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ABIM Board Review: Pulmonary Medicine. Overview. Topics Respiratory Infections Airway Disease Restrictive Lung Diseases Pulmonary Vascular Disease Pleural Disease Sleep Potpourri. Hints. Stress certain topics ASTHMA, TB, SARCOID, ILD’s,PFT’s

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Abim board review pulmonary medicine

ABIM Board Review:Pulmonary Medicine


Overview
Overview

  • Topics

    • Respiratory Infections

    • Airway Disease

    • Restrictive Lung Diseases

    • Pulmonary Vascular Disease

    • Pleural Disease

    • Sleep

    • Potpourri


Hints
Hints

  • Stress certain topics

    • ASTHMA, TB, SARCOID, ILD’s,PFT’s

  • ‘Things marked with these things are pearls to remember’

  • Disclaimer: A 3 year fellowship is difficult to condense into a 1 hour lecture…


Respiratory infections
Respiratory Infections

  • Community Acquired PNA (CAP)

  • HealthCare Assocoiated PNA

    • Hospital Acquired PNA (HAP)

    • Ventilator Associated PNA (VAP)

    • Nursing Home Associated PNA

  • TB


Types of pneumonia
Types of Pneumonia

  • Community Acquired

    • Bacterial

    • Atypical

  • Hospital Acquired >72 hours after admission

  • Ventilator Associated

  • Aspiration Syndromes


Physical signs of pneumonia
Physical Signs of Pneumonia

  • Bronchial Breath sounds

  • Dullness to percussion

  • Egophony


Community acquired pneumonia bugs
Community Acquired Pneumonia Bugs

  • Strep pneumoniae

  • mycoplasma

  • viral

  • Chlamydia

  • H. influenzae

  • Staph aureus

  • Legionella

  • Anerobic?


Hospital acquired pna bugs
Hospital Acquired PNA Bugs

  • Gram negative enterics

  • Staph aureus (MRSA)

  • H. influenzae

  • Strep pneumonia


Indicators of severe pneumonia
Indicators of Severe Pneumonia

  • Multilobar

  • Advanced age

  • Elevated BUN

  • Elevated Respiratory rate

  • High or Low WBC

  • High or Low Temp.

  • Hypotension


Antibiotics
Antibiotics

  • Outpatient younger than 60

  • ATS

    • Macrolide or Tetracycline

  • IDSA

    • Macrolide or Fluoroquinolone or Doxycycline

    • Alternative: Oral second-generation cephalosporin or Augmentin

  • E-mycin does not cover H. flu (COPD)


Antibiotics cont
Antibiotics Cont.

  • Outpatient older than 60 or with co-morbid conditions

  • ATS

    • Second generation cephalosporin, Bactrim, Augmentin with or without a macrolide

  • IDSA

    • Macrolide or Fluoroquinolone or Doxycycline

    • Alternative: Oral second-generation cephalosporin or Augmentin


Antibiotics cont1
Antibiotics Cont.

  • Inpatient Ward

    • ATS

      • Second or third generation cephalosporin or beta lactam/beta lactamase inhibitor with a macrolide

    • IDSA

      • Beta lactam with a macrolide or fluoroquinolone alone


Antibiotics cont2
Antibiotics Cont.

  • Inpatient Severe

    • ATS

      • Macrolide with antipseudomonal agent plus an aminoglycoside

    • IDSA

      • Cefotaxime, ceftriaxone, or Beta-lactam/ Beta-lactamase inhibitor with macrolide or fluoroquinolone


Follow up cxr
Follow-Up CXR

  • Fifty percent of pneumonias clear within 2 weeks and 75 percent clear with in 6 weeks

  • <5% of 20 year olds, 10-20% of 40 year olds, 30% of 60 year olds and 50% of 80 year olds will continue to have infiltrates at 12 weeks

  • Multilobar pneumonias are slower to resolve


Pneumovax
Pneumovax

  • Persons older than the age of 50

  • Persons with asplenia, high risk environments, immunosuppression and chronic illness.

  • Give vaccine if status is unknown

  • Repeat vaccination should be considered for patients at high risk and those vaccinated before 65 if not given with in 5 years.


Tb for another time
TBFor Another Time…

  • Extra-Pulmonary Tuberculosis

    • Lungs> Kidneys> Bone> Brain

  • Mycobacterium Other Than Tuberculosis (MOTT) AKA Non-Tuberculous Mycobacteria (NTM)


AKA

  • Phthisis- “wasting”; chronic pulmonary tuberculosis

  • “Consumption”

  • “White Plague”


Nomenclature
Nomenclature

  • Phthisiology- the study of tuberculosis of the lungs

  • Converter- patient who has experienced an increase of > 10mm of induration in PPD test size within a two-year period, regardless of age.

  • Reactor- a non-converter patient with a positive skin test.

  • LTBI- latent tuberculosis infection. “Treatment of Latent Tuberculosis Infection” has replaced “preventative therapy” and “chemoprophylaxis”.


Epidemiology
Epidemiology

  • An estimated 1/3 of the world’s population is believed to be infected with M. Tuberculosis (roughly 2 billion people).

  • Because actual reporting is generally unreliable, several surrogate values have been used, including:

    • Average annual risk of MTB infection (ARTI)

    • Estimated incidence of smear positive MTB

    • Case Notifications

    • Estimated Case-Fatality rates.


Re emerging scourge
Re-Emerging Scourge?

  • Although MTB experienced a resurgence in the mid-late 80’s, the incidence has actually continued to decline since 1993 and, as of 2005 was at an all-time low…


Location location location
Location, Location, Location

  • In 1998 active TB reported in every state.

  • Seven states (CA, FL, GA, IL, NJ, NY and TX) accounted for 60% of all cases.

  • 40% of all cases in America’s 64 largest cities.


A disease of import
A Disease of Import

  • Incidence of MTB among Foreign-born persons varies by country of origin:

    • Latin America (57% from Mexico)

    • Philippines

    • Vietnam

    • South Korea

    • China


Hiv tb s not so silent partner
HIV: TB’s Not-So Silent Partner

  • HIV’s effect on cell-mediated immunity uniquely positions it as a dominant factor in susceptibility to MTB in SE Asia and Sub-Saharan Africa.

  • Rates of co-infection have increased as high as 45-fold between 1990 and 1994 (Thailand)


Where the money is
Where the Money is…

  • Active MTB cases: 1990-1999

    • North America: 320,000

    • Sub-Saharan Africa: 15,000,000

    • Asia and the Sub-Continent:

      55,000,000


High risk groups infection
High-Risk Groups: Infection

  • HIV+

  • Foreign-born in endemic regions (4-6X)

  • Children of foreign-born from endemic regions

  • Homeless

  • Veterans

  • IV Drug users

  • Congregate living- Nursing homes, prisons, etc.


High risk groups infection con t
High-Risk Groups: Infectioncon’t

  • Close contacts of individuals known, or suspected, to have active MTB.

  • Health care workers (i.e. you)


High risk groups disease
High Risk Groups: Disease

  • HIV+ (100X)

  • Diabetes Mellitus (3X)

  • Post-Gastrectomy or Intestinal Bypass

  • Silicosis (30X)

  • Certain Cancers- Leukemia, Lymphomas, HEENT(16X)

  • Pharmacologically Immunosuppressed

    • Post-chemotherapy, DMARD, Steroids

      • Post solid-organ transplant (20-74X)

  • Recent infection (within 2 years)


High risk groups disease con t
High-Risk Groups: Disease con’t

  • CXR consistent with prior disease without adequate treatment.

  • ESRD (10-25X)

  • Chronic malabsorption syndromes

  • Low Body Weight (<10% below ideal) (2X)


Clinical pathogenesis
Clinical Pathogenesis

  • Although one organism per 12,000 cu ft has been shown to produce infection, only up to 1/3 of individuals in close contact with patient with active MTB develop infection.

  • Most infected aerosolized droplets are cleared by upper airway mechanisms.

  • Those less than 5 microns reach the alveolus, and are phagocytosed by macrophages (MTB infection).


  • Bacilli multiply at this primary site of infection and within 2 weeks are transported to lymphatics to establish secondary site.

  • Within 4 weeks delayed-type hypersensitivity develops leading to granuloma formation and subsequent decrease in bacterial burden.

  • However, sterilization rarely occurs, even though host displays acquired immunity, rapidly clearing subsequent exposures.




By the numbers
By the Numbers… prolonged courses of therapy so effective drug levels are persistent for months as latent organisms reactivate, rendering themselves susceptible.

  • Once infected with MTB 3-5% of immunocompetent hosts develop active disease within one year. A further 3-5% will develop active disease within their lifetime.

  • Said another way: Once primarily infected, lifetime risk of active MTB is 10%; half of those within the following year.


More numbers
More Numbers prolonged courses of therapy so effective drug levels are persistent for months as latent organisms reactivate, rendering themselves susceptible.

  • For immunosuppressed, risk of developing active MTB is 7-10% annually.


Diagnosis symptoms
Diagnosis: Symptoms prolonged courses of therapy so effective drug levels are persistent for months as latent organisms reactivate, rendering themselves susceptible.

  • Pulmonary

    • Prolonged productive cough

    • Hemoptysis

    • Chest pain

  • Systemic

    • Fevers/Chills

    • Drenching Night Sweats

    • Anorexia/Weight loss

    • Easy Fatigability


Diagnosis h p
Diagnosis: H&P prolonged courses of therapy so effective drug levels are persistent for months as latent organisms reactivate, rendering themselves susceptible.

  • After considering diagnosis of MTB (and putting a mask on you or patient), focus history on risk factors for MTB infection or disease (see previous) as well as past exposure and treatment history.

  • Don’t forget to perform adequate review of systems as only 73% of pulmonary MTB cases are exclusively pulmonary.


Diagnosis the laboratory
Diagnosis: The Laboratory prolonged courses of therapy so effective drug levels are persistent for months as latent organisms reactivate, rendering themselves susceptible.

