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Pulmonology

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Pulmonology

Pulmonology

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  • 1.
    • Pulmonology
    • http://crisbertcualteros.page.tl
  • 2.
    • Bronchial asthma
    • COPD
    • Pneumonia
    • Bronchiectasis
    • Cystic fibrosis
    • ILD
  • 3.  
  • 4. Asthma
    • Chronic inflammatory disease of the airways characterized by increased responsiveness of the TBT to a variety of stimuli
  • 5. Pathophysiologic hallmark
    • Widespread narrowing of airways
        • Smooth muscle contraction
        • Vascular congestion
        • Bronchial wall edema
        • Epithelial denudation
        • BM thickening
        • Eosinophilic infiltration
  • 6.
        • Sm contraction
        • Vascular congestion
        • Bronchial wall edema
        • Epithelial denudation
        • BM thickening
        • Eosinophilic infiltration
     Airway resistance  FEV 1 Hyperinflation  Work of breathing Altered resp muscle mechanics Blood gas abnormalities
  • 7. Stimuli that Incite asthma
    • Allergenic – causal in 25-35%; contributory in 1/3 of cases
      • Seasonal; children/young adults
  • 8.
    • Pharmacologic
      • Aspirin, coloring agents, B 2 agonists, NSAIDs
      • Often begins with perennial vasomotor rhinitis --- full blown asthma
      • May be treated with desensitization
  • 9.
    • Environmental
    • Occupational
      • HMW - immunologic mechanism
      • LMW compounds – haptines
      • Tx: antiinflammatory agents prior to exposure
  • 10.
    • Infections
      • Most common
      • Viruses
        • Children – RSV & parainfluenza
        • Adults – rhinovirus & influenza
        • The only stimuli that can produce constant symptoms for weeks
  • 11.
    • Exercise-related
      • Due to thermally induced hyperemia & capillary leakage
      • Typically follows exertion
      • Higher ventilation & lower heat content of air
      • Does not evoke long-term sequelae
      • Does not increase airway reactivity
  • 12.
    • Emotional
      • Fluctuations in vagal afferent activities
  • 13.
    • Relieved spontaneously or with therapy
    • Episodic
    • Atopy – single largest risk factor
    • Triad: dyspnea, cough & wheezing
    • Nocturnal awakenings with dyspnea &/ wheezing
  • 14.
    • Hypoxia universal finding during acute exacerbations
    • Frank ventilatory failure relatively uncommon
    • Hypocapnia & respiratory alkalosis in early/mild attacks
    • Normal pCO 2 – warning!!!
  • 15.
    • D/Dx
    • Dx Established by demonstrating reversible airway obstruction - > 15% increase in FEV 1
    Upper airway obstruction Heart failure TB COPD Recurrent pulmonary emboli
  • 16. Therapy
      • Quick-relief - inhibit sm contraction
        •  -adrenergic agonists
        • Methylxanthines
        • Anticholinergics
      • Long-term controllers
        • Steroids
        • LABA
        • Leukotriene modifiers
        • Mast cell stabilizers
        • Methylxanthines
    Table 236-1 & 236-2
  • 17. C O P D
  • 18. COPD
    • Disease state characterized by airflow limitation that is not fully reversible.
    • The airflow limitation is usually progressive and associated with an abnormal inflammatory response of the lungs to noxious particles & gases
            • - Global Initiative for Obstructive Lung Disease (GOLD)
  • 19. COPD
    • Chronic Obstructive Pulmonary Disease (COPD) is a preventable and treatable disease with some significant extrapulmonary effects that may contribute to the severity in individual patients. Its pulmonary component is characterized by airflow limitation that is not fully reversible . The airflow limitation is usually progressive and associated with an abnormal inflammatory response of the lung to noxious particles or gases.
    -GOLD, 2006
  • 20.
    • 4 th leading cause of death in US
    • >16M people in US
    • Increasing public health importance
    • 2020 – 5 th leading cause of death worldwide
  • 21. What are the Risk Factors for Developing COPD?
  • 22.
    • Direct dose relationship between smoking intensity (expressed in pack-years) and rate of decline in lung function (expressed in FEV 1 )
  • 23.
