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.
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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
• 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)
• 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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References • Barkley, T., & Myers, C. (2015). Practice Considerations for Adult-Gerontology Acute Care
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