  • The gold standard for diagnosis, the sputum smear, is neither sensitive nor specific.

    • >10,000 organisms/ml are required for detection, leaving the smear positive in only 50% of active MTB cases

    • Any acid-fast bacilli present will cause the test to be positive.


The sputum
The Sputum prolonged courses of therapy so effective drug levels are persistent for months as latent organisms reactivate, rendering themselves susceptible.

  • Early AM specimens on three consecutive days are ideal. Induced sputum with inhaled saline may be required in patients unable to provide adequate lower airway samples.

  • Alternatives

    • Bronchoscopy (choose wisely)

    • Early AM Gastric aspiration


Sensitivities
Sensitivities prolonged courses of therapy so effective drug levels are persistent for months as latent organisms reactivate, rendering themselves susceptible.

  • All initially positive MTB cultures must be tested for sensitivities to guide anti-microbiologic treatment and identify Multi-Drug Resistant-TB (MDRTB).

  • Sensitivities should be repeated if patient experiences clinical treatment failure or cultures remain positive despite two months of treatment.


Purified protein derivative
Purified Protein Derivative prolonged courses of therapy so effective drug levels are persistent for months as latent organisms reactivate, rendering themselves susceptible.

  • First recognized as potential tool for diagnosis by Sir Arthur Conan Doyle.

  • Later perfected by Mantoux.

  • Though fairly accurate for diagnosing infection (not disease), limited by false positive rate around 10% and false negative rates around 20-30% (higher in immunocompromised).


Ppd con t
PPD con’t prolonged courses of therapy so effective drug levels are persistent for months as latent organisms reactivate, rendering themselves susceptible.

  • A PPD may take up to 10 weeks to turn positive after initial infection.

  • The PPD is the only way to diagnose MTB infection prior to MTB disease.

    • Role of Interferon-Gamma…


The ppd itself
The PPD Itself prolonged courses of therapy so effective drug levels are persistent for months as latent organisms reactivate, rendering themselves susceptible.

  • 0.1 ml of PPD tuberculin containing 5 TU is injected intradermally on the inner surface of the forearm producing a 6-10 mm wheal.

  • A reading 48-72 hours from PPD placement should be obtained:

    • Positive readings may be obtained up to one week after placement.

    • Failure to obtain reading within 72 hours indicates need for repeat testing


More ppd
More PPD prolonged courses of therapy so effective drug levels are persistent for months as latent organisms reactivate, rendering themselves susceptible.

  • The area of induration (not erythema) is measured in millimeters perpendicular to the long-axis of the forearm.

  • “Conversion”- defined as an increase of >10mm within a 2-year period.


A positive ppd
A Positive PPD prolonged courses of therapy so effective drug levels are persistent for months as latent organisms reactivate, rendering themselves susceptible.

  • >5 mm

    • HIV+

    • Recent contacts of active MTB case

    • CXR consistent with healed MTB

    • Patients with organ transplants or immunosuppression > 15mg/day of prednisone > 1 month


  • > prolonged courses of therapy so effective drug levels are persistent for months as latent organisms reactivate, rendering themselves susceptible.10 mm

    • Recent arrivals (<5 years) from endemic regions.

    • IVDU

    • Residents/Employees of:

      • Prisons/jails

      • Nursing home/shelters

      • Hospitals, including mycobacterial labs

    • High-Risk of Progressing to MTB disease

    • Children <4 yo


  • > prolonged courses of therapy so effective drug levels are persistent for months as latent organisms reactivate, rendering themselves susceptible. 15mm

    • No known risk factors for MTB.


Ppd false positives
PPD: False Positives prolonged courses of therapy so effective drug levels are persistent for months as latent organisms reactivate, rendering themselves susceptible.

  • MOTT

  • BCG vaccination


Ppd false negatives
PPD: False Negatives prolonged courses of therapy so effective drug levels are persistent for months as latent organisms reactivate, rendering themselves susceptible.

  • Recent MTB infection

  • Very Young (< 6mos)

  • Live-Virus vaccination

  • Overwhelming MTB disease

  • HIV+ or other viral infection

  • Immunosuppressive Therapy


BCG prolonged courses of therapy so effective drug levels are persistent for months as latent organisms reactivate, rendering themselves susceptible.

  • Bottom line: prior vaccination with BCG should be ignored and the patient treated appropriately if the PPD is positive.


Boost effect
Boost Effect? prolonged courses of therapy so effective drug levels are persistent for months as latent organisms reactivate, rendering themselves susceptible.

  • Delayed-Type Hypersensitivity may fade over time, resulting in subsequent negative testing in those previously infected. This exposure to tuberculin may “re-awaken” sensitivity and lead to potential misinterpretation of future positive testing as a new infection.


Two step testing
Two-Step Testing prolonged courses of therapy so effective drug levels are persistent for months as latent organisms reactivate, rendering themselves susceptible.

  • This “Boost” phenomenon, and subsequent misinterpretation, may be sidestepped by performing two-step testing.

  • This entails a second test 1-3 weeks after the first with positive tests indicating past infection and treated appropriately


Who not to test
Who Not to Test prolonged courses of therapy so effective drug levels are persistent for months as latent organisms reactivate, rendering themselves susceptible.

  • Pregnant women without specific high-risk.

  • Previously positive PPD patients should not receive repeat testing (including yearly CXR’s); instead, these patients should be followed symptomatically.


Other testing
Other Testing prolonged courses of therapy so effective drug levels are persistent for months as latent organisms reactivate, rendering themselves susceptible.

  • Some populations may require screening for active MTB disease which is more appropriately performed by CXR.

    • Prisoners

    • New accessions to congregate living

    • POW’s/Detainees


Targeted testing
Targeted Testing prolonged courses of therapy so effective drug levels are persistent for months as latent organisms reactivate, rendering themselves susceptible.

  • Screening should be limited to previously described high-risk groups.

  • Prior to testing a follow-up plan for further testing and treatment must be considered:

    • “The decision to test is the decision to treat.”


The chest radiograph
The Chest Radiograph prolonged courses of therapy so effective drug levels are persistent for months as latent organisms reactivate, rendering themselves susceptible.

  • Though traditionally relied upon to assist in making diagnosis, HIV and other forms of immunosuppression have impacted its utility.

    • Old-school:

      • Primary: Middle or lower lung field infiltrates with ipsilateral lymphadenopathy.

      • Reactivation: Upper-lobe infiltrates and cavities in 98% of non-AIDS cases.

        • Predilection for apical and posterior segments of upper lobe and superior segments of lower lobes


Cxr con t
CXR con’t prolonged courses of therapy so effective drug levels are persistent for months as latent organisms reactivate, rendering themselves susceptible.

  • New: Up to 35% of AIDS patients with active MTB may have clear CXR; frequent findings include lymphadenopathy or effusion alone.


Old granulomatous disease ogd
Old Granulomatous Disease (OGD) prolonged courses of therapy so effective drug levels are persistent for months as latent organisms reactivate, rendering themselves susceptible.

  • Common radiographic term used to describe stigmata of prior infection, frequently MTB.

    • Implies dense, smaller nodules without or without visible calcification or fibrotic scarring typically seen in the upper lobes.

    • Bronchiectasis, volume loss or pleural scarring may accompany OGD.


Diagnosis lab
Diagnosis: Lab prolonged courses of therapy so effective drug levels are persistent for months as latent organisms reactivate, rendering themselves susceptible.

  • Smear/Cultures

    • AFB+/MTB culture growth from sputum, pleural fluid or pleural biopsy

  • Pathology

    • Demonstration of caseating granulomas in pleural tissue.

  • Pleural Fluid Analysis


Diagnosis lab pleural fluid
Diagnosis: Lab prolonged courses of therapy so effective drug levels are persistent for months as latent organisms reactivate, rendering themselves susceptible.Pleural Fluid

  • Exudative with higher total protein levels (esp.> 5.0g/dl) adding to specificity.

  • Lymphocyte pre-dominance (though early effusions may be neutrophil pre-dominant).

  • > 10% eosinophils virtually excludes MTB as diagnosis (unless prior thoracentesis or PTX).

  • Likewise, the presence of > 5% mesothelial cells makes MTB less likely (does not apply to HIV+ individuals).


Pleural fluid ada
Pleural Fluid: ADA prolonged courses of therapy so effective drug levels are persistent for months as latent organisms reactivate, rendering themselves susceptible.

  • Adenosine Deaminase levels may correspond directly with likelihood of MTB infection.

    • < 40 U/L- unlikely MTB

    • 40-70 U/L- questionable

    • > 70 U/L- likely MTB

  • Other clinical conditions (RA and empyema) may have elevated ADA levels, but should be easy to clinically differentiate.


Treatment
Treatment prolonged courses of therapy so effective drug levels are persistent for months as latent organisms reactivate, rendering themselves susceptible.

  • Several different nuances to treatment modalities:

    • LTBI

    • Empiric (4 drug)

    • Therapeutic

    • MDRTB


Treatment of ltbi
Treatment of LTBI prolonged courses of therapy so effective drug levels are persistent for months as latent organisms reactivate, rendering themselves susceptible.

  • Essential for any program aimed at reducing future spread of MTB.

  • MTB disease must be considered and ruled out prior to treating LTBI.


Regimens
Regimens prolonged courses of therapy so effective drug levels are persistent for months as latent organisms reactivate, rendering themselves susceptible.

  • Isoniazid (INH) alone

  • Rifampin/Pyrazinamide (PZA)

  • Rifampin alone

  • Known exposure to MDRTB


Inh alone
INH alone prolonged courses of therapy so effective drug levels are persistent for months as latent organisms reactivate, rendering themselves susceptible.

  • Daily INH for 12 months reduces the risk of MTB disease by 90%.

  • 6 months of therapy reduces risk by 70%.