    • More common in males; incidence in females increasing
    ~15% of smokers develop COPD What proportion of smokers develop COPD?
  • 24. Airway Responsiveness & COPD
    • Many patients with COPD also have hyperreactive airways
    • Dutch hypothesis
      • Asthma & COPD are variations of the same disease
      • Modulated by genetic & environmental factors
      • Considerable overlap in airway hyperresponsiveness, airflow obstruction & pulmonary symptoms among COPD & asthma patients
    • British hypothesis
      • Asthma largely allergic; COPD mainly smoking –related
  • 25. Risk Factors: Respiratory Infections
    • Childhood respiratory infections potential predisposing factor to COPD?
  • 26. Risk Factors: Occupational Exposure
    • Occupational exposure to different substances leads to chronic airflow obstruction
    • Coal, gold, textile dust
    • Independent risk factor?
  • 27. Risk Factors: Ambient Air Pollution
    • Indoor pollution, emissions/smoke from biomass fuels
  • 28. Risk factors: Passive, or 2 nd -hand smoking (ETS)
  • 29. Genetic Considerations
    • Development of airflow obstruction highly variable
    • ~15% smokers develop COPD
    •  1 antitrypsin (  1 AT) deficiency
  • 30.  
  • 31. MMP Serine proteinases MMP Cysteine proteinases Proteinase inhibitors ECM degradation: lung destruction Emphysema Repair Inflammatory cell recruitment
  • 32. Transcription of cytokines Inactivation of antiproteinases Lipid peroxidation Depletion of antioxidant defenses Neutrophil sequestration OXIDATIVE STRESS I N F L A M M A T I O N I N J U R Y &
  • 33. What are the Major Categories of COPD?
  • 34. Chronic Bronchitis
    • Chronic productive cough for 3 months during each of 2 successive years in a patient in whom others causes of chronic cough have been excluded
  • 35. Emphysema
    • Abnormal permanent enlargement of the air spaces distal to the terminal bronchioles accompanied by destruction of their walls & without obvious fibrosis
  • 36. - What are the clinical manifestations of COPD? - What is the most common symptom which prompts patients to seek consultation?
  • 37. Clinical Features
    • Cough
    • Sputum production
    • Hemoptysis
    • Dyspnea with exertion
    • Health status (quality of life)
    • Acute exacerbations
  • 38.  
  • 39. What are the physiologic abnormalities in COPD?
  • 40. Physiologic Abnormalities in COPD
    • Accelerated decline in FEV 1
    • Mucus hypersecretion
    • Mucociliary dysfunction
    • Airflow limitation
    • Hyperinflation
    • Gas exchange abnormality
    • Hypoxemia
    • Pulmonary hypertension
    • Cor pulmonale
  • 41.  
  • 42. Airway obstruction & low elastic recoil Expiratory flow limitation Hyperinflation at rest, worsened by exercise Limited inspiratory “space”/”depth of breath” Dyspnea
  • 43. Hyperinflation
  • 44. How do you stage the severity of COPD? What are the recommended therapies?
  • 45.  
  • 46. Treatment: Stable COPD
    • Oxygen supplementation & smoking cessation
      • The only interventions proven to influence natural history of COPD
    • Other therapies only improve symptoms &/or reduce exacerbations
  • 47. Pharmacotherapy: Bronchodilators
    • For symptomatic relief
    • Inhaled route preferred; lesser side effects
    • Anticholinergics
    • Beta agonists
  • 48. Pharmacotherapy: Glucocorticoids
    • No benefit in preventing decline of lung function
    • Reduce frequency of exacerbations
    • Parenteral steroids
      • Chronic use is not recommended
      • For acute exacerbations
  • 49. Pharmacotherapy: Theophylline
    • Modest improvements in flowrates & arterial oxygen & CO 2 levels
    • Narrow therapeutic window
    • Side effects
  • 50. Pharmacotherapy: Oxygen
    • The only therapy demonstrates to decrease mortality in COPD
    • Indications
      • Resting O 2 saturation < 88% with signs of pulmonary hypertension or right heart failure
  • 51. Exacerbations of COPD
    • Increased dyspnea
    • Increased cough
    • Change in sputum character
    • +/- other illness
    • Heavy social & economic burden
  • 52. Exacerbations
    • Assessment of severity, both chronic & acute components
    • Identify precipitating causes
    • Institution of therapy
  • 53. Patient Assessment
    • Establish severity of exacerbation
    • Establish severity of preexisting COPD
    • Thorough history & PE
    • Special focus on respiratory mechanics
    • CXR, ABG, routine lab exams
    • May need to hospitalize if
      • Respiratory acidosis
      • Hypoxemia
      • Severe underlying disease
      • Poor home care
  • 54. Therapy
    • Bronchodilators, inhaled
      • Β 2 agonist + anticholinergics
    • Steroids, systemic
    • Antibiotics
    • Oxygen
      • SaO 2 > 90%
    • Mechanical ventilation
  • 55. Pneumonia
    • Infection of alveoli, distal airways & epithelium
    • Possible routes of entry of pathogen into lungs
      • Gross & microaspiration
      • Aerosolization
      • Hematogenous
      • Contiguous/direct extension from adjacent infection
  • 56.  
