Bone and joint infections

BONE S AND JOINTS INFECTIONSDR: MAHMOOD ABED ALJUMAILYPROFESSOR AND CONSULTANT IN ORTHOPEDIC SURGERY

LEARNING OBJECTIVES

To achieve 1- Early diagnosis depending on : history clinical examination imaging investigations 2- Early effective treatment.

BONES INFECTIONS

Osteomylitis is infection of bone and its marrow by pyogenic organisms

Acute infections of bones and joints can be life or limb threatening, while undiagnosed or incompletely treated infection can persist for decades, causing pain and interfering with activities of daily living.

EPIDEMIOLOGY OF BONE INFECTION

●● Bone and joint infections from haematogenous spread remain common worldwide●● The increased use of implants for joint replacement and fracture fixation is an important source of new infections●● Immunocompromised patients are another increasing source (e.g. diabetes, cancer treatment, Aids….)

MICROORGANISM MAY REACH BONE AND JOINT BY:

1 - indirect spread via blood( haematogenous) from far focus of infection 2 - direct introduction. ( open wound, surgical infection, pinprick, injection----) 3 - direct spread from nearby infection. Bacteria can adhere to dead bone or implant surfaces, forming a complex envelop of a polysaccharide matrix, known as a biofilm, making them more resistant both to the host immune system and to antibiotics.

ACUTE HAEMATOGENOUS OSTEOMYELITIS

It is acute pyogenic infection of bone and its marrow, the infecting microorganism reach bone via blood . It is mainly disease of children 2-6 years, but any age might be affected. When adult affected it is secondary to other diseases impaired the immunity

CAUSATIVE MICROOGANISM OF ACUTE HAEMATOGENOUS OSTEOMYELITIS

Staphylococcus areus is usually the causative in 70%.Sreptococcusis other causeHaemophilus influenzae may causative in children between 1-4 years.G – ve microorganism( e-coli, psuedomonus, proteus and bacteriod) in neonatesAnaerobic (peptococcus) is rare cause.Salmonella in sickle cell anemia.Pseudomonus in adult drug addict.

PATHOLOGY OF ACUTE HAEMATOGENOUS OSTEOMYELITIS

In children Acute haematogenous osteomyelitis starts in metaphysis of long bone because of : Blood vessels is terminal and sinusoidal and newly formed with relative stasis, and low oxygen tension. Local immunity is impaired, weak structure predispose to hematoma

EIPHYSEAL PLATE IN CHILDREN AND INFANTS

ACUTE HAEMATOGENOUS OSTEOMYELITIS PATHOLOGY SHOW CHARACTERISTIC PROGRESSION
Pathology1- Inflammation (congestion, exudation, cellular infiltration, increased intraosseous pressure and intravascular thrombosis).2- Suppuration: pus formation and spread of pus through Volkmann's canals to form subperiosteal abscesses. 3- Bone necrosis by the effect of ischemia, pressure, toxic materials, periosteal stripping lead to necrosis of segment of bone (sequestrum).4 –Reactive new bone formation under elevated periostium, the layer of new bone enclosing sequestrum called (involcrum).5- resolution and healing or chronicity. If bone infection persist, sinus continue to discharge pus through perforation in bone called cloacae and tract extend from skin to bone (sinus).

If acute haematogenous osteomyelitis treated early these changes will be controlled and progression can be prevented, and changes limited to small area or even normality restored (resolution). Chronic osteomyelitis is common sequalae for delayed treatment. Acute haematogenous osteomyelitis in infants may complicated by septic arthritis.

CLINICAL FEATURES OF ACUTE HAEMATOGENOUS OSTEOMYELITIS

Clinical features in children: sever pain, malaise, ill, fever, inability to move and toxemia. Any bone my be affected, the Common side is proximal tibia, distal femur and proximal femur. Child look ill ,feverish, tachycardia, locally worm, there is acute tenderness near end of bone, movement restricted ( pseudo paralysis) limb held still. Local redness, local edema is late sign and indicate pus collection in soft tissue. All these features might be attenuated by antibiotics.


In infants and especially neonates' constitutional symptoms might be mild, irritable , drowsy, failure to thrive, metaphyseal tenderness and restricted movement (pseudo paralysis). In adults the common site is thoracolumbar vertebrae following urological procedures. Fever and backache and local tenderness. Adult with osteomyelitis may be immune compromised.