  • Two acceptable regimens:

    • 300mg once daily

    • 15mg/kg twice weekly (DOT) (900mg max)

  • Though a 6 month regimen is acceptable, 9 months of therapy is considered optimal in both HIV+ and HIV- individuals.


Post exposure to mdrtb
Post-exposure to MDRTB prolonged courses of therapy so effective drug levels are persistent for months as latent organisms reactivate, rendering themselves susceptible.

  • Regimens should consist of two drugs to which the organism has demonstrated susceptibility.

    • PZA

    • Ethambutol

    • Quinalone


Monitoring
Monitoring prolonged courses of therapy so effective drug levels are persistent for months as latent organisms reactivate, rendering themselves susceptible.

  • Though baseline laboratory testing is not indicated at the start of treatment for LTBI, baseline liver function tests should be obtained in those whose initial evaluation suggests a liver disorder, pregnant women, and HIV+ patients.

  • Though advancing age increases risk of hepatotoxicity, routine screening of LFT’s is not recommended in the elderly.


Monitoring con t
Monitoring con’t prolonged courses of therapy so effective drug levels are persistent for months as latent organisms reactivate, rendering themselves susceptible.

  • Monthly evaluations should address:

    • Adherence to prescribed regimen.

    • Signs and Symptoms of active MTB disease.

    • Signs and Symptoms of hepatitis

    • Other potential side effects from individual regimens.


Empiric 4 drug therapy
Empiric (4-drug) Therapy prolonged courses of therapy so effective drug levels are persistent for months as latent organisms reactivate, rendering themselves susceptible.

  • Clinical Dogma

    • Adherence must be ensured.

    • Multiple drugs to which the organism is susceptible must be used for prolonged periods.

    • Never add a single drug to a failing regimen.


Pires
PIRES prolonged courses of therapy so effective drug levels are persistent for months as latent organisms reactivate, rendering themselves susceptible.

  • 4-drug therapy should be administered for the initial 2 months of therapy; potential agents include:

    • Pyrazinamide (PZA)

    • Isoniazid (INH)

    • Rifampin (RIF)

    • Ethambutol (EMB)

    • Streptomycin (SM)


More pires
More PIRES prolonged courses of therapy so effective drug levels are persistent for months as latent organisms reactivate, rendering themselves susceptible.

  • Each agent plays a special role in the initial 2-month course of therapy.

    • INH and RIF allow for short-course regimens with high cure rates.

    • PZA has potent sterilizing ability allowing for shortening from 9 to 6 mos

    • EMB (or SM) is added to prevent emergence of further drug resistance if primary INH resistance is possible.


Continuation of treatment
Continuation of Treatment prolonged courses of therapy so effective drug levels are persistent for months as latent organisms reactivate, rendering themselves susceptible.

  • As culture and sensitivity data return, regimens may be tailored, recalling that at least two drugs must be used at all times.

  • Typical minimal length of therapy is six months:

    • “4 drugs for 2 months, followed by 2 drugs for 4 months”

      • If RIF is not used, 18 months of therapy is required.

  • INH therapy should be discontinued if:

    • LFT’s > 3X nl and Pt is symptomatic

    • LFT’s > 5X nl and Pt is asymptomatic


  • End of therapy
    End of Therapy prolonged courses of therapy so effective drug levels are persistent for months as latent organisms reactivate, rendering themselves susceptible.

    • A chest x-ray should be obtained to establish baseline for future examinations.

    • Sputum sample should be obtained at end of therapy to document cure.


    Mtb treatment pregnancy
    MTB Treatment: Pregnancy prolonged courses of therapy so effective drug levels are persistent for months as latent organisms reactivate, rendering themselves susceptible.

    • The preferred initial treatment is INH, RIF and EMB.

      • SM has proven harmful fetal effects.

      • PZA’s effect are unknown

    • Since PZA is excluded treatment must continue for 9 months.


    Multi drug resistant tb mdrtb
    Multi-Drug Resistant TB prolonged courses of therapy so effective drug levels are persistent for months as latent organisms reactivate, rendering themselves susceptible.(MDRTB)

    • Definition: MTB resistant to both INH and rifampin.

    • Always treated with daily DOT therapy.

    • XDRTB not likely to be tested…


    MDR TB Cases, 1993 - 1998 prolonged courses of therapy so effective drug levels are persistent for months as latent organisms reactivate, rendering themselves susceptible.


    Mdrtb high risk groups
    MDRTB: High-Risk Groups prolonged courses of therapy so effective drug levels are persistent for months as latent organisms reactivate, rendering themselves susceptible.

    • Prior treatment with MTB drugs.

    • Contacts with known carriers of MDRTB

    • Foreign-born persons from MDRTB endemic regions

    • Remains smear or culture positive despite 2 months of treatment

    • Received inadequate therapy for > 2 weeks

    • Cavitary Disease


    Public health
    Public Health prolonged courses of therapy so effective drug levels are persistent for months as latent organisms reactivate, rendering themselves susceptible.

    • Assume infectiousness in persons known, or suspected to have pulmonary or laryngeal MTB if they are:

      • Coughing or are “smear-positive” and

      • Not receiving therapy, just started therapy or have a poor response to therapy.

    • Mask on you or them and ISOLATE.


    Public health con t
    Public health con’t prolonged courses of therapy so effective drug levels are persistent for months as latent organisms reactivate, rendering themselves susceptible.

    • Patients with drug-susceptible MTB disease are no longer considered infectious if they meet all of the following:

      • On adequate therapy.

      • Have experienced a clinical response to therapy.

      • Three consecutive negative sputum smears from three different days.


    Home isolation
    Home Isolation prolonged courses of therapy so effective drug levels are persistent for months as latent organisms reactivate, rendering themselves susceptible.

    • Isolation is not required to occur in a hospital. In fact, an estimated 60% of all costs spent in the US treating MTB are due to hospitalization.

    • Must ensure that others in the home are not at high risk for developing MTB disease and that simple precautions (physical isolation, surgical masks, etc) are followed until non-infectivity can be assured.


    Directly observed therapy dot
    Directly-Observed Therapy (DOT) prolonged courses of therapy so effective drug levels are persistent for months as latent organisms reactivate, rendering themselves susceptible.

    • Health Care Worker watches patient swallow each and every dose of MTB meds

    • Considered for patients with:

      • Concerns for non-adherence.

      • Intermittent dosing regimen.

      • Household member on DOT for active MTB disease.


    Airway disease
    Airway Disease prolonged courses of therapy so effective drug levels are persistent for months as latent organisms reactivate, rendering themselves susceptible.

    • Asthma

    • COPD

    • Bronchiectasis

      • CF

      • ABPA


    Definition
    Definition prolonged courses of therapy so effective drug levels are persistent for months as latent organisms reactivate, rendering themselves susceptible.

    • Asthma is an inflammatory disorder manifested by a clinical syndrome of episodic dyspnea, wheeze, and cough with reversible airflow obstruction and bronchial hyper-responsiveness.


    Initial assessment and diagnosis of asthma
    Initial Assessment and prolonged courses of therapy so effective drug levels are persistent for months as latent organisms reactivate, rendering themselves susceptible. Diagnosis of Asthma

    • Determine that:

      • Patient has history or presence of episodic symptoms of airflow obstruction

      • Airflow obstruction is at least partially reversible

      • Alternative diagnoses are excluded


    Initial assessment and diagnosis of asthma continued
    Initial Assessment and prolonged courses of therapy so effective drug levels are persistent for months as latent organisms reactivate, rendering themselves susceptible.Diagnosis of Asthma (continued)

    Is airflow obstruction at least partially

    reversible?

    • Use spirometry to establish airflow obstruction:

      • FEV1 < 80% predicted;

      • FEV1/FVC <65% or below the lower limit of normal

    • Use spirometry to establish reversibility:

      • FEV1 increases >12% and at least 200 mL after using a short-acting inhaled beta2-agonist


    Bronchoprovocation testing
    Bronchoprovocation Testing prolonged courses of therapy so effective drug levels are persistent for months as latent organisms reactivate, rendering themselves susceptible.

    • Methacholine Challenge

    • Exercise Induced Bronchospasm

    • Increased sensitivity

    • Decreased specificity

    • Very high negative predictive value


    Methacholine challenge
    Methacholine Challenge prolonged courses of therapy so effective drug levels are persistent for months as latent organisms reactivate, rendering themselves susceptible.

    • Increasing doses of methacholine given by inhalation

    • Repeated spirometry performed

    • Decrement of FEV1 by 20% is diagnostic of bronchial hyper-reactivity at dose < 4 mg/ml.

      • 4-16 mg/ml is considered by most to be borderline

      • Clinical interpretation in requires correlation with symptoms.