  • 57.
    • Pathology
      • Lobar – congestion, red & gray hepatization, resolution
      • Bronchopneumonia – patchy consolidation centered around bronchi & bronchioles
      • Interstitial
      • Miliary
  • 58.  
  • 59.  
  • 60.  
  • 61.
    • Pulmonary complications
      • Necrotizing pneumonia
      • Abscess formation
      • Vascular invasion
      • Empyema
      • BPF
  • 62. Community-acquired pneumonia
    • Risk factors (Table 239-3, p 1531)
      • Alcoholism
      • Asthma
      • Immunosuppression
      • Age > 70 yo
      • Seizures
      • Dementia
      • COPD
      • Cigarette smoking
      • Diabetes
      • Hematologic malignancies
      • ESRD
  • 63. Etiology
      • S. pneumoniae – most common
    • Dx
      • CXR
      • Sputum Gm staining & culture
      • Blood culture
      • Bronchoalveolar lavage
      • Urine antigen test for Legionella
      • Serology for Mycoplasma & Chlamydia
  • 64. Clinical Manifestations
      • Fever, cough, dyspnea, chest pain
      • The single most useful clinical sign of the severity of pneumonia is RR> 30/min in a person without underlying lung disease
  • 65. Hospital-acquired pneumonia
    • > 48H after admission & not incubating at the time of admission
    • New or progressive infiltrates on CXR, plus at least 2 of the ff:
      • Fever (> 37.8 o C)
      • Leukocytosis
      • Production of purulent sputum
    • 2 nd most common nosocomial infection
    • Highest morbidity & mortality
    • Highest in ICU px who are undergoing MV
    • S. aureus – most common cause in US
    • Tx: Table 239-13, p 1540
  • 66. Bronchiectasis
    • Abnormal & permanent dilation of bronchi
      • Destructive & inflammatory changes in airway walls
      • Focal or diffuse
      • Thick purulent sputum
      • Fibrosis
      • Increased vascularity of bronchial wall
      • Impaired mucociliary clearance
  • 67.
    • Cylindrical – uniformly dilated
    • Varicose – irregular, beaded
    • Saccular/cystic – ballooned
  • 68. Etiology
    • Infection- S. aureus, K. pneumoniae , adenovirus, influenza, TB
    • Inhalation/aspiration – ammonia, gastric contents
    • Immunologic – ABPA,  1 -antitrypsin deficiency
    • Impaired host defenses --- recurrent infections
      • Endobronchial obstruction
  • 69. Clinical manifestations
      • Persistent/recurrent purulent sputum production
      • Hemoptysis
      • Dyspnea
      • Wheezing
      • Symptoms worsen/increase during exacerbations
      • Recurrent infections
  • 70. PE & Diagnosis
      • Crackles, ronchi, wheezing
      • Clubbing, hypoxemia, RV failure
    • CXR: “tram tracks” , “ring shadows”
    • CT scan – better resolution
  • 71.  
  • 72. Goals of therapy
      • Elimination of underlying problem
      • Improve clearance of tracheobronchial secretions
      • Control of infection
      • Reversal of airflow obstruction
  • 73. Cystic Fibrosis
    • Monogenic disorder that presents as a multisystem disease
    • Autosomal recessive – mutation in CFTR
    • CFTR
      • Volume absorption – airways & distal intestinal epithelia
      • Salt absorption – sweat glanbds
      • Volume secretory – proximal intestinal & pancreas
  • 74.