DIAGNOSTIC IMAGING IN ACUTE HAEMATOGENOUS OSTEOMYELITIS.
1- Plain X -ray: in first week no finding except soft tissue swelling, in second week periosteal reaction as a faint line over the bone become visible, patchy rarefaction in metaphysis. Area of decreased and increased bone density may be seen. 2- Ultrasound can detect fluid collection. 3- Radioactive isotope scanning is highly sensitive but has low specificity. 4- MRI is the investigation of choice, it detect marrow inflammation, It is highly sensitive and specific. MRI scanning showing all components of the disease 5- Computed tomography (CT) and PT scans are helpful

LABORATORY INVESTIGATION IN ACUTE HAEMATOGENOUS OSTEOMYELITIS.

1- The most certain way to confirm diagnosis is aspiration of pus or fluid from subperiosteal abscess. Aspirate examined for cells, gram stain and culture sensitivity. 2- blood cultures is positive in less than half of patients. 3- ESR and C reactive protein CRP elevated. 4- CBP show leuckocytosis, neutrophilia and anemia.


Superficial samples from wounds or spontaneously draining pus are unreliable for culture, because the organisms colonizing the surface may bear no relation to those causing the invasive infection in the deeper tissues. Microbiological samples may be falsely negative if antibiotics are given first. - INFECTED TISSUE samples are particularly important , the growth of causative organism is 94% specific for infection , if three or more tissue culture samples are used.

CARDINAL FEATURES OF ACUTE HAEMATOGENOUS

Pain Fever Tenderness Refusal to bear weight. Elevated WBCs. Elevated ESR. Elevated CRP.

PRINCIPLES OF DIAGNOSIS

ESR and CRP are neither sensitive nor specific in making a diagnosis of bone infection Plain radiographs may be normal in the early phase Ultrasound is valuable for identifying fluid/pus collections MRI is usually the investigation of choice Superficial swabs are of no value in identifying the organism causing deep infection If the patient is on antibiotics, cultures may be falsely negative Multiple biopsy specimens should be obtained to optimise microbiological diagnosis A neutrophil infiltrate on histology is strongly indicative of infection

DIFFERENTIAL DIAGNOSIS OF ACUTE HAEMATOGENOUS OSTEOMYELITIS IN CHILDREN

1- Pyogenic arthritis ( absolute stiffness of affected joint , pus in joint, tenderness in joint line). 2- Cellulitis : redness and swelling early with lymphangitis.3-Acute rheumatism.4- Sickle cell crises and Gaucher’s disease.5- Primary bone tumors ( osteosarcoma, Ewing’s sarcoma).


TREATMENT OF ACUTE HAEMATOGENOUS OSTEOMYELITIS
ACUTE osteomyelitis is suspected on clinical base, blood and fluid samples should be taken for laboratory investigation, and then treatment started immediately without waiting for final confirmation of diagnosis.

TREATMENT

1- Supportive treatment for pain and dehydration; analgesia, rest, antipyretics, fluid therapy, septicemia management. 2- Splintage; skin traction, back slab or slings . 3- Antibiotics: intravenous antibiotics started immediately on clinical bases and then changed on cultures and sensitivity. Antibiotics should cover expected microorganism especially staphylococcus.

ANTIBIOTICS SELECTION ON CLINICAL BASES

In children: flucloxacillin+ fusidic acid and or 3rd generation of cephalosporin. Antibiotics continue intravenously until patient improved and CRP return to normal for about 2-4 weeks and continue orally for other 4- 6 weeks. CRP, ESR , and WBCs values checked frequently and antibiotics stopped when be normal. .

4- SURGICAL DRAINAGE

If antibiotics start early in first 48 hours drainage may be unnecessary. Surgical drainage indicated if: 1- condition not improved after 36 hours of treatment. 2- sign of pus collection present in delayed presentation ( swelling, edema, fluctuation). 3- if pus aspirated . Drainage done by open operation under general anesthesia, window done in cortex , splintage applied post operatively. Weight bearing delayed for one month or even more.

COMPLICATIONS OF ACUTE HAEMATOGENOUS OSTEOMYELITIS

1- Septicemia. 2- Epiphyseal damage and altered bone growth. 3- Suppurative arthritis; infants or when metaphysis in side join like hip. 4- Metastatic infection. 5- Pathological fractures. 6- Chronic osteomyelitis.

SUBACUTE HAEMATOGENOUS OSTEOMYELITIS BRODIE'S ABSCESSES

When microorganism virulence is low or the patient more resistant or both Subacute haematogenous osteomyelitis occur. The common microorganism is staph. aureus. Commonly affect distal femur or proximal tibia or distal tibia.


There is a well define cavity in metaphysis of long bone or in flat bone. The cavity contain acute and chronic inflammatory cell infiltration with fluid. Patient usually child had pain, limping, swelling and tenderness, there is no fever, WBCs is normal and ESR elevated.