    Monitoring symptoms
    Monitoring Symptoms Treatment

    • Symptom history should be based ona short (2 to 4 weeks) recall period

    • Symptom history should include:

      • Daytime asthma symptoms

      • Nocturnal wakening as a result ofasthma symptoms

      • Exercise-induced symptoms

      • Exacerbations


    Monitoring lung function spirometry
    Monitoring Lung Function: Spirometry Treatment

    • Spirometry is recommended:

      • At initial assessment

      • After treatment has stabilized symptoms

      • At least every 1 to 2 years


    Monitoring lung function peak flow monitoring continued
    Monitoring Lung Function: TreatmentPeak Flow Monitoring (continued)

    Patients should:

    • Measure peak flow on waking before taking a bronchodilator

    • Use personal best

    • Be aware that a peak flow <80% of personal best indicates a need for additional medication

    • Use the same peak flow meter over time


    Monitoring pharmacotherapy
    Monitoring Pharmacotherapy Treatment

    • Monitor:

      • Patient adherence to regimen

      • Inhaler technique

      • Frequency of inhaled short-actingbeta2-agonist use

      • Frequency of oral corticosteroid “burst” therapy

      • Side effects of medications


    Control of factors contributing to asthma severity
    Control of Factors TreatmentContributing to Asthma Severity

    • Assess exposure and sensitivity to:

      • Inhalant allergens

      • Occupational exposures

      • Irritants:

        • Indoor air (including tobacco smoke)

        • Air pollution


    Control other factors that can influence asthma severity
    Control Other Factors That TreatmentCan Influence Asthma Severity

    • Rhinitis

      • Intranasal corticosteroids are most effective

    • Sinusitis

      • Promote drainage; antibiotics for complicating acute bacterial infection

    • Gastroesophageal reflux

      • Medications; no food before bedtime; elevate head of bed

    • Influenza vaccine annually


    Overview of asthma medications
    Overview of TreatmentAsthma Medications

    • Daily: Long-Term Control

      • Corticosteroids (inhaled and systemic)

      • Cromolyn/nedocromil

      • Long-acting beta2-agonists

      • Methylxanthines

      • Leukotriene modifiers


    Overview of asthma medications continued
    Overview of TreatmentAsthma Medications (continued)

    • As-needed: Quick Relief

      • Short-acting beta2-agonists

      • Anticholinergics

      • Systemic corticosteroids


    Inhaled corticosteroids
    Inhaled Corticosteroids Treatment

    • Most effective long-term-control therapy for persistent asthma

    • Small risk for adverse events at recommended dosage

    • Reduce potential for adverse events by:

      • Using spacer and rinsing mouth

      • Using lowest dose possible

      • Using in combination with long-acting beta2-agonists

      • Monitoring growth in children


    Inhaled corticosteroids continued
    Inhaled Corticosteroids Treatment(continued)

    • Benefit of daily use:

      • Fewer symptoms

      • Fewer severe exacerbations

      • Reduced use of quick-relief medicine

      • Improved lung function

      • Reduced airway inflammation


    Long acting beta 2 agonists
    Long-Acting Beta Treatment2-Agonists

    • Not a substitute for anti-inflammatory therapy

    • Not appropriate for monotherapy

    • Beneficial when added to inhaled corticosteroids

    • Not for acute symptoms or exacerbations


    Short acting beta 2 agonists
    Short-Acting Beta Treatment2-Agonists

    • Most effective medication for relief of acute bronchospasm

    • More than one canister per month suggests inadequate asthma control

    • Regularly scheduled use is not generally recommended


    Leukotriene modifiers
    Leukotriene Modifiers Treatment

    • Mechanisms

      • 5-LO inhibitors

      • Cysteinyl leukotriene receptor antagonists

    • Indications

      • Long-term-control therapy in mildpersistent asthma

        • Improve lung function

        • Prevent need for short-acting beta2-agonists

        • Prevent exacerbations

      • Further experience and research needed

      • Do not replace inhaled corticosteroids

      • Not for monotherapy


    Stepwise approach to therapy gaining control
    Stepwise Approach to Therapy: Gaining Control Treatment

    1. Start high and step down.

    2. Start at initial level of severity; gradually step up.

    STEP 4

    Severe Persistent

    2

    STEP 3

    1

    Moderate Persistent

    STEP 2

    Mild Persistent

    STEP 1

    Mild Intermittent


    Indicators of poor asthma control
    Indicators of Poor TreatmentAsthma Control

    • Step up therapy if patient:

      • Awakens at night with symptoms

      • Has an urgent care visit

      • Has increased need for short-acting inhaled beta2-agonists

      • Uses more than one canister of short-acting beta2-agonist in 1 month


    Indicators of poor asthma control continued
    Indicators of Poor Treatment Asthma Control (continued)

    • Before increasing medications, check:

      • Inhaler technique

      • Adherence to prescribed regimen

      • Environmental changes

      • Also consider alternative diagnoses


    Managing exercise induced bronchospasm eib
    Managing Exercise-Induced Bronchospasm (EIB) Treatment

    • Anticipate EIB in all patients

    • Teachers and coaches need to be notified

    • Diagnosis

      • History of cough, shortness of breath, chest pain or tightness, wheezing, or endurance problemsduring exercise

      • Conduct exercise challenge OR have patientundertake task that provoked the symptoms

      • 15% decrease in PEF or FEV1 is compatible with EIB


    Managing exercise induced bronchospasm eib continued
    Managing Exercise-Induced Bronchospasm (EIB) Treatment(continued)

    • Management Strategies

      • Short-acting inhaled beta2-agonists used shortly before exercise last 2 to 3 hours

      • Salmeterol may prevent EIB for 10 to 12 hours

      • Cromolyn and nedcromil are also acceptable

      • A lengthy warmup period before exercise may preclude medications for patients who can tolerate it

      • Long-term-control therapy, if appropriate


    Management of asthma exacerbations
    Management of TreatmentAsthma Exacerbations

    • Inhaled beta2-agonist to provide prompt relief of airflow obstruction

    • Systemic corticosteroids to suppress and reverse airway inflammation

      • For moderate-to-severe exacerbations, or

      • For patients who fail to respond promptly and completely to an inhaled beta2-agonist


    Risk factors for death from asthma
    Risk Factors for TreatmentDeath From Asthma

    • Past history of sudden severe exacerbations

    • Prior intubation or admission to ICUfor asthma

    • Two or more hospitalizations for asthmain the past year

    • Three or more ED visits for asthmain the past year


    Risk factors for death from asthma continued
    Risk Factors for TreatmentDeath From Asthma (continued)

    • Hospitalization or an ED visit for asthmain the past month

    • Use of >2 canisters per month of inhaled short-acting beta2-agonist

    • Current use of systemic corticosteroidsor recent withdrawal from systemic corticosteroids


    Risk factors for death from asthma continued1
    Risk Factors for TreatmentDeath From Asthma (continued)

    • Difficulty perceiving airflow obstructionor its severity

    • Co-morbidity, as from cardiovascular diseases or chronic obstructive pulmonary disease

    • Serious psychiatric disease or psychosocial problems


    Risk factors for death from asthma continued2
    Risk Factors for TreatmentDeath From Asthma (continued)

    • Low socioeconomic status andurban residence

    • Illicit drug use

    • Sensitivity to Alternaria


    Aspirin sensitive asthma
    Aspirin Sensitive Asthma Treatment

    • Sampter’s Triad

      • Asthma

      • ASA sensitivity

      • Nasal polyps

    • Difficult to control

    • Probable role for leukotriene modifiers

    • Role for ASA desensitization


    Difficult to control asthma
    Difficult to Control Asthma Treatment

    • Consider alternative or complicating diagnoses

      • Rhinitis, Sinusitis, GERD

      • Allergic Bronchopulmonary Aspergillosis

      • Churg-Strauss Vasculitis

      • Vocal Cord Dysfunction

      • Non-pulmonary Disorders


    Copd epidemiology
    COPD- Epidemiology Treatment

    • Rising Mortality rates now place COPD 4th in US

    • Tobacco use responsible for 85-90% of cases

      • Alpha-1 AT def < 1%

    • ~20% of smokers develop COPD

      • ~20% of COPDer’s develop CO2 retention

    • FEV1 < 0.75L Mortality

      • 1 year = 30%

      • 10 year = 95%


    COPD Treatment

    • Emphysema

      • Centrilobular

        • Tobacco Related

      • Panacinar

        • Alpha-1 AT def

    • Chronic Bronchitis

      • ‘Two tablespoons of sputum daily for three months of any 2 year period’


    Emphysema dx
    Emphysema- Dx Treatment

    • Suspected in patients with sig tobacco exposure and sx’s

      • Dx: SPIROMETRY!

    • DLCO reduction with emphysema vice CB

    • Imaging reveals bullous lung disease

      • Only severe disease on CXR


    Emphysema dx1
    Emphysema- Dx Treatment

    • Alpha1- AT def- Suspect in patients with sx’s and age < 50.

      • May have no tobacco exposure, but smoking will accelerate sx presentation

      • May have family hx of lung or liver involvement

      • ‘Basilar Predominance to Bullous lung disease’


    Emphysema tx
    Emphysema- Tx Treatment

    • ‘Tobacco Cessation and Oxygen’

    • Symptom relief

      • Bronchodilators

      • Anti-inflammatories

      • Methylxanthines

      • Oral steroids as tx of last resort

    • Pulmonary Rehabilitation

    • Surgery

      • Bullectomy- Bullae > 1/3 hemithorax

      • LVRS- Upper lobe predom with low exercise cap

      • Transplant-


    Emphysema tx acute exacerbations
    Emphysema- Tx TreatmentAcute Exacerbations

    • Pt’s with 2/3 ‘Winnipeg Criteria’ deserve Abx

      • Increased SOB

      • Increased Sputum volume

      • Sputum purulence

    • Trump card = Hospitalization

    • Any abx will do…


    Indications for o 2
    ‘Indications for O Treatment2’

    • Resting Sp02 < 88%

    • Resting Pa02 < 55mmHg

    • Resting Pa02 56 to 59 mmHg if

      • Cor pulmonale (including peripheral edema)

      • Polycythemia

    • Remember to re-eval for O2 requirements ~4-6 weeks after acute exacerbation.