    • Chronic airways infection – bronchiectasis, bronchiolectasis,
    • Exocrine pancreatic insufficiency, intestinal dysfunction, abnormal sweat gland function & urogenital dysfunction
    • Upper respiratory tract (chronic sinusitis) disease almost universal
    • Chronic persistent cough – viscous, purulent, greenish sputum
      • S. aureus, H. influenzae, P. aeruginosa
  • 75. Diagnosis
    • Clinical criteria
    • Analysis of sweat Cl values (>70 mEq/L)
  • 76. Therapy
    • Promote clearance of secretions
    • Control infection
  • 77.  
  • 78. Disorders of the Pleura
    • Pleural Effusions
      • Definition
      • Diagnostic approach
    • Pneumothorax
  • 79. Pleural Effusion
      • Accumulation of excessive quantity of fluid in the pleural space
    • Etiology
      • Formation / accumulation > absorption
  • 80. Diagnostic Approach
    • Transudate vs exudate
    • Transudate
      • Systemic factors that influence formation and absorption are altered
      • LV failure, pulmonary embolism, cirrhosis
    • Exudate
      • Local factors that influence pleural fluid formation & absorption are altered
      • Pneumonia
      • Malignancy
      • Pulmonary embolism
      • TB
      • Additional diagnostic procedures indicated
  • 81. Exudative Pleural Effusion
    • At least 1 of the ff
      • PF CHON/serum CHON > 0.5
      • PF LDH/serum LDH > 0.6
      • PF LDH > 2/3 upper normal limit for serum
    • If still in doubt ( > 1 above criteria met but clinically thought to be transudate)
      • Serum albumin - PF albumin > 1.2 g/dL --- TRANSUDATIVE
  • 82. Exudative Pleural Effusion
    • Description
    • Glucose
    • Differential cell count
    • Microbiologic studies
    • Cytologic studies
  • 83. Exudate Further diagnostic procedure Approach to the Diagnosis of Pleural Effusions Pleural effusion Perform diagnostic thoracentesis Measure PF CHON & LDH Any of the ff met? PF/serum CHON >0.5 PF/serum:LDH >0.6 PF LDH > 2/3 upper normal serum limit Transudate Treat CHF, cirrhosis, nephrosis
  • 84. Measure PF glucose, amylase Obtain PF cytology Differential cell count Culture, stain PF PF markers for TB Exudate Further diagnostic procedure
  • 85. Effusion Due to Heart Failure
    • Most common cause of pleural effusion is LV failure
    •  amount of fluid exits across the visceral pleural
    • Indications for diagnostic thoracentesis (to verify if transudative)
      • If not bilateral & not comparable in size
      • Febrile
      • Pleruitic chest pain
      • If persists despite diuretic therapy
  • 86. Hepatic Hydrothorax
    • ~ 5% of px with cirrhosis & ascites
    • Direct movement of peritoneal fluid across small holes in the diaphragm
    • Usually right-sided & large
    • Medical treatment
    • Liver transplant
    • TIPS
  • 87. Parapneumonic Pleural Effusion
    • Bacterial pneumonia
    • Lung abscess
    • Bronchiectasis
    • Empyema – grossly purulent
  • 88.
    • Aerobic pneumonia
      • Acute febrile illness
    • Anaerobic bacterial pneumonia
      • Subacute illness
      • Anemia
      • Wt loss
      • Brisk leukocytosis
      • Predisposing factors to aspiration
  • 89.
    • Pneumonia + effusion = parapneumonic effusion
    • Diagnosis
      • CXR
      • UTZ
      • CT scan
    • If > 10 mm fluid between lung & chest wall
      • therapeutic thoracentesis
  • 90. Factors indicating the likely need for a procedure more invasive than thoracentesis
    • Loculated PF
    • PF pH <7.20
    • PF glucose < 3.3 mmol/L (60 mg/dL)
    • (+) Gram staining or culture
    • Gross pus
    *increasing order of importance
  • 91.
