Pulmonology http://crisbertcualteros.page.tl

Pulmonology

http://crisbertcualteros.page.tl

Bronchial asthma COPD Pneumonia Bronchiectasis Cystic fibrosis ILD

Bronchial asthma

COPD

Pneumonia

Bronchiectasis

Cystic fibrosis

ILD

Asthma Chronic inflammatory disease of the airways characterized by increased responsiveness of the TBT to a variety of stimuli

Chronic inflammatory disease of the airways characterized by increased responsiveness of the TBT to a variety of stimuli

Pathophysiologic hallmark Widespread narrowing of airways Smooth muscle contraction Vascular congestion Bronchial wall edema Epithelial denudation BM thickening Eosinophilic infiltration

Widespread narrowing of airways

Smooth muscle contraction

Vascular congestion

Bronchial wall edema

Epithelial denudation

BM thickening

Eosinophilic infiltration

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

Sm contraction

Vascular congestion

Bronchial wall edema

Epithelial denudation

BM thickening

Eosinophilic infiltration

Stimuli that Incite asthma Allergenic – causal in 25-35%; contributory in 1/3 of cases Seasonal; children/young adults

Allergenic – causal in 25-35%; contributory in 1/3 of cases

Seasonal; children/young adults

Pharmacologic Aspirin, coloring agents, B 2 agonists, NSAIDs Often begins with perennial vasomotor rhinitis --- full blown asthma May be treated with desensitization

Pharmacologic

Aspirin, coloring agents, B 2 agonists, NSAIDs

Often begins with perennial vasomotor rhinitis --- full blown asthma

May be treated with desensitization

Environmental Occupational HMW - immunologic mechanism LMW compounds – haptines Tx: antiinflammatory agents prior to exposure

Environmental

Occupational

HMW - immunologic mechanism

LMW compounds – haptines

Tx: antiinflammatory agents prior to exposure

Infections Most common Viruses Children – RSV & parainfluenza Adults – rhinovirus & influenza The only stimuli that can produce constant symptoms for weeks

Infections

Most common

Viruses

Children – RSV & parainfluenza

Adults – rhinovirus & influenza

The only stimuli that can produce constant symptoms for weeks

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

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

Emotional Fluctuations in vagal afferent activities

Emotional

Fluctuations in vagal afferent activities

Relieved spontaneously or with therapy Episodic Atopy – single largest risk factor Triad: dyspnea, cough & wheezing Nocturnal awakenings with dyspnea &/ wheezing

Relieved spontaneously or with therapy

Episodic

Atopy – single largest risk factor

Triad: dyspnea, cough & wheezing

Nocturnal awakenings with dyspnea &/ wheezing

Hypoxia universal finding during acute exacerbations Frank ventilatory failure relatively uncommon Hypocapnia & respiratory alkalosis in early/mild attacks Normal pCO 2 – warning!!!

Hypoxia universal finding during acute exacerbations

Frank ventilatory failure relatively uncommon

Hypocapnia & respiratory alkalosis in early/mild attacks

Normal pCO 2 – warning!!!

D/Dx Dx Established by demonstrating reversible airway obstruction - > 15% increase in FEV 1 Upper airway obstruction Heart failure TB COPD Recurrent pulmonary emboli

D/Dx

Dx Established by demonstrating reversible airway obstruction - > 15% increase in FEV 1

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

Quick-relief - inhibit sm contraction

 -adrenergic agonists

Methylxanthines

Anticholinergics

Long-term controllers

Steroids

LABA

Leukotriene modifiers

Mast cell stabilizers

Methylxanthines

C O P D

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)

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)

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

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.

4 th leading cause of death in US >16M people in US Increasing public health importance 2020 – 5 th leading cause of death worldwide

4 th leading cause of death in US

>16M people in US

Increasing public health importance

2020 – 5 th leading cause of death worldwide

What are the Risk Factors for Developing COPD?

Direct dose relationship between smoking intensity (expressed in pack-years) and rate of decline in lung function (expressed in FEV 1 )

Direct dose relationship between smoking intensity (expressed in pack-years) and rate of decline in lung function (expressed in FEV 1 )

More common in males; incidence in females increasing ~15% of smokers develop COPD What proportion of smokers develop COPD?

More common in males; incidence in females increasing

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

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

Risk Factors: Respiratory Infections Childhood respiratory infections potential predisposing factor to COPD?

Childhood respiratory infections potential predisposing factor to COPD?

Risk Factors: Occupational Exposure Occupational exposure to different substances leads to chronic airflow obstruction Coal, gold, textile dust Independent risk factor?

Occupational exposure to different substances leads to chronic airflow obstruction

Coal, gold, textile dust

Independent risk factor?