    Emphysema tx acute exacerbations1
    Emphysema- Tx TreatmentAcute Exacerbations

    • Steroids

      • Oral = IV (equivalent to 40-60mg prednisone)

      • Rapidly tapered over 2 weeks

    • Aggressive BD tx’s


    Bronchiectasis defined
    ‘Bronchiectasis’ Defined Treatment

    • Bronchial dilatation frequently associated with:

      • Bronchial wall thickening

      • Fluid retention within the bronchi

      • Chronic inflammation/infection

    • Can be localized or diffuse


    Bronchiectasis
    Bronchiectasis Treatment


    Restrictive lung diseases
    Restrictive Lung Diseases Treatment

    • Pleural Disease

    • Alveolar Diseases

    • Interstitial Diseases

    • Neuromuscular Diseases

    • Thoracic Cage Diseases


    Parenchymal disease
    Parenchymal Disease Treatment

    • Interstitial Lung Disease

      • Idiopathic Interstitial PNA’s

      • Sarcoidosis

      • Collagen Vascular Disorders

      • Eosinophilic Lung Diseases

    • Alveolar Lung Disease

      • Pulmonary Edema Syndromes

      • Pulmonary Alveolar Proteinosis


    Nomenclature1
    Nomenclature Treatment

    • Pneumonia vs Pneumonitis

    • Alphabet Soups

      • COP, BOOP, BO, BOS, OB, CB

    • Name Game

      • That was then, this is now…

    • Disease’s Clinical name vs Histologic name


    New names
    New Names Treatment

    • Hypersensitivity Pneumonitis

      • Extrinsic Allergic Alveolitis (EAA)

    • Eosinophilic Granuloma or Histiocytosis X

      • Langerhan’s Cell Histiocytosis (LCH)

    • Idiopathic Bronchiolitis Obliterans Organizing Pneumonia

      • Cryptogenic Organizing Pneumonia (COP)


    An alphabet soup of new names
    An Alphabet Soup of New Names Treatment

    • Idiopathic Interstitial Pneumonias (IIP’s)

      • Idiopathic Pulmonary Fibrosis (IPF)

      • Non-Specific Interstitial Pneumonia (NSIP)

      • Desquamative Interstitial Pneumonia (DIP)

      • Respiratory Bronchiolitis Interstitial Lung Disease (RBILD)

      • Cryptogenic Organizing Pneumonia (COP)

      • Acute Interstitial Pneumonia (AIP)


    Clinical name vs histologic name
    Clinical Name vs TreatmentHistologic Name

    • Same entity may be referred to by different names by different specialists or in different circumstances.

      • Idiopathic Pulmonary Fibrosis -Clinical

        • Usual Interstitial Pneumonia (UIP)- Histologic


    Blood pus water
    Blood,Pus, Water… Treatment

    • Blood

    • Mineral

    • Water

    • Cells

    • Proteins


    Blood
    Blood Treatment

    • Diffuse Alveolar Hemorrhage Syndromes

    • Hemosiderosis


    Minerals
    Minerals Treatment

    • Calcium

      • Pulmonary Alveolar Microlithiasis

      • Metastatic Calcinosis

    • Pneumoconioses

      • Asbestos

      • Silicosis

      • Talc

      • Coal Worker’s Pneumoconiosis


    Water
    Water Treatment

    • Cardiogenic Pulmonary Edema

    • ARDS

    • Radiation Toxicity


    Cells
    Cells Treatment

    • Lymphocytes

      • LIP, most Collagen Vascular Dz assoc. ILD

    • Eosinophils

      • Eosinophilic Pneumonias, ABPA, CSS

    • Multi-Nucleated Giant Cells (Granuloma)

      • Sarcoid/Berylliosis, EAA

    • Histiocytes

      • Langerhan’s Cell Histiocytosis

    • Malignant

      • Lymphangitic CA, BAC


    Protein
    Protein Treatment

    • Amyloidosis

    • Gaucher’s Disease

    • Pulmonary Alveolar Proteinosis


    When to think interstitial lung disease
    When to Think “Interstitial Lung Disease?” Treatment

    • Dyspnea evaluation

      • +/- Hypoxemia

    • Chronic Cough

    • Refractory “CHF”

    • Abnormal radiograph

      • Exceptions: Stage 0/1 Sarcoid, EAA, DIP/RBILD

    • Abnormal PFT’s

      • Isolated DLCO defect


    Epidemiology1
    Epidemiology Treatment

    • Previously felt to occur in 5 per 100,000

    • Recently estimated to occur in 31.5 per 100,000 males in US (by death certificate diagnosis of ILD).

      • 26.1/100,000 females

    • Most common ILD is “Idiopathic Pulmonary Fibrosis” accounting for up to 45% of ILD diagnoses.


    Epidemiology con t
    Epidemiology Con’t Treatment

    • Accounts for approx. 100,000 hospital admissions annually in US.

    • Represents approx. 15% of office visits to pulmonologists.

    • Expanding populations of patients at risk for ILD ( AIDS, post-chemotherapy, etc.) is likely to lead to higher incidence of these diseases.


    Idiopathic pulmonary fibrosis
    Idiopathic Pulmonary Fibrosis Treatment

    • Prevalence: 13–20/100,000 in US (approximately 35,000-55,000 cases)

    • Onset: Usually between 50 and 70 yr

    • Clinical presentation

      • Progressive dyspnea on exertion

      • Paroxysmal cough, usually nonproductive

      • Abnormal breath sounds on chest auscultation

      • Abnormal chest x-ray or HRCT

      • Restrictive pulmonary physiology with reduced lung volumes and DLCO and widened AaPO2

    • Coultas DB et al. Am J Respir Crit Care Med. 1994;150:967.

    • ATS/ERS. Am J Respir Crit Care Med. 2000;161:646.


    Diagnosis of ipf
    DIAGNOSIS OF IPF Treatment

    • Major criteria

      • Exclusion of other known causes of ILD

      • Abnormal pulmonary function studies

      • Bibasilar reticular abnormalities on HRCT scan

      • No histologic or cytologic features on transbronchial lung biopsy or BAL analysis supporting another diagnosis

    • Minor criteria

      • Age >50 yr

      • Insidious onset of otherwise unexplained exertional dyspnea

      • Duration of illness 3 mo

      • Bibasilar, dry (“Velcro”) inspiratory crackles


    Sarcoidosis
    Sarcoidosis Treatment

    • “Sarcoidosis is a multi-system disorder of unknown cause…” characterized by “…histological evidence of noncaseating epithelioid cell granulomas. Granulomas of known causes and local sarcoid reactions must be excluded.”ATS Statement on Sarcoidosis. AJRCCM 1999.

    • First described in 1877 by Hutchinson

    • Boeck coined the term “sarkoid” in 1899

    • Organs that may be involved:

      • Lung, skin, eyes, liver, spleen, lymph nodes, salivary glands, heart, nervous system, muscles, bones, kidneys, joints, stomach


    Epidemiology2
    Epidemiology Treatment

    • Most commonly affects < 40 years old

    • Slightly higher disease rates in women

    • Swedes, Danes, and US AA’s highest prevalence rates

      • Lifetime risk US white: .85%, US black: 2.4%

    • Significant variability in disease presentation and severity among different groups

      • More severe disease in AA’s, caucasians with asx disease

      • EN in Europeans

      • Cardiac and ocular more common in Japan


    Skin Treatment

    • Approx 20% of patients

    • Most common subacute finding => maculopapular eruption

      • Nares, lips, eyelids, neck, previous trauma (‘scars and tatoos’)

    • Erythema Nodosum

      • Hallmark of acute sarcoidosis

      • Red, raised, tender nodules on anterior legs

      • Adjacent joints may be painful, swollen

      • Lasts 6-8wks and rarely recurs

      • ‘Lofgren’s syndrome – fever, arthralgia, EN, bilat hilar LAN’

    • Lupus pernio

      • Marker of chronic sarcoidosis

      • Indurated plaques located on cheeks, lips, nose, ears

      • Prolonged course with rare spontaneous remission



    Pulmonary
    Pulmonary Treatment

    • >90% of patients

    • 1/3-1/2 describe dyspnea, dry cough, vague chest tightness

    • <20% with “crackles”, clubbing is rare

    • Rare findings – effusion, chylothorax, PTX, cavitary lesions, calcified LAN

    • 5 stages based on CXR findings

      • Stage 0 – no intrathoracic findings


    Stage 1
    Stage 1 Treatment

    • Bilateral hilar adenopathy – 50% of patients

    • 60-80% spontaneous remission


    Stage 2
    Stage 2 Treatment

    • Bilateral hilar adenopathy with parenchymal infiltrate – 25% of patients

    • 50-60% spontaneous remission


    Stage 3
    Stage 3 Treatment

    • Parenchymal infiltrate without hilar LAN

    • <30% spontaneous remission


    Stage 4
    Stage 4 Treatment

    • Advanced fibrosis

      • Honey-combing, hilar retraction, bullae, cysts, emphysema


    Diagnostic evaluation
    Diagnostic evaluation Treatment

    • Diagnosis:

      • Compatible clinical picture

      • Compatible histology

      • Exclusion of other causes

    • Goals of work-up:

      1 – histologic confirmation

      2 – assess extent and severity of organ involvement

      3 – assess disease stability and whether will progress

      4 – determine if therapy will benefit patient


    Diagnostic evaluation1
    Diagnostic evaluation Treatment

    • Biopsy

      • Lymph node

      • Skin lesions

      • Bronchoscopy

        • 40- 90+% yield

      • Mediastinoscopy

      • VATS

      • Open lung bx


    Natural history
    Natural history Treatment

    • Highly variable and influenced by race and genetic factors

      • 4-7% present with serious extrapulm involvement

    • Spontaneous remission in 2/3

      • >85% within 2yrs

      • If remission or stabilization, 2-8% relapse

    • Chronic or progressive in 10-30%

      • Failure to remit in 24 mos

    • Mortality 1-5%

    • Poor prognostic indicators

      • Lupus pernio - chronic high Ca

      • AA race - nephrocalcinosis

      • age onset >40 - chronic uveitis

      • neurosarcoid - cardiac involvement

      • progressive pulm dz - cystic bone lesions

      • nasal mucosal involvement


    Treatment1
    Treatment Treatment

    • Controversial and unclear

      • Large number of spont remissions or benign clinical course

        • Stg 1 – 60-80%, 2 – 50-60%, 3 – 30%

      • No good method to assess activity

      • Variability in presentation and course not amenable to developing guidelines

      • Cause is unknown, no specific tx


    Treatment2
    Treatment Treatment

    • Steroids first line therapy

    • Topical therapy

      • Uveitis, skin, cough

    • Systemic therapy

      • Definite indications- heart, neuro, ocular not responding, hyperCa


    Treatment of pulmonary sarcoid
    Treatment of pulmonary sarcoid Treatment

    • Observation

      • Asx or mild sx stage 1, 2, 3

      • Eval q6mth stage 1, q3mth stage 2, 3

      • Tx if worsening sx’s, deteriorating lung fxn, progressive xray findings

    • Treatment

      • .5 – 1mg/kg for 4-6 wks

      • If response, taper by 5-10mg every 4-8wks to maintenance of 5-10mg/d

      • If no response after 3mths then taper off steroids

      • Total duration of therapy 12mths then taper off

      • Relapse rate high – 60-90%


    Surveillance
    Surveillance Treatment

    • If no treatment, most intense in first 2 yrs then annual

    • If treated, most intense in first 3 yrs after discontinuation of therapy then “at least annually”


