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Pneumonia - what is it?
an acute inflammation of the lung parenchyma (caused by an infectious agent) that can lead to alveolar consolidation
CAUSATIVE AGENTS - bacterial, viral, fungal, parasitic
Pneumonia - community acquired pneumonia (CAP)
OUTSIDE the hospital
common pathogens - Streptococcus pneumoniae, Legionella pneumophila, Klebsiella pneumoniae, Haemophilus influenzae, Staphylococcus aureus, Mycoplasma pneumoniae, Pseudomonas aeruginosa
Pneumonia - hospital acquired pneumonia (HAP)
pneumonia that developed in acute care, long-term care, or a nursing home
Pneumonia - ventilator associated pneumonia
develops 48 hours or more after admission to the hospital
common pathogens: P. aeruginosa, E. coli, K. pneumoniae, Acinetobacter baumannii, S. aureus (especially diabetes and head trauma), MRSA
HIGHER MORTALITY THAN COMMUNITY ACQUIRED PNEUMONIA
Pneumonia - risk factors
age
preexisting pulmonary disease
smoking
decreased LOC
artificial airways
chronic illness
malnutrition
immunocompromised
increased secretions
atelectasis
immobility
depressed cough or gag reflex
concurrent antibiotic therapy
aspiration
organisms spread from another site (gut, wound) to the lungs
multiple organ dysfunction syndrome (MODS)
Pneumonia - signs and symptoms
chills, diaphoresis, fever, malaise
tachycardia, chest pain
confusion (ESPECIALLY OLDER ADULTS)
productive cough
use of accessory muscles
dehydration
over area of consolidation on chest:
INCREASED tactile fremitus (how well sound is transmitted through the lungs)
dull to percussion
bronchial breath sounds or diminished breath sounds
bronchophony (louder/clearer)
egophony (“e” to “a”)
whispered pectoriloquy (whisper heard better with a stethoscope)
Pneumonia - DIAGNOSIS
CXR: consolidation or diffuse patchy infiltrates
sputum culture with Gram stain
blood cultures
WBC: high but may be normal or low in immunocompromised or elderly people
WBC differential: increased bands >10%
ABGs - hypoxemia
thoracentesis for effusions
Pneumonia - treatments
optimize oxygenation/ventilation → titrate FiO2
POSITIONING - GOOD lung DOWN
bronchial hygiene, chest physiotherapy
prone positioning for severe hypoxemia
noninvasive ventilation or intubation/mechanical ventilation as needed
bronchoscopy (with lavage, if needed)
mobilize, clear secretions
identify organisms → sputum culture/sensitivity; blood cultures
antibiotic therapy
system support (hydration, fever management, glucose control, nutrition)
general preventative measures (smoking cessation, pneumonia vaccine for those who are 65 and older; flu vaccine)
Pneumonia - antibiotic therapy (empiric therapy, timing, organism-specific therapy)
empiric therapy - choice of agent is based on the likely causative organism (as determined by a patient assessment and the types of pneumonia seen in the community and in the institution) and whether that organism may be resistant to therapy
timing - first dose within 4 hours if the patient first presents to the ED (and is later admitted to the hospital); the first ABX dose should be given in the ED
organism-specific therapy - AS SOON AS THE RESULTS OF THE CULTURE AND SENSITIVITY ARE AVAILABLE
Pneumonia - PREVENTION of Hospital-Acquired Pneumonia
practice hand hygiene
keep HOB elevated 30 degrees or more
prevent bacterial translocation from GI tract: use the gut, feed the patient
practice oral hygiene
provide education on common institution pathogens and the rates of nosocomial pneumonia
use evidence-based confirmation of feeding tube placement (confirm with x-ray prior to using for feeding; mark exist site with marker; assess patency Q4; observe for change in length; review routine chest/abd xrays; observe changes in volume of aspirate; use pH strips; observe appearance of feeding tube aspirates)
Pneumonia - PREVENTION OF VENTILATOR-ASSOCIATED PNEUMONIA
drain accumulated condensate from tubing
prevent backflow of tubing condensate into ETT
change ventilator tubing only when it is contaminated
mobilize the patient
utilize aseptic technique for ETT, tracheostomy suctioning
adhere to mouth care protocol, chlorhexidine mouth rinse
brush teeth to remove plaque
keep ETT cuff inflated
perform subglottic suctioning prior to cuff deflation
perform routine oropharyngeal suctioning
Aspiration - what is it?