    • Recurrence after initial thoracentesis + any of above characteristics
      • Repeat thoracentesis
    • 2 nd recurrence
      • Tube thoracostomy
    • Incomplete removal
      • thrombolytic instillation (e.g. streptokinase)
      • Thoracoscopy with breakdown of adhesions
      • Decortication
  • 92. Effusion Secondary to Malignancy
    • Malignant pleural effusion
      • 2 nd most common cause of exudative effusion
    • ~ 75% lung CA, breast CA & lymphoma
    • Dyspnea out of proportion to size of effusion
    • Diagnosis
      • Cytology
      • Thorascopy
      • Needle biopsy of pleura
    • Treatment
      • Symptomatic
      • Tube thoracostomy with instillation of sclerosing agent
      • Outpatient insertion of indwelling catheter
  • 93. Mesothelioma
    • Primary tumors from mesothelial cells
    • Symptoms
      • Chest pain, SOB
    • CXR
      • Pleural effusion, diffuse pleural thickening, shrunken hemithorax
    • Diagnosis
      • Thoracoscopy & pleural biopsy
    • Therapy
      • Surgery, chemotherapy, radiation
    • Prognosis
      • Poor
  • 94. Effusion Secondary to Pulmonary Embolism
    • Pulmonary embolism
      • Most commonly overlooked differential diagnosis in undiagnosed pleural effusion
    • Dyspnea most common symptom
    • Exudative or transudative
    • Diagnosis
      • Spiral CT or pulmonary angiography
    • Treatment
      • Same as pulmonary embolism
    • If effusion increases in size after anticoagulation
      • Recurrent emboli
      • Hemothorax
      • Infection
  • 95. Tuberculous Pleuritis
    • Hypersensitivity reaction to TB CHON in the pleural space
    • Symptoms
      • Dyspnea, fever, wt loss, pleuritic chest pain
    • Exudate with predominantly small lymphocytes
    • Diagnosis
      • TB markers in PF (ADA, interferon  , (+) PCR for TB DNA
      • Culture of PF
      • Pleural biopsy
      • Thoracoscopy
    • Therapy
  • 96. Effusion Secondary Viral Infection
    • ~ 20% of undiagnosed exudative PE
  • 97. AIDS
    • Uncommon
    • Most common cause – Kaposi’s sarcoma
  • 98. Chylothorax
    • Disruption of thoracic duct - accumulation of chyle
    • Trauma most common cause
    • Presentation – dyspnea, large effusions
    • Milky fluid
    • Triglyceride >1.2 mmol/L (110 mg/dL)
    • Lymphagiogram or CT scan to assess mediastinal LN
    • Treatment
      • Pleuroperitoneal shunt
      • Avoid prolonged thoracostomy – malnutrition & immunologic incompetence
  • 99. Hemothorax
    • Blood in pleural space
    • PF Hct > 50% peripheral Hct
    • Trauma, rupture of blood vessels, tumor
    • Tube thoracostomy – continuous quantification of bleeding
    • >200 ml/H – consider thoracotomy
  • 100. Miscellaneous Causes of Pleural Effusion
    • Transudative Pleural Effusions
      • CHF
      • Cirrhosis
      • Pulmonary embolism
      • Nephrotic syndrome
      • Peritoneal dialysis
      • Superior vena cava obstruction
      • Myxedema
      • Urinothorax
  • 101.
    • Neoplastic diseases
      • metastatic, mesothelioma
    • Infectious diseases
      • Bacterial infectionis
      • TB
      • Fungal
      • Viral
      • Parasitic
    • Pulmonary embolism
    Exudative Pleural Effusions
  • 102.
    • GI diseases
      • Esophageal perforationi
      • Pancreatic disease
      • Intraabdominal abscesses
      • Diaphragmatic hernia
      • After abdominal surgery
      • Endoscopic variceal sclerotherapy
      • After liver transplant
    • Collagen-vascular diseases
      • Rheumatoid pleuritis
      • SLE
      • Drug-induced lupus
      • Immunoblastic lymphadenopathy
      • Sjogren’s syndrome
      • Wegener’s granulomatosis
      • Churg-Strauss Syndrome
  • 103.