    Pulmonary edema syndromes
    Pulmonary Edema Syndromes Treatment

    • Cardiogenic

      • High-Output Failure

      • Low-Output Failure

        • Systolic Dysfunction

        • Diastolic Dysfunction

    • Noncardiogenic

      • Pulmonary

      • Non-pulmonary


    Pulmonary etiologies
    Pulmonary Etiologies Treatment

    • PNA

    • Aspiration

    • Acute Interstitial Pneumonia (Hamman-Rich)

    • Acute Eosinophilic Pneumonia

    • Diffuse Alveolar Hemorrhage Syndrome


    Non pulmonary etiologies

    ‘Surgical’ Treatment

    Burns

    Trauma

    Surgical SIRS

    Re-perfusion PE

    Negative Pressure PE

    Narcotic-Related PE

    General Anesthesia PE

    ‘Medical’

    MICU

    TRALI

    Pancreatitis

    Sepsis

    Neurogenic

    Emboli

    Fat

    Amniotic

    Air

    Other

    HAPE

    SIPE

    Drugs

    Non-Pulmonary Etiologies


    Fat emboli
    Fat Emboli Treatment

    • Patients:

      • ‘Post-Trauma, esp. long bone fracture’

      • Sickle Cell patients, exp post-partum

    • Signs

      • Central Nervous System

      • Renal Failure

      • Acute Lung Injury

      • Petechiae


    Eosinophilic lung diseases
    Eosinophilic Lung Diseases Treatment

    • Pulmonary Infiltrates w/Eosinophilia (PIE)

      • Primary

        • Acute vs. Chronic Eosinophilic PNA

        • Simple Pulmonary Eosinophilia (Loeffler’s)

        • Idiopathic Hypereosinophilic Syndrome

      • Secondary

        • ILD’s

        • ‘Asthma syndromes’

        • Malignancies

        • Infections

        • Drugs


    Acute vs chronic eosinophilic pna

    Acute Treatment

    Presents acutely like PNA/ARDS

    CXR mimics PNA/ARDS

    Peripheral Eosinophilia rare; High count on BAL

    Prompt, lasting response to steroids

    Chronic

    Presents subacutely with Mild Hypoxemia

    CXR- ‘Photographic negative of CHF’

    Peripheral Eosinophilia common; High count on BAL

    Prompt response to steroids, but recurrence common

    Acute vs. Chronic Eosinophilic PNA


    Simple pulmonary eosinophilia loeffler s
    Simple Pulmonary Eosinophilia (Loeffler’s) Treatment

    • Migratory Pulmonary Infiltrates

    • Eosinophilia

    • Cause:

      • Ascaris Lumbricoides


    Ild s
    ILD’s Treatment

    • Sarcoidosis

    • Langerhans Cell Histiocytosis

    • Idiopathic Pulmonary Fibrosis

    • Collagen Vascular Diseases

    • Bronchioloitis Obliterans Organizing Pneumonia (BOOP/COP)


    Asthma syndromes
    ‘Asthma syndromes’ Treatment

    • Allergic Angiitis & Granulomatosis

    • Allergic Bronchopulmonary Mycosis

    • Allergic Reaction


    Allergic angiitis granulomatosis
    Allergic Angiitis & Granulomatosis Treatment

    • AKA Churg-Strauss Syndrome

      • Diagnostic Criteria (4/6)

        • Migratory Pulmonary Infiltrates (‘fleeting’)

        • Eosinophilia (>10%)

        • Peripheral Neuropathy

        • Sinus disease

        • Asthma

        • Biopsy findings

          • Extravascular eosinophils

          • Granuloamtous Angiitis

          • Extravascular Necrotizing Granulomas


    Allergic bronchopulmonary mycosis

    Diagnostic Criteria Treatment

    Asthma

    + skin test to fungus

    + IgG precipitins

    + IgE precipitins

    Elevated IgE

    Central BTX

    Eosinophilia with CXR ASO’s

    ‘Central or Proximal Bronchiectasis’

    ‘Coughs up brown, plugs’

    ‘Finger-in-gloves-’ X-ray

    Allergic Bronchopulmonary Mycosis


    Malignancies
    Malignancies Treatment

    • NHL

    • NSCLCA

    • Leukemias


    Infections
    Infections Treatment

    • Parasites

    • PCP

    • Mycobacteria

    • Fungal

      • Especially Cocci


    Other ild s
    Other ILD’s Treatment

    • Wegener’s

      • ‘ELK’

      • ‘c-ANCA’

    • Goodpasture’s

      • Bleeding Kidneys and lungs

      • ‘Anti-GBM ab’

    • Langerhans Cell Histiocytosis

      • ‘Young, male smokers with recurrent PTX’

    • LAM

      • ‘Young, female non-smokers with recurrent PTX’


    Drugs and lung disease
    ‘Drugs and Lung Disease’ Treatment

    • ARA-c = ARDS

    • Bleomycin = ARDS/Fibrosis worsened with oxygen exposure

    • Amiodarone = Pulm fibrosis, typically dose-dependant

    • Hydralazine/Procainamide = SLE-like

    • Crack-lung = hemorrhage, ARDS, vaculitis


    Pulmonary vascular disease
    Pulmonary Vascular Disease Treatment

    • Venous Thromboembolic Disease (VTE)

      • DVT

      • PE

      • CTEPH

    • Pulmonary Hypertension (PH)


    DVT Treatment

    • Etiologies

    • Diagnosis

    • Treatment


    Dvt etiologies
    DVT: Etiologies Treatment

    • Trauma

    • Recent Surgery

    • Medical Immobility

    • Medications- e.g. OCP’s

    • Medical conditions- Behcet’s, IBD, SCD, CA, Nephrotic syn

    • Hypercoaguable States


    Hypercoaguable states
    Hypercoaguable States Treatment

    • APC resistance (Factor V Leiden)

    • APLS

    • Protein C def

    • Protein S def

    • AT III def

    • Homocystenemia

    • Prothrombin Gene mutation


    Diagnosis
    Diagnosis Treatment

    • Duplex compression U/S

      • Role of serial testing in low-risk setting

    • Venography

    • CT


    Treatment3
    Treatment Treatment

    • Anticoagulation

      • UFH vs LMWH

        • Look for HIT/HAT

      • Warfarin

    • Vena Caval Filter

    • Stockings


    PE Treatment


    Total incidence 630 000
    Total Incidence Treatment630,000

    11%

    Death within

    1 hr

    67,000

    89%

    Survival

    > 1 hr

    563,000

    71%

    Diagnosis not

    made

    400,000

    29%

    Diagnosis made,

    therapy instituted

    163,000

    70%

    Survival

    280,000

    30%

    Death

    120,000

    92%

    Survival

    150,000

    8%

    Death

    13,000


    Pathophysiology of acute pe
    Pathophysiology of Acute PE Treatment

    • Related to reduction in cross-sectional area of pulmonary vasculature

      • increase in PVR=> impedance of RV ejection of blood => decreased filling of LV

        Predicting the Severity of Pulmonary Embolism

        PE Severity PA PA mean RA mean CI

        obstruction pressure pressure

        Mild <50 <20 <10 >2.5

        Mod or Submassive 50-75 25-40 <10 >2.5

        Massive >75 40-45 >10 <2.5


    Acute pe cont
    Acute PE (cont.) Treatment

    • Thrombolysis or embolectomy

      • massive PE with hemodynamic instability or refractory hypoxemia

    • Heparin/Lovenox

    • Oral anticoagulation

    • IVC filter

      • patients with contraindication to anticoagulation

      • recurrent embolism despite anticoagulation

      • unable to tolerate further emboli


    Pulmonary hypertension symptoms and signs
    Pulmonary Hypertension Symptoms and Signs Treatment

    • Dyspnea on exertion in a young female

    • Fatigue

    • Shortness of Breath and Chronic Hypoxia

    • About 10% of primary and >50% of secondary P-HTN patients have Raynaud's phenomenon


    Symptoms and signs
    Symptoms and Signs Treatment

    • Chest pain

      • Secondary to RV ischemia in the face of RV hypertrophy and increased sys and dias pressures

    • Syncope

      • Usually exertional or post exertional implies a severely restricted CO with deminished cerebral blood flow


    Symptoms and signs1
    Symptoms and Signs Treatment

    • Symptoms of right sided heart failure

      • Peripheral edema and hepatic congestion (abdominal pain)

      • Distended neck veins and fluid retention

      • Ineffective filling of Left ventricle, with resultant hypotension


    The demise in pulmonary hypertension
    The Demise in Pulmonary Hypertension Treatment

    • Progressive RV failure leads to dyspnea, hypoxemia, and progressive decrease in CO

    • This leads to death from RV failure or fatal dysrhythmias

    • Arterial hypoxemia and acidosis predispose to fatal dysrhythmias


    The demise in primary pulmonary hypertension
    The Demise in Primary Pulmonary Hypertension Treatment

    • Common causes of death include:

