Abdiminal tuberculosis

Abdiminal tuberculosis

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  ABDOMINAL TUBERCULOSIS DR SASIDHAR Postgraduate Department of pediatric surgery
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  HEADINGS ABDOMINAL TUBERCULOSIS DEFINITION1 • The termabdominal tuberculosis refers to tuberculous infection of the gastrointestinal tract, mesenteric lymph nodes, peritoneum and omentum, and of solid organs related to the gastrointestinal tract such as the liver, spleen and pancreas . Definition history Agent Epidemiology Routes of transmission Pathology and Pathogenesis Classification of abdominal TB Individual types Investigations management Note on HIV and tuberculosis
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  History1 • Tuberculosis wasfirst recognized in the fourth century BC • Hippocrates described a condition resembling tuberculosis in a patient with pulmonary lesions and intestinal disease. • major cause of intestinal strictures and bowel obstruction In the nineteenth century and the early part of twentieth century,
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  1882 - identificationof the causative organism, Mycobacterium tuberculosis, by Robert Koch Koch’s Postulates 1998 - the complete genetic sequence of M. tuberculosis was identified.
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  Bacterial agent1, 2 •Mycobacterium tuberculosis (90%), M. bovis (largely eliminated ) • The tubercle bacillus is a Gram-positive, aerobic, non-motile, non- spore-bearing organism that is identified by the Ziehl–Neelson acid- fast differential staining method (high content of mycolic acids in the cell wall) • Culture of the organism is Löwenstein–Jensen medium, which requires an incubation period of 4 to 6 weeks. • Liquid culture medium, may provide faster results and is more sensitive. • The virulence of M. tuberculosis is established by guinea-pig inoculation.
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  Mycobacterium tuberculosis: Ziehl-Neelsen stain Lowenstein-JensenMedium.
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  Epidemiology • It iscommon in India and developing countries, more frequently in people of poor socioeconomic circumstances. • It is the 6th most common type of extrapulmonary tuberculosis following lymph nodes, pleura, genitourinary tract, bones and joints, meninges2. • Its incidence is high in HIV infected patients • 24th March - World Tb day3. • TB declared as notifiable disease by INDIAN GOVERNMENT on may 9th 2012
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  Routes of transmission •6 Routes. 1. Ingestion of contaminated food may cause primary intestinal tuberculosis. 2. Hematogenous spread- during the bacteraemic phase that may follow primary pulmonary tuberculosis 3. swallowed sputum containing tuberculous bacilli 4. spread from adjacent organs or Retrograde spread from female genital tuberculosis. 5. Through lymph channels from infected nodes. 6. disseminated in the bile, since they are sequestrated and excreted from granulomas in the liver.
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  Pathology and pathogenesis •Abdominal tuberculosis is either primary or secondary. • Primary abdominal tunerculosis results from the ingestion of the milk or food infected with M.bovis. • Secondary abdominal tuberculosis is caused by M.tuberculosis and is due to the other routes described.
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  Pathogenesis of M.tuberculosis
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  Pathogenesis Bacilli in depthof mucosal glands  Inflammatory reaction  Phagocytes carry bacilli to Peyer’s Patches  Formation of tubercle Submucosal tubercles enlarge  undergo necrosis  Endarteritis & edema  Sloughing  Ulcer formation  Accumulation of collagenous tissue Thickening & Stenosis Inflammatory process in submucosa penetrates to serosa Tubercles on serosal surface  Bacilli reach lymphatics •Lymphatic obstruction of mesentery and bowel •Thick fixed mass •Regional lymph nodes •Hyperplasia •Caseation necrosis •Calcification
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  Types4 1. Intestinal – Ileocaecalregion  Ulcerative—60%.  Hyperplastic.  Ulcero-hyperplastic. – Ileal region, commonly:  Stricture type. 2. Peritoneal tuberculosis • a. Acute. • b. Chronic. – i. Ascitic type. – ii. Encysted (loculated) type. – iii. Plastic (fi brous/adhesive) type. – iv. Purulent type. 3. Tuberculosis of mesentery and its lymph nodes 4. Ano-recto-sigmoidal—present as fistula, fissure, abscess, mass. 5. Involvement of liver, spleen and other organs as a part of miliary tuberculosis. 6. Tuberculosis of the omentum. 7. Rare types: – Oesophageal (0.2% of abdominal tuberculosis) – gastroduodenal (1% of abdominal tuberculosis) – retroperitoneal tuberculosis. Intestinal tuberculosis is called as Konig’s syndrome (1892)5.
