Chapter 17 Tuberculosis.ppt

1、Chapter 17 Tuberculosis,Figure 17-1. Tuberculosis. A, Early primary infection. B, Cavitation of a caseous tubercle and new primary lesions developing. C, Further progression and development of cavitations and new primary infections. Note the subpleural location of some of these lesions. D, Severe lu

2、ng destruction caused by tuberculosis.,A,C,B,D,Anatomic Alterations of the Lungs,(Three categories) Primary tuberculosis Primary infection stage Postprimary tuberculosis Secondary or reinfection TB Disseminated tuberculosis Extrapulmonary TB,Anatomic Alterations of the Lungs (Mainly Primary TB),Alve

3、olar consolidation Alveolar-capillary destruction Caseous tubercles or granulomas Fibrosis and secondary calcification of the lung parenchyma Distortion and dilation of the bronchi Increased bronchial airway secretions,Etiology,In human, TB primarily caused by Mycobacterium tuberculosis Others Mycob

4、acterium bovis Mycobacterium ulcerans Mycobacterium kansasii Mycobacterium avium-intracellulare Highly aerobic organisms,Diagnosis,Intradermal tuberculin skin testing Mantoux test Injection of purified protein derivative (PPD) Wheal 5 mm: negative Wheal 5 mm to 9 mm: considered suspicious Wheal 10 m

5、m or greater: positive,Diagnosis,Acid-fast stain and sputum culture Ziehl-Neelsen stain Reveals bright red acid-fast bacilli against a blue background Fluorescent acid-fast stain Reveals luminescent yellow-green bacilli against a dark brown background A culture is necessary to differentiate M. tuber

6、culosis form other acid-fast organisms Results take as long as 6 to 8 weeks,Diagnosis,Identification of Mycobacterium species Polymerase chain reaction (PCR) Quick identification of organisms in expectorated or bronchoscopically obtained sputumDeoxyribonucleic acid (DNA) probe,Nontuberculosis Mycoba

7、cteria,Mycobacterial infection caused by species other than M. tuberculosis are called nontuberculosis mycobacteria (NTM)also called: Mycobacteria other than tuberculosis (MOTT) Atypical mycobacterial infection Found in soil and water,Overview of the Cardiopulmonary Clinical Manifestations Associate

8、d with TUBERCULOSIS,The following clinical manifestations result from the pathophysiologic mechanisms caused (or activated) by Alveolar Consolidation (see Figure 9-8), and Increased Alveolar-Capillary Membrane Thickness (see Figure 9-9)the major anatomic alterations of the lungs associated with tube

9、rculosis (see Figure 17-1).,Figure 9-8. Alveolar consolidation clinical scenario.,Figure 9-9. Increased alveolar-capillary membrane thickness clinical scenario.,Clinical Data Obtained at the Patients Bedside,Vital signs Increased respiratory rate Increased heart rate, cardiac output, blood pressure,

10、Clinical Data Obtained at the Patients Bedside,Chest pain/decreased chest expansion Cyanosis Digital clubbing Peripheral edema and distention Distended neck veins Pitting edema Enlarged and tender liver,Digital Clubbing,Figure 2-46. Digital clubbing.,Distended Neck Veins,Figure 2-48. Distended neck

11、veins (arrows).,Figure 2-47. Pitting edema. From Bloom A, Ireland J: Color atlas of diabetes, ed 2, London, 1992, Mosby-Wolfe.,Clinical Data Obtained at the Patients Bedside,Cough, sputum production, and hemoptysis Chest assessment findings Increased tactile and vocal fremitus Dull percussion note B

12、ronchial breath sounds Crackles, rhonchi, and wheezing Pleural friction rub Whispered pectoriloquy,Figure 2-11. A short, dull, or flat percussion note is typically produced over areas of alveolar consolidation.,Figure 2-16. Auscultation of bronchial breath sounds over a consolidated lung unit.,Figur

13、e 2-19. Whispered voice sounds auscultated over a normal lung are usually faint and unintelligible.,Clinical Data Obtained from Laboratory Tests and Special Procedures,Pulmonary Function Study: Expiratory Maneuver Findings,FVC FEVT FEF25%-75% FEF200-1200 N or N or NPEFR MVV FEF50% FEV1% N N or N N o