      • Brady and tachy dysrhythmias

      • PE

      • Massive pulmonary hemorrhage

      • Sudden RV ischemia / infarction


    Diagnosis1
    Diagnosis Treatment

    • Clinical Definition

    • Presence of pulmonary HTN: mean PA pressure >25mm Hg at rest (or 30mm in exercise)

      • Normal pulmonary capillary wedge pressure (PCWP)

      • Absence of secondary etiology (for primary P-HTN)


    Diagnosis2
    Diagnosis Treatment

    • Evaluate for secondary etiology

      • Echocardiography

      • Ventilation-Perfusion (V/Q) Scanning

      • Pulmonary Angiography

      • Autoantibody serologies

      • Pulmonary Function Testing

      • Note that many patients with primary P-HTN have low titer autoantibodies


    Diagnosis3
    Diagnosis Treatment

    • CXR: Evidence of pulmonary hypertension

      • Prominent main pulmonary artery

      • Enlarged hilar and pulmonary vessels

      • Enlarged R heart structures

      • 6-10% of patients have a normal CXR


    Diagnosis4
    Diagnosis Treatment

    • EKG

      • May show right axis deviation

      • RVH

      • R Heart strain pattern

      • Peaked P waves in lead II

      • Findings do not correlate with the severity of disease


    Diagnosis5
    Diagnosis Treatment

    • Echocardiography

      • Elevated pulmonary pressures

      • May reveal RA and RV enlargement

      • May reveal a normal to decreased LV chamber size

      • Loss of normal septal curvature and decreased LV filling may reflect disease severity


    Treatment4
    Treatment Treatment

    • Overview of Vasodilator Therapy

      • In general, response to acute vasodilator administration predicts chronic response

      • Chronic prostacyclin may be beneficial in absence of acute response

      • Diltiazem combined with oxygen may have synergistic chronic effects

      • Invasive monitoring a must during acute infusions in patients


    Treatment5
    Treatment Treatment

    • Other Therapies

      • Oxygen - usually improves function, acts as vasodilator

      • Digoxin - may be useful in setting of atrial fibrillation, improved inotropy

      • Note that diltiazem may also reduce ventricular response in atrial fibrillation

      • Lung (± heart) transplantation may be only other treatment at present


    Treatment6
    Treatment Treatment

    • Anticoagulation

      • Patients with PPH are at increased risk for intrapulmonary thrombosis and thromboembolism due to:

        • Sluggish pulmonary blood flow

        • Dilated right heart chambers

        • Venous stasis

        • Sedentary lifestyle

        • Increased risk of atrial fibrillation


    Internship
    Internship Treatment


    Pleural disease
    Pleural Disease Treatment

    • Pleural Effusions

      • Transudates

      • Exudates

    • Pneumothorax (PTX)


    Light s criteria
    ‘Light’s Criteria’ Treatment

    • Any one of the following qualifies the effusion as exudative:

      • Protein P/S > 0.5

      • LDH P/S > 0.6

      • Pleural LDH > 200 or > 2/3 upper limits of serum normal


    Transudates
    Transudates Treatment

    • ‘-Oses’

      • Nephrosis- Nephrotic syn

      • Cirrhosis

      • Cardiosis- Pulmonary Venous HTN (CHF)

    • Other

      • Hypo-Thyroid, PE, ATX, pericardial disease, trapped lung, urinothorax, SVC syn


    Exudates
    Exudates Treatment

    • Parapneumonic Effusions

    • Malignancy

    • Chylothorax


    Lymphocyte predominant exudates
    Lymphocyte Predominant Exudates Treatment

    • Chylothorax

    • Rheumatoid

    • Yellow Nail

    • Sarcoid

    • TB

    • Acute Rejection

    • Lymphoma

    • Post CABG


    Eosinophilic exudates
    Eosinophilic Exudates Treatment

    • Air

    • Benign Asbestos Pleural Effusion (BAPE)

    • Cancer, esp lymphomas

    • Drugs

    • Embolism

    • Fungus

    • Granulomatous Disease

    • Hemothorax

    • Infection (Parasite, TB?)


    Parapneumonic effusions
    Parapneumonic Effusions Treatment

    • Predictors for Poor Outcomes (i.e. should be drained)

      • Low Glucose

      • Low pH

      • + gram stain

      • + culture

      • Complicated appearance (i.e. loculated) on CT or US


    Malignancy
    Malignancy Treatment

    • Usually proven with cytology

    • Poor prognostic indicator

      • IIIb disease

      • Average life expectancy ~ 6 mos

    • Low pH implies poor response to pleurodesis


    Chylothorax
    Chylothorax Treatment

    • ‘Milky Appearance’

    • Triglycerides > 110 or chylomicrons on lipid analysis

    • DDx- post-trauma > tumor > idiopathic

    • High cholesterol implicates ‘pseudochylous effusion’

    • Do NOT drain repeatedly- leads to immunocompromise and malnutrition


    Pneumothorax
    Pneumothorax Treatment

    • Spontaneous

    • Secondary

      • Traumatic

      • COPD

      • CF

      • TB

      • Diffuse Parenchymal Lung Disease


    Ptx treatment
    PTX: Treatment Treatment

    • ASX PTX < 15% of hemithorax = observe

    • >15% = simple aspiration

      • Failure of aspiration will require tube thoracostomy.

      • BPF’s may require large bore tube.

    • A 2nd spontaneous PTX deserves pleurodesis


    Sleep
    Sleep Treatment

    • Sleep-Disordered Breathing

      • OSA

      • Central Apneas

    • Narcolepsy

    • Insomnia


    OSA Treatment

    • Incidence- ~3% of all Americans, mostly undiagnosed.

    • Signs/Sx’s- Excessive daytime somnolence, morning headaches, HTN, caffeine dependence, snoring, witnessed apneas

    • AHI > 5 arousals/hour


    Osa treatment
    OSA: Treatment Treatment

    • CPAP

    • Oral appliances

    • Surgery


    Central apneas
    Central Apneas Treatment

    • ‘Cheynes-Stokes is associated with CHF.’


    Narcolepsy
    Narcolepsy Treatment

    • EDS

    • Cataplexy- sudden loss of tone in weight-bearing muscles.

    • Hypnagogic Hallucinations- visual/auditory hallucinations occuring as patient falls asleep.

    • Sleep Paralysis- total paralysis while falling asleep or waking up.


    Narcolepsy dx
    Narcolepsy: Dx Treatment

    • Multiple Sleep Latency Test- demonstrates sleep onset in < 5 minutes and two episodes of Rapid Onset REM sleep.


    Narcolepsy tx
    Narcolepsy: Tx Treatment

    • Avoid excessive sleep deprivation.

    • Stimulants

      • Amphetamines

      • Modafinil


    Potpourri
    Potpourri Treatment

    • Lung Transplant

    • Lung Cancer

    • Perioperative Lung Eval

    • PFT’s

    • Hemoptysis


    Lung transplant
    Lung Transplant Treatment

    • Lung Transplant may be considered for end-stage Lung Disease.

      • Post-Transplant Survival

        • 1 month- 88%

        • 1 year- 72%

        • 3 year- 56%

        • 5 year- 43%


    Lung cancer epidemiology
    Lung Cancer TreatmentEpidemiology

    • Estimated in 2004, 174,000 Americans will be diagnosed

    • In 2003, approximately 157,200 deaths due to lung cancer

    • Leading cause of cancer death in both men and women in U.S.

    • Causes more deaths than colon, breast, and prostate combined

    • 5 year survival for all patients newly diagnosed is 15% (colon – 61%, breast – 86%, prostate – 96%)


    Epidemiology3
    Epidemiology Treatment

    • Rare disease beginning 20th century; sharp rise in 1930’s; by mid-century leading cancer death in men

    • Rise in women followed in 1960’s to present when is now leading cancer death

    • Similar rates among African-American and white women, but 50% more frequent among AA males

    • More common in developed countries


    Epidemiology4
    Epidemiology Treatment

    • Histologic subtype has shifted with adenocarcinoma replacing squamous cell as most common

    • Median survival untreated metastatic non-small cell 4-5 months (8 mths with state-of-the-art treatment)

    • 5 year survival for potentially resectable disease:

      • IA – 67%

      • IB – 57%

      • IIA – 55%

      • IIB – 39%

      • IIIA – 23%


    Cigarette smoking
    Cigarette Smoking Treatment

    • Leading cause of lung cancer and accounts for approximately 90% of cases in U.S.