X-ray show well- define, rounded or oval cavity surrounded by sclerosis( Brodies abscess) Differential diagnosis is osteoid osteoma and malignant bone tumors. If diagnosis, clear patient treated by rest and flucloxacillin and fusidic acid for 8 weeks If there is doubt in diagnosis, biopsy and debridement done with flucloxacillin and fusidic acid for 8 weeks


GARRE’S SECLEROSING OSTEOMYELITIS This type characterized by marked sclerosis and cortical thickening in diaphysis. Patient usually young complain of pain and swelling. X-ray show increased bone density. It should differentiated from bone tumors. Treatment is surgical resection and antibiotics

POST TRAUMATIC OSTEOMYELITIS

It followed open fractures. It is the commonest cause of chronic osteomyelitis. Staph. aureus is the usual pathogen ; many other type microorganism or mixed infection may occur.

Patients develop pain, swelling, fever, wound inflamed, WBCs increased, ESR increased. Early effective treatment of open fractures is the best to prevent this type of infection by : ( debridement, antibiotics, splintage, leave wound open, good wound care and external fixations) .

POSTOPERATIVE OSTEOMYELITIS

Osteomyelitis may follows any type of bone operation, it occur in about 1- 5% of bone surgery. Organisms is mixture of pathogens ( staph, protus, pseudomonas ---- Microorganism introduce from atmosphere, instrument, patients, surgeon or haemetogenous. Local factors favor infection is soft tissue damage, hematoma, and bone death.

It may occur early, delayed or late after surgery. Prevention is the most important. Treatment include supportive treatment, proper antibiotic , debridement and stabilization of bone. If fixation stable , it is preserved until fracture healed, If fixation unstable , it is removed and replaced by external fixation.

IMPLANT-ASSOCIATED INFECTION

Good centres should have an infection rate of <1% per joint per year Internal fixation of open fractures remains a high infection risk Late infection may present with low-grade symptoms ( pain and start-up stiffness) Radiographs may show lucency around the implant Multiple specimens need to be taken at surgery for reliable diagnosis

PROSTHETIC JOINT INFECTION

Well-fixed prostheses may be debrided, treated with antibiotics and the implant retained. Loose prostheses must be removed. Replacement can be made at the initial surgery (one-stage) or after a delay to allow infection to be eradicated with a course of antibiotics (two-stage) Multiple surgical samples are crucial for identifying a pathogen Thorough excision of infected tissue is a key determinant of outcome Long-term antibiotics may be used for patients who are not suitable for major revision surgery



CHRONIC OSTEOMYELITISIT MAY FOLLOW ACUTE OSTEOMYELITIS, OPEN FRACTURES, AND POSTOPERATIVE INFECTIONS
It may caused by staph aureus, strept, proteus, pseudomonas, staph epidermidis or mixed infection. There is segments of dead bones, sclerosis, cavities and chronic inflammatory infiltration.


Clinically either presented with: 1- Flare-up of infection ( acute on chronic) : pain, fever, swelling and redness. 2- Chronic Discharging sinus Investigations include culture and sensitivity from infected tissues in depth of sinus , x-ray, sinogram, and other imaging studied. Treatment include supportive treatment, proper antibiotic , surgical drainage of abscesses and debridement, filling cavities by viable tissues ( muscle flap or autogenous cancellous bone graft) and stabilization of bone and reconstruction.

CHRONIC OSTEOMYELITIS

CHRONIC OSTEOMYELITIS TO 1- Medullary. 2- Superficial. 3- Localized. 4- Diffused. Chronic osteomyelitis requires specialist surgery. Host status should be optimized before surgery Following surgery, antibiotic therapy is typically continued for at least 6 weeks.

COMPLICATIONS OF CHORIC OSTEOMYELITIS ARE :

1- Repeated reactivation, 2- Septic arthritis, 3- Soft tissue scaring and deformities, 4- Joint stiffness, 5- Amyloidosis, 6- Malignancy, 7- Disseminations to other site.

ACUTE SUPPURATIVE ARTHRITISIT IS ACUTE PYOGENIC INFECTION OF JOINTS .

Microorganism may reach joint by: 1- direct introduction. ( wound, pinprick, injection, arthroscopy, or following surgery) 2- direct spread from nearby infection, especially osteomyelitis. 3- indirect spread via blood (haematogenous) from far focus of infection

CAUSAL ORGANISM IN ACUTE SUPPURATIVE ARTHRITIS

The usual causative organism is staphylococcus. In children 1-4 years haemophilus influenzae may be a cause. Streptococcus, e.coli, proteus occasionally. Gonococcus may be a cause in young adults.