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  Types
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  ILEOCAECAL TUBERCULOSIS • Mostcommon site of abdominal tuberculosis • due to: – Stasis – Abundant payer’s patches – Alkaline media – Bacterial contact time is more – Minimal digestive activity – Maximum absorption in the area • Types  Ulcerative—60%.  Hyperplastic.  Ulcero-hyperplastic.
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  Ileocaecal tuberculosis withrolled up omentum. Note the sites and tubercles in ileocaecal valve, which will be incompetent due to fibrosis.
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  Ileocaecal tuberculosis. (A)Note the multiple transverse undermined ulcers. (B) Note the ileocaecal tuberculosis with stricture. A B
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  Types A. Ulcerative— • mostcommon 60%. • Circumferential transverse ulcers—with skip lesions. • common in old, malnourished people. • Long-standing ulcers cause fibrosis and later stricture formation. (Napkin ring stricture-- is common in ileal part). • Bowel adhesions are common. • Patient mainly presents with diarrhea, blood in stool, loss of appetite and reduced weight.
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  B. Hyper plastic---- • 10% common, less virulent, seen in young well nourished individuals • Fibroblast reaction in submucosa and subserosa causes thickening of bowel wall and lymph node enlargement, leading to nodular mass (tumor-like) formation. • It is common in caecal part. • It causes extensive chronic inflammation, fibrosis, bowel adhesions, nodal enlargement, often presents with mass in the right iliac fossa. • When present as a mass, it can cause sub acute intestinal obstruction. • Commonly primary form.
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  Differences between ulcerativeand hyperplasic types • ULCERATIVE (60%) 1.Secondary to pulmonary tuberculosis 2. Virulent organism 3. Poor body resistance, old people 4. Multiple transverse ulcers commonly in the ileum, often in the caecum 5. Clinically presents with diarrhoea, bleeding P/R, loss of appetite and reduced weight 6. Complications: Stricture, intestinal obstruction 7. Chest X-ray shows primary lesion. 8. Barium study shows ileal strictures with hypermotility • HYPERPLASTIC (10%) 1. Primary GIT tuberculosis, could be due to bovine bacilli 2. Less virulent organism 3. Good body resistance, young individual 4. Chronic granulomatous lesion in the ileocaecal region 5. Presents as a mass in right iliac fossa 6. Complication: Subacute intestinal obstruction 7. No primary lesion in chest X-ray 8. Barium study—pulled-up caecum, obtuse ileocaecal angle
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  Ileocaecal and mesenterictuberculosis. Ileocaecal tuberculosis or tuberculous mesenteric lymphadenitis presenting as mass in the right iliac fossa
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  ILEAL TUBERCULOSIS • Itis usually stricture type. • It may be multiple. • It presents usually with intestinal obstruction. • Bowel adhesion, localisation, fibrosis, secondary infections are quiet common. • Perforation (5%) though rare may lead to peritonitis.
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  PERITONEAL TUBERCULOSIS Pathology inPeritoneal Tuberculosis Enormous thickening of the parietal peritoneum with multiple tiny yellowish tubercles.  Dense adhesions in peritoneum and omentum with content inside as small bowel looking like abdominal cocoon. It may precipitate intestinal obstruction.  Multiple dense adhesions between bowel loops and between bowel and peritoneum and omentum
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  A B C A to C:On-table findings in intestinal tuberculosis, of extensive involvement with multiple tiny tubercles, thickening, adhesions and involvement of mesenteric lymph nodes.
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  PERITONEAL TUBERCULOSIS • a.Acute. • b. Chronic. – i. Ascitic type. – ii. Encysted (loculated) type. – iii. Plastic (fibrous/adhesive) type. – iv. Purulent type.
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  Acute type • MimicsAcute Abdomen • It is an on-table diagnosis • Presents with features of peritonitis. • It is due to perforation or rupture of mesenteric tuberculous lymph nodes
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  Chronic type – Types a)Ascitic form b) Encysted form c) Plastic form d) Purulent form
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  Ascitic form distension ofabdomen with dilated veins +. presents with hydrocele in male with patent processus vaginalis, umbilical hernia, shifting dullness, fluid thrill Ascitic tap reveals straw coloured fluid from which AFB can be isolated. Fluid is pale yellow, clear, rich in lymphocytes, with high specific gravity.