Risk Factors: Ambient Air Pollution Indoor pollution, emissions/smoke from biomass fuels

Indoor pollution, emissions/smoke from biomass fuels

Risk factors: Passive, or 2 nd -hand smoking (ETS)

Genetic Considerations Development of airflow obstruction highly variable ~15% smokers develop COPD  1 antitrypsin (  1 AT) deficiency

Development of airflow obstruction highly variable

~15% smokers develop COPD

 1 antitrypsin (  1 AT) deficiency

MMP Serine proteinases MMP Cysteine proteinases Proteinase inhibitors ECM degradation: lung destruction Emphysema Repair Inflammatory cell recruitment

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 &

What are the Major Categories of COPD?

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

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

Emphysema Abnormal permanent enlargement of the air spaces distal to the terminal bronchioles accompanied by destruction of their walls & without obvious fibrosis

Abnormal permanent enlargement of the air spaces distal to the terminal bronchioles accompanied by destruction of their walls & without obvious fibrosis

- What are the clinical manifestations of COPD? - What is the most common symptom which prompts patients to seek consultation?

Clinical Features Cough Sputum production Hemoptysis Dyspnea with exertion Health status (quality of life) Acute exacerbations

Cough

Sputum production

Hemoptysis

Dyspnea with exertion

Health status (quality of life)

Acute exacerbations

What are the physiologic abnormalities in COPD?

Physiologic Abnormalities in COPD Accelerated decline in FEV 1 Mucus hypersecretion Mucociliary dysfunction Airflow limitation Hyperinflation Gas exchange abnormality Hypoxemia Pulmonary hypertension Cor pulmonale

Accelerated decline in FEV 1

Mucus hypersecretion

Mucociliary dysfunction

Airflow limitation

Hyperinflation

Gas exchange abnormality

Hypoxemia

Pulmonary hypertension

Cor pulmonale

Airway obstruction & low elastic recoil Expiratory flow limitation Hyperinflation at rest, worsened by exercise Limited inspiratory “space”/”depth of breath” Dyspnea

Hyperinflation

How do you stage the severity of COPD? What are the recommended therapies?

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

Oxygen supplementation & smoking cessation

The only interventions proven to influence natural history of COPD

Other therapies only improve symptoms &/or reduce exacerbations

Pharmacotherapy: Bronchodilators For symptomatic relief Inhaled route preferred; lesser side effects Anticholinergics Beta agonists

For symptomatic relief

Inhaled route preferred; lesser side effects

Anticholinergics

Beta agonists

Pharmacotherapy: Glucocorticoids No benefit in preventing decline of lung function Reduce frequency of exacerbations Parenteral steroids Chronic use is not recommended For acute exacerbations

No benefit in preventing decline of lung function

Reduce frequency of exacerbations

Parenteral steroids

Chronic use is not recommended

For acute exacerbations

Pharmacotherapy: Theophylline Modest improvements in flowrates & arterial oxygen & CO 2 levels Narrow therapeutic window Side effects

Modest improvements in flowrates & arterial oxygen & CO 2 levels

Narrow therapeutic window

Side effects

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

The only therapy demonstrates to decrease mortality in COPD

Indications

Resting O 2 saturation < 88% with signs of pulmonary hypertension or right heart failure

Exacerbations of COPD Increased dyspnea Increased cough Change in sputum character +/- other illness Heavy social & economic burden

Increased dyspnea

Increased cough

Change in sputum character

+/- other illness

Heavy social & economic burden

Exacerbations Assessment of severity, both chronic & acute components Identify precipitating causes Institution of therapy

Assessment of severity, both chronic & acute components

Identify precipitating causes

Institution of therapy

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

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

Therapy Bronchodilators, inhaled Β 2 agonist + anticholinergics Steroids, systemic Antibiotics Oxygen SaO 2 > 90% Mechanical ventilation

Bronchodilators, inhaled

Β 2 agonist + anticholinergics

Steroids, systemic

Antibiotics

Oxygen

SaO 2 > 90%

Mechanical ventilation

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

Infection of alveoli, distal airways & epithelium

Possible routes of entry of pathogen into lungs

Gross & microaspiration

Aerosolization

Hematogenous

Contiguous/direct extension from adjacent infection

Pathology Lobar – congestion, red & gray hepatization, resolution Bronchopneumonia – patchy consolidation centered around bronchi & bronchioles Interstitial Miliary

Pathology

Lobar – congestion, red & gray hepatization, resolution

Bronchopneumonia – patchy consolidation centered around bronchi & bronchioles

Interstitial

Miliary

Pulmonary complications Necrotizing pneumonia Abscess formation Vascular invasion Empyema BPF

Pulmonary complications

Necrotizing pneumonia

Abscess formation

Vascular invasion

Empyema

BPF

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

Risk factors (Table 239-3, p 1531)