    • Post-coronary artery bypass
    • Asbestos exposure
    • Sarcoidosis
    • Uremia
    • Meig’s syndrome
    • Yellow nail syndrome
    • Drug-induced pleural disease
    • Trapped lung
    • Radiation therapy
    • Post-cardiac injury syndrome
    • Hemothorax
    • Iatrogenic injury
    • Ovarian hyperstimulation syndrome
    • Pericardial disease
    • Chylothorax
  • 104.
    • Esophageal rupture or pancreatitis -  amylase
    • Intraabdominal abscess
      • Febrile, PF predominantly lymphocytic, no parenchymal infiltrates
    • Asbestos pleural effusion – diagnosis is one of exclusion
    • PE commonly occur after coronary bypass surgery
  • 105. Pneumothorax
    • Gas in the pleural space
    • Spontaneous pneumothorax
      • Without antecedent trauma
    • Primary spontaneous pneumothorax
      • No underlying disease
    • Secondary spontaneous pneumothorax
    • Traumatic
      • Due to penetrating or non-penetrating injuries
    • Tension pneumothorax
      • Pressure in the pleural space is positive throughout the respiratory cycle
  • 106. Primary Spontaneous Pneumothorax
    • Rupture of apical pleural blebs
    • Almost exclusively in smokers – subclinical lung disease (?)
    • ~50% will recur
    • Initial therapy – simple aspiration
    • Recurrent – thoracoscopy with stapling of blebs
  • 107. Secondary Spontaneous Pneumothorax
    • Most are due to COPD
    • Virtually in every lung disease
    • In patients with lung disease – more life-threatening
    • Treatment – tube thoracostomy with instillation of sclerosis agent
    • If with persistent air leak or unexpanded lung > 3 days after tube thoracostomy or recurrent
      • Thoracoscopy with bleb resection and pleural abrasion
  • 108. Traumatic Pneumothorax
    • Should be treated with tube thoracostomy unless very small
    • If with hemothorax – insert 2 tubes
    • Iatrogenic pneumothorax
      • Caused by needle aspiration, thoracentesis, central intravenous catheters
      • Treated by O 2 , aspiration or tube thoracostomy
  • 109. Tension Pneumothorax
    • During mechanical ventilation or resuscitative efforts
    • Life-threatening
      • Ventilation severely compromised
      • Reduced cardiac output
    • Suspect if
      • Difficulty in ventilation
      • High peak inspiratory pressures
    • Clinical diagnosis
      • Enlarged hemithorax with no breath sounds
      • Contralateral shift of mediastinum
    • Treatment
      • “ Needling”
      • If large amounts of gas escape from needle – diagnosis confirmed
      • Needle should be left until thoracostomy tube inserted
  • 110. Disorders of the Mediastinum
  • 111. Mediastinal Masses
    • Anterior
      • Thymomas
      • Lymphomas
      • Thyroid masses
      • Teratoma
    • Middle
      • Vascular masses
      • Lymph nodes
      • Pleuropericardial cyst
      • Bronchogenic cyst
    • Posterior
      • Neurogenic tumors
      • Meningomyeloceles
      • Meningoceles
      • Esophageal diverticula
  • 112. Evaluation of Mediatinal Masses
    • CT scan – most valuable
    • Barrium studies – posterior lesions
    • I 131 nuclear scan – intrathoracic goiter
    • Definite diagnosis
      • Mediastinoscopy, mediastinostomy, needle aspiration biopsy, VATS
  • 113. Acute Mediastinitis
    • Most commonly caused by esophageal perforation or occur after median sternotomy for cardiac surgery
    • Esophageal rupture
      • Acutely ill, chest pain, dyspnea
      • Treatment
        • Exploration and antibiotics
    • Following cardiac surgery
      • Wound drainage, sepsis, widened mediastinum
      • Diagnosis established with needle aspiration
      • Treatment
        • Immediate drainage
        • Debridement
        • Antibiotics
      • High mortality (~20%)
  • 114. Chronic Mediastinitis
    • Granulomatous inflammation of LN – fibrosing mediatinitis
    • Causes
      • TB
      • Histoplasmosis
      • Sarcoidosis
      • Silicosis
      • Fungal diseases
    • Granulomatous mediastinitis – asymptomatic
    • Fibrosing mediastinitis
      • Signs of obstruction
    • Therapy
      • Anti-TB
      • Supportive
      • Medical/surgical (?)