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  Encysted (Loculated) ascites •Ascites gets loculated because of the fibrinous deposition. • Dullness, which is not shifting, is the typical feature. • They may present as intra-abdominal mass, which may mimic ovarian cyst, retroperitoneal cyst or mesenteric cyst.
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  Plastic type wide spreadadhesions c/o recurrent colicky abdominal pain, diarrhoea, wasting, and loss of weight, mass abdomen, and doughy abdomen Differential diagnosis: Peritoneal carcinomatosis
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  Purulent form • Itis invariably due to tuberculous salpingitis • presents as a mass in the lower abdomen containing pus, omentum, fallopian tubes, small and large bowel. • Cold abscess gets adherent to the abdominal wall, umbilicus and may form an umbilical fistula. • Patient commonly has got genitourinary tuberculosis
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  TUBERCULOUS MESENTERIC LYMPHADENITIS • Infectionis usually through the Peyer‘s patches • Commonly right-sided lymph nodes are involved • presents with general symptoms, Pain in umbilical region and right iliac fossa, mass in right iliac fossa, or features of acute appendicitis. • Often coils of intestine get adherent to the caseated mesenteric lymph nodes leading to intestinal obstruction.
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  caseating material maycollect between the layers of the mesentery, forming a cold abscess -- Pseudomesenteric cyst Massive enlargement of mesenteric lymph nodes due to tuberculosis is called as tabes mesenterica. more common in children, Present with anaemia, fever, loss of appetite and reduced weight, failure to thrive, palpable mass in right iliac fossa which is firm and nodular.
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  Differential Diagnosis • Carcinomacaecum. • Lymphoma. • Retroperitoneal tumour. • Nonspecific lymphadenitis. (Acute nonspecific mesenteric lymphadenitis is called as nurses’ syndrome).
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  ANO-RECTO-SIGMOIDAL TUBERCULOSIS • It mimicscarcinoma rectum. • It presents as tenesmus, diarrhoea, and discharge from the fistula and occasionally as mass per abdomen. • Rectal tuberculosis occurs usually within 10 cm of anal verge. • Fistulas are painful and characteristically not indurated. • Tuberculous fistulas are commonly multiple. • Tuberculous anal ulcers when occur are shallow, bluish, with undermined edges.
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  TUBERCULOSIS OF THEOMENTUM • It usually occurs as a part of the other types of abdominal tuberculosis. • Rolled up omentum with thickening is characteristic. • Often cold abscess can develop -- can be dealt with laparoscopy safely under the cover of ATDs. • In all abdominal tuberculosis, drug treatment is for one year • In adrenal tuberculosis and severe adhesions steroids may be beneficial.
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  Omental tuberculosis showingtubercles
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  Different clinical presentationsof abdominal tuberculosis • Clinical presentation may be: – Acute – Acute on chronic – Chronic • Common in 25-50 years age group. Equal in both sexes. • Constitutional symptoms: – Anaemia, loss of weight and appetite (80%). – Diarrhoea—10-20%. – Fever—50-70%. – Over all Observed in 30% of patients
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  • Abdominal pain-most common symptom (90%), dull in mesenteric type; colicky in intestinal type • Mass in right iliac fossa, (35%) which is hard, nodular,nonmobile, nontender with impaired resonance ---may mimic carcinoma caecum. • can be associated with adenocarcinoma of caecum, or large bowel lymphoma or HIV.
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  Types: • Ulcerative—diarrhoea andmalabsorption • Stricture—subacute or acute intestinal obstruction • Hyperplastic—mass abdomen (RIF) and obstruction • Ascites—generalised distension of abdomen • Localised -- intra-abdominal mass, which may mimic ovarian cyst, retroperitoneal cyst or mesenteric cyst. • Peritoneal—abdominal cocoon; vague abdominal pain, • parietal peritoneal thickening as doughy abdomen; mass abdomen • Mesenteric—tabes mesenterica, obstruction, mass • Associated tuberculosis of other organs is seen in 30% of cases
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  Atypical presentations: • LowerGI bleed, fistula-in-ano, PID like pain, gastric disease symptoms, dysphagia, GI fistulae, perforation
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  Investigations 1. Chest Xray– for primary focus 2. Blood investgations: Mantoux, ELISA, serum IgG 3. ESR- raised 4. Plain X-ray abdomen I. Intestinal obstruction II. Calcified lymph nodes III. Hollow viscous perforation IV. Calcified Granuloma in liver
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  Barium study X-ray(Enteroclysis followed by barium enema or barium meal follow through X-ray) (efficacy—75%)  Pulled up caecum, conical caecum, pulled down hepatic flexure,  Obtuse ileocaecal angle  Steirlin sign --Hurrying of barium due to rapid flow and lack of barium in inflamed segment due to Incompetent ileocaecal valve, ileocaecal spasm  Napkin lesions --Ulcers and strictures in the terminal ileum and caecum  Earliest signs are—increased transit time; hyper segmentation (chicken intestine); flocculation of barium  Other signs are—persistent narrow stream (string sign); multiple strictures with enormous dilatation of proximal ileum (mega ileum); straightening of ileocaecal junction with ‘goose neck’ deformity.