Alcoholism

Asthma

Immunosuppression

Age > 70 yo

Seizures

Dementia

COPD

Cigarette smoking

Diabetes

Hematologic malignancies

ESRD

Etiology S. pneumoniae – most common Dx CXR Sputum Gm staining & culture Blood culture Bronchoalveolar lavage Urine antigen test for Legionella Serology for Mycoplasma & Chlamydia

S. pneumoniae – most common

Dx

CXR

Sputum Gm staining & culture

Blood culture

Bronchoalveolar lavage

Urine antigen test for Legionella

Serology for Mycoplasma & Chlamydia

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

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

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

> 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

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

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

Cylindrical – uniformly dilated Varicose – irregular, beaded Saccular/cystic – ballooned

Cylindrical – uniformly dilated

Varicose – irregular, beaded

Saccular/cystic – ballooned

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

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

Clinical manifestations Persistent/recurrent purulent sputum production Hemoptysis Dyspnea Wheezing Symptoms worsen/increase during exacerbations Recurrent infections

Persistent/recurrent purulent sputum production

Hemoptysis

Dyspnea

Wheezing

Symptoms worsen/increase during exacerbations

Recurrent infections

PE & Diagnosis Crackles, ronchi, wheezing Clubbing, hypoxemia, RV failure CXR: “tram tracks” , “ring shadows” CT scan – better resolution

Crackles, ronchi, wheezing

Clubbing, hypoxemia, RV failure

CXR: “tram tracks” , “ring shadows”

CT scan – better resolution

Goals of therapy Elimination of underlying problem Improve clearance of tracheobronchial secretions Control of infection Reversal of airflow obstruction

Elimination of underlying problem

Improve clearance of tracheobronchial secretions

Control of infection

Reversal of airflow obstruction

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

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

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

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

Diagnosis Clinical criteria Analysis of sweat Cl values (>70 mEq/L)

Clinical criteria

Analysis of sweat Cl values (>70 mEq/L)

Therapy Promote clearance of secretions Control infection

Promote clearance of secretions

Control infection

Disorders of the Pleura Pleural Effusions Definition Diagnostic approach Pneumothorax

Pleural Effusions

Definition

Diagnostic approach

Pneumothorax

Pleural Effusion Accumulation of excessive quantity of fluid in the pleural space Etiology Formation / accumulation > absorption

Accumulation of excessive quantity of fluid in the pleural space

Etiology

Formation / accumulation > absorption

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

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

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

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

Exudative Pleural Effusion Description Glucose Differential cell count Microbiologic studies Cytologic studies

Description

Glucose

Differential cell count

Microbiologic studies

Cytologic studies

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

Measure PF glucose, amylase Obtain PF cytology Differential cell count Culture, stain PF PF markers for TB Exudate Further diagnostic procedure

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

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

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

~ 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

Parapneumonic Pleural Effusion Bacterial pneumonia Lung abscess Bronchiectasis Empyema – grossly purulent

Bacterial pneumonia

Lung abscess

Bronchiectasis

Empyema – grossly purulent

Aerobic pneumonia Acute febrile illness Anaerobic bacterial pneumonia Subacute illness Anemia Wt loss Brisk leukocytosis Predisposing factors to aspiration

Aerobic pneumonia

Acute febrile illness

Anaerobic bacterial pneumonia

Subacute illness

Anemia

Wt loss

Brisk leukocytosis

Predisposing factors to aspiration

Pneumonia + effusion = parapneumonic effusion Diagnosis CXR UTZ CT scan If > 10 mm fluid between lung & chest wall therapeutic thoracentesis

Pneumonia + effusion = parapneumonic effusion

Diagnosis

CXR

UTZ

CT scan

If > 10 mm fluid between lung & chest wall

therapeutic thoracentesis

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

Loculated PF

PF pH <7.20

PF glucose < 3.3 mmol/L (60 mg/dL)

(+) Gram staining or culture

Gross pus

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

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

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

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

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

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

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

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

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

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

Effusion Secondary Viral Infection ~ 20% of undiagnosed exudative PE

~ 20% of undiagnosed exudative PE

AIDS Uncommon Most common cause – Kaposi’s sarcoma

Uncommon

Most common cause – Kaposi’s sarcoma

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

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

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

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

Miscellaneous Causes of Pleural Effusion Transudative Pleural Effusions CHF Cirrhosis Pulmonary embolism Nephrotic syndrome Peritoneal dialysis Superior vena cava obstruction Myxedema Urinothorax

Transudative Pleural Effusions

CHF

Cirrhosis

Pulmonary embolism

Nephrotic syndrome

Peritoneal dialysis

Superior vena cava obstruction

Myxedema

Urinothorax

Neoplastic diseases metastatic, mesothelioma Infectious diseases Bacterial infectionis TB Fungal Viral Parasitic Pulmonary embolism Exudative Pleural Effusions

