What’s New in Managing Pneumonias

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1 What’s New in Managing Pneumonias Anne Dabrow Woods, DNP, RN, CRNP, ANP-BC, AGACNP-BC Chief Nurse Wolters Kluwer Philadelphia, PA Acute Care Nurse Practitioner Critical Care Service, Penn Medicine, Chester County Hospital West Chester, PA Adjunct Faculty Drexel University, College of Nursing & Health Sciences Philadelphia, PA Copyright Anne Dabrow Woods; all rights reserved Disclosure: I have nothing to disclose. Objectives: At the conclusion of this session you will be able to: Identify the definitions and causes of community-acquired pneumonia (CAP), healthcare-associated pneumonia (HCAP), hospital-acquired pneumonia (HAP), and ventilator-associated pneumonia (VAP). Identify the presentation and the diagnostic studies for each type of pneumonia. Identify the treatment and prevention plans for each type of pneumonia and respiratory failure.

Transcript of What’s New in Managing Pneumonias

Page 1: What’s New in Managing Pneumonias

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What’s New in Managing Pneumonias

Anne Dabrow Woods, DNP, RN, CRNP, ANP-BC, AGACNP-BC Chief Nurse

Wolters Kluwer Philadelphia, PA

Acute Care Nurse Practitioner

Critical Care Service, Penn Medicine, Chester County Hospital West Chester, PA

Adjunct Faculty

Drexel University, College of Nursing & Health Sciences Philadelphia, PA

Copyright Anne Dabrow Woods; all rights reserved

Disclosure:

• I have nothing to disclose.

Objectives:

• At the conclusion of this session you will be able to:

• Identify the definitions and causes of community-acquired pneumonia (CAP), healthcare-associated pneumonia (HCAP), hospital-acquired pneumonia (HAP), and ventilator-associated pneumonia (VAP).

• Identify the presentation and the diagnostic studies for each type of pneumonia.

• Identify the treatment and prevention plans for each type of pneumonia and respiratory failure.

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Definition of pneumonia

• Acute, febrile inflammatory disorder of the lungs associated with cough and exertional dyspnea

• Infiltrate on chest x-ray

• Appearance on CXR may lag 24 to 48 hours behind clinical presentation

• Leukocytosis – elevated WBCs

Types of pneumonia

• Community-acquired pneumonia

• Hospital-acquired pneumonia

• Healthcare-associated pneumonia

• Ventilator-associated pneumonia

• Other ways to look at pneumonias

• Organism

• Bacterial

• Viral

• Fungal

• Mode of entry

• Aspiration

Let’s look at Bacteria…

• Classification

• Morphology: (cocci, bacilli, spirochetes)

• Gram Stain: cell wall presence and properties (gram-positive vs. gram-negative),

• Colony clustering: clusters, pairs or chains

• Growth requirements (aerobic vs. anaerobic)

• Presence of a capsule (e.g., encapsulated bacteria) or spores (e.g., spore-forming bacteria).

• Biochemistry and appearance on agar

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Gram + vs. Gram - Organisms

• Selective staining of the cell walls with crystal violet

• Gram positives absorb the stainpurple

• Gram negative organisms the stain easily washes awaypink

Gram positive cocci in clusters, Gram negative bacilli

Comparing organisms • Gram –

• Cocci – neisseria, moraxella

• Bacilli • Aerobic – vibrio,

enterobacter, acinetobacter, ecoli, klebsiella, haemophilus, proteus, salmonella, shigella, pseudomonas, acinobacter

• Anerobic – bacteroides, prevotella, fusobacterium

• Gram + • Cocci

• Aerobic • clusters (staph)

• chains/pairs (strep), enterococcus

• Anerobic – peptococcus

• Bacilli • Aerobic – lactobacillus,

gardenella, cornybacter, listeria

• Anerobic – actinomyces, clostridium

Atypical bacteria

• Colorless – do not color with gram staining

• Responsible for 20 to 30% of CAP

• The big 3 atypicals

• Mycoplasma pneumoniae

• Chlamydia pneumoniae

• Legionella pneumonphilia

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Let’s look at the alphabet soup of pneumonia…

Community-acquired pneumonia (CAP) • Acquired in the community; most common type of pneumonia

• 4 to 5 million cases per year • 25% of cases require hospitalization • In hospital mortality 10-12% (mild cases not admitted - < 1%)

• If patient gets admitted to the hospital and develops pneumonia within 48 hours – CAP • Cause: defense mechanism failure

• Cough reflex • Mucociliary clearance system • Immune response

• Organisms • Bacteria

• Strep pneumoniae (most common in adults) – gm + • Haemophilus influenza – gm - • Klebsiella pneumoniae – gm -

• Atypical • Chlamydia pneumoniae • Mycoplasma pneumoniae • Mycobacterium tuberculosis

• Viruses • Respiratory syncytial virus • Adenovirus • Rhinovirus

Hospital-acquired pneumonia (HAP)

• Definition:

• Occurs 48 hours after admission to the hospital and it wasn’t incubating at time of admission

• We gave it to the patient!

• Most common organisms

• Staphylococcus aureus – gram +

• Streptococcus pneumoniae – gram +

• Haemophilus influenzae – gram -

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Ventilator-associated pneumonia (VAP)

• Definition

• Pneumonia that occurs 48 to 72 hours post intubation

• Risk increases with poor oral care

• Most common organism

• Pseudomonas aeruginosa – gram -

Healthcare-associated pneumonia (HCAP)

• Definition

• Patient was in hospital or a healthcare setting for 2 or more days within 90 days of infection and develop pneumonia

• Long-term care facilities

• Assisted living

• Rehabilitation

• Nursing home

• IV therapy including antibiotics

• Chemotherapy – within 30 days of current infection

• Wound care – within 30 days of current infection

• Hemodialysis clinic

HCAP organisms

• More similar to HAP than CAP

• Staphylococcus aureus (gram +)

• Pseudomonas aeruginosa (gram -)

• Less likely but possible

• Streptococcus pneumoniae (gram +)

• Haemophilus influenzae (gram -)

• MRSA (gram +)

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Pneumonia categorized by risk factors

• Aspiration pneumonia or pneumonitis

• R upper and R middle lobe most commonly affected

• Obstruction of the airway

• Tumor

• Secretions

• Inhalation injury

• Hypersensitivity pneumonia

• Near drowning

Comorbidities that increase mortality…

• COPD

• Heart Failure

• Diabetes

• Chronic liver disease

• Chronic kidney disease

• Very old

• Very young

Patient presentation

• “Typical pneumonia”

• Fever

• Chills or Rigors

• Leukocytosis (increased WBCs)

• Cough

• Sputum production

• Increased fremitus

• CXR

• Usually involves one lung and one lobe

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Patient Presentation

• “Atypical pneumonia”

• Fever or low temperature

• Leukocytosis – may be absent or have left shift on CBC (presence of bands)

• Dry cough

• Sore throat

• Headache

• Excessive sweating

• Soreness in chest or with cough

• CXR

• More diffuse pattern on CXR

• May involve more than one lung and multiple lobes

Diagnostics

• Chest Xray

• Sputum culture

• Blood cultures

• CBC with diff

• Chem 20

• PT/INR – for those on warfarin

• ABG – if worried about acute respiratory failure

A word about CXR

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Normal CXR

RML pneumonia

LLL pneumonia

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Multilobar pneumonia – RUL,RML, RLL

To admit or not to admit…

• CURB-65 (predicts mortality)

• Confusion - 1 point

• Uremia (BUN > 19) – 1 point

• Respiratory Rate (> 30/min) – 1 point

• Blood pressure (SBP< 90 or DBP < 60) – 1 point

• Age (> 65 years) – 1 point

• Action

• 0 to 1: treat as outpatient

• 2: consider short stay in hospital or watch closely as outpatient

• 3-5: requires hospitalization

Pneumonia severity scale (PSI)

Step 1: Stratify to Risk Class I vs. Risk Classes II-V

Presence of:

Over 50 years of age Yes/No

Altered mental status Yes/No

Pulse ≥125/minute Yes/No

Respiratory rate >30/minute Yes/No

Systolic blood pressure

<90 mm Hg Yes/No

Temperature <35°C or ≥40°C Yes/No

History of:

Neoplastic disease Yes/No

Congestive heart failure Yes/No

Cerebrovascular disease Yes/No

Renal disease Yes/No

Liver disease Yes/No

If any "Yes", then proceed to

Step 2

If all "No" then assign to Risk

Class I

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Step 2: Stratify to Risk Class II vs III vs IV vs V

Demographics Points Assigned

If Male +Age (yr)

If Female +Age (yr) - 10

Nursing home

resident +10

Comorbidity

Neoplastic

disease +30

Liver disease +20

Congestive

heart failure +10

Cerebrovascula

r disease +10

Renal disease +10

Physical Exam Findings

Altered mental

status +20

Pulse

≥125/minute +10

Respiratory rate

>30/minute +20

Systolic blood

pressure <90 mm

Hg +20

Temperature

<35°C or ≥40°C +15

Lab and Radiographic Findings

Arterial pH <7.35 +30

Blood urea nitrogen

≥30 mg/dl (9 mmol/liter) +20

Sodium <130 mmol/liter +20

Glucose ≥250 mg/dl

(14 mmol/liter) +10

Hematocrit <30% +10

Partial pressure of arterial O2

<60mmHg +10

Pleural effusion +10

∑ <70 = Risk Class II

∑ 71-90 = Risk Class III

∑ 91-130 = Risk Class IV

∑ >130 = Risk Class V

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Treatment for pneumonia

• Right drug for the right bug – antibiotics, antivirals, antifungals

• Hydration

• NSS and LR for volume replacement

• Supplemental oxygen – keep SpO2 > 93%

• Nasal cannula

• HFNC

• Bipap

• Ventilator

• Fever management – fever helpful; don’t treat unless over 101.5 or symptomatic

• Acetaminophen – antipyretic and analgesic

• NSAIDS – antipyretic, analgesic, anti-inflammatory

• Bronchoscopy

• Supportive care

A word about …

• Antihistamines • Works for allergies not pneumonia

• Decongestants • Works for rhinitis and nasal congestion

• Cough suppressants • Only use at night to sleep

• If cough is productive – do not use

• Expectorants • Liquefies secretions

• Use if has nasal congestion or need to loosen secretions

Right bug…

• Gram –

• Cocci – neisseria, moraxella

• Bacilli

• Aerobic – vibrio, enterobacter, acinetobacter, ecoli, klebsiella, haemophilus, proteus, salmonella, shigella, pseudomonas, acinobacter

• Anerobic – bacteroides, prevotella, fusobacterium

• Gram + • Cocci

• Aerobic • clusters (staph)

• chains/pairs (strep), enterococcus

• Anerobic – peptococcus

• Bacilli • Aerobic – lactobacillus,

gardenella, cornybacter, listeria

• Anerobic – actinomyces, clostridium

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Atypical bacteria

• Colorless – do not color with gram staining

• Responsible for 20 to 30% of CAP

• The big 3 atypicals

• Mycoplasma pneumoniae

• Chlamydia pneumoniae

• Legionella pneumonphilia

Kill fast or kill slow…

• Bacteriostatic agent prevents growth (slower kill) of bacteria, keeping them in the stationary phase of growth.

• Bactericidal agents kill more than 99.9% of bacteria found in an inoculum.

• Always use bactericidal in these cases:

• Endocarditis secondary to cardiac vegetation

• Meningitis due to the poor immune competence of CNS

• Neutropenia due to the immunocompromised status of the host

Death or slow kill

• Cidals

• PCN

• Cephalosporin

• Carbapenems

• Vancomycin

• Quinalones

• Metrondiazole

• Static

• Macrolides

• Tetracyclines

• linezolid

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Right drug…

• Gram –

• Piperacillin/tazobactam – (Zosyn) – pseudomonas

• Cephalosporins – 3,4,5

• Aztreonam

• Quinalones (Levaquin)

• Metrondiazole

• Macrolides for CAP and travelers diarrhea

• Gram +

• Penicillins and Penicillin with Clavulanate (Augmentin)

• good for strep but not staph

• Zosyn

• Cephalosporins 1,2,3?

• Vancomycin – MRSA

• linezolid

Suspect Infection

Culture Suspected Sites

Begin empiric Therapy

Gram Stain

Identification of Organisms

Susceptibilities

Adjust to definitive therapy

Steps to antibiotic prescribing and use…

Antibiotic stewardship • Right drug for the right bug

• Only use antibiotics for bacterial infections

• Empiric coverage and then specific coverage

• Give antibiotics as ordered

• If on warfarin, watch INR

• INR prolonged with many antibiotics

• Instruct patient to take as instructed and for the full course of therapy

• Work with team to make sure sensitivities are monitored

• Re-culture if spikes temp over 101.5 after being on antibiotics for 48 hours

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Right drug: CAP treatment • CAP (no comorbid conditions) – macrolide (Azithromycin)

• CAP with risk factors – respiratory fluoroquinolone – (Levaquin)

• CAP inpatient (not ICU) –

• respiratory fluoroquinolone (Levaquin) OR

• Macrolide (Azithromycin) + beta-lactam antibiotic (amoxicillin/clavulanate; Augmentin)

• CAP requiring ICU

• respiratory fluoroquinolone (Levaquin) OR

• Macrolide (Azithromycin) + antipseudomonal coverage (piperacillin/tazobactam; Zosyn)

Right drug: HAP treatment

• Low risk of multiple drug-resistant pathogens; use one of the following

• Ceftriaxone (Rocephin)

• Moxifloxacin (Avelox)

• Levofloxacin (Levaquin)

• Ampicillin/sulbactam (Unasyn)

• Pipercillin/tazobactam (Zosyn)

Right drug: HAP/VAP: high risk of multi-drug resistance

• Chose one agent from each category

• Antipseudomonal coverage

• Cefipime

• Piperacillin/tazobactam (Zosyn)

• PCN allergic patients: aztreonam

• A second antipseudomonal coverage

• Levoflaxacin

• Coverage for MRSA

• Vancomycin IV (dosed based on renal function to achieve trough of 15-20 mcg/ml)

• Linezolid

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COPD exacerbation secondary to Pneumonia

Definition of COPD

• A preventable, progressive disease of the lungs caused by airflow limitation that is not fully reversible

• Cause – smoking!

• Chronic bronchitis

• Emphysema

Inflammation

Small airway remodeling and

alveolar destruction

Airflow limitation

The pathophysiology behind COPD

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Chronic bronchitis versus emphysema

The picture of COPD

Stages of COPD and treatment • I. Mild – Reduce risk factors, influenza vaccine, SABA if needed

• II. Moderate – SABA + anticholinergic + LABA + Rehab

• III. Severe – SABA + LABA + ICS (for repeated exacerbations

• IV. Very Severe – SABA + LABA + ICS + O2 + consider surgical treatment

• Understanding the acronyms

• SABA – short acting beta-agonist (albuterol)

• LABA – long acting beta-agonist [(salmeterol (Serevent)]

• Anticholinergic – ipratropium (atrovent) or tiotropium (Spiriva)

• ICS – inhaled corticosteroid (beclomethasone, budesonide, fluticasone, triamcinolone)

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What defines a COPD exacerbation?

• Increased sputum production

• Increased sputum purulence

• Increased dyspnea

Treatment • Oxygen – keep SpO2 88-92% • Hydration • Noninvasive ventilation

• HFNC • Bipap

• Albuterol – episodic symptoms • Duonebs – albuterol + atrovent every 4 to 6 hours (then switch to long

acting once exacerbation under control)- conflicting evidence • Antibiotics or antivirals if has underlying bacterial/viral infection • Flutter valve • Chest percussion • Steroids

• Oral 40-60 mg prednisolone x 5 days (taper if used over 7 days) • For impending respiratory failure

• IV: methylprednisolone 60 mg 1 to 4 times per day up to 240 mg/day; 5-14 days (taper if used over 7 days)

• Ventilatory support

Acute respiratory failure

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Etiology of Acute Respiratory Failure

• Failure of oxygenation or carbon dioxide elimination

• Reduced lung capacity and increased ventilation/perfusion mismatch

• Reduced chest wall compliance and diaphragmatic and intercostal muscle strength

• Reduced clearance of airway secretions

• Altered responsiveness to hypoxemia and hypercarbia

• Acute versus chronic

• Acute – occurs over minutes to hours

• Chronic – occurs over days – usually see renal compensation

Understanding the causes… • Type 1 – hypoxemia (PaO2 < 60 mm Hg)

• Cardiogenic cause

• Pulmonary edema

• Noncardiogenic cause

• Pneumonia

• Pulmonary hemorrhage

• Pulmonary embolism

• Type 2 – Hypercarbia (PaCO2 > 50 mm Hg)

• Hypoventilation secondary to

• Drug overdose

• Neuromuscular disease

• Hypercarbia secondary to

• Asthma

• COPD

• Pulmonary embolism

Acute respiratory failure…

• Type 1 – hypoxemic respiratory failure

• Problem is oxygen!

• PaO2 < 60 mm Hg with normal PaCO2

• Type 2 – hypercarbic respiratory failure

• Problem is carbon dioxide!

• PaCO2 > 50 mm Hg

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Identify the causes…

It’s all about the pump…

It’s all about the circulation…

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It’s all about gas exchange…

Arterial blood gases • pH

• Normal 7.35-7.45

• Below 7.35 – acidosis

• Above 7.45 - alkalosis

• PaCO2

• Normal 35-45 mm Hg

• Above 45 means – hypoventilation causing CO2 retention

• Below 35 means – hyperventilation, blowing off CO2

• PaO2

• Normal 80-100 mm Hg

• HCO3

• Normal 22-26 mEq/L ( metabolic compensation by the kidneys)

• High level – kidneys are increasing HCO3 in blood for alkalosis

• Low level – kidneys are decreasing HCO3 in blood for acidosis

• SaO2 – Normal is > 95% (doesn’t always correlate to the SpO2)

ABG interpretation • Step 1: Analyze the pH

• pH < 7.35 = acidosis • pH > 7.45 = alkalosis

• Step 2: Analyze the PaCO2 • PaCO2 > 45 = acidosis • PaCO2 < 35 = alkalosis

• Step 3: Analyze the HCO3 • HCO3 < 22 = acidosis • HCO3 > 26 = alkalosis

• Step 4: Match the PaCO2 or HCO3 with pH • pH < 7.35, PaCO2 > 45 and HCO3 normal = respiratory acidosis (pulmonary issue)

• Hypoventilation, respiratory infection, COPD, Asthma, pulmonary edema, central nervous system or spinal cord injury • Treat by increasing ventilation rate, tidal volume

• pH < 7.35, HCO3 < 22 and PaCO2 normal = metabolic acidosis (kidneys trying to buffer) • Renal failure, DKA, lactic acidosis, sepsis, drugs – ethylene glycol

• pH > 7.45, PaCO2 < 35 and HCO3 normal = respiratory alkalosis (pulmonary issue) • Hyperventilation, pain, anxiety, early stages of pneumonia or PE, excessive mechanical

ventilation • Treat by decreasing ventilation rate

• pH > 7.45, HCO3 > 26 and PaCO2 normal = metabolic alkalosis (kidneys trying to buffer) • Diuretics, steroids, excessive vomiting, dehydration, Cushings, liver failure, hypokalemia

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Acute Lung Injury versus Acute Respiratory Distress Syndrome

Acute Lung Injury (ALI) versus Acute Respiratory Distress Syndrome (ARDS)