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  Pulled-up caecum, obtuse ileocaecalangle— ileocaecal tuberculosis multiple strictures with enormous dilatation of proximal ileum (mega ileum);
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   Fleischner signor Inverted umbrella sign -- Narrow ileum with thickened ileocaecal valve string sign-- persistent narrow stream
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  hyper segmentation- chicken intestine
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  Ultrasound features observedin abdominal tuberculosis • Thickened bowel wall, mesentery, omentum, peritoneum • Loculated ascites with fine septae • Interloop ascites with alternate echogenic and echofree areas— Club- sandwich appearance • Bowel loop radiates from its mesenteric root—stellate sign • Mesenteric thickness more than 15 mm • Hepatosplenomegaly • Lymph nodal enlargement matted • Pulled up caecum presenting with a mass in subhepatic region— “pseudokidney sign”( also seen in intussuception) • Concentric uniform mural thickening Club-sandwich appearance
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  CT scan inabdominal tuberculosis It is very useful and reliable investigation It is done with oral contrast- CT enteroclysis Findings are: – Thickened bowel wall, thickened peritoneum – Ileocaecal valve thickening – Enlarged/necrosed/matted mesenteric nodes often with cold abscess – Adhesions – Mesenteric thickening and nodules – Nodules in the peritoneum/solid organs like liver – Adhesions in the bowel/stricture/dilatations of the bowel/ features of obstruction – Loculated ascites CT guided FNAC/biopsy/aspiration of fl uid can be done
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  Colonoscopy •To rule outcarcinoma •Shows mucosal nodules, ulcers, strictures, deformed ileocaecal valve, mucosal oedema and diffuse colitis •Biopsy can be taken to eslablish the diagnosis Capsule endoscopy is also useful to see small intestinal (tuberculous) pathology in difficult cases. Can cause obstrction at stricture site.
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  Laparoscopy •aids in directvisualisation, •to collect ascitic fluid for analysis •to take biopsy Blind percutaneous needle peritoneal biopsy using Cope’s/ Abraham’s needle is also practiced. Ascitic tap fluid analysis Bactec MGIT broth culture
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  Recent serological investigationsare • Interferon-γ Release Assays -- IGRAs Based on the detection of IFN-γ - Released by sensitized T cells on stimulation with very specific Ags . – T-Spot TB test - Directly count the number of IFN-γ- secreting T cells – Quantiferon TB Gold In-Tube test - Measures the concentration of IFN-γ secretion • Early secretory antigen target-6 (ESAT 6) & Culture filtrate protein-10 (CFP 10) – Both derived from a very specific region of MTb, the region of difference 1 (RD1). This segment (RD1) is deleted from all strains of BCG and the majority of environmental mycobacteria. – Advantage - Discriminate between MTB infection and previous use of BCG vaccine.
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  • polymerase chainreaction (PCR) -- molecular tests for detection of nucleic acids • Nucleic acid amplification assays – – assays amplify M. tuberculosis-specific nucleic acid sequences using a nucleic acid probe – major limitation of NAA tests is that they give no drug-susceptibility information. – Require as few as IO bacilli from a given sample – specificity in the range of 98% to 99%. – various types • AMPLICOR M. TUBERCULOSIS assay • Amplified M.tuberculosis Direct (AMTD2) assay • LCx MTB assay, ABBOTT LCx probe system • BD ProbeTec energy transfer (ET) system (DTB) • INNO-LiPA RIF.TB assay • 16S rRNA gene sequence analysis
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  Ascitic fluid inabdominal tuberculosis • Exudate with protein level > 2.5 g/dl • Serum-ascitic fluid albumin gradient is < 1.1 • Lymphocyte predominant cells with count as high as 4000/mm3 >250/cumm • AFB in ascitic fluid is seen only < 3% cases • ADA (Adenosine deaminase activity) in ascitic fluid (95% specificity and 98% sensitivity) • Specific gravity >1.016 • Glucose < 30 mg • Decreased pH • LDH more than 90 units/litre
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  Complications of abdominal tuberculosis •Obstruction—20% • Malabsorption, blind loop syndrome • Dissemination of tuberculosis to other areas of abdomen as well as extra-abdominal sites • Faecal fistula • Cold abscess formation • Haemorrhage, perforation (rare)
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  treatment • Medical – firstline of management – Anti tuberculous therapy (ATT) • surgical
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  Medical management2 DRUG DOSAGE (mg/kg) ADVERSEEFFECTS ISONIAZID 5 PERIPHERAL NEURITIS, hepatitis, fever, rashes, acne. RIFAMPACIN 10 HEPATITIS, orange urine, skin rashes, ‘flu syndrome’, purpura ETHAMBUTOL 15 OPTIC NEURITIS,hyperurecemia PYRAZINAMIDE 25 Hepatotoxicity, hyperurecemia, arthralgia, rashes. STREPTOMYCIN 15 OTOTOXICITY, NEPHROTOXICITY -WHO recommends 6-9 months course -Commonly patient presents with complications and late presentations are also common in many. So, more often treatment for one year may be required in these patients.
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  SECOND LINE DRUGS Amikacin Kanamycin  Paraaminosalicylic acid  Ciprofloxacin  Ofloxacin  levofloxacin  Clarithromycin  Azithromycin  Rifabutin In drug resistance cases second line drugs are needed. Directly observed therapy (DOT-S) If facilities for directly observed therapy are available, initial treatment is the same as in short-term therapy
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  Indications for steroidsin tuberculosis • Miliary tuberculosis • Tuberculous meningitis • Adrenal tuberculosis • Tuberculous pericarditis • Pleural and endobronchial tuberculosis • In abdominal tuberculosis to prevent adhesions • Tuberculosis of the mediastinal lymph nodes (Rapidly • progressive) • Genitourinary tuberculosis • Ocular tuberculosis
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  Surgical management • Indicationsare Intestinal obstruction Severe haemorrhage.  Acute abdominal presentation like perforation.  Intra-abdominal abscess formation or fistula formation.  Uncertain diagnosis.
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  Surgical Management 1. Ileocaecalresection with 5 cm margin 2. Stricturoplasty- single stricture
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  3. Single strictutrewith friable bowel or Multiple Strictures or stricture within 10 cm of ileocaecal valve : Resection and anastomosis 4. Multiple strictures with long segment gaps: Multiple stricturoplasty 5. If Perforation - resection and anastomosis is done, In severely contaminated peritoneum, resection and exteriorisation is done. Bowel continuity is maintained after proper antituberculous chemotherapy and proper nutritional improvement. 6. During therapy, if patient develops ileocaecal obstruction, ileotransverse colon anastomosis (bypass) can be done. 7. Adhesive obstruction may be released through laparoscopic adhesiolysis. 8. Drainage of intra-abdominal abscess, perianal abscess and treatment for tuberculous fistula-in-ano is done when necessary.
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  Exploratory laparotomy --revealsstraw-coloured fluid with tubercles in the peritoneum, greater omentum and bowel wall. Fluid is evacuated and collected for AFB study and culture. Omental biopsy is taken. Abdomen is closed (without a drain) with tension sutures to prevent burst abdomen and ATD is started. Management of acute type of peritoneal tuberculosis include:
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  9. Treatment ofloculated form of peritoneal tuberculosis is U/S guided aspiration or laparoscopic aspiration along with ATD‘s. Laparoscopic picture of loculated ascites due to abdominal tuberculosis. Fluid is getting aspirated using a needle under laparoscopic vision. Straw coloured ascitic fluid
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  Treatment of purulentform of peritoneal tuberculosis is ATD, exploration of umbilicus, exploration of fistula and bowel by pass is done. Prognosis is poor in this type. ANO-RECTO-SIGMOIDAL TUBERCULOSIS : Treatment is ATD‘s, fistulectomy, often sigmoid resection.
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  Rarer types ofGI tuberculosis
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  TB- Oesophagus (0.2%) Mimicsoesophageal carcinoma Mid oesophageal ulcer, dysphagia and odynophagia, Low grade fever Pathology: Extension from nearby tubercular lymph nodes into esophagus. Barium Swallow •Patient with mediastinal lymphadenopathies that produced a fistula demonstrated by endoscopy. •Extensive esofageal ulceration (black arrows). • Extrinsic compression due to lymphadenopathies is appraised (white arrow).
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  TB- Gastroduodenum • occurringin 0.3 to 2.3 per cent of patients with pulmonary tuberculosis. • Uncommon – Acidic environment – Rapid gastric emptying – Paucity of Peyer’s patches in stomach. • Gastric TB- May mimic Peptic ulcer not relieving to anti-secretory therapy or gastric carcinoma, or gastric sarcoidosis. Similar appearances are also seen in syphilis of the stomach. • Tuberculosis of the stomach presents as an ulcerative, granulomatous, or fibrosing lesion. the last two types may result in gastric-outlet obstruction. • Duodenal TB- Obstruction due to extrinsic compression by lymph nodes.
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  Other presentations: – Perforation –Fistula – Ulcer excavation into pancreas – Obstructive jaundice due to CBD compression • Antituberculous chemotherapy should be initiated in all patients; this is curative in most, especially those with ulcerative lesions. • Surgical intervention is required if gastric-outlet obstruction persists despite treatment. • usual surgical approach is a partial gastric resection such as a Billroth gastrectomy or a sleeve resection.
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  Jejunal TB • Presentswith – Single or multiple strictures – Intestinal obstruction – Perforation (proximal to the stricture)
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  Segmental Colonic TB(9.2%) • It is involvement of colon without ileocaecal region. • Involves sigmoid, ascending and transverse colon. • Pain and hematochezia is common.
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  Appendiceal • Tuberculosis ofthe appendix is reported in 0.1 to 3 per cent of patients with tuberculosis. • Isolated tuberculosis of the appendix is rare. • Appendectomy followed by antituberculosis chemotherapy is the treatment of choice.
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  TUBERCULOSIS OF SOLIDABDOMINAL ORGANS Hepatic tuberculosis – exceedingly rare these days – diagnosis is usually made accidentally during exploratory laparotomy or at autopsy – lesions typically are granulomas, with or without central caseating necrosis,calcified masses, and biliary strictures – Tuberculous periportal lymph nodes may cause obstructive jaundice by compressing the bile duct – usually have hepatomegaly, with or without jaundice – Liver enzymes, in particular serum alkaline phosphatase, are usually elevated • differentiated from other conditions associated with hepatic granulomas such as leprosy, sarcoidosis,Hodgkin disease, brucellosis, infectious mononucleosis, inflammatory bowel disease, drug-induced liver damage, and syphilis
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  • treatment ofhepatic tuberculosis is chemotherapy It should be remembered that most antituberculous drugs (except ethambutol) are hepatotoxic, and may aggravate the liver damage and worsen the jaundice. These patients therefore should be kept under close observation during antituberculous chemotherapy.
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  Splenic tuberculosis rare andmay present as a splenic abscess or with hypersplenism presence of multiple hypoechoic lesions on ultrasonography of the spleen in a HIV-positive patient is highly suggestive of disseminated tuberculosis. The diagnosis is usually made following surgical resection of the diseased spleen.
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  Tuberculosis of pancreas: Likeor part of miliary tuberculosis Common in immunocompromised Usually presents as acute or chronic pancreatitis Pancreatic mass or abscess may develop Can mimic malignancy
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  HIV & TUBERCULOSIS •Progresses faster • Fatal – Left untreated • TB occurs earlier in the course of HIV • TB is the only major AIDS-related opportunistic infection that poses a risk to HIV-negative people
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  • The mostcommon cause of death in patients with AIDS. • Accelerate the clinical course of HIV infection. • Atypical radiographic manifestations. • More frequent extrapulmonary involvement • Multi drug resistant
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  Thank you
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  References 1. Oxford Textbookof Surgery 2nd ed. 2. Harrisons priciples of internal medicine, 18th edition 3. https://en.wikipedia.org/wiki/World_Tuberculosis_Day 4. SRB's Manual of Surgery 4th edition 5. https://en.wikipedia.org/wiki/K%C3%B6nig%27s_syndrome