RISK FACTORS FOR JOINT SEPTIC ARTHRITIS.
● Extremes of age● Underlying joint abnormality, especially rheumatoid arthritis● Immunocompromise (e.g. diabetes mellitus, human immunodeficiency virus infection, immunosuppressive therapy)●Joint instrumentation (e.g. steroid injection, arthroscopy)● Intravenous drug abuse● Indwelling central venous catheter● Bacteraemia (especially Staphylococcus aureus)

PATHOLOGY OF ACUTE SUPPURATIVE ARTHRITIS

1- Acute inflammatory reaction (synovitis) with serious or seropurulent exudate. 2- Arthritis: Articular cartilage is eroded and destroyed by the effect of bacterial and cellular enzymes. 3- if the infection untreated it will spread to bone and soft tissues to form abscesses and sinuses. Joint may end by bony ankylosis and deformity. Depending on stage of treatment, Joint may end by complete resolution when treated early, partial loss of articular surface and joint fibrosis, bony ankylosis after complete damage to articular surfaces, or permanent deformity to joint and limb.

PRESENTATION OF SEPTIC ARTHRITIS

Children may be toxic and febrile, but adults may only have a low-grade feverThe joint is swollen and held in a characteristic ‘position of comfort’ Any movement causes extreme pain

CLINICAL FEATURES OF SEPTIC ARTHRITISDIFFER ACCORDING TO THE AGE OF THE PATIENTS

1- In children: acute pain in single large joint, reluctant to move the limb, fever, the child is ill, tachycardia, overlying skin is hot, swelling and red. All movements are restricted. 2- In newborn infants: septicemia is more common , the baby irritable and refuses feeding reluctant to move the limb ( pseudo paralysis). There is rapid pulse and sometimes fever. It may complicate early by osteomyelitis. 3- In adults: pain and swelling in affected joints. There is warmth and marked tenderness and movement restricted. 4- In Rheumatoid Arthritis, especially after injection of steroid the infection may be silent.

IMAGING OF ACUTE SUPPURATIVE ARTHRITIS

1- Ultrasonography, septic arthritis are positively echogenic. 2- X-ray examination. ( soft tissue swelling, widening joint space, Subluxation, gas in joint, or narrowing and irregularity of the joint space in late features. 3- MRI and radionuclide imaging in difficult cases.

INVESTIGATION OF ACUTE SUPPURATIVE ARTHRITIS

1- ESR, WBCs, CRP elevated. Aspirate the joint and examine fluid directly, chemically, bacteriological and for cultures and sensitivity.

DIFFERENTIAL DIAGNOSIS OF ACUTE SUPPURATIVE ARTHRITIS

1- Acute osteomyelitis.2- Traumatic synovitis, history of trauma and aspiration used.3-Traumatic Haemarthrosis, history of trauma and aspiration used.4- Irritable joint (US of hip useful).5- Hemophilic bleed.6- Rheumatic disorders.7- Sickle cell disease, and Gaucher’s disease.8- Gout and pseudogout in adults.


TREATMENT OF ACUTE SUPPURATIVE ARTHRITISTHE FIRST PRIORITY IS TO ASPIRATE THE JOINT AND EXAMINE THE FLUID
1- general supportive care.( analgesia and fluid) 2- splintage (rest, skin traction or cast). 3- antibiotics. Start immediately on clinical base. Infant and children treated by flucloxacillin with 3rd generation cephalosporin.

Older teenager and adults treated by flucloxacillin with fusidic acid , if g-ve present add 3rd generation cephalosporin. Antibiotics can be changed on result of culture sensitivity test. Antibiotics should be given intravenously for 4-7 days and then orally for another 3 weeks.

TREATMENT OF ACUTE SUPPURATIVE ARTHRITIS

Surgical drainage by open surgery or arthroscopy. Joint drained and washed and suction irrigation system left in joint. Surgical drainage indicated 1- Very young infants. 2- When hip involved. 3-When aspirated pus thick. 4- When patient not respond to conservative treatment. Splintage in the optimum position is necessary

COMPLICATIONS OF ACUTE SUPPURATIVE ARTHRITIS

Infant have the highest incidence of complications, most of which affect the hip. 1- Osteomyelitis (proximal femur). 2- Subluxation and dislocation of hip and instability of knee. 3- damage to the cartilaginous physis or the epiphysis in the growing child. 4- Articular cartilage erosion (chondrolysis). 5- ankylosis of the joint.

