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Tuberculosis of Hip joint FULL PPT.pptx

The document provides a comprehensive overview of hip tuberculosis, emphasizing its historical context, anatomical features, risk factors, and clinical presentation. It explains the pathogenesis, diagnosis, classification, and various investigative techniques for osteoarticular tuberculosis, highlighting the importance of biopsies and imaging in confirming the diagnosis. Management strategies and potential complications related to hip tuberculosis are also discussed, underlining its prevalence and significance in public health, particularly among certain high-risk populations.

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TUBERCULOSIS OF HIP
HISTORY • Tuberculosis is one of the oldest infection. • India: Rig Veda, Charaka Samhitha and Sushrutha Samhitha – mention of disease by the name “Yakshma”. • Greco-Roman civilization – phthisis or consumption. • Tuberculosis lesions recorded in Egyptian mummies.
• Robert Koch discovered Mycobacterium tuberculosis in1882. • Hence also called Koch Bacilli.
Anatomy of Hip • It is the largest joint of human body. • Ball and socket type of synovial joint. • It is synovial articulation between head of Femur and acetabulum.
ACETABULUM • It has Horse-shoe shaped articular surface. • Fibrocartilaginous labrum attached to acetabulum, makes the socket deeper. • Opening of acetabulum directed laterally, downwards and forward. • The acetabular rim is circular but deficient inferiorly which is bridged by transverse acetabular ligament.
FEMUR • Head of femur is globular and forms 2/3 of sphere. • Covered by hyaline cartilage (except the fovea). • Neck/shaft angle: 120-135°. • Femoral anteversion: 10-15°.
Capsule • Medially-Attached circumferentially around acetabular labrum and transverse ligament. • Laterally- to the neck of Femur, front to the Inter Trochanteric line but posteriorly 1 cm proximal to trochanteric crest. • Whole of anterior half of femoral neck and proximal part of its posterior half is
3 ligaments strengthen the capsule, which spiral around long axis of femoral neck. Iliofemoral ligament (Y-shaped ligament of Bigelow) • stem of ‘Y’ arises from anterior inferior iliac spine(AIIS) and adjacent superior rim of Acetabulum. Pubofemoral ligament • from ilio-pubic eminence. Ischio-femoral ligament • weakest • arises from posterior- inferior margin of acetabulum. These ligaments are relaxed in flexion, external rotation and taut in extension, internal rotation. Haversion fat pad- fill the non-articular depression of acetabulum.
Arterial Blood Supply Of Head Of Femur a) Introsseous vessels running up the neck b) Retinacular vessels- arise as upward continuation of vascular anastomosis around the trochanteric region. c) Vessels in ligament teres- minor contribution.
Introduction • Chronic granulomatous infectious disease. • Osteoarticular TB 1-3 % of all TB cases • TB hip constitutes 15-20% of osteoarticular tuberculosis. • 2nd most common , next only to TB spine. • Transmission-Air borne spread droplet nuclei by patients with pulmonary tuberculosis. • Increased incidence have been noted with prevalence with AIDS.
Regional Distribution of osteoarticular Tuberculosis • Spine - 50% • Hip - 20% • Knee - 10% • Ankle Joint - 5% • Elbow - 2% • Metatarsal and Phalanges –1%
Risk factors • HIV patients • IV drug abusers • Alcoholics • Elderly • Over crowding. • People with Poor Nutrition • Therapeutically Immunosupressed Patients • Organ transplant receipients • Patients on Cancer chemotherapy.
Organism • Mycobacteriaceae family. • Species: • Tuberculosis m/c human pathogen. • M bovis – bovine tuberculosis. • Atypical – Kansasii, Marinum, Avium, Scrofulaceum, Ulcerans.
• Rod shaped, gram positive • Aerobic • Acid fast bacilli – due to mycolic acid in cell wall. • Slow growing aerobic organism.
• PATHOLOGY: • Osteoarticular TB is result of Hematogenous spread. • Primary focus: Active or Latent Lungs Lymph node Mediastinum Mesentery Kidney
Pathogenesis Insemination of infection Accumulation of macrophages/monocytes TB bacilli – phagocytosed, broken down Lipid dispersed throught the cytoplasm EPITHELOID cells – large pale cells, large vesicular nucleus, abundant cytoplasm Langhans gaint cell
• Lymphocytes appear and form ring around the lesion. • Mass formed by reactive cells – nodule /tubercle. Central caseous necrosis. • Soft tubercle – caseous necrosis. • Hard tubercle – no caseous necrosis – atypical organism. 2 weeks
Pathogenesis and Pathology Primary focus (active/quiescent) haemotogenous spread Osteoarticular TB
• Organism reaches joint space through Sub synovial vessels • Lesions in the epiphyseal bones • Articular cartilage destruction from periphery. • Tubercular arthritis – no proteolytic enzymes – central cartilage intact for long time.
Cold abscess • Collection of products of liquefaction and reactive exudation. • Contains – serum, leukocytes, caseous material, bone debris, TB bacilli. • Feels warm – not as high as in pyogenic infection. • Bursts – sinus /ulcer formation. • Wall of sinus/ulcer covered – tubercular granulation. • Ulcer – undermined edges.
• Cold abscess forms within joint – inferior capsule weak Perforated • Cold abscess presents anywhere around hip – • Femoral triangle. • Medial , lateral, posterior aspect of thigh. • Ischiorectal fossa • Pelvis
Intrapelvic abscess Below the levator ani Above levator ani Ischiorectal fossa Upwards into inguinal region
Type of disease Caseous exudative • More destructive • More exudative and abscess formation • Insidious onset • Marked constitutional features • Generally in children Granular • Less destructive • Abscess formation rare • Insidious onset. • Dry lesion • More likely in adults.
Fate of tubercle • Resolve completely. • Heal completely with residual deformities/ loss of function. • Heal by Fibrous ankylosis. • Lesion completely walled off, caseous tissue calcified • Low grade chronic fibromatous, granulating and caseating lesion may persist. • Infection spreads – contiguous, systemically
Common sites • Acetabular roof(common) • Epiphysis/ femoral head • Metaphyseal region • Greater trochanter – least common
• TB of greater trochanter may involve overlying trochanteric bursa without involving hip joint. • Upper end of femur – intracapsular - joint involvement early • Acetabular roof – joint involvement late.
Clinical features • Commonest age: 1st to 3rd decade • Insideous onset. • Limp - earliest and commonest, antalgic gait. • Pain – maximum towards end of the day Referred to medial aspect of thigh • Night cries-Spasm relaxes and permits movement and causes pain. • Deformity • Fullness around the hip
• Constitutional symptoms – low grade fever, cough with expectorant, anorexia, loss of weight, night sweats, evening rise of temperature. • Regional lymph nodes enlargement. • Tenderness – joint line, Bitrochanteric pressure.
Classification • Tubercular Synovitis • Early arthritis • Advanced arthritis • Advanced arthritis with subluxation/ dislocation.
Synovitis stage • Position of max joint capacity – FABER • Apparent lengthening. • No true shortening. • Extremes of movement painful.
Early arthritis • Articular damage starts • Severe muscle spasm – FADIR • Apparent shortening • True shortening <1 cm. • Restriction of joint movement
Advanced arthritis • FADIR. • Apparent shortening. • True shortening >1cm. • Increased severity of symptoms • Capsule further destroyed, thickened and contracted.
Advance arthritis with subluxation/dislocation • With further destruction of acetabulum , femur head , capsule and ligaments, upper end of femur – displaced upwards and dorsally wandering acetabulum. • pathological dislocation of femur • Shenton’s arc broken. • Movements are grossly restricted.
• The classical deformity of Flexion, Adduction and Internal rotation may not be seen in severe arthritis when destruction of Iliofemoral ligament and the thigh resting on extreme external rotation for long time.
• Investigations • Management • Complications
Clinico-radiological classification
Synovitis
Early arthritis • A child with tuberculosis of the left hip joint, early arthritis (stage II) resembling the normal hip appearance. Note slight diminution of the joint space and a juxtaarticular lytic lesion in the acetabular roof
Advanced arthritis • Active tubercular arthritis of right hip joint. Note localized osteoporosis, break in the Shenton’s arc, widened acetabulum, protrusio acetabuli, avascular capital femoral epiphysis (Perthes type) and mild coxa vara
Advanced arthritis with subluxation or dislocation
Shanmugasundaram’s Classification
Modified classification
• Campbell and Hoffman (1995) while treating children with tuberculosis of hip joint observed a close relationship between the radiological type and the therapeutic outcome; • Good-results were obtained in 92 percent of “normal type”, 80 percent of Perthes’ type, 50 percent of dislocating type, 29 percent of travelling- acetabulum and mortar-pestle type. If the joint space was reduced to 3 mm or less the outcome could be predicted as poor.
Differentials • transient synovitis of the hip, • Legg–Calve–Perthes disease, • osteomyelitis of the upper end of the femur, • injury hip • acute infective arthritis of infancy and childhood • osteoid osteoma of the neck of the femur with synovial involvement, • villonodular synovitis, • rheumatoid arthritis, • AVN of the head of the femur, • giant cell variants of upper femur, etc.
Blood • Low haemoglobin, relative • lymphocytosis, raised erythrocytic • sedimentation rate (ESR) are often found • in active stage Raised ESR, however, is not necessarily a proof of activity of infection. Its repeated estimation at 3 to 6 months intervals gives a valuable index to the activity of the disease
Mantoux test • Stantard dose of 5 tuberculin units (TU-0.1 ml) is injected intradermally & read 48 to 72 hrs later. • Person who has been exposed to the bacteria is expected to mount an immune response in skin containing bacterial protiens. • A positive reaction (induration more than 10 mm) is present in tuberculous disease. • A negative test, in general, rules out the disease. • The tuberculin test may be negative in disseminated T.B, after vaccination, recent viral infection or steroid therapy, or in immunocompromised individuals [20]. • This test in not recommended, currently.
Immunological test • Interferon gamma release assays (IGRAs by quantiferon assay) • blood – based assays rely on the stimulation of host blood cells with M. tuberculosis- specific antigens & measure the production of interferon gamma. • Although it more specific than the mantoux test, but they are currently unable to distinguish between active disease & latent TB infection & hence not recommended
Ziehl-Neelsen staining • This test is rapid, easy & requires minimal infrastructure; however, minimum load of 5,000-10,000 bacilli/ml is required & species differentiation is not possible. • It may be helpful in sputum smears, but as osteoarticular TB is paucibacillary, hence this test has limited value .
Fluorescence microscopy • It utilizes fluorescent dye to stain the organisms and when excited by UV light using special microscope, bacteria appear as bright rods in a dark back ground. • It is used successfully for rapid diagnosis of pulmonary TB; but in osteoarticular TB, particularly paucibacillary disease, use is not clearly established. • Fluorescence microscopy is faster & more sensitive than conventional light microscopy, but the expense, need for a dark room & poor specificity limit its usefulness
Culture • Isolation of organism on culture is gold standard for diagnosis of TB. Culture media used are egg based (Lowenstein – Jensen medium), agar based (Middlebrook 7H10,7H11) or liquid based (Mycobacterium growth indicator tube). • Culture can detect as little as 10 bacilli/ml of sputum, differentiate different mycobacterial species, can be used for drug sensitivity testing & is useful in symptomatic smear negative cases. •
• But drawbacks of conventional culture methods are time consuming (6 to 8 weeks) & require strict quality control. Rapid culture methods like BACTEC which detect mycobacteria based on metabolism (detects C14 labelled CO2 & reports as growth index(GI) value) rather than visible growth give results within 7-14 days. • MGIT(mycobacteria growth indicator tube) method, detects growth early in 7 to 12 day by nonradioactive detection system using flurochrome for detection & drug screening, hence is useful for drug susceptibility testing
Tissue biopsy • TB guidelines TAC subcommittee for bone & joint TB recommends that wherever possible, all patients should have a biopsy of the lesion, to provide a specimen for culture to confirm the diagnosis, perform drug susceptibility testing, and to rule out other diagnoses. • Tissue biopsy can be done under radiological guidance, arthroscopy or via open surgical biopsy. • Arthroscopic biopsy is advantageous as it visualizes the lesion, helps excision of affected tissue for diagnostic testing, & simultaneous therapeutic intervention if required. • Percutaneous CT-guided biopsy is preferred, but some patients may require open biopsy.
• Regional enlarged lymph nodes / sinus tract curettage/edge biopsy can be sent for culture & • histopathology, but microbiological result may be misleading due to contamination/colonization/secondary infection. • Biopsy is not needed for culture and microbiologically confirmed TB, but if • patient is microbiological negative for TB then percutaneous biopsy is advised and • if the foci is not easily accessible percutaneously or needs surgical • management, then should undergo open surgical biopsy.
• Specimens should also be collected, when therapeutic invasive • procedure is done. Specimens collected should be sent for: • a. Microscopy & culture for pyogenic bacteria • b. Microscopy & culture for MTB • c. Histopathology / cytology.
Cytological examination of smears • Direct smears may be stained with MayGrunwald-Giemsa (or Romanowsky dyes) • & ZN stain for cytopathologic examination allowing recognition of inflammatory • patterns & acid – fast organisms and making a tentative diagnosis in a day, but • the diagnosis is always circumstantial and never definitive. This can be done for • intraoperative consultation also .
Serological testing • This test can be used for antigen & antibody detection; however • serological tests are expensive, require trained personnel, have low senstivity, • are affected by BCG vaccination, previous infection & cannot distinguish between • MTB & non-tubercular mycobacteria. Serological tests have so banned in India • for TB
Molecular methods (PCR) • Detection &identification of mycobacteria directly from samples can be done by polymerase chain reaction (PCR) & nucleic acid amplification test. • PCR provides rapid diagnosis within 48 hrs, has high senstivity, can identify the species & requires very small volume of specimen; • However it cannot differentiate between live & dead mycobacteria. High cost, availability & infrastructure required limits its usage.
Line Probe assay • Another molecular assay LPA (line probe assay) is based on reversed hybridization principle. • DNA material is hybridized with specific oligonucleotide probes & after addition of enzyme substrate complex with chromogen results in purple/brown precipitates, which is visually interpreted. It is useful to detect resistance against rifampicin & isoniazid
CBNAT • Gene Xpert (CBNAT) MTB/RIF automates & integrates sample processing & PCR in a single disposable plastic cartridge, giving accurate results within 2 hrs. It simultaneously detects MTB & resistance to rifampicin. • WHO recommends its use as initial diagnostic test in adults & children suspected of having MDR-TB or HIV associated TB
Imaging • 1. X-rays – as described before for each stage 2. Computed Tomography- It detects disease earlier even when destroyed areas of bone erosion is small and in areas of skeleton not appreciated on plain X- rays . • CT guided biopsy/aspiration provides tissue for histological/cytological/microbiological diagnosis. • Further, swelling in soft tissues caused by edema, granulations, exudations or abscess formation can be demonstrated, earlier. • Calcification in abscess, as seen on CT is pathognomic of TB
MRI • 3. It is more sensitive & specific than X-rays & CT scan to detect tuberculous lesion and can diagnose disease in predestructive stage. • MRI can show abscess/granulation tissue/caseous tissue, localized tuberculoma & generalized granuloma in multiple planes & can delineate soft tissue masses in both sagittal & coronal plane.
PET- CT • It helps in picking, residual inflammation in cases where the signs of healing are ambiguous on contrast MRI.
USG • It is a useful non-invasive modality to detect soft tissue • mass (solid or liquid), deep-seated abscesses & to perform USG guided • aspiration. It is particularly useful in follow-up evaluation of psoas abscess • when patient is under cover of ATT to document resolution of psoas abscess.
Diagnosis ( index TB guidelines ) • (a) High suspicision in patients with signs of joint infection with insidious onset & • charaterisitic imaging features. • (b) Refer such patient to orthopaedian who can assess the joint & perform a biopsy for • culture & histopathology • (c) Whenever possible and safe for patient take pus/fluid/aspirate/specimens and sent it • for microscopy, culture (for all mycobacterial, pyogenic and fungal testing) and • histopathology because it confirms diagnosis; drug susceptibility testing can be done to • guide ATT and alternative diagnoses can be picked up .
The hierarchy of evidence for the diagnosis of TB • 1. Culture • 2. Molecular testing, PCR, other tests in development. • 3. Demonstartion of AFB in direct smears or tissue sections. • 4. Tissue reaction patterns: granulomas necrotising/non–caseating, necrosis • without AFB • 5. Radiological examination & imaging studies. • 6. Physical examination of the patient. • 7. Therapeutic response
MANAGEMENT • Early diagnosis and effective chemotherapy are vital to save the joint. In view of the nonspecific findings early in the course of the disease, failure to consider TB can lead to devastating outcomes. • We recommend the standard chemotherapy as accepted universally with four anti tubercular drugs to start with in all the stages of presentation .
• In addition to medical treatment, traction preferably skeletal is recommended to all patients. In the case of the abduction deformity, traction on the other limb is also applied to stabilize the pelvis. • Traction relieves the muscle spasm, prevents or corrects deformity and subluxation, maintains the joint space, minimizes the chances of development of migration of acetabulum and permits close observation of the hip region. • Another advantage with traction is that it keeps the joint surfaces apart; hence with an early start of mobilization exercises of the hip, functional range of movements can be achieved. With late presentation, the deformities may become permanent.
• The TB heals with fibrosis, hence may not respond to traction. Unlike pyogenic infections, proteolytic enzymes are not produced in tubercular infection; articular cartilage survives for a long time thus preserving mobility in many patients. • Tuli earlier was recommending partial weight-bearing only after 4-6 months of treatment, and full weight-bearing only at 18 months. • However, in the present day scenario, we recommend weight-bearing earlier, whenever patient can tolerate the pain.
• Moon et al. Recommends early rehabilitation regimen for ambulation as it boosted the patients’ confidence and activity level. • In addition to ATT, nutritional supplementation and traction, the specific treatment depends upon the stage of involvement at the time of diagnosis.
DRUGS ( ATT ) • 1. Rifampicin: is semisynthetic antibiotic, acts on dormant intracellular mycobacterium, has good absorption in empty stomach. • It causes red-brown discolouration of body fluids. 10mg kg is daily recommended dose with adult dose between 450-600 mg • 2. Isoniazid: has ability to penetrate cell which contain tubercle bacillus. Toxic effects • include rashes, fever, vitamin B- deficiency & neurologic effects on reflexes & bladder • function. The daily recommended dose is 3- 8 mg/kg .
• 3. Pyrazinamide: It is bactericidal drug, which is well absorbed orally & eliminated by • hepatic metabolism. • It may cause nausea, flushing, arthralgia & hepatotoxic reactions. It is prescribed as 35 mg/kg/day . • 4. Ethambutol: has replaced para-amino salicylic acid (PAS) as it has fewer toxic • reactions & is well tolerated. Dose is 2.5 mg/kg for 60 days, then 15 mg/kg single • daily dose .
• 5 . Streptomycin: it acts best at 9.0 pH & so it should be accompanied by a buffered • alkaline solution when injected intra synovially. Permanent toxic effects are • related to 8th nerve palsy causing deafness & vertigo. The daily recommended dose is • 1gm .
• 1. Synovitis. 2RHZE/10–16RHE with appropriate analgesia and rest to • the joint in above-knee skin traction or skeletal traction for around • 4 weeks. Active assisted exercises to mobilize thereafter. Surgery is • rarely required. • 2. Early arthritis. 2RHZE/10–16RHE with appropriate analgesia and rest • to the joint in above-knee skin traction or skeletal traction until spasm • is relieved, and non-weight bearing exercises as tolerated.
• 3. Advanced arthritis. • 2RHZE/10-16RHE with appropriate analgesia and rest to the joint in traction. • Arthrolysis with joint debridement is usually indicated, followed by a period of skeletal traction, with early supervised mobilization of the hip as tolerated. • 4. Advanced arthritis with subluxation/dislocation. • 2RHZE/10–16RHE with appropriate analgesia and rest to the joint in traction. • Gross bony destruction at this stage requires surgical management with excision arthroplasty, arthrodesis or total hip replacement.
Arthrolysis • Arthrolysis aims to achieve the useful range of movements in the cases with gross limitation of movements not responding to traction and exercises. • The arthrolysis helps in the cases where limitation of movement is because of fibrous ankylosis and not to mechanical restriction as a result of mainly alteration in the anatomy of the joint. • For example, it may not help in wandering acetabulum type or pathological dislocation or even in pestle and mortal appearance.
• All pathological and fibrous tissues are excised carefully without compromising with vascularity of remaining part of the upper end of the femur. It is wise to leave the posterior capsule undisturbed because it carries vital blood supply to the femoral head. • Posterior capsule is generally not shortened as most of the patients have flexion deformity. Before the completion of the operative procedure, ensure that adequate range has been achieved by passive movements (while under anesthesia).
Excision arthroplasty • In the Indian subcontinent and in many Asian countries, people do not accept a stiff hip joint as squatting, sitting cross-legged, and kneeling are essential socioeconomic actives in their day to day life. • Girdlestone’s excisionarthroplasty can be safely carried out in healed or active disease after the completion of growth potential of bones of the hip joint .
• This procedure provides a mobile, painless hip joint with control of infection and correction of deformity. However, some degree of shortening and instability is unavoidable. • Postoperatively traction in 30 to 50 degrees of abduction was maintained for 3 months.The patient was encouraged to sit soon after the peration, and repetitive active assisted movements of the hip and knee were started during the first week.
• During the period of traction active and assisted physiotherapy helped to develop good muscle power, maximal range of hip movements, and encouraged the patients to place the operated limb in the tailor’s position and squatting posture. • After 3 months of traction the patients were encouraged to walk using a weightrelieving orthosis or crutches. • The orthosis and crutches were usually discarded 6 to 9 months after the operation and the patient was advised to use a walking stick generally in the contralateral hand.
Arthrodesis • Arthrodesis of the hip, though relieves the pain, and corrects the deformity. However it is at the cost of loss of movements. • Its acceptance in Indian subcontinent is very low due to socio cultural reasons. • Young adult with sound bony ankylosis in functioning position has to learn to adopt himself for the active life. • One has however to resort to chairand commode toilet system for whole life.
• In cases where the patient reports with healed disease with a painless fused hip joint in unacceptable deformity all that is needed to obtain sound fusion is an upper femoral corrective osteotomy. The ideal site for corrective osteotomy is as near the deformed joint as practicable. • The best position for fusion of the hip joint is one to 30 degrees of flexion (depending upon age), no abduction or abduction (in adults), and 5 to 10 degrees of external rotation. Diagrammatic representation of Brittain’s extra-articular operation for tuberculous disease of the hip joint.
Total Hip Arthroplasty
• In tubercular arthritis, as acetabulum is involved, there is no role of hemi replacement. • Total hip arthroplasty (THA) in the hip with active tuberculous infection is a controversial issue due to the potential risk of reactivation of TB. • The acceptability of the THA is gradually increasing globally with reports that metal can be safely used in tuberculous lesions . • THA in a patient with healed TB of the hip is now an accepted procedure
• Majority perform it in the stage of the advance arthritis or in sequalae of advance arthritis when the joint is unsalvageable. • Babhulkar and Pande recommended it to be performed after 10 years or more between active infection and replacement surgery. Its role in active TB is debatable. • Wang et al. recommend a combination of antituberculous drugs for at least 2 weeks prior to the operation and subsequently for at least 12 months after operation.
• Sidhu et al. performed cemented THR in 23 patients with active tuberculous arthritis of the hip. His patients had received at least 3 months of antitubercular therapy before surgery and treatment were continued for a total of 18 months. • With a mean followup of 4.7 years, no activation of the infection or implant-loosening was recorded. • They concluded that hip replacement in the presence of active tuberculous arthritis of the hip may be a safe procedure when peri operative chemotherapy was used .
TUBERCULOSIS OF KNEE JOINT
• Knee Joint is the largest joint in the body having the largest intra articular space. • It is the 3rd most common site for osteoarticular tuberculosis. • Accounts for nearly 10% of all skeletal tuberculous lesion.
Pathology • The initial focus occurring by hematogenous dissemination may start in the synovium, or in the subchondral bone (Distal femur, proximal Tibia, Patella). • The synovium lesion may for many months remain purely as tubercular synovitis. • The synovial membrane gets congested, edematous and studded with tubercles. • The synovial lining which is normally a single cell layer in thickness becomes hypertrophied and thickened with granulation tissue.
• The joint fluid in the initial stages is increased (Serous, Opaque, turbid, yellowish and may contain fibrinous flakes). • In advanced stage of the disease tuberculous process becomes osteoarticular. • The Tuberculous granulation tissue like the pannus erodes the articular margins, destroys the bone and involves the cruciate ligament, periarticular tissues, capsule and ligaments.
• The Pannus may erode the margins of the articular cartilage, grow between the articular cartilage and the subchondral bone, thus detaching the cartilage from the bone. • Nutrition of the articular cartilage is thus interfered. • It looses its smooth glistening appearance, there may be fibrillation of its surface, it becomes roughened, pitted and erosion of the cartilage exposes the subchondral bone.
• As the disease advances large areas at pressure points show osseous destruction and the whole joint is obliterated with granulation/fibrous tissue, capsular apparatus and ligaments are disrupted and joint gets a triple deformity. • Triple deformity I. Flexion deformity II. Posterior subluxation III. Lateral rotation
Clinical Features • The onset and course is insidious • The knee shows – Swelling • warm • patellar tap is present due to synovial effusion • the thickened synovium – filling up all parapatellar fossa appreciated earliest in medial parapatellar fossa. • When the arthritis has set – movements are grossly restricted, – painful – accompanied by muscle atrophy. • regional lymphadenopathy.
• Quadricep muscle shows gross wasting • In the neglected case – triple deformity • Once the flexion deformity established – tensor fasciae latae further increases the deformity. • In long case – Posterior capsule of the knee joint gets contracted
Differential Diagnosis • Monoarticular affections – rheumatic arthritis (in children) – chronic traumatic synovitis due to chronic internal derangement of knee (e.g. • meniscal tears • loose bodies • osteochondritis dissecans • chondromalaciapatellae • Rheumatoid arthritis (in adults) • subacute pyogenic arthritis/synovitis
• Hemarthrosis • villonodular synovitis • synovial chondromatosis
Staging of the tuberculosis of the joints Stages Clinical Radiology Treatment Synovitis ROM >75% Soft tissue swelling, Osteoporosis Chemotherapy Early Arthritis ROM 50-75% Above + moderate diminution of joint space + marginal erosion Chemotherapy + Movements Advanced arthritis Movements restricted >75% Above + marked diminution of J.Space +destruction of J. surface Chemotherapy +surgery (Generally arthrodesis in lower limb) Advanced arthritis + sub/dislocation Ankylosis Joint is disorganized with sub/dislocation Chemotherapy +surgery (Corrective Osteotomy/ Arthrodesis)
Treatment • Non operative treatment with antitubercular drugs is employed in – tubercular synovitis • Traction is applied to – prevent (or correct) flexion and subluxation deformity – keep the joint surfaces distracted. • In addition to the systemic drugs, the joint may be aspirated
• With the quiescence of acute local signs, gently active and assisted knee bending should be. • Usually after 12 weeks of treatment the patient may be permitted ambulation with suitable orthosis and crutches. • After 6 to 12 months of treatment, in cases with favorable response, the crutches or orthosis may be discarded. • Unprotected weight bearing is usually permitted 9 to 12 months after the start of treatment.
• Arthrodesis of the grossly destroyed knee in children should be deferred till the completion of growth potential of the distal femur and proximal tibia.
Operative Treatment • In the synovial stage – arthrotomy and synovectomy should be carried out. • In early arthritis, – synovectomy, – removal of loose bodies, debris, pannus, loose articular cartilage and – careful curettage of osseous juxta-articular foci • Postoperatively antitubercular drug therapy, – traction, – intermittent active and assisted exercises, – suitable brace ambulation should be continued
• In adults with advanced arthritis or in cases which resulted in painful fibrous ankylosis during the process of healing, the knee joint may be treated by arthrodesis. • This option provides  painless stable knee  prevents recrudescence  corrects deformity  patients can do long hours of standing and walking. • However it imposes a lot of restrictions in sitting, using public transport and many other social activities.
Arthroplasty
References • Tuberculosis of skeletal system – S M Tuli • Campbell operative orthopaedics • Textbook of orthopaedics – Tureks . • Robbins and Cotran pathological basis of disease
THANK YOU

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Tuberculosis of Hip joint FULL PPT.pptx

  • 1.
  • 2.
    HISTORY • Tuberculosis isone of the oldest infection. • India: Rig Veda, Charaka Samhitha and Sushrutha Samhitha – mention of disease by the name “Yakshma”. • Greco-Roman civilization – phthisis or consumption. • Tuberculosis lesions recorded in Egyptian mummies.
  • 3.
    • Robert Kochdiscovered Mycobacterium tuberculosis in1882. • Hence also called Koch Bacilli.
  • 4.
    Anatomy of Hip •It is the largest joint of human body. • Ball and socket type of synovial joint. • It is synovial articulation between head of Femur and acetabulum.
  • 5.
    ACETABULUM • It hasHorse-shoe shaped articular surface. • Fibrocartilaginous labrum attached to acetabulum, makes the socket deeper. • Opening of acetabulum directed laterally, downwards and forward. • The acetabular rim is circular but deficient inferiorly which is bridged by transverse acetabular ligament.
  • 7.
    FEMUR • Head offemur is globular and forms 2/3 of sphere. • Covered by hyaline cartilage (except the fovea). • Neck/shaft angle: 120-135°. • Femoral anteversion: 10-15°.
  • 8.
    Capsule • Medially-Attached circumferentially aroundacetabular labrum and transverse ligament. • Laterally- to the neck of Femur, front to the Inter Trochanteric line but posteriorly 1 cm proximal to trochanteric crest. • Whole of anterior half of femoral neck and proximal part of its posterior half is
  • 9.
    3 ligaments strengthenthe capsule, which spiral around long axis of femoral neck. Iliofemoral ligament (Y-shaped ligament of Bigelow) • stem of ‘Y’ arises from anterior inferior iliac spine(AIIS) and adjacent superior rim of Acetabulum. Pubofemoral ligament • from ilio-pubic eminence. Ischio-femoral ligament • weakest • arises from posterior- inferior margin of acetabulum. These ligaments are relaxed in flexion, external rotation and taut in extension, internal rotation. Haversion fat pad- fill the non-articular depression of acetabulum.
  • 14.
    Arterial Blood SupplyOf Head Of Femur a) Introsseous vessels running up the neck b) Retinacular vessels- arise as upward continuation of vascular anastomosis around the trochanteric region. c) Vessels in ligament teres- minor contribution.
  • 15.
    Introduction • Chronic granulomatousinfectious disease. • Osteoarticular TB 1-3 % of all TB cases • TB hip constitutes 15-20% of osteoarticular tuberculosis. • 2nd most common , next only to TB spine. • Transmission-Air borne spread droplet nuclei by patients with pulmonary tuberculosis. • Increased incidence have been noted with prevalence with AIDS.
  • 16.
    Regional Distribution ofosteoarticular Tuberculosis • Spine - 50% • Hip - 20% • Knee - 10% • Ankle Joint - 5% • Elbow - 2% • Metatarsal and Phalanges –1%
  • 17.
    Risk factors • HIVpatients • IV drug abusers • Alcoholics • Elderly • Over crowding. • People with Poor Nutrition • Therapeutically Immunosupressed Patients • Organ transplant receipients • Patients on Cancer chemotherapy.
  • 18.
    Organism • Mycobacteriaceae family. •Species: • Tuberculosis m/c human pathogen. • M bovis – bovine tuberculosis. • Atypical – Kansasii, Marinum, Avium, Scrofulaceum, Ulcerans.
  • 19.
    • Rod shaped,gram positive • Aerobic • Acid fast bacilli – due to mycolic acid in cell wall. • Slow growing aerobic organism.
  • 20.
    • PATHOLOGY: • OsteoarticularTB is result of Hematogenous spread. • Primary focus: Active or Latent Lungs Lymph node Mediastinum Mesentery Kidney
  • 21.
    Pathogenesis Insemination ofinfection Accumulation of macrophages/monocytes TB bacilli – phagocytosed, broken down Lipid dispersed throught the cytoplasm EPITHELOID cells – large pale cells, large vesicular nucleus, abundant cytoplasm Langhans gaint cell
  • 22.
    • Lymphocytes appearand form ring around the lesion. • Mass formed by reactive cells – nodule /tubercle. Central caseous necrosis. • Soft tubercle – caseous necrosis. • Hard tubercle – no caseous necrosis – atypical organism. 2 weeks
  • 24.
    Pathogenesis and Pathology Primaryfocus (active/quiescent) haemotogenous spread Osteoarticular TB
  • 25.
    • Organism reachesjoint space through Sub synovial vessels • Lesions in the epiphyseal bones • Articular cartilage destruction from periphery. • Tubercular arthritis – no proteolytic enzymes – central cartilage intact for long time.
  • 26.
    Cold abscess • Collectionof products of liquefaction and reactive exudation. • Contains – serum, leukocytes, caseous material, bone debris, TB bacilli. • Feels warm – not as high as in pyogenic infection. • Bursts – sinus /ulcer formation. • Wall of sinus/ulcer covered – tubercular granulation. • Ulcer – undermined edges.
  • 27.
    • Cold abscessforms within joint – inferior capsule weak Perforated • Cold abscess presents anywhere around hip – • Femoral triangle. • Medial , lateral, posterior aspect of thigh. • Ischiorectal fossa • Pelvis
  • 28.
    Intrapelvic abscess Below thelevator ani Above levator ani Ischiorectal fossa Upwards into inguinal region
  • 29.
    Type of disease Caseousexudative • More destructive • More exudative and abscess formation • Insidious onset • Marked constitutional features • Generally in children Granular • Less destructive • Abscess formation rare • Insidious onset. • Dry lesion • More likely in adults.
  • 30.
    Fate of tubercle •Resolve completely. • Heal completely with residual deformities/ loss of function. • Heal by Fibrous ankylosis. • Lesion completely walled off, caseous tissue calcified • Low grade chronic fibromatous, granulating and caseating lesion may persist. • Infection spreads – contiguous, systemically
  • 31.
    Common sites • Acetabularroof(common) • Epiphysis/ femoral head • Metaphyseal region • Greater trochanter – least common
  • 32.
    • TB ofgreater trochanter may involve overlying trochanteric bursa without involving hip joint. • Upper end of femur – intracapsular - joint involvement early • Acetabular roof – joint involvement late.
  • 33.
    Clinical features • Commonestage: 1st to 3rd decade • Insideous onset. • Limp - earliest and commonest, antalgic gait. • Pain – maximum towards end of the day Referred to medial aspect of thigh • Night cries-Spasm relaxes and permits movement and causes pain. • Deformity • Fullness around the hip
  • 34.
    • Constitutional symptoms– low grade fever, cough with expectorant, anorexia, loss of weight, night sweats, evening rise of temperature. • Regional lymph nodes enlargement. • Tenderness – joint line, Bitrochanteric pressure.
  • 35.
    Classification • Tubercular Synovitis •Early arthritis • Advanced arthritis • Advanced arthritis with subluxation/ dislocation.
  • 36.
    Synovitis stage •Position of max joint capacity – FABER • Apparent lengthening. • No true shortening. • Extremes of movement painful.
  • 37.
    Early arthritis •Articular damage starts • Severe muscle spasm – FADIR • Apparent shortening • True shortening <1 cm. • Restriction of joint movement
  • 38.
    Advanced arthritis •FADIR. • Apparent shortening. • True shortening >1cm. • Increased severity of symptoms • Capsule further destroyed, thickened and contracted.
  • 39.
    Advance arthritis withsubluxation/dislocation • With further destruction of acetabulum , femur head , capsule and ligaments, upper end of femur – displaced upwards and dorsally wandering acetabulum. • pathological dislocation of femur • Shenton’s arc broken. • Movements are grossly restricted.
  • 40.
    • The classicaldeformity of Flexion, Adduction and Internal rotation may not be seen in severe arthritis when destruction of Iliofemoral ligament and the thigh resting on extreme external rotation for long time.
  • 41.
  • 42.
  • 43.
  • 44.
    Early arthritis • Achild with tuberculosis of the left hip joint, early arthritis (stage II) resembling the normal hip appearance. Note slight diminution of the joint space and a juxtaarticular lytic lesion in the acetabular roof
  • 45.
    Advanced arthritis • Activetubercular arthritis of right hip joint. Note localized osteoporosis, break in the Shenton’s arc, widened acetabulum, protrusio acetabuli, avascular capital femoral epiphysis (Perthes type) and mild coxa vara
  • 46.
    Advanced arthritis withsubluxation or dislocation
  • 47.
  • 49.
  • 50.
    • Campbell andHoffman (1995) while treating children with tuberculosis of hip joint observed a close relationship between the radiological type and the therapeutic outcome; • Good-results were obtained in 92 percent of “normal type”, 80 percent of Perthes’ type, 50 percent of dislocating type, 29 percent of travelling- acetabulum and mortar-pestle type. If the joint space was reduced to 3 mm or less the outcome could be predicted as poor.
  • 51.
    Differentials • transient synovitisof the hip, • Legg–Calve–Perthes disease, • osteomyelitis of the upper end of the femur, • injury hip • acute infective arthritis of infancy and childhood • osteoid osteoma of the neck of the femur with synovial involvement, • villonodular synovitis, • rheumatoid arthritis, • AVN of the head of the femur, • giant cell variants of upper femur, etc.
  • 52.
    Blood • Low haemoglobin,relative • lymphocytosis, raised erythrocytic • sedimentation rate (ESR) are often found • in active stage Raised ESR, however, is not necessarily a proof of activity of infection. Its repeated estimation at 3 to 6 months intervals gives a valuable index to the activity of the disease
  • 53.
    Mantoux test • Stantarddose of 5 tuberculin units (TU-0.1 ml) is injected intradermally & read 48 to 72 hrs later. • Person who has been exposed to the bacteria is expected to mount an immune response in skin containing bacterial protiens. • A positive reaction (induration more than 10 mm) is present in tuberculous disease. • A negative test, in general, rules out the disease. • The tuberculin test may be negative in disseminated T.B, after vaccination, recent viral infection or steroid therapy, or in immunocompromised individuals [20]. • This test in not recommended, currently.
  • 54.
    Immunological test • Interferongamma release assays (IGRAs by quantiferon assay) • blood – based assays rely on the stimulation of host blood cells with M. tuberculosis- specific antigens & measure the production of interferon gamma. • Although it more specific than the mantoux test, but they are currently unable to distinguish between active disease & latent TB infection & hence not recommended
  • 55.
    Ziehl-Neelsen staining • Thistest is rapid, easy & requires minimal infrastructure; however, minimum load of 5,000-10,000 bacilli/ml is required & species differentiation is not possible. • It may be helpful in sputum smears, but as osteoarticular TB is paucibacillary, hence this test has limited value .
  • 56.
    Fluorescence microscopy • Itutilizes fluorescent dye to stain the organisms and when excited by UV light using special microscope, bacteria appear as bright rods in a dark back ground. • It is used successfully for rapid diagnosis of pulmonary TB; but in osteoarticular TB, particularly paucibacillary disease, use is not clearly established. • Fluorescence microscopy is faster & more sensitive than conventional light microscopy, but the expense, need for a dark room & poor specificity limit its usefulness
  • 57.
    Culture • Isolation oforganism on culture is gold standard for diagnosis of TB. Culture media used are egg based (Lowenstein – Jensen medium), agar based (Middlebrook 7H10,7H11) or liquid based (Mycobacterium growth indicator tube). • Culture can detect as little as 10 bacilli/ml of sputum, differentiate different mycobacterial species, can be used for drug sensitivity testing & is useful in symptomatic smear negative cases. •
  • 58.
    • But drawbacksof conventional culture methods are time consuming (6 to 8 weeks) & require strict quality control. Rapid culture methods like BACTEC which detect mycobacteria based on metabolism (detects C14 labelled CO2 & reports as growth index(GI) value) rather than visible growth give results within 7-14 days. • MGIT(mycobacteria growth indicator tube) method, detects growth early in 7 to 12 day by nonradioactive detection system using flurochrome for detection & drug screening, hence is useful for drug susceptibility testing
  • 59.
    Tissue biopsy • TBguidelines TAC subcommittee for bone & joint TB recommends that wherever possible, all patients should have a biopsy of the lesion, to provide a specimen for culture to confirm the diagnosis, perform drug susceptibility testing, and to rule out other diagnoses. • Tissue biopsy can be done under radiological guidance, arthroscopy or via open surgical biopsy. • Arthroscopic biopsy is advantageous as it visualizes the lesion, helps excision of affected tissue for diagnostic testing, & simultaneous therapeutic intervention if required. • Percutaneous CT-guided biopsy is preferred, but some patients may require open biopsy.
  • 60.
    • Regional enlargedlymph nodes / sinus tract curettage/edge biopsy can be sent for culture & • histopathology, but microbiological result may be misleading due to contamination/colonization/secondary infection. • Biopsy is not needed for culture and microbiologically confirmed TB, but if • patient is microbiological negative for TB then percutaneous biopsy is advised and • if the foci is not easily accessible percutaneously or needs surgical • management, then should undergo open surgical biopsy.
  • 61.
    • Specimens shouldalso be collected, when therapeutic invasive • procedure is done. Specimens collected should be sent for: • a. Microscopy & culture for pyogenic bacteria • b. Microscopy & culture for MTB • c. Histopathology / cytology.
  • 62.
    Cytological examination ofsmears • Direct smears may be stained with MayGrunwald-Giemsa (or Romanowsky dyes) • & ZN stain for cytopathologic examination allowing recognition of inflammatory • patterns & acid – fast organisms and making a tentative diagnosis in a day, but • the diagnosis is always circumstantial and never definitive. This can be done for • intraoperative consultation also .
  • 63.
    Serological testing • Thistest can be used for antigen & antibody detection; however • serological tests are expensive, require trained personnel, have low senstivity, • are affected by BCG vaccination, previous infection & cannot distinguish between • MTB & non-tubercular mycobacteria. Serological tests have so banned in India • for TB
  • 64.
    Molecular methods (PCR) •Detection &identification of mycobacteria directly from samples can be done by polymerase chain reaction (PCR) & nucleic acid amplification test. • PCR provides rapid diagnosis within 48 hrs, has high senstivity, can identify the species & requires very small volume of specimen; • However it cannot differentiate between live & dead mycobacteria. High cost, availability & infrastructure required limits its usage.
  • 65.
    Line Probe assay •Another molecular assay LPA (line probe assay) is based on reversed hybridization principle. • DNA material is hybridized with specific oligonucleotide probes & after addition of enzyme substrate complex with chromogen results in purple/brown precipitates, which is visually interpreted. It is useful to detect resistance against rifampicin & isoniazid
  • 66.
    CBNAT • Gene Xpert(CBNAT) MTB/RIF automates & integrates sample processing & PCR in a single disposable plastic cartridge, giving accurate results within 2 hrs. It simultaneously detects MTB & resistance to rifampicin. • WHO recommends its use as initial diagnostic test in adults & children suspected of having MDR-TB or HIV associated TB
  • 67.
    Imaging • 1. X-rays– as described before for each stage 2. Computed Tomography- It detects disease earlier even when destroyed areas of bone erosion is small and in areas of skeleton not appreciated on plain X- rays . • CT guided biopsy/aspiration provides tissue for histological/cytological/microbiological diagnosis. • Further, swelling in soft tissues caused by edema, granulations, exudations or abscess formation can be demonstrated, earlier. • Calcification in abscess, as seen on CT is pathognomic of TB
  • 68.
    MRI • 3. Itis more sensitive & specific than X-rays & CT scan to detect tuberculous lesion and can diagnose disease in predestructive stage. • MRI can show abscess/granulation tissue/caseous tissue, localized tuberculoma & generalized granuloma in multiple planes & can delineate soft tissue masses in both sagittal & coronal plane.
  • 69.
    PET- CT • Ithelps in picking, residual inflammation in cases where the signs of healing are ambiguous on contrast MRI.
  • 70.
    USG • It isa useful non-invasive modality to detect soft tissue • mass (solid or liquid), deep-seated abscesses & to perform USG guided • aspiration. It is particularly useful in follow-up evaluation of psoas abscess • when patient is under cover of ATT to document resolution of psoas abscess.
  • 71.
    Diagnosis ( indexTB guidelines ) • (a) High suspicision in patients with signs of joint infection with insidious onset & • charaterisitic imaging features. • (b) Refer such patient to orthopaedian who can assess the joint & perform a biopsy for • culture & histopathology • (c) Whenever possible and safe for patient take pus/fluid/aspirate/specimens and sent it • for microscopy, culture (for all mycobacterial, pyogenic and fungal testing) and • histopathology because it confirms diagnosis; drug susceptibility testing can be done to • guide ATT and alternative diagnoses can be picked up .
  • 72.
    The hierarchy ofevidence for the diagnosis of TB • 1. Culture • 2. Molecular testing, PCR, other tests in development. • 3. Demonstartion of AFB in direct smears or tissue sections. • 4. Tissue reaction patterns: granulomas necrotising/non–caseating, necrosis • without AFB • 5. Radiological examination & imaging studies. • 6. Physical examination of the patient. • 7. Therapeutic response
  • 73.
    MANAGEMENT • Early diagnosisand effective chemotherapy are vital to save the joint. In view of the nonspecific findings early in the course of the disease, failure to consider TB can lead to devastating outcomes. • We recommend the standard chemotherapy as accepted universally with four anti tubercular drugs to start with in all the stages of presentation .
  • 74.
    • In additionto medical treatment, traction preferably skeletal is recommended to all patients. In the case of the abduction deformity, traction on the other limb is also applied to stabilize the pelvis. • Traction relieves the muscle spasm, prevents or corrects deformity and subluxation, maintains the joint space, minimizes the chances of development of migration of acetabulum and permits close observation of the hip region. • Another advantage with traction is that it keeps the joint surfaces apart; hence with an early start of mobilization exercises of the hip, functional range of movements can be achieved. With late presentation, the deformities may become permanent.
  • 75.
    • The TBheals with fibrosis, hence may not respond to traction. Unlike pyogenic infections, proteolytic enzymes are not produced in tubercular infection; articular cartilage survives for a long time thus preserving mobility in many patients. • Tuli earlier was recommending partial weight-bearing only after 4-6 months of treatment, and full weight-bearing only at 18 months. • However, in the present day scenario, we recommend weight-bearing earlier, whenever patient can tolerate the pain.
  • 76.
    • Moon etal. Recommends early rehabilitation regimen for ambulation as it boosted the patients’ confidence and activity level. • In addition to ATT, nutritional supplementation and traction, the specific treatment depends upon the stage of involvement at the time of diagnosis.
  • 77.
    DRUGS ( ATT) • 1. Rifampicin: is semisynthetic antibiotic, acts on dormant intracellular mycobacterium, has good absorption in empty stomach. • It causes red-brown discolouration of body fluids. 10mg kg is daily recommended dose with adult dose between 450-600 mg • 2. Isoniazid: has ability to penetrate cell which contain tubercle bacillus. Toxic effects • include rashes, fever, vitamin B- deficiency & neurologic effects on reflexes & bladder • function. The daily recommended dose is 3- 8 mg/kg .
  • 78.
    • 3. Pyrazinamide:It is bactericidal drug, which is well absorbed orally & eliminated by • hepatic metabolism. • It may cause nausea, flushing, arthralgia & hepatotoxic reactions. It is prescribed as 35 mg/kg/day . • 4. Ethambutol: has replaced para-amino salicylic acid (PAS) as it has fewer toxic • reactions & is well tolerated. Dose is 2.5 mg/kg for 60 days, then 15 mg/kg single • daily dose .
  • 79.
    • 5 .Streptomycin: it acts best at 9.0 pH & so it should be accompanied by a buffered • alkaline solution when injected intra synovially. Permanent toxic effects are • related to 8th nerve palsy causing deafness & vertigo. The daily recommended dose is • 1gm .
  • 80.
    • 1. Synovitis.2RHZE/10–16RHE with appropriate analgesia and rest to • the joint in above-knee skin traction or skeletal traction for around • 4 weeks. Active assisted exercises to mobilize thereafter. Surgery is • rarely required. • 2. Early arthritis. 2RHZE/10–16RHE with appropriate analgesia and rest • to the joint in above-knee skin traction or skeletal traction until spasm • is relieved, and non-weight bearing exercises as tolerated.
  • 81.
    • 3. Advancedarthritis. • 2RHZE/10-16RHE with appropriate analgesia and rest to the joint in traction. • Arthrolysis with joint debridement is usually indicated, followed by a period of skeletal traction, with early supervised mobilization of the hip as tolerated. • 4. Advanced arthritis with subluxation/dislocation. • 2RHZE/10–16RHE with appropriate analgesia and rest to the joint in traction. • Gross bony destruction at this stage requires surgical management with excision arthroplasty, arthrodesis or total hip replacement.
  • 82.
    Arthrolysis • Arthrolysis aimsto achieve the useful range of movements in the cases with gross limitation of movements not responding to traction and exercises. • The arthrolysis helps in the cases where limitation of movement is because of fibrous ankylosis and not to mechanical restriction as a result of mainly alteration in the anatomy of the joint. • For example, it may not help in wandering acetabulum type or pathological dislocation or even in pestle and mortal appearance.
  • 83.
    • All pathologicaland fibrous tissues are excised carefully without compromising with vascularity of remaining part of the upper end of the femur. It is wise to leave the posterior capsule undisturbed because it carries vital blood supply to the femoral head. • Posterior capsule is generally not shortened as most of the patients have flexion deformity. Before the completion of the operative procedure, ensure that adequate range has been achieved by passive movements (while under anesthesia).
  • 84.
    Excision arthroplasty • Inthe Indian subcontinent and in many Asian countries, people do not accept a stiff hip joint as squatting, sitting cross-legged, and kneeling are essential socioeconomic actives in their day to day life. • Girdlestone’s excisionarthroplasty can be safely carried out in healed or active disease after the completion of growth potential of bones of the hip joint .
  • 85.
    • This procedureprovides a mobile, painless hip joint with control of infection and correction of deformity. However, some degree of shortening and instability is unavoidable. • Postoperatively traction in 30 to 50 degrees of abduction was maintained for 3 months.The patient was encouraged to sit soon after the peration, and repetitive active assisted movements of the hip and knee were started during the first week.
  • 86.
    • During theperiod of traction active and assisted physiotherapy helped to develop good muscle power, maximal range of hip movements, and encouraged the patients to place the operated limb in the tailor’s position and squatting posture. • After 3 months of traction the patients were encouraged to walk using a weightrelieving orthosis or crutches. • The orthosis and crutches were usually discarded 6 to 9 months after the operation and the patient was advised to use a walking stick generally in the contralateral hand.
  • 87.
    Arthrodesis • Arthrodesis ofthe hip, though relieves the pain, and corrects the deformity. However it is at the cost of loss of movements. • Its acceptance in Indian subcontinent is very low due to socio cultural reasons. • Young adult with sound bony ankylosis in functioning position has to learn to adopt himself for the active life. • One has however to resort to chairand commode toilet system for whole life.
  • 88.
    • In caseswhere the patient reports with healed disease with a painless fused hip joint in unacceptable deformity all that is needed to obtain sound fusion is an upper femoral corrective osteotomy. The ideal site for corrective osteotomy is as near the deformed joint as practicable. • The best position for fusion of the hip joint is one to 30 degrees of flexion (depending upon age), no abduction or abduction (in adults), and 5 to 10 degrees of external rotation. Diagrammatic representation of Brittain’s extra-articular operation for tuberculous disease of the hip joint.
  • 89.
  • 90.
    • In tuberculararthritis, as acetabulum is involved, there is no role of hemi replacement. • Total hip arthroplasty (THA) in the hip with active tuberculous infection is a controversial issue due to the potential risk of reactivation of TB. • The acceptability of the THA is gradually increasing globally with reports that metal can be safely used in tuberculous lesions . • THA in a patient with healed TB of the hip is now an accepted procedure
  • 91.
    • Majority performit in the stage of the advance arthritis or in sequalae of advance arthritis when the joint is unsalvageable. • Babhulkar and Pande recommended it to be performed after 10 years or more between active infection and replacement surgery. Its role in active TB is debatable. • Wang et al. recommend a combination of antituberculous drugs for at least 2 weeks prior to the operation and subsequently for at least 12 months after operation.
  • 92.
    • Sidhu etal. performed cemented THR in 23 patients with active tuberculous arthritis of the hip. His patients had received at least 3 months of antitubercular therapy before surgery and treatment were continued for a total of 18 months. • With a mean followup of 4.7 years, no activation of the infection or implant-loosening was recorded. • They concluded that hip replacement in the presence of active tuberculous arthritis of the hip may be a safe procedure when peri operative chemotherapy was used .
  • 93.
  • 94.
    • Knee Jointis the largest joint in the body having the largest intra articular space. • It is the 3rd most common site for osteoarticular tuberculosis. • Accounts for nearly 10% of all skeletal tuberculous lesion.
  • 95.
    Pathology • The initialfocus occurring by hematogenous dissemination may start in the synovium, or in the subchondral bone (Distal femur, proximal Tibia, Patella). • The synovium lesion may for many months remain purely as tubercular synovitis. • The synovial membrane gets congested, edematous and studded with tubercles. • The synovial lining which is normally a single cell layer in thickness becomes hypertrophied and thickened with granulation tissue.
  • 96.
    • The jointfluid in the initial stages is increased (Serous, Opaque, turbid, yellowish and may contain fibrinous flakes). • In advanced stage of the disease tuberculous process becomes osteoarticular. • The Tuberculous granulation tissue like the pannus erodes the articular margins, destroys the bone and involves the cruciate ligament, periarticular tissues, capsule and ligaments.
  • 97.
    • The Pannusmay erode the margins of the articular cartilage, grow between the articular cartilage and the subchondral bone, thus detaching the cartilage from the bone. • Nutrition of the articular cartilage is thus interfered. • It looses its smooth glistening appearance, there may be fibrillation of its surface, it becomes roughened, pitted and erosion of the cartilage exposes the subchondral bone.
  • 98.
    • As thedisease advances large areas at pressure points show osseous destruction and the whole joint is obliterated with granulation/fibrous tissue, capsular apparatus and ligaments are disrupted and joint gets a triple deformity. • Triple deformity I. Flexion deformity II. Posterior subluxation III. Lateral rotation
  • 99.
    Clinical Features • Theonset and course is insidious • The knee shows – Swelling • warm • patellar tap is present due to synovial effusion • the thickened synovium – filling up all parapatellar fossa appreciated earliest in medial parapatellar fossa. • When the arthritis has set – movements are grossly restricted, – painful – accompanied by muscle atrophy. • regional lymphadenopathy.
  • 100.
    • Quadricep muscleshows gross wasting • In the neglected case – triple deformity • Once the flexion deformity established – tensor fasciae latae further increases the deformity. • In long case – Posterior capsule of the knee joint gets contracted
  • 101.
    Differential Diagnosis • Monoarticularaffections – rheumatic arthritis (in children) – chronic traumatic synovitis due to chronic internal derangement of knee (e.g. • meniscal tears • loose bodies • osteochondritis dissecans • chondromalaciapatellae • Rheumatoid arthritis (in adults) • subacute pyogenic arthritis/synovitis
  • 102.
    • Hemarthrosis • villonodularsynovitis • synovial chondromatosis
  • 103.
    Staging of thetuberculosis of the joints Stages Clinical Radiology Treatment Synovitis ROM >75% Soft tissue swelling, Osteoporosis Chemotherapy Early Arthritis ROM 50-75% Above + moderate diminution of joint space + marginal erosion Chemotherapy + Movements Advanced arthritis Movements restricted >75% Above + marked diminution of J.Space +destruction of J. surface Chemotherapy +surgery (Generally arthrodesis in lower limb) Advanced arthritis + sub/dislocation Ankylosis Joint is disorganized with sub/dislocation Chemotherapy +surgery (Corrective Osteotomy/ Arthrodesis)
  • 104.
    Treatment • Non operativetreatment with antitubercular drugs is employed in – tubercular synovitis • Traction is applied to – prevent (or correct) flexion and subluxation deformity – keep the joint surfaces distracted. • In addition to the systemic drugs, the joint may be aspirated
  • 105.
    • With thequiescence of acute local signs, gently active and assisted knee bending should be. • Usually after 12 weeks of treatment the patient may be permitted ambulation with suitable orthosis and crutches. • After 6 to 12 months of treatment, in cases with favorable response, the crutches or orthosis may be discarded. • Unprotected weight bearing is usually permitted 9 to 12 months after the start of treatment.
  • 106.
    • Arthrodesis ofthe grossly destroyed knee in children should be deferred till the completion of growth potential of the distal femur and proximal tibia.
  • 107.
    Operative Treatment • Inthe synovial stage – arthrotomy and synovectomy should be carried out. • In early arthritis, – synovectomy, – removal of loose bodies, debris, pannus, loose articular cartilage and – careful curettage of osseous juxta-articular foci • Postoperatively antitubercular drug therapy, – traction, – intermittent active and assisted exercises, – suitable brace ambulation should be continued
  • 108.
    • In adultswith advanced arthritis or in cases which resulted in painful fibrous ankylosis during the process of healing, the knee joint may be treated by arthrodesis. • This option provides  painless stable knee  prevents recrudescence  corrects deformity  patients can do long hours of standing and walking. • However it imposes a lot of restrictions in sitting, using public transport and many other social activities.
  • 109.
  • 110.
    References • Tuberculosis ofskeletal system – S M Tuli • Campbell operative orthopaedics • Textbook of orthopaedics – Tureks . • Robbins and Cotran pathological basis of disease
  • 111.