation cephalosporin (such as ceftriaxone) is an alternative choice.
Surgical therapy in Chronic Osteomyelitis
Surgical therapy for chronic osteomyelitis ranges from open drainage of abscesses, simple sequestrectomy or amputation. The operation most likely to eradicate osteomyelitis and maintain good function include adequate drainage, extensive debridement of all necrotic tissue, obliteration of dead spaces, stabilization, adequate soft tissue coverage, and restoration of an effective blood supply. The number and nature of the required surgical procedures increases with the severity of the infection, which can be divided into 4 categories, as follows:
This involves removal of necrotic tissue by extensive debridement, sequestrectomy and saucerization. The goal of debridement is to reach healthy, viable tissue, but even when all necrotic tissue has been adequately debrided; the remaining bed of tissue must be considered contaminated with the responsible organism. Surgical excision of bone is carried down to uniform haversian or cancellous bleeding, known as the paprika sign. It is important to carry out radionucleotide studies to know the extent of necrotic tissue.
This involves the Dead space obliteration with flaps, antibiotic beads and bone grafts. The goal of dead space management is to replace dead bone and scar tissue with durable vascularized tissue to maintain skeletal integrity. Local tissue flaps or free flaps may be used to fill dead space. An alternative technique is to place cancellous bone grafts beneath local or transferred tissues where structural augmentation is necessary. Antibiotic-impregnated acrylic beads can be used to sterilize and temporarily maintain dead space. The beads are usually removed within 2 to 4 weeks and replaced with a cancellous bone graft. The most commonly used antibiotics in beads are vancomycin, tobramycin, and gentamicin. Local delivery of antibiotics (amikacin, clindamycin)to dead space can also be achieved with an implantable pump.
This is the provision of soft tissue coverage of the bone. In the presence of a large soft tissue defect or an inadequate soft tissue envelope, local muscle flaps and free vascularized muscle flaps may be placed in a 1 or 2-stage procedure. However, most soft tissue defects are closed primarily, but small soft tissue defects may be covered with a split thickness skin graft.
This involves the stabilization of bone by external or open reduction and internal fixation. Stability can be achieved with plates, screws, rods and/or an external fixator. One type of external fixation allows bone reconstruction of segmental defects and difficult infected nonunion. The Ilizarov external fixation method uses the theory of distraction histogenesis, in which bone is fractured in the metaphyseal region and slowly lengthened. The growth of new bone in the metaphyseal region pushes a segment of healthy bone into the defect left by surgery. When osteomyelitis is characterized by a full thickness cortical sequestration, patients usually can be treated with removal of the dead infected bone (bone saucerization). Bone grafting may be necessary to augment structural support. If the whole segment of bone is involved then bone segment excision with bone grafting and external fixation by illizarov technique may be necessary.
This requires Amputation; long segment bone involvement may require an amputation.
Osteomyelitis Follow up
Local examination and documentation of pain, wound condition, tenderness, swelling, and discharges from wounds should be made in all visits. Repeat Complete Blood Count (CBC), C – reactive protein, Erythrocyte Sedimentation test and plain radiographs to evaluate the progression and behavior of the infection. Physiotherapy is an essential part of follow-up care; isometric exercises should be started early
- Bone abscess such as Brodie abscess
- Septicemia: this can be a cause of dead in osteomyelitis
- Pathological Fracture
- Loosening of prosthetic implant
- Soft tissue infection such as cellulitis
- Spread through epiphyseal plate and into joint causing septic arthritis or may spread to the brain to cause brain abscess
- Acute osteomyelitis cannot heal on its own but progresses to Chronic osteomyelitis evidenced by non-healing ulcers and draining soft-tissue sinus tracts
- Altered bone growth when growth plate is affected.
- Recurrence of osteomyelitis may occur, especially chronic osteomyelitis because it is very serious and more difficult to treat
- Osteomyelitis involving long segment of bone may lead to amputation of the limb involved
- Neurologic impairment following abscess formation or bony collapse may occur causing Vertebral osteomyelitis
- Major bone loss hinders limb length and results in permanent disability
- Chronic Osteomyelitis may cause a form of cancer known as Squamous Cell Carcinoma (SCC) of the skin around the site of the skin draining the pus known as the draining sinus.
- May cause Amyloidosis
- Fistula or sinus formation