TUBERCULOSIS OF BONE AND JOINTS

Tuberculosis is still a major cause of death and disability in developing countries.  Tuberculosis again on the increase in last two decade, bones or joints are affected in about 5% of patients .

TUBERCULOSIS 

Mycobacterium tuberculosis, enter via the lung or gut or rarely through the skin. Tuberculosis may appear in any bone, synovial or bursal sheath.

PATHOLOGY OF TB

1- Primary complex 2- Secondary spread 3- Tertiary lesion: Mycobacterium tuberculosis gained a foot hold in bone or joint. There is predilection to vertebral bodies ( 50%), and the large synovial joints ( hip ,knee, less often shoulder or ankle). These changes affected either the synovium (SYNOVITIS) or the bone (OSTITIS) is affected and then spread to the near by structure and whole joint affected ( ARTHRITIS). Fibrous ankylosis of joint. Spread to soft tissue lead to cold abscess. Followed with sinus and end with secondary pyogenic infection.



In endemic area skeletal TB is seen mainly in children. In non endemic area is seen in chronic debilitating disease (AIDS). 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 FEATURES OF TB IN LARGE JOINTS

History of previous infection. The patient usually a child ,or young adult Pain . Swelling. Fever . Lassitude . d Loss of weight. Night cries (the joint splinted by muscle spasm during the day, relaxes with sleep and irritate the joint cause sharp pain and cries ). Muscle wasting. Movement in all direction limited.

IN T B SPINE

BACKACHEKyphosis (gibbus). Occasionally the presenting feature is weakness or loss of sensibility in the lower limb.In neglected cases patient presented with paralysis (Pott’s paraplegia).

RADIOLOGICAL FEATURES

early changes: Soft tissue swelling, Periarticular osteoporosisLocalized osteoporosis (Bone ends ‘washed – out’ or localized decalcification ).Narrowing and irregularity of the articular ends.Late changes: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 shadow of paravertebral abscess.

INVESTIGATIONS
E S R increased. Relative lymphocytosis. Mantoux test positive. Synovial fluid aspirate (high protein). Polymerase chain reaction ( PCR ) is sensitive and specific . Acid fast bacilli isolation and cultures is diagnostic. Synovial biopsy is the more valuable .


CARDINAL FEATURES OF TB
Long history. Involvement only one joint. Marked synovial thickening. Marked muscle wasting. Periarticular osteoporosis.

DIFFERENTIAL DIAGNOSIS OF TUBERCULOSIS.

1- transient synovitis. 2- Monoarticular rheumatoid arthritis. 3- subacute arthritis ( reactive or brucellosis) 4- haemorrhagic arthritis. 5- pyogenic arthritis 6- multiple myeloma and secondary metastases. 7- fungal infection and sarcodosis. 8- bone tumors.

TREATMENT OF TUBERCULOSIS.

1- Rest; splintage or skin traction, restricted activity continue for 6-12 months if diagnosis is early until joint resolved. Those with progressive joint destruction may need prolonged period of splintage to prevent ankylosis in bad position. 2 - chemotherapy of TB A- isoniazid , rifampicin, pyrazinamide, ethambutol for 2 months. B- isoniazid and rifampicin fore another 4 . This is the recommendation of WHO, and BMRC. C- some authors recommend to give chemotherapy for 18 months ( 4 HRZE, 14 HR)

3-SURGERY FOR TB

3- operative drainage or clearance of tuberculous foci may used. Arthrodesis or replacement arthroplasty may considers if articular surface is destroyed, years after healing, chemotherapy given 3 months before and after the operation.

ARTHRODESIS

ARTHROPLASTY

TUBERCULOSIS

TB tenosynovitis – compound ganglion. TB BURSITIS – trochrenteric bursitis. TB dactylitis – in children hand and feet digits , it should be differentiated from sickle cell anemia,

BRUCELLOSIS

It cause subacute or chronic arthritis. It has intermediate picture between pyogenic and TB. Positive agglutination test is diagnostic. Tissue culture positive if spine affected. Treatment by rifampicin and 3rd generation cephalosporin.

SPIROCHAETAL INFECTIONS

Syphilis Yaws Lyme disease

HYDATID DISEASE OF BONE

Hydatid disease affect bone in 1-2%. The cyst slowly enlarged in bone with little respect to cortical or epiphyeseal boundaries. The bones most commonly affected are the vertebrae, pelvis, femur, scapula and ribs. Patients may complain of pain and swelling or pathological fractures. It most differentiated from benign and malignant bone tumors. Treatment by radical resection if possible with prolonged courses of albendazole.