  • 115. Pneumomediastinum
    • Gas in the mediastinal interstices
    • 3 main causes
      • Alveolar rupture
      • Perforation/rupture of trachea, bronchi, esophagus
      • Dissection of air from neck or abdomen
    • PE
      • Subcutaneous emphysema in suprasternal notch
      • Hamman’s sign
    • Diagnosis
      • CXR
    • Therapy
      • Usually none
      • High O 2 concentration
      • Needle aspiration if with compression of mediastinal structures
  • 116. Acute Respiratory Distress Syndrome
    • Severe dyspnea
    • Hypoxemia
    • Diffuse pulmonary infiltrates
    • Heterogeneous etiology
    Respiratory Failure
  • 117. Clinical Disorders Commonly Associated with ARDS Post-cardiopulmonary bypass Pancreatitis Toxic inhalation injury Drug overdose Near-drowning Multiple transfusions Pulmonary contusion Severe trauma Aspiration of gastric contents Sepsis Pneumonia Indirect Lung Injury Direct Lung Injury
  • 118. Diagnostic Criteria for ALI & ARDS ARDS: PaO 2 /FIO 2 < 200 PCWP < 18 mmHg or no clinical evidence of left atrial HPN Bilateral alveolar or interstitial infiltrates Acute ALI: PaO 2 /FIO 2 < 300 Absence of Left Atrial HPN CXR Onset Oxygenation
  • 119. Acute Lung Injury
    • Less severe
    • May evolve into ARDS
  • 120. Clinical Course & Pathophysiology
    • 3 phases
      • Exudative
      • Proliferative
      • Fibrotic
    Exudative Proliferative Fibrotic Hyaline membranes Interstitial inflammation Interstitial fibrosis Fibrosis 0 2 7 14 21…
  • 121. Exudative
    • 1 st 7 days; symptoms appear during 1 st 12-36 H
    • Cellular injury
    • Loss of normally tight alveolar barrier
    • Protein-rich edema fluid in interstitial & alveolar spaces
    • Cytokine accumulation
    • Surfactant dysfunction – hyaline membrane formation
    • Vascular injury
    • Edema in dependent areas
  • 122.
    • Atelectasis
    • Intrapulmonary shunting & hypoxemia
    • Hypercapnea 2 o to increase dead space
    • DDx
      • Cardiogenic pulmonary edema
      • Diffuse pneumonia
      • Alveolar hemorrhage
  • 123. Proliferative
    • 7-21 D
    • Most patients recover during this phase
    • Initiation of lung repair
    • Organization of alveolar exudates
    • Proliferation of type II pneumocytes
  • 124. Fibrotic
    • Exudates converted to extensive fibrosis
    • Emphysematous changes
    • Vascular occlusion – pulmonary hypertension
    • Increased risk of pneumothorax
    • Decreased lung compliance
    • Increased dead space
    • Protracted course
    • Increased mortality
  • 125. Therapy
    • General Principles
      • Recognition & treatment of underlying cause
      • Minimize procedures & their complications
      • Prophylaxis vs venous thromboembolism
      • Prompt recognition of nosocomial infections
      • Adequate nutrition
  • 126. Mechanical Ventilation
    • Low tidal volume (6 mL/kg predicted body wt)
    • Optimal PEEP for alveolar recruitment
  • 127. Others
    • Fluid Management
    • Steroids – current evidence does not support its use in early ARDS
  • 128. Prognosis
    • Mortality rate: 41 – 65%
    • Largely due to nonpulmonary causes
      • Sepsis
      • Nonpulmonary organ failure
    • Age
    • Preexisting organ dysfunction
    • Pulmonary causes of ARDS (pneumonia, pulmonary contusion, aspiration of gastric contents) – higher mortality
  • 129. Neoplasms of the Lung
    • Lung cancer
      • Arise from respiratory epithelium
      • Leading cause of cancer deaths
      • Incidence decreasing in males; increasing in females
      • (table 75-1, p 506)
      • Squamous, small cell, adenoCA, large cell CA – 88% of all primary lung cancer
      • Small cell vs non-small cell CA (squamous, adenoCA, large cell CA)
      • ~90% of patients are current or former smokers
  • 130.