14、r ,Pulmonary Function Study: Lung Volume and Capacity Findings,VT RV FRC TLCN or VC IC ERV RV/TLC% N,Arterial Blood Gases,Mild to Moderate Tuberculosis Acute alveolar hyperventilation with hypoxemia,pH PaCO2 HCO3- PaO2 (Slightly) ,Time and Progression of Disease,100,50,30,80,0,PaCO2,10,20,40,Alveola

15、r Hyperventilation,60,70,90,Point at which PaO2 declines enough to stimulate peripheral oxygen receptors,PaO2,Disease Onset,PaO2 or PaCO2,Figure 4-2. PaO2 and PaC02 trends during acute alveolar hyperventilation.,Arterial Blood Gases,Extensive Tuberculosis with Pulmonary Fibrosis Chronic ventilatory

16、failure with hypoxemia,pH PaCO2 HCO3- PaO2 Normal (Significantly) ,Time and Progression of Disease,100,50,30,80,0,PaO2,10,20,40,Alveolar Hyperventilation,60,70,90,Point at which PaO2 declines enough to stimulate peripheral oxygen receptors,PaCO2,Chronic Ventilatory Failure,Disease Onset,Point at whi

17、ch disease becomes severe and patient begins to become fatigued,Pa02 or PaC02,Figure 4-7. PaO2 and PaCO2 trends during acute or chronic ventilatory failure.,Acute Ventilatory Changes on Chronic Ventilatory Failure,Acute alveolar hyperventilation on chronic ventilatory failure Acute ventilatory failu

18、re on chronic ventilatory failure,Oxygenation Indices,QS/QT DO2 VO2 C(a-v)O2 Normal NormalO2ER SvO2 ,Hemodynamic Indices (Severe Tuberculosis),CVP RAP PA PCWP NormalCO SV SVI CINormal Normal Normal Normal RVSWI LVSWI PVR SVR Normal Normal,Abnormal Laboratory Tests and Procedures,Positive tuberculosi

19、s skin test (PPD) Positive acid-fast bacillus stain of sputum and sputum culture,Radiologic Findings,Chest radiograph Increased opacity Ghons complex Cavity formation Pleural effusion Calcification and fibrosis Retraction of lung segments or lobe Right ventricular enlargement,Figure 17-2. Cavitary r

20、eactivation TB showing a left upper lobe cavity and localized pleural thickening (arrows). (From Armstrong P et al: Imaging of diseases of the chest, ed 2, St. Louis, 1995, Mosby.),General Management of Tuberculosis,Pharmacologic agents Consists of 2 to 4 drugs for 6 to 12 months First-line agents (

21、first 9 months) Isoniazid (INH) and rifampin (Rifadin) INH most effective Often supplemented with: Ethambutol Streptomycin Pyrazinamide,General Management of Tuberculosis,Respiratory care treatment protocols Oxygen therapy protocol Bronchopulmonary hygiene therapy protocol Hyperinflation therapy pro

22、tocol Mechanical ventilation protocol,Review,The protective cell wall that surrounds and encases the TB bacilli is called -? Tubercle or granuloma What is primary TB? Reaction following first exposure to pathogen Inflammation leading to alveolar consolidation Formation of tubercle Fibrosis and calci

23、fication, development of bronchiectasis,What is postprimary TB? Reactivation of TB after initial infection has been controlled What is dissemminated TB? Infection that spreads to sites outside the lung via pulmonary lymphatic system or bloodstreamThe presence of numerous small tubercles scattered th

24、roughout the body is called - ? Miliary tuberculosis,How long can TB bacillus remain suspended in the air after a sneeze or a cough? Several hoursWhat is a Ghons complex? Combination of tubercles and hilar lymphadenopathy seen on CXRTypical ABGs from a patient with extensive TB and fibrosis would be

25、 describe as - ? Chronic Ventilatory failure and hypoxemia,What hemodynamic indices reflect right-side heart failure in a patient with advanced TB? Increased CVP Increased RAP Increased mean PA Increased PVR Increased RVSWI What respiratory care treatments/protocols are used for TB? O2 Therapy BHT H

26、yperinflation Therapy,True or False,Pleural space complications such as empyema and pneumothorax are common in patients with tuberculosis. True A positive reaction to the tuberculin skin test confirms that a patient has active tuberculosis False Tuberculosis commonly develops in the apices of the lungs True,Classroom Discussion Case Study: Tuberculosis,