      • Leading cause of preventable death (1 out of 5 deaths)

      • ½ of regular smokers die prematurely of tobacco-related disease

    • First scientific report associating cigarette smoking with increased risk of premature death in 1938

    • Doll and Hill in 1950 demonstrated clear epidemiologic evidence linking smoking and lung cancer

    • Compared to never smokers, 20 fold increase in risk


    Cigarette smoking1
    Cigarette Smoking Treatment

    • Risk increases with duration and number of cigarettes per day

      • Models show duration of smoking even stronger risk than number per day

      • Those starting younger, most likely to develop cancer and to do so at younger age

    • Risk decreased in those who quit compare to those who continue

      • As period of abstinence increases, risk decreases

      • Never returns to level of risk of never smokers


    Occupational environmental
    Occupational/Environmental Treatment

    • Lung cancer attributed to occupational exposure approximately 9-15%

    • Asbestos

      • Approximately 7 fold increased risk

      • Acts synergistically with cigarettes to increase to 16 fold

      • Dose dependent and fiber dependent

    • Radon

      • Formed from breakdown of uranium

      • Found in soil, groundwater, rock – can accumulate in homes

    • Ionizing radiation

    • Approx 1-2% attributed to atmospheric pollution


    Histology
    Histology Treatment

    • Adenocarcinoma

      • Neoplastic gland formation or intracytoplasmic mucin

      • Peripheral in 75% of cases

    • Squamous cell

      • Proximal tracheobronchial tree 60-80% of cases

      • Can demonstrate central necrosis with cavitation

    • Small cell

      • Neuroendocrine features

      • Commonly proximal airways with involvement of hilum and mediastinum

    • Large cell

      • Diagnosis of exclusion

      • Commonly peripheral


    Signs symptoms due to intrathoracic spread
    Signs/Symptoms Due to Intrathoracic Spread Treatment

    • Due to lymphatic spread or direct extension

    • Nerve involvement

      • Recurrent laryngeal, phrenic, Pancoast tumor, Horner’s syndrome

    • Chest wall and pleura

    • Vascular invasion

      • SVC syndrome

    • Visceral invasion

      • Esophagus, heart and pericardium


    Paraneoplastic syndromes
    Paraneoplastic Syndromes Treatment

    • Occur in approximately 10% of patients

    • Unrelated to size of tumor

    • Can sometimes precede the diagnosis of the tumor

    • Can mark the recurrence of malignancy



    Evaluating suitability for surgery
    Evaluating suitability for surgery Treatment

    • FEV1 most commonly used parameter

    • If FEV1 > 2L for pneumonectomy or >1.5L for lobectomy, no further eval (low risk)

    • If suitable FEV1, but suspect ILD or patient with excessive DOE, can use DLCO (more testing if <60%)

    • If patient does not meet above, then testing to evaluate post-op FEV1 and DLCO

      • Post-op predicted FEV1 or DLCO <40% indicates high risk

    • Can use exercise testing to further assist

      • VO2 max >20ml/kg/min – low risk

      • VO2 max <15ml/kg/min – increased risk of perioperative complications

      • <10ml/kg/min – very high risk


    Perioperative lung eval effects of surgery
    Perioperative Lung Eval Treatment Effects of Surgery

    • Lung volumes

    • Diaphragm function

    • Gas exchange

    • Control of breathing

    • Lung defense mechanisms


    Lung volumes
    Lung Volumes Treatment

    • Dependent on site of surgery

    • Restrictive

    • Reduction in vital capacity (VC) and functional residual capacity (FRC) up to 70 and 50 percent respectively


    Frc and cc
    FRC and CC Treatment

    • FRC = lung volume at end of normal expiration

    • CC = lung volume at which small airways in bases begin to close during expiration because of reduction in airway radial traction

    • Normally FRC > CC and airways remain open throughout tidal breath


    Diaphragm
    Diaphragm Treatment

    • Temporary dysfunction following thoracic or upper abdominal surgery


    Gas exchange
    Gas Exchange Treatment

    • Arterial hypoxemia

      • First phase: initially post-op secondary to residual anesthesia, shunting, V/Q mismatch

      • Second phase: CC > FRC


    Control of breathing
    Control of Breathing Treatment

    • Anesthetic agents inhibit respiratory drive and reduce ventilatory response to hypercapnia, hypoxia, and acidemia

    • Narcotics decrease sighs and may precipitate OSA


    Pulmonary complications
    Pulmonary Complications Treatment

    • Incidence 5-90 percent

    • 528 patients underwent elective abdominal surgery

    • Pulmonary complications >> cardiac complications

    • Pulmonary complications associated with longer hospitalization

    • Healthy non-obese, non-smoker < 1 percent

    J Gen Intern Med, 1995.


    Pulmonary complications1
    Pulmonary Complications Treatment

    • Atelectasis

    • Infection (tracheobronchitis and pneumonia)

    • Prolonged mechanical ventilation or respiratory failure

    • Exacerbation of underlying pulmonary disease

    • Thromboembolic disease


    Pre operative risk factors
    Pre-operative Risk Factors Treatment

    • Chronic lung disease

    • Smoking

    • General health

    • Age

    • Obesity

    • Antecedent respiratory infection

    • Obstructive sleep apnea


    Asthma
    Asthma Treatment

    • If under good control, minimal complications

    • Tracheal intubation can initiate bronchospasm

    • Consider regional anesthesia in severe asthma

    • Consider stress dose steroids

    • Treat acute bronchospasm

    • Delay surgery if necessary


    Smoking
    Smoking Treatment

    • 200 consecutive CABG patients stratified by smoking history

    • Significant reduction in complications if patient stops at least 8 weeks prior to surgery1

    • Stop 12-18 hours pre-op to allow for sufficient carboxyHB clearance

    • Evidence for decreased HR, BP, and cathecholamine levels within 60 minutes after smoking

    Mayo Clin Proc 1989.


    Obesity
    Obesity Treatment

    • Common false assumption

    • 10 series of gastric bypass surgery found no increased incidence of pneumonia or atelectasis

    • Meta-analysis of 6 studies (4526 patients) demonstrated equal rate of complications in obese and non-obese

    Ann Intern Med 1986.


    Post operative risk factors
    Post-operative Risk Factors Treatment

    • Inadequate post-operative analgesia

    • Immobilization


    Inadequate post operative analgesia
    Inadequate post-operative analgesia Treatment

    • Pain inhibits coughing and deep breathing

    • Pain discourages mobility

    • Hesitancy to report pain

    • Anxiety of prescribing narcotics


    Immobilization
    Immobilization Treatment

    • FRC decreases 500-1000cc when moving from upright to supine position

    • Increased risk of thromboembolic disease

    • Ambulation is associated with clearance of secretions


    Pulmonary function tests
    Pulmonary Function Tests Treatment

    • Not indicated for routine pre-operative screening

    • Indications:

      • Persistent cough or unexplained dyspnea

      • Hx of chronic lung disease

      • Hx of smoking

      • Planned lung resection


    Incentive spirometer
    Incentive spirometer Treatment

    • Non-invasive

    • Inexpensive

    • Decreased atelectasis

    • Decreased hospital stay


    Pft s indications
    PFT’s TreatmentIndications

    • Detect presence or absence of lung dysfunction suggested by history, physical or presence of other abnormal tests.

    • Quantify severity of known lung disease.

    • Assess change in function over time or effect of therapy.

    • Assess effects of environmental or occupational exposure.

    • Pre-surgical evaluation.

    • Assess impairment or disability




    Obstructive fvl
    Obstructive FVL Treatment



    Restrictive fvl
    Restrictive FVL Treatment





    Determining normal flows
    Determining “Normal” TreatmentFlows

    • The use of “80% of predicted” as a cutoff between normal and abnormal is arbitrary.

      • Extremes of age and height are frequently mislabeled

      • Lower limits of normal for flows

        (e.g. ‘FEF25-75’) is closer to 50%.


    Determining normal fev 1 fvc ratio
    Determining “Normal” TreatmentFEV1/FVC Ratio

    • This ratio is inversely related to age and height; therefore, use of a fixed ratio (i.e. 80%) will result in increased labeling of impairment in older patients.

    • Athletes and workers in demanding occupations frequently have disproportionately high FVC compared to FEV1.


    Definition of an obstructive defect
    Definition of An Obstructive Defect Treatment

    • A disproportionate reduction of maximal airflow from the lung with respect to the maximal volume that can be displaced from the lung.

      • Low FEV1/ FVC.


    Significant bd response
    ‘Significant BD Response’ Treatment

    • Many different definitions looking at different flows, volumes or ratios.

    • ATS:

      • Increase in FVC or FEV1 of 12% from baseline

        AND

        - an absolute increase of 200ml.


    Definition of a restrictive defect
    Definition of a Restrictive Defect Treatment

    • One may infer the presence of a restrictive defect when VC is reduced and FEV1/FVC is preserved, but…

      • A restrictive defect is physiologically defined by a reduction in TLC.

    • If a contradiction between TLC and VC arises, defining restriction should be based on TLC.


    When to obtain lung volumes
    When to Obtain Lung Volumes Treatment

    • To confirm and help stage the severity of disease suspected by spirometry.

    • To provide evidence of lung dysfunction not clearly evident from spirometric tests.

    • To trend the course of a disease or response to therapy.


    Lung volumes in restrictive lung disease
    Lung Volumes in Restrictive Lung Disease Treatment

    • Since Restrictive Lung Diseases are defined by a decrease in VC and TLC, measurements of lung volumes are most helpful in detecting, confirming and staging restrictive lung defects.

    • Lung Volumes may suggest the physiologic type of disease from the pattern of lung volume alterations.


    Restrictive lung disease differential diagnosis
    Restrictive Lung Disease: TreatmentDifferential Diagnosis

    • Pleural- Effusion

    • Alveolar- PAP, PNA

    • Interstitial- ILD’s, IPF

    • Neuromuscular-

    • Thoracic Wall- Kyphoscoliosis, AS


    Low dlco differential diagnosis
    Low DLCO: TreatmentDifferential Diagnosis

    • Obstructive Lung Disease- COPD, CF

    • Interstitial Lung Disease-

    • Pulmonary Vascular Disease- Pulm HTN,

      Venous Thromboembolic Disease

    • Cardiovascular Disease- Pulm Edema

    • Anemia


    Elevated dlco differential diagnosis
    Elevated DLCO: TreatmentDifferential Diagnosis

    • Polycythemia

    • Alveolar Hemorrhage

    • Asthma

    • Increased Pulmonary Blood Flow

      • Left  Right Intracardiac shunt

      • Exercise

      • Mild CHF


    Hemoptysis
    Hemoptysis Treatment

    • DDx:

      • Bronchitis

      • Lung Cancer

      • Idiopathic

      • Bronchiectasis

      • TB


    Hemoptysis1
    Hemoptysis Treatment

    • ‘Massive Hemoptysis’ = > 100-150ml

    • Requires Emergent imaging and bronchoscopy because:

      • Mortality due to asphyxiation > exsanguination


    Hemoptysis2
    Hemoptysis Treatment

    • Tx:

      • Hemodynamic management

      • Reverse coagulopathies

      • Triage the DDx

      • Consider FOB, IR, Surgical intervention

      • ‘Bleeding side down if hemoptysis persists’


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