• Definition

• Mild (ALI) – PaO2/FiO2 ratio 200-300

• Moderate ARDS – PaO2/FiO2 ratio 100-200

• Severe ARDS – PaO2/FiO2 ratio < or equal to 100

• Mortality rate - 40-45%

• Complications

• 2/3 of survivors have impairment of pulmonary function

• Barotrauma – secondary to pressure

• Volutrauma – secondary to volume of air used to inflate lungs

• Bacterial infections

• Delirium

• Goal: Prevent cellular ischemia and death while correcting the cause

Causes of ALI/ARDS • SIRS – systemic inflammatory response syndrome • Bacteremia • Pancreatitis • Massive trauma • Shock • Pneumonia – including aspiration • Transfusion related lung injury (TRALI)

• Cytokine mediated response • Inflammation • May occur after single blood product but more common with multiple

blood products

• Transfusion related circulatory overload (TACO) • No inflammation • Signs of volume overload • Elevated BNP

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Three phases of ARDS • Exudative phase

• 2 to 4 days post acute lung injury, up to 7 days

• Capillary leaking causes alveolar flooding • Atelectasis

• Inflammation

• No high dose steroids – does not improve outcomes

• Fibroproliferative/proliferative phase

• Connective tissue proliferation in response to initial injury

• Steroids maybe helpful in the first 7-14 days of ARDS – improves survivability; steroids may breakdown collagen and inhibit fibrosis

• Resolution and Recovery

• 6 to 12 months of recovery

Clinical presentation

• Tachypnea

• Dyspnea - Breathlessness

• Crackles

• Cyanosis

• Tachycardia

• Anxiety

• Confusion

• Somnolence

• CXR shows alveolar flooding!

Diagnostic studies • ABG

• CXR

• Sometimes helpful to get ECG

• Diagnostic tests to determine cause and to monitor clinical improvement

• CBC with diff

• PTT, PT/INR

• Fibrinogen, FDP

• Chem 20 – includes LFTs

• UA

• Blood, sputum, urine cultures

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Treatment • Treat the cause!

• Hypoxemia is major threat to organ dysfunction!

• Oxygen – keep SaO2 > 90%

• Permissive hypercapnia (PaCO2 60-70) with pH of 7.2-7.25

• Bipap

• Vent support • Goal is to increase PaO2 and decrease PaCO2

• Prevent barotrauma – keep TV around 6 ml/kg

• Maintain minimum of 5 cm peep

• Avoid dopamine – constricts the pulmonary capillary beds

• Transfuse as needed

Prevention of pneumonia • Pneumonia vaccine

• Influenza vaccine

• Hand hygiene

• Good oral care

• Stay away from sick people especially if high risk

• HOB elevated 30-45%

• Swallowing evaluation

• Increase activity • OOB

• increase mobility

• Incentive spirometry

• See healthcare provider if has URI

Questions?

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Nurse Practitioners, Vol. 1. Barkley & Associates: West Hollywood, CA. • Burnham, E., Janssen, W., Riches, D., Moss, M., Downey, G. (2014). The fibroproliferative

response in acute respiratory syndrome: Mechanisms and clinical significance. European Respiratory Journal, 43(1): 276-285.

• Camargo, C., Rachelefsky, G., & Schatz, M. (2009). Managing asthma exacerbations in the emergency department. Proceedings American Thoracic Society; (6), 357-366.

• DeCramer, M., & Vestibo, J. (2014). Global initiative for Chronic Obstructive Pulmonary Disease.

• File, T. (2016). Treatment of communicty-acquired pneumonia in adults who require hospitalization. UptoDate.

• Kaynar, A., & Pinsky, M. (2015). Respiratory failure; Medscape; updated April 1, 2015. • Mandell, L., & Wunderlink R. (2007). Infectious Disease Society of America/American

Thoracic Society Consensus guidelines on the management of community-acquired pneumonia in adults. Clinical Infectious Disease. Suppl. 2:s27.

• NAEPP (2016). National Asthma Education and Prevention Guideline. • Papadarkis, M. & McPhee, S. (2015). Current Medical Diagnosis & Treatment. McGraw Hill:

New York, NY. • Stoller, J. (2016). Managing COPD Exacerbations. UptoDate. Accessed March 24,2016. • Wunderlink, R. (2014). Clinical Practice. Community-acquired pneumonia. New England

Journal of Medicine; 370:543.