    • AdenoCA - #1
      • Most common in lifetime nonsmokers, women & young patients
    • Squamous & small cell CA – central lesions with endobronchial growth
    • adenoCA & large cell CA – peripheral masses; frequent pleural involvement
    • Squamous & large cell - cavitate in ~10-20%
  • 131.
    • Bronchoalveolar CA – subtype of adenoCA
      • Peripheral airways
      • Single mass
      • Diffuse multinodular
      • Fluffy infiltrate
  • 132. Etiology/Risk Factors
    • Strongest risk factor: cigarette smoking
    • RR: 13-fold for active smokers; 1.5-fold for passive smokers
    • COPD
    • Death rate related to total amount of cigarette smoked (pack-years)
    • Risk decreases with smoking cessation; may never return to normal
    • Women with higher relative risk; more susceptible?
    • Molecular genetics & tumor markers (table 75-2, p 507)
  • 133. Clinical Manifestations
    • Local tumor growth
    • Tumor invasion
    • Obstruction
    • LN spread
    • Distant metastasis
    • Paraneoplastic syndromes
  • 134.
    • 5-15% identified while asymptomatic
    • Central/endobronchial growth
      • cough, hemoptysis, wheeze, stridor, dyspnea, postobstructive pneumonitis
    • Peripheral growth
      • Pain, cough, dyspnea, lung abscess/cavitation
    • Extension to contiguous structures or LN
      • Tracheal obstruction, esophageal compression, recurrent laryngeal nerve compression, sympathetic nerve paralysis (Horner’s syndrome)
      • Pancoast’s tumor (superior sulcus tumor)
  • 135.
    • Superior vena cava syndrome
    • Extrathoracic metastatic disease
      • >50% in squamous
      • 80% in adenoCA & large cell CA
      • >95% in small cell CA
    • Paraneoplastic syndromes
      • May be presenting finding or fist sign of recurrence
      • May mimic metastatic disease
      • May be relieved with successful treatment
      • Endocrine syndromes
    • Skeletal-CT syndromes
        • Eaton-Lambert syndrome
        • Myopathy
  • 136. Diagnosis & Staging
    • Screening of asymptomatic high risk patients has not improved survival rate
    • Tissue diagnosis
      • FOB
      • Pleural biopsy
      • LN biopsy during mediastinoscopy
      • Cell block of pleural effusion
    • Resectability/ pathologic staging vs operability/ physiologic staging
    • Tables 75-3, 509; 75-4, p 510
  • 137. Therapy
    • Stages IA, IB, IIA, IIB – treatment of choice is pulmonary resection
    • IIIA – team approach
    • Palliative approach
  • 138. Solitary Pulmonary Nodule (SPN)
    • X-ray density completely surrounded by normal aerated lung, with circumscribed margins, of any shape, 1-6 cm in diameter
    • ~35% malignant
    • <1% malignant in nonsmokers ,35 yo
    • Complete hx & PE, routine labs, CT, FOB, CXRs
  • 139. When to Resect SPN?
    • History of cigarette smoking
    • > 35 yo
    • Relatively large lesion
    • Lack of calcification
    • Chest symptoms
    • Atelectasis, pneumonitis or adenopathy
    • Growth of lesion
    • (+) PET scan
  • 140. Reliable radiographic criteria for benignity of lesion
      • “ Popcorn” & “bull’s eye” calcification
      • Lack of growth over 2 years
    For px >35 and all px who smoke – histologic diagnosis mandatory Algorithm (Fig 75-2, p 513)
  • 141. Benign Lung Neoplasms
    • <5% of all primary lung tumors
    • Bronchial adenoma & hamartomas – 90%
    • Surgery – diagnostic & therapeutic
    • Produce symptoms due to obstruction
  • 142. Bronchial Adenomas
    • 80% central in location
    • Slow growing, endobronchial
    • ~50% of all benign pulmonary tumors
    • 80-90% are carcinoids
      • May express neuroendocrine phenotype
    • Carcinoids must be considered potentially malignant
    • Good survival rate; decreased if with LN spread
  • 143. Hamartomas
    • Peak incidence: 60 yo
    • More common on males
    • Normal pulmonary tissue components in a disorganized fashion