Neoplastic diseases

metastatic, mesothelioma

Infectious diseases

Bacterial infectionis

TB

Fungal

Viral

Parasitic

Pulmonary embolism

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Disorders of the Mediastinum

Mediastinal Masses Anterior Thymomas Lymphomas Thyroid masses Teratoma Middle Vascular masses Lymph nodes Pleuropericardial cyst Bronchogenic cyst Posterior Neurogenic tumors Meningomyeloceles Meningoceles Esophageal diverticula

Anterior

Thymomas

Lymphomas

Thyroid masses

Teratoma

Middle

Vascular masses

Lymph nodes

Pleuropericardial cyst

Bronchogenic cyst

Posterior

Neurogenic tumors

Meningomyeloceles

Meningoceles

Esophageal diverticula

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

CT scan – most valuable

Barrium studies – posterior lesions

I 131 nuclear scan – intrathoracic goiter

Definite diagnosis

Mediastinoscopy, mediastinostomy, needle aspiration biopsy, VATS

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%)

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%)

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 (?)

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 (?)

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

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

Acute Respiratory Distress Syndrome Severe dyspnea Hypoxemia Diffuse pulmonary infiltrates Heterogeneous etiology Respiratory Failure

Severe dyspnea

Hypoxemia

Diffuse pulmonary infiltrates

Heterogeneous etiology

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

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

Acute Lung Injury Less severe May evolve into ARDS

Less severe

May evolve into ARDS

Clinical Course & Pathophysiology 3 phases Exudative Proliferative Fibrotic Exudative Proliferative Fibrotic Hyaline membranes Interstitial inflammation Interstitial fibrosis Fibrosis 0 2 7 14 21…

3 phases

Exudative

Proliferative

Fibrotic

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

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

Atelectasis Intrapulmonary shunting & hypoxemia Hypercapnea 2 o to increase dead space DDx Cardiogenic pulmonary edema Diffuse pneumonia Alveolar hemorrhage

Atelectasis

Intrapulmonary shunting & hypoxemia

Hypercapnea 2 o to increase dead space

DDx

Cardiogenic pulmonary edema

Diffuse pneumonia

Alveolar hemorrhage

Proliferative 7-21 D Most patients recover during this phase Initiation of lung repair Organization of alveolar exudates Proliferation of type II pneumocytes

7-21 D

Most patients recover during this phase

Initiation of lung repair

Organization of alveolar exudates

Proliferation of type II pneumocytes

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

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

Therapy General Principles Recognition & treatment of underlying cause Minimize procedures & their complications Prophylaxis vs venous thromboembolism Prompt recognition of nosocomial infections Adequate nutrition

General Principles

Recognition & treatment of underlying cause

Minimize procedures & their complications

Prophylaxis vs venous thromboembolism

Prompt recognition of nosocomial infections

Adequate nutrition

Mechanical Ventilation Low tidal volume (6 mL/kg predicted body wt) Optimal PEEP for alveolar recruitment

Low tidal volume (6 mL/kg predicted body wt)

Optimal PEEP for alveolar recruitment

Others Fluid Management Steroids – current evidence does not support its use in early ARDS

Fluid Management

Steroids – current evidence does not support its use in early ARDS

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

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

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

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

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%

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%

Bronchoalveolar CA – subtype of adenoCA Peripheral airways Single mass Diffuse multinodular Fluffy infiltrate

Bronchoalveolar CA – subtype of adenoCA

Peripheral airways

Single mass

Diffuse multinodular

Fluffy infiltrate

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)

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)

Clinical Manifestations Local tumor growth Tumor invasion Obstruction LN spread Distant metastasis Paraneoplastic syndromes

Local tumor growth

Tumor invasion

Obstruction

LN spread

Distant metastasis

Paraneoplastic syndromes

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)

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)

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

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

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

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

Therapy Stages IA, IB, IIA, IIB – treatment of choice is pulmonary resection IIIA – team approach Palliative approach

Stages IA, IB, IIA, IIB – treatment of choice is pulmonary resection

IIIA – team approach

Palliative approach

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

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

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

History of cigarette smoking

> 35 yo

Relatively large lesion

Lack of calcification

Chest symptoms

Atelectasis, pneumonitis or adenopathy

Growth of lesion

(+) PET scan

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)

“ Popcorn” & “bull’s eye” calcification

Lack of growth over 2 years

Benign Lung Neoplasms <5% of all primary lung tumors Bronchial adenoma & hamartomas – 90% Surgery – diagnostic & therapeutic Produce symptoms due to obstruction

<5% of all primary lung tumors

Bronchial adenoma & hamartomas – 90%

Surgery – diagnostic & therapeutic

Produce symptoms due to obstruction

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

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

Hamartomas Peak incidence: 60 yo More common on males Normal pulmonary tissue components in a disorganized fashion

Peak incidence: 60 yo

More common on males

Normal pulmonary tissue components in a disorganized fashion