the inhalation of toxic substances into the lung, with an injury to the lung that is the result of the chemical, mechanical, and/or bacterial characteristics of aspirate
oropharyngeal is most common; may or may not involve an infection; may be acute or chronic; micro or massive
Aspiration - emergent management (witnessed vs. ALL aspirations)
witnessed - place patient in slight trendelenburg and turned to the RIGHT side to aid drainage; suction mouth and pharyngeal areas; bronchoscopy for large particles
ALL aspirations - O2 (titrate as needed); intubation/mechanical ventilation as needed; monitor for the onset of noncardiogenic pulmonary edema (ARDS) or pneumonia; monitor for decreased BP
Aspiration - why do we turn the patients to the right for a witnessed aspiration?
due to the anatomy of the right mainstem bronchus (shorter, wider, and with less of an angle), most aspirations occur in the RIGHT lung
the GOAL is to keep the aspiration from spreading/protect the airway!!
Aspiration - ETIOLOGIES
altered LOC
drug or alcohol abuse
depressed gag, cough, or swallowing reflexes
presence of feeding tubes (ALL TYPES)
improper patient positioning
presence of artificial airways
ileus or gastric distension
history of dysphagia, GERD, esophageal strictures, decreased GI motility
increased secretions
Aspiration - signs and symptoms
acute respiratory distress
presence of gastric contents in oropharynx
tachycardia
hypoxemia
crackles
copious secretions due to alveolar edema
hypotension (massive fluid shifts may occur)
ARDS/ALI - what are they?
syndromes caused by acute conditions that trigger an inflammatory response, resulting in an increase in permeability of pulmonary capillary membranes, allowing transudation of proteinaceous fluid into interstitial/alveolar spaces
“NONcardiogenic pulmonary edema”
DAMAGE to type II alveolar cells is one of the pathological consequences, as these are the cells that are responsible for production of surfactant → MASSIVE ATELECTASIS!!
ARDS/ALI - both involve a shunt. What does this MEAN? what is NEEDED to help with this?
pathologic shunting → blood goes through the lungs but does NOT get oxygenated, resulting in refractory hypoxia (FiO2 is increased to the maximum 100% and hypoxemia is still present)
PEEP needs to be provided in order to increase alveolar recruitment/prevents alveolar collapse and treat the refractory hypoxemia
ARDS/ALI - differentiation with PaO2/FiO2 ratio
ARDS - less than OR equal to 200 mmHg regardless of PEEP level
ALI - between 201 and 300 mmHg regardless of PEEP level
ARDS/ALI - PaO2/FiO2 examples
patient receiving 50% FiO2 and PaO2 is 90
90 / 0.50 = 180
ARDS/ALI - what is surfactant? why is it important?
phospholipid/lipoprotein produced by Type II alveolar cells that stabilizes alveoli by keeping them open
helps increase lung compliance/eases work of breathing
ARDS - type II alveolar cells are destroyed, resulting in massive atelectasis/alveolar collapse, decreased compliance, INCREASED WOB, and decreased functional residual capacity (decreased amount of air remaining in lungs after normal exhalation)
ARDS/ALI - PATHOPHYSIOLOGY
DIFFUSE alveolar-capillary membrane injury (inflammatory response)
→damage to Type II alveolar cells → decreased surfactant → ALVEOLAR COLLAPSE/decreased FRC/lung compliance → HYPOXEMIA
→damage to capillary endothelial cells → capillary leak →alveolar edema/pulmonary interstitial edema → diffusion defect → ALVEOLAR COLLAPSE/HYPOXEMIA
ARDS/ALI - ETIOLOGIES (direct vs. indirect)
direct
aspiration; pneumonia, pulmonary contusion, fat/air embolism, O2 toxicity, inhalation injury, drowning, transthoracic radiation
indirect
sepsis, shock, head injury, non-thoracic trauma, blood transfusion, pancreatitis, burns, heart bypass, DIC
ARDS/ALI - EARLY signs/symptoms
tachycardia
apprehension/restlessness
mild dyspnea
respiratory ALKALOSIS (breathing fast)
few crackles
chest x-ray → isolated infiltrate or “ground glass” appearance
PaO2 on room air ABOUