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Prof, Magd Galal Professor of Pulmonary Medicine Faculty of Medicine For Girls Al-Azhar University 2015 Definition • Tuberculosis (TB) is caused by Mycobacterium tuberculosis. • In many cases, M tuberculosis becomes latent before it reactivates. Patients who are infected but who have no clinical, bacteriological, or radiographic evidence of active TB are said to have latent TB infection. Definition • When there is progression from latent infection to disease, it most commonly involves the lungs and is communicable in this form, • But may affect almost any organ system including the lymph nodes, CNS, bones/joints, genito-urinary tract, abdomen (intra-abdominal organs, peritoneum), and pericardium. Definition A case with TB in any site other than pulmonary is considered an extra pulmonary TB (EPTB) case. Epidemiology EPTB constitutes about 15 to 20 per cent of all cases of tuberculosis in immunocompetent patients and accounts for more than 50 per cent of the cases in HIV-positive individuals. Epidemiology Epidemiology Epidemiology Introduction In the 1980s, after a steady decline during preceding decades, there was a resurgence in the rate of tuberculosis in the World Wide that coincided with the acquired immunodeficiency syndrome epidemic. Disease patterns since have changed, with a higher incidence of disseminated and extra pulmonary disease now found. Introduction The diagnosis of extra pulmonary tuberculosis can be elusive, necessitating a high index of suspicion. Introduction Physicians should obtain a thorough history focusing on risk behaviors for human immunodeficiency virus (HIV) infection and tuberculosis. Antituberculous therapy can minimize morbidity and mortality but may need to be initiated empirically. A negative smear for acid-fast bacillus, a lack of granulomas on histopathology, and failure to culture Mycobacterium tuberculosis do not exclude the diagnosis. Introduction Novel diagnostic modalities such as adenosine deaminase levels and polymerase chain reaction can be useful in certain forms of extra pulmonary tuberculosis. In general, the same regimens are used to treat pulmonary and extra pulmonary tuberculosis, and responses to anti tuberculous therapy are similar in patients with HIV infection and in those without. Introduction Treatment duration may need to be extended for central nervous system and skeletal tuberculosis, depending on drug resistance, and in patients who have a delayed or incomplete response. Adjunctive corticosteroids may be beneficial in patients with tuberculous meningitis, tuberculous pericarditis, or miliary tuberculosis with refractory hypoxemia. Clinical Clues to Prompt Suspicion of EPTB Ascites with lymphocyte predominance and negative bacterial cultures Chronic lymphadenopathy (especially cervical) CSF lymphocytic pleocytosis with elevated protein and low glucose Differential diagnosis of Crohn’s disease and amebiasis Exudative pleural effusion with lymphocyte predominance, negative bacterial cultures, and pleural thickening Clinical Clues to Prompt Suspicion of EPTB HIV infection Joint inflammation (monoarticular) with negative bacterial cultures Persistent sterile pyuria Tuberculosis-endemic country of origin Unexplained pericardial effusion, constrictive pericarditis, or pericardial calcification Vertebral osteomyelitis involving the thoracic spine 1. Airborne infection control 2. Intensive case finding and treatment of TB 3. Diagnosis and treatment of LTBI Principles of Management Patients with suspected tuberculosis should have appropriate specimens sent for acid-fast bacillus (AFB) staining, mycobacterial culture, and histology. Hospitalization is not necessary for tuberculosis to be diagnosed unless clinically indicated. Hospitalized patients in whom infectious (i.e., pulmonary or laryngeal) tuberculosis is suspected should be placed in an airborne-infection isolation room and should wear a surgical mask during transport and in waiting areas.7 Principles of Management Health care workers and visitors entering the isolation room should wear at least N95 disposable respirators, as should health care workers performing procedures such as sputum induction, bronchoscopy, jet irrigation of abscesses, and autopsies. All patients with tuberculosis should have counseling and testing for HIV infection. The local health department should be notified of all confirmed cases of tuberculosis.7 Pathophysiology Infection with Mycobacterium tuberculosis requires inhalation of droplet nuclei. In the course of primary infection, a period of subclinical bacillaemia usually occurs and a small number of M tuberculosis organisms are contained in various body organs. Exposure may be followed by clearance, persistent latent infection, or progression to primary disease. Pathophysiology Successful containment of TB is dependent on the cellular immune system, mediated primarily through T-helper cells (TH1 response). T cells and macrophages form a granuloma with a centre that contains necrotic material (caseous centre) and M tuberculosis, and peripheral granulation tissue consisting primarily of macrophages and lymphocytes. The granuloma serves to prevent further growth and spread of M tuberculosis. These individuals are not infectious and have latent TB infection; the majority of these patients will have a normal chest x-ray and positive tuberculin skin test and positive interferon-gamma release assays. Pathophysiology Pleural TB (particularly primary disease) may occur from a few mycobacteria gaining access to the pleural space with a resultant T cell response and delayed hypersensitivity reaction. The effusion is due to increased capillary permeability and decreased lymphatic drainage. As TB pleural effusion results from intensive inflammatory response, recovery of M tuberculosis from the pleural fluid occurs in about 40% of cases. Pathophysiology Skeletal TB is an osteomyelitis that starts in the growth plates of bones where the blood supply is the richest, and from there spreads into joint spaces. Vertebral disease usually starts in the subchondral cancellous bone, from where it spreads to the cortex and on to the disc. Bone destruction is more extensive on the ventral aspect leading to anterior wedging. Paraspinous collections may also develop. Spinal or vertebral TB has been known historically as Pott's disease. Pathophysiology TB meningitis results from haematogenous spread of M tuberculosis with the development of submeningeal or intrameningeal foci called Rich foci. With rupture of a Rich focus into the subarachnoid space, meningitis develops. This may result from reactivation (more common in adults) or primary infection (more common in children). BCG vaccination is about 64% effective against TB meningitis in young children. Pathophysiology Abdominal TB includes disease of the intestines, peritoneum, and mesenteric lymph nodes. In peritoneal TB, the peritoneum becomes studded with tubercles. As protein-rich fluid is exuded, ascites accumulate. More than 90% of patients with peritoneal TB will have ascites; the remainder generally have more advanced disease and present with fibroadhesions ('doughy abdomen'). TB enteritis may occur secondary to ingestion of infected sputum or initial haematogenous spread. If the enteric source spreads to the mesenteric lymph nodes, they may rupture into the peritoneum. TB enteritis occurs most frequently in the ileocecal region. Its appearance may be ulcerative or hypertrophic. Pathophysiology Pericardial TB results from contiguous spread from adjacent mediastinal lymph nodes, or progression of a primary or latent focus within the pericardium. Some patients present with signs of cardiac constriction without an acute phase of pericarditis being noticed. Disseminated TB refers to simultaneous involvement of multiple organ sites that may occur with primary infection (particularly in immunocompromised individuals) or with reactivation. Disseminated TB is sometimes called miliary TB; its lesions are yellowish granulomas 1 to 2 mm in diameter that resemble millet seeds on chest x-ray. It is due to haematogenous spread of M tuberculosis. Tuberculous Lymphadenitis Tuberculous Lymphadenitis Lymphadenitis is the most commonly occurring form of extrapulmonary tuberculosis. Cervical adenopathy is most common, but inguinal, axillary, mesenteric, mediastinal, and intramammary involvement all have been described. Tuberculous Lymphadenitis Although previously considered a disease of childhood, lymphadenitis has a peak age of onset of 20 to 40 years Tuberculous Lymphadenitis Patients without HIV infection typically present with chronic, non tender lymphadenopathy. Patients with HIV infection usually present with fever, night sweats, and weight loss. The nodes are discrete, firm, and non tender; with time, a firm mass of matted nodes becomes visible . Tuberculous Lymphadenitis If untreated, the nodes become fluctuant and drain spontaneously with sinus tract formation. Tuberculous Lymphadenitis Excisional biopsy of the lymph nodes with histology, AFB stain, and mycobacterial culture is the diagnostic procedure of choice. Fine-needle aspiration is more reliable in patients with HIV infection because of the higher mycobacterial burden, and in these patients should be the initial diagnostic procedure. Polymerase chain reaction (PCR) for Mycobacterium tuberculosis on the fine-needle aspiration specimen enhances test sensitivity. Tuberculous Lymphadenitis During antituberculous therapy, affected nodes may enlarge or new nodes may appear, representing an immune response to killed mycobacteria. A similar phenomenon in patients with HIV infection who begin concurrent antiretroviral therapy is a result of immune reconstitution. Lymph node excision usually is not indicated. When lymph nodes are fluctuant and ready to drain, aspiration or incision and drainage appear to be beneficial. Pleural Tuberculosis Pleural Tuberculosis Chest radiography typically reveals a small to moderate, unilateral pleural effusion; about 20 percent of patients have associated pulmonary lesions. Computed tomography (CT) of the chest may show lymphadenopathy, pulmonary infiltrates, or cavitation not obvious on chest radiography . Pleural thickening of more than 1 cm is seen in most instances. Pleural Tuberculosis Pleural fluid is exudative with a lymphocyte predominance (i.e., more than 50 percent of white blood cells in more than 90 percent of effusion; in patients with less than two weeks of symptoms, an initial predominance of neutrophils may be seen. Pleural fluid glucose and pH can be low or normal. AFB smears of pleural fluid are seldom positive (5 percent of cases) unless the patient has tuberculous empyema. Pleural fluid cultures for M. tuberculosis are positive in less than 40 percent of cases. Pleural Tuberculosis The combined sensitivity of the analyses of pleural biopsy specimens (i.e., observation for caseating granulomas, AFB smear, and culture) is more than 90 percent. Tuberculin skin test results are positive in two thirds of patients. Biochemical markers such as adenosine deaminase, interferon gamma, and lysozyme in the pleural fluid can be useful A high level of adenosine deaminase (greater than 47 U per L [783 nkat per L]) was seen in 99 per cent of tuberculous effusions. Pleural Tuberculosis In countries with a low prevalence of tuberculosis, such as the United States, a normal or low level of pleural fluid adenosine deaminase has a high negative predictive value and can be used to exclude tuberculous pleurisy. Pleural fluid PCR for M. tuberculosis has a sensitivity of 80 percent and a specificity of 100 percent. Pleural Tuberculosis Tuberculous pleurisy responds well to medical therapy, with resorption of pleural fluid in six to 12 weeks. The effusion may resolve without therapy, but tuberculosis later recurs. Rare complications include bronchopleural fistula, empyema, and fibrothorax. Skeletal Tuberculosis Skeletal Tuberculosis Bone and joint tuberculosis may account for up to 35 percent of cases of extrapulmonary tuberculosis. Skeletal tuberculosis most often involves The spine, Tuberculous arthritis in weight-bearing joints and Extraspinal tuberculous osteomyelitis. Skeletal Tuberculosis Spinal tuberculosis (Pott’s disease) most commonly involves the thoracic spine. Infection begins in the anteroinferior aspect of the vertebral body with destruction of the intervertebral disc and adjacent vertebrae. Skeletal Tuberculosis The resulting anterior wedging and angulation of adjacent vertebral bodies with disc space obliteration are responsible for the palpable spinal prominence (gibbus) and a classic radiographic appearance. Paraspinal and psoas abscesses can develop, with extensions to the surface or adjacent tissues . Skeletal Tuberculosis Articular tuberculosis is a slowly progressive monoarthritis of the hip or knee. Presentation is indolent with pain, joint swelling, and decreased range of motion. Draining sinuses and abscesses are seen in chronic cases. Systemic symptoms usually are absent. Skeletal Tuberculosis Radiographic changes are nonspecific and include soft tissue swelling, juxtaarticular osteopenia, joint space narrowing, and sub chondral erosions Skeletal Tuberculosis Extra spinal tuberculous osteomyelitis often presents with local pain and can involve any bone. Involvement of adjacent structures may result in complications such as carpal tunnel syndrome, tenosynovitis, and facial palsy. Skeletal Tuberculosis Chest radiography shows pulmonary disease in one half of patients with osteoarticular tuberculosis, but active pulmonary disease is uncommon. Magnetic resonance imaging may be helpful to assess the degree of bony destruction and to identify soft tissue extension and encroachment on adjacent structures such as the spinal cord. Skeletal Tuberculosis Physicians should consider skeletal tuberculosis in patients with An indolent clinical course manifesting as osteomyelitis involving the thoracic spine or monoarticular septic arthritis With negative bacterial cultures. Skeletal Tuberculosis Arthrocentesis with mycobacterial cultures of synovial fluid yields positive results in up to 80 percent of patients with tuberculous arthritis. Synovial biopsy also may be diagnostic (caseating granulomas on histology or positive mycobacterial culture). Bone biopsy for culture and histology is required for diagnosis of tuberculous osteomyelitis. Skeletal Tuberculosis SOFT TISSUE TUBERCULOSIS ALONG THE MEDIAL ASPECT OF THE LEFT KNEE High-signal-intensity soft tissue abscess(white arrow), with adjacent bone marrow edema involving the medial condyle and a T2 hyperintense focus in the medial proximal tibia (black arrow) due to the associated osteomyelitis Skeletal Tuberculosis spina ventosa. (A) 99m Tc- methylene diphosphonte (MDP) whole body anterior and (B) posterior sweep views in a patient presenting with backache and low-grade fever showing diffuse increased radiotracer localization in the body of L4 and 5 vertebrae (arrows) suggestive of spinal TB. (Kind courtesy: Dr TC Kalawat, Department of Nuclear Medicine, Sri Venkateswara Institute of Medical Sciences, Tirupati) Skeletal Tuberculosis Aim of the treatment is to Control of the infection Care of the diseased part In the absence of neurologic impairment, unstable spine, or spinal cord compression, medical therapy alone should result in an excellent response. Surgery may be necessary to drain abscesses, debride infected tissue, or stabilize the spine and relieve spinal cord compression Skeletal Tuberculosis Antibiotic for secondary infection(for persistently draining sinus which gets secondary infections) . Bed sore care and treat other comorbid condition Building up of patient’s resistance – High protein diet . Excision of sinus tract - if sinus are persisting. Skeletal Tuberculosis Affected part should be rested during active stage of the disease. In upper limbs this can be done with the help of plaster slab and in lower limbs traction can be applied. As the disease comes under control and the pain reduces , joint mobilization is begun. Gradual mobilization should be encouraged with the help of suitable braces/appliances after 3-6 months of start of treatment when the healing is progressing, which are gradually discarded after about 2 years. Skeletal Tuberculosis Exercise is started as the joint regains movement and weight bearing started gradually as osteoporosis secondary to disease is reversed In presence of gross destruction especially in weight bearing joints, immobilization may be continued to obtain sound ankylosis . Skeletal Tuberculosis To summarise Distribution Spinal Tuberculosis (Pott's Disease) Thoracic Spine most commonly involved Associated with paraspinous abscess Destroys anterior Vertebral body and adjacent disc Results in anterior wedging Forms prominence of spine known as Gibbus May compress central cord Skeletal Tuberculosis Articular Tuberculosis (most common involvement) Monoarticular Arthritis of weight bearing joints Presents with insidious monoarticular pain, swelling May form superficial abscesses and drain to skin Poncet's Disease (rare) Acute sterile Polyarthritis Associated with visceral involvement Tuberculous Osteomyelitis May involve any bone Central Nervous System Tuberculosis Central Nervous System Tuberculosis Central nervous system tuberculosis includes Tuberculous meningitis (the most common presentation), Intracranial tuberculomas, and Spinal tuberculous arachnoiditis. Central Nervous System Tuberculosis Meningitis results from intense inflammation following rupture of a subependymal tubercle into the subarachnoid space. The ensuing arachnoiditis encases both cranial nerves and penetrating vessels, leading to cranial nerve palsies and communicating hydrocephalus. Cranial vasculitis may lead to focal neurologic deficits. Central Nervous System Tuberculosis Hypersensitivity to tuberculoproteins may cause meningismus and typical cerebrospinal fluid (CSF) findings. Cerebral edema causes impairment of consciousness, seizures, and raised intracranial pressure, whereas tuberculomas can manifest as spaceoccupying lesions. Central Nervous System Tuberculosis Meningitis An initial phase of malaise, headache, fever, or personality change is followed in two to three weeks by protracted headache, meningismus, vomiting, confusion, and focal neurologic findings. If untreated, mental status deteriorates into stupor or coma. Atypical presentations include a rapid progression simulating pyogenic meningitis, subtle cognitive decline mimicking dementia, and a predominant syndrome of encephalitis. Convulsions can occur at all stages of the illness. Central Nervous System Tuberculosis CSF typically reveals moderate lymphocytic pleocytosis (100 to 500 cells per μL [0.10 to 0.50×109 per L] initially, a neutrophilic predominance can be seen. CSF protein levels range from 100 to 500 mg per dL (1,000 to 5,000 mg per L) and can be extremely high (2 to 6 g per dL [20 to 60 g per L]), with xanthochromia in the presence of subarachnoid block. CSF glucose concentration usually is less than 45 mg per dL (2.50 mmol per L). Central Nervous System Tuberculosis AFB smears on CSF are positive in 10 to 90 percent of patients; sensitivity can be improved if large volumes of CSF from multiple lumbar punctures are examined, CSF is centrifuged and AFB smears are performed on the pellicle, or an experienced reviewer examines several high-powered fields Central Nervous System Tuberculosis CSF culture for M. tuberculosis is positive in 45 to 90 percent of cases but takes four to six weeks. CSF PCR for M. tuberculosis has a sensitivity of 56 percent and a specificity of 98 percent, and therefore should not be used to exclude tuberculous meningitis. An elevated CSF adenosine deaminase level supports the diagnosis in the appropriate clinical setting. A CT scan of the head with contrast may reveal basilar arachnoiditis, infarction, hydrocephalus, or tuberculomas. Central Nervous System Tuberculosis Empiric antituberculous therapy should be initiated as soon as clinical, laboratory, or imaging findings suggest tuberculous meningitis. Delay in initiation of therapy has been directly associated with adverse outcomes. Antituberculous therapy is recommended for at least nine to 12 months. Central Nervous System Tuberculosis Adjunctive corticosteroid therapy with dexamethasone (Decadron) for the initial six to eight weeks in patients with tuberculous meningitis has been associated with reduced mortality and fewer neurologic sequelae. Mortality is highest in patients younger than five years, those older than 50 years, and those in whom illness has been present for longer than two months. Abdominal Tuberculosis Abdominal Tuberculosis Abdominal tuberculosis may involve the gastrointestinal tract, peritoneum, mesenteric lymph nodes, or genito-urinary tract. Other organs (e.g., liver, spleen, adrenal glands) usually are affected as a consequence of miliary tuberculosis. GASTROINTESTINAL TUBERCULOSIS Symptoms include abdominal pain, diarrhea, weight loss, and fever. Melena, rectal bleeding, and abdominal tenderness also can be present. A mass in the right lower quadrant is palpable in 25 to 50 percent of patients. GASTROINTESTINAL TUBERCULOSIS Pathophysiology Involves any part of Gastrointestinal tract Ileocecal most commonly affected Risk of contracting gastrointestinal Tb Parallels severity of pulmonary disease GASTROINTESTINAL TUBERCULOSIS Tuberculous enteritis can result from swallowing of infected sputum, ingestion of contaminated food, hematogenous spread, and direct extension from adjacent organ The intestinal lesions can be ulcerative (most common), hypertrophic, or ulcero-hypertrophic. s.35 GASTROINTESTINAL TUBERCULOSIS The ileocecal area and jejunoileum are the most common sites of involvement. Complications include obstruction, perforation, and fistula formation. Rectal lesions usually present as anal fissures, fistulas, or perirectal abscesses. Barium contrast studies and colonoscopy may show ulcers, strictures, a deformed cecum, incompetent ileocecal valve, or fistulas. An abdominal CT scan can define extraluminal pathology, especially lymphadenopathy. GASTROINTESTINAL TUBERCULOSIS Differential Diagnosis Crohn's Disease Critical to differentiate from Tuberculosis Crohn's Treatment disseminates Tuberculosis Infection Yersinia Actinomyces Amebiasis Colon Cancer GASTROINTESTINAL TUBERCULOSIS Diagnosis Endoscopy Mucosal injury Ulcerations Hypertrophic lesions Dense bandlike fibrosis Mucosal biopsy shows Acid Fast Bacilli (low yield) Culture of biopsy specimens CT Abdomen Barium Enema Shortened and retracted cecum GASTROINTESTINAL TUBERCULOSIS Complications Intestinal Obstruction Bowel perforation Enteric fistulas GASTROINTESTINAL TUBERCULOSIS A six-month course of antituberculous therapy is recommended. Surgery is reserved for patients with complications TUBERCULOUS PERITONITIS Risk Factors HIV Infection. Cirrhosis. Ambulatory Peritoneal Dialysis. Pathophysiology Results from peritoneal Tuberculosis reactivation Symptoms Abdominal Pain Fever Signs Ascites TUBERCULOUS PERITONITIS Laboratory: Peritoneal fluid Exudative: Serum to Ascites albumin <1.1 g/dl White Blood Cells >150/mm3 with Lymphocytes predominance. A neutrophilic pleocytosis may be seen with tuberculous peritonitis complicating continuous ambulatory peritoneal dialysis. Send fluid for AFB smear and culture One liter is preferred to increase Test Sensitivity Measures with highest sensitivity and Specificity Adenosine deaminase >33 U/L Peritoneal biopsy GENITOURINARY TUBERCULOSIS GENITOURINARY TUBERCULOSIS GENITOURINARY TUBERCULOSIS Renal disease may be the result of direct infection of the kidney and lower urinary tract or may present as secondary amyloidosis. Patients present with dysuria, hematuria, or flank pain. More than 90 percent of asymptomatic patients have sterile pyuria with or without microscopic hematuria GENITOURINARY TUBERCULOSIS Chest X-ray Abnormal in 50% Active pulmonary TB in 5-10% Sequelae of old TB of past infection. GENITOURINARY TUBERCULOSIS Fluoroscopy: IVP Traditional plain film IVP is quite sensitive to renal tuberculosis with only 10% of affected patients having normal imaging. Features include: parenchymal scars 50% moth eaten calyces: early finding Irregular caliectasis phantom calyx hydronephrosis GENITOURINARY TUBERCULOSIS Lower urinary tract signs (see bladder and ureteric tuberculosis) also recognised include: Kerr kink3 sawtooth ureter pipe-stem ureter beaded or corkscrew ureter thimble bladder GENITOURINARY TUBERCULOSIS Excretory urography in a patient with renal tuberculosis shows an irregular cavity at the upper pole calyx of the right kidney. Note the multiple tiny calcifications in the liver, spleen, and right adrenal gland due to calcified tuberculous granuloma. GENITOURINARY TUBERCULOSIS Excretory urography in a woman with a history of tuberculosis of the breast. The film shows irregular cavitation in the lower pole calyx of the left kidney due to renal tuberculosis. GENITOURINARY TUBERCULOSIS Lobar calcification in a large destroyed right kidney in a patient with renal tuberculosis. Note the involvement of the right ureter. GENITOURINARY TUBERCULOSIS Excretory urography in a patient with tuberculosis of the ureter and bladder. The lower end of the right ureter demonstrates an irregular caliber with an irregular stricture at the right vesico-ureteric junction. Note the asymmetric contraction of the urinary bladder, with marked irregularity due to edema and ulceration. GENITOURINARY TUBERCULOSIS CT is the most sensitive modality for visualising renal calcifications and CT IVP is more sensitive at identifying all manifestations of renal tuberculosis 4. early papillary necrosis (single or multiple) resulting in uneven caliectasis progressive multifocal strictures can affect any part of the collecting system generalised or focal hydronephrosis mural thickening and enhancement poorly enhancing renal parenchyma, either due to direct involvement or due to hydronephrosis endstage progressive hydronephrosis results in very thin parenchyma, mimicking multiple thin walled cysts amorphous dystrophic calcification eventually involves the entire kidney (known as putty kidney) GENITOURINARY TUBERCULOSIS GENITOURINARY TUBERCULOSIS The role of nephrectomy is controversial and depends on the degree of renal impairment, bilateral vs unilateral disease and the status of the lower urinary tract. Nephrectomy, partial nephrectomy or cavernostomy can be performed both open and endoscopically 5. GENITOURINARY TUBERCULOSIS Male genital tuberculosis usually is associated with renal tuberculosis. It involves the prostate, seminal vesicles, epididymis, and testes, in order of incidence. Patients usually present with a scrotal mass , and diagnosis is made by surgery. Oligospermia is common and may be persistent. GENITOURINARY TUBERCULOSIS Female genital tuberculosis begins in the endosalpinx and can spread to the peritoneum, endometrium, ovaries, cervix, and vagina. Patients present with pelvic pain, infertility, and vaginal bleeding. Response to chemotherapy is excellent for all forms of genital tuberculosis; surgery in women is necessary for large tuboovarian abscesses. MILIARY TUBERCULOSIS MILIARY TUBERCULOSIS Miliary tuberculosis : refers to any progressive, disseminated form of tuberculosis; the disease can occur during primary dissemination or after years of untreated tuberculosis. Miliary disease is seen in 10 % of patients who have AIDS and pulmonary tuberculosis, 38 %of those who have AIDS and extra-pulmonary tuberculosis.5 MILIARY TUBERCULOSIS Presenting symptoms include fever, chills, night sweats, weight loss, and anorexia. Clinical manifestations depend on the organs involved. Fulminant disease including septic shock, acute respiratory distress syndrome, and multiorgan failure has been described. MILIARY TUBERCULOSIS A chest radiograph or CT scan reveals numerous 2to 3-mm nodules scattered throughout the lung in more than 85 percent of patients MILIARY TUBERCULOSIS Common laboratory abnormalities include normochromic anemia, leukopenia or leukocytosis, elevated sedimentation rate, and hyponatremia. MILIARY TUBERCULOSIS Examination of the sputum, bronchoalveolar lavage, gastric washings, CSF, blood culture, or biopsies of liver and bone marrow may be necessary for diagnosis. A tuberculin skin test result is positive in less than 50 percent of patients. Antituberculous therapy (and corticosteroids in select situations) is as previously outlined TUBERCULOUS PERICARDITIS TUBERCULOUS PERICARDITIS Tuberculous pericarditis develops secondary to contiguous spread from mediastinal nodes, lungs, spine, or sternum, or during miliary dissemination. The onset may be abrupt or insidious with symptoms such as chest pain, dyspnea, and ankle edema . Cardiomegaly, tachycardia, fever, pericardial rub, pulsus paradoxus, or distended neck veins may be found on examination. Pericardial biopsy yields a definitive diagnosis more often than pericardial fluid alone TUBERCULOUS PERICARDITIS In addition to antituberculous therapy, corticosteroids are recommended to hasten resolution of symptoms and to reduce reaccumulation of fluid. The risk of progression to constrictive pericarditis or mortality is not altered by corticosteroids. Open pericardial drainage is favoured over repeated pericardiocentesis. TNF-α INHIBITOR–ASSOCIATED TUBERCULOSIS TNF-α INHIBITOR–ASSOCIATED TUBERCULOSIS Two recent reports describe several cases of active tuberculosis occurring after treatment with the TNFα inhibitors infliximab (Remicade) and etanercept (Enbrel), mainly in patients with rheumatoid arthritis or Crohn’s disease. Tuberculosis was diagnosed sooner after initiation of infliximab than after initiation of etanercept (median of 12 weeks versus 12 months). TNF-α INHIBITOR–ASSOCIATED TUBERCULOSIS Extra pulmonary tuberculosis accounted for 52 to 57 percent of cases. As a result, it is now recommended that patients be screened for latent tuberculosis infection or active disease before initiation of therapy with a TNF-α inhibitor. Treatment of extra pulmonary TB Treatment of extra pulmonary TB Provider-initiated HIV testing is recommended as part of the evaluation of all TB patients and patients in whom the disease is suspected. HIV testing is especially important in persons with or suspected of having EPTB because of the increased frequency of extrapulmonary involvement in persons with immunosuppression. Extrapulmonary TB is considered to be WHO clinical stage 4 HIV disease Treatment of extra pulmonary TB Pulmonary and extra pulmonary disease should be treated with the same regimens Recommend duration 9–12 months of treatment for TB meningitis given the serious risk of disability and mortality, and 9 months of treatment for TB of bones or joints because of the difficulties of assessing treatment response . Treatment of extra pulmonary TB Unless drug resistance is suspected, adjuvant corticosteroid treatment is recommended for TB meningitis and pericarditis. In tuberculous meningitis, ethambutol should be replaced by streptomycin. Treatment of extra pulmonary TB Although sometimes required for diagnosis, surgery plays little role in the treatment of extrapulmonary TB. It is reserved for management of late complications of disease such as hydrocephalus, obstructive uropathy, constrictive pericarditis and neurological involvement from Pott's disease (spinal TB). For large, fluctuant lymph nodes that appear to be about to drain spontaneously, aspiration or incision and drainage appear beneficial Key Points Diagnosis of EPTB poses challenges due to the diversity of symptoms with which EPTB may present, the low level of suspicion among clinicians, and the difficulty in obtaining an adequate sample for confirmation. Raising awareness among non-pulmonary physicians about EPTB and guidelines for diagnosis and treatment of EPTB may result in more timely and adequate diagnosis. Key Points TB can spread from the lungs through the bloodstream to many sites. Symptoms depend on the affected organ but typically include fever, malaise, and weight loss. Diagnose based identification of bacilli in infected fluid or tissue by microscopic examination and culture and/or nucleic acid amplification tests. Treat with multiple drugs for several months and sometimes with surgery. Drug resistance is a major concern and is increased by poor adherence, use of too few drugs, and inadequate susceptibility testing. Prof; Magd Galal Cough Etiquette