(兒科學(xué)英文課件）18 tuberculersis

1、( (兒科學(xué)英文課件）兒科學(xué)英文課件）18 18 tuberculersistuberculersisPrimary pulmonary tuberculosislPrimary pulmonary TB is a tuberculosis that is caused by primary pulmonary infection of M. tuberculosis. lPrimary pulmonary TB includes: Primary complexTuberculosis of trachebronchial lymphnodes Droplet nuclei inhalati

2、onalveoliIngestion by PAMSIntracellular replication of bacilliDestruction of bacillidestruction of PAMSTubercle formationLymphogenic spreadHilar lymph nodesPrimary focuslymphangitislymphadenitisPrimary complexPathogenesisPAM: pulmonary alveolar macrophages typicalTuberculosis of trachebronchial lymp

3、hnodesPrimary palmonary tuberculosisatypicalprimary complexLymphadenitisPrimary focusLymphangitisPathologypLocation of primary focus : l low zones of lobus superior pulmonis or upper zone of lobus inferior pulmonisl subpleurall right lung mostlypBasic lesions ： pepithelioid cells, lymphocytes, and f

4、ibroblasts l caseous necrosis1. Tuberculosis toxic symptomsLow fever, night sweats, anorexia, weight loss,and fatigue 2. Lung clinical manifestatios：Symptoms is mild:dry coughSigns are not obvious generally (signs in lung is not consistent with the lesions in lung lesions not consistent)Clinical man

5、ifestations 3. Oppression symptoms of Bronchial lymph node4. Extrapulmonary clinical manifestations：5. others：Clinical manifestations Deterioration :Hematogenic spreadHealing with u obsorptionu calcificationu scleromaProgression Expansion of lesionsPrimary complexPrognosis of primary palmonary tuber

6、culosis:Diagnosis 1. Epidemiology history ：History of contact with tuberculosis personBCG vaccination historyHistory of infectious diseases recently2. Clinical manifestations ：Tuberculosis toxic symptomsRespiratory symptoms Manifestations of tuberculosis hypersensitivity Diagnosis 3. auxiliary exami

7、nation (1) PPD testStrong positivePPD test result is from negative to positive PPD test result is positive in 3 years old children uninoculated BCGsuggest active tuberculosis in body 3. auxiliary examination (2) Chest X-ray radiograph: the main diagnostic basis3. auxiliary examination (3) CT scan (4

8、) Flexible bronchofiberscope examination(5) Finding tubercle bacillus in sputum or gastric aspirates(6) ESR(7) Antibody of TBTreatment 1. Antitubercular treatment (1) Principles： early treatment, appropriate doses, drug combination, standard medication, adhere to full course of treatment, two phases

9、 (2) Treatment regimen Active primary pulmonary tuberculosis INH + RFP + PZA or+ SM/EMB Intensive treatment phase : 3m 3m 3m 3mConsolidate treatment phase: 6-9m 3-6m 0-3mTotal treatment 9-12m 6-9m 3-6m 3m兒童時期結(jié)核病的特點(diǎn)兒童時期結(jié)核病的特點(diǎn)( (重點(diǎn)重點(diǎn)、掌握）、掌握） 原發(fā)型肺結(jié)核病理（原發(fā)型肺結(jié)核病理（熟悉熟悉、了解）、了解）發(fā)病機(jī)理（了解）發(fā)病機(jī)理（了解）臨床表現(xiàn)（臨床表現(xiàn)（重點(diǎn)重點(diǎn)

10、、掌握）、掌握）診斷（診斷（重點(diǎn)重點(diǎn)、掌握）、掌握）轉(zhuǎn)歸轉(zhuǎn)歸（重點(diǎn)重點(diǎn)、掌握）、掌握）治療（治療（熟悉熟悉、掌握方案及總療程掌握方案及總療程）Summary:Tuberculous MeningitisWangyuting MDTuberculous meningitis (TBM)nTuberculous meningitis is the most serious TB and is uniformly fatal without treatmentnTBM is 2540% of all types of TB in childrennThe younger the children,

11、the more common to develop TBM. 60% of TBM in Children is under 3 years old and it is always a part of systemic disseminated tuberculosis.nTBM often occurs within 1 year of initial infection, especially in the first 26 months of infection.nHigh rates of sequelae and high case-fatality(15-30%)Tubercl

12、e BacilliPrimary ComplexTuberculous MeningitisLung, CNS, liver, spleen, bone, ect Miliary TBPrimary Complex deteriorationFormation Rich foci in Meninges & brain parenchymaRupture into subarachnoid space Immuno-compromised:such as measles, pertussis in distant future forceacute generalized hematogeni

13、c spreadoccult hematogenic spreadPATHOPHYSIOLOGY 1. Brief DescriptionsnChronic meningitis.ncharacterized as a meningoencephalitisPATHOLOGYA. Leptomeningesndiffuse hyperemianedemaninflammatory exudatesntubercles (Rich focus): discrete and white granules scattered over the leptomeninges ncaseous necro

14、sis 2. Gross FindingsPATHOLOGYB. Subarachnoid SpacenThere are inflammatory exudates in subarachnoid spaces, particularly over the ventral surface of the brain stem( at the base of the brain), obliterating arteries and encasing cranial nerves(VII, III, VI,etc.). -Basal meningitis2. Gross FindingsPATH

15、OLOGYC. brain parenchymaTubercle, tuberculoma, and caseous necrosisPATHOLOGY2. Gross Findings3. Micro FindingsPATHOLOGIC EFFECTSnThree general processes produce the subsequent neurological pathology: adhesion formation obliterative vasculitis encephalitis1. Adhesions formation - Cranial nerve palsyn

16、Basal meningitis, there are adhesions around the interpeduncular fossa and related structures, can compromise cranial nerves. nCranial nerves can be compromised, particularly CN III (Oculomotor nerve) CN VI (abducens nerve) CN VII (Facial nerve) PATHOLOGIC EFFECTS1. Adhesions formation - Hydrocephal

17、usPATHOLOGIC EFFECTS1. Adhesions formation - HydrocephalusHyperemia of choroids overproduction of CSF Inflammatory adherence of Arachnoid granulations defective absorption of CSF Communicating hydrocephalus The route of CSF flow is obstructedObstructive hydrocephalusAtrophyPATHOLOGIC EFFECTSanterior

18、 cerebral artery arteria cerebri media posterior communicating arterybasal artery vertebral artery cervical internal carotid artery pontine arteries 2. Obliterative vasculitisPATHOLOGIC EFFECTSnExudates, vasculitis, and hydrocephalus each exert their own effect on brain parenchyma and cause encephal

19、itis in TBM. nThe intensity of the basal inflammatory process extends into the parenchyma resulting in encephalitis 3. Encephalitis PATHOLOGIC EFFECTS exudatesadhesion formation obliterative vasculitisencephalitisedema intracranial hypertensionPATHOLOGIC EFFECTS4. Edema A. Stage 1(Prodrome stage) 1-

20、2 weeks1. Tuberculous toxic symptoms :ulow to moderate grade fever, fatigue, malaise, anorexia, loss of weight, night sweat2. Mental status changes: alternant of irritability and drowsiness3. Headache, vomiting 4. Focal neurologic signs are absent5. CSF is abnormal CLINICAL MANIFESTIONSB. Stage 2 (M

21、eningeal Irritation Stage) 1-2 weeks1. More serious TB toxic symptoms 2. Neurologcal symptoms and signs: (1) Meningeal Irritation: nuchal rigidity, Kernig sign or Brudzinski sign (2) Intracranial hypertension:usevere headache, irritation, projectile vomiting, seizures, etc (3) Altered consciousness:

22、 such as lethargy (4) Cranial neuropathies: palsy of cranial nerve 3, 6, 7,etc. (5) Minor focal neurological deficits: umonoplegia, hemiplegia, aphasia, hemiparesis, tetraparesis, etc. Cranial nerve III palsy Cranial nerve VII palsyCLINICAL MANIFESTIONSC. Stage 3(Coma Stage) 1-3 weeksnDepletion: ext

23、remely maransisnNeurological symptoms and signs are more sever (1) progressive altered state of consciousness: coma, decerebrate rigidity (2) frequent convulsion (3) hyponatraemia due to inappropriate ADH secretion by hypophysis (4) severe focal neurological deficits: hemiplegia or paraplegia (5) de

24、terioration in vital signs and dead from cerebral hernia eventuallyCLINICAL MANIFESTIONSThe whole process lasts for 34 weeksCLINICAL MANIFESTIONSCharacteristics of TBM in infants and young childrennA rapid onset with abruptly high fever or convulsionnThe progression is rapidnAtypical meningeal irrit

25、ationnIntracranial hypertension manifests as bulging of anterior fontanelle and widening of cranial sutures in infant CLINICAL MANIFESTIONS 1. Cerebrospinal FluidINVESTIGATIONS- Lab Studies2. Tuberculin Skin Test 3. CT/MRI, Chest radiograph DIAGNOSIS nDiagnosis of TBV is made based on TB toxic sympt

26、oms, neurological symptoms and signs, CSF findings Neuroimaging characteristicsnEvidence of extra-neural TB with appropriate microbiological, radiological or histopathological findings will add to the confirmation of the diagnosis. nA history of recent TB contact is also an important supporting feat

27、ure of tuberculous etiology. nA definitive diagnosis of TB etiology depends upon detection of Tubercle bacilli in CSF either by microscopy or in culture. DIFFERENTIAL DIAGNOSISnPyogenic meningitisnViral meningoencephalitisnCryptococcal meningitisTREATMENT1.Supportive and Symptomatic treatmentnBed re

28、st and keep away from patients with pulmonary tuberculosis nNutritional support are paramount nKeep good hygiene for the coma children to prevent secondary infections, help them to change position frequently to prevent decubitinManagement of electrolyte abnormalities nAntipyreticsnControl of seizure

29、s: Diazepam (Valium)TREATMENT2.Anti-tubercular treatmentA. Intensification phase of treatment : 3 months INH, RFP, PZA, SM/EMBB. Continuation phase of treatment : 912months INH, RFP or EMB In order to eliminate tubercle bacilli completely and prevent relapse in the host (I3R3P3E3 or I3R3P3S3 ) +I912

30、R36The total course is 1 year at leastPay close attention to the side effects TREATMENT 3. Management of intracranial hypertensionElevated intracranial pressure can be life-threateningnDehydrant: Mannitol (MNT)nDiuretic agent: furosemide4.Management of hydrocephalus Hydrocephalus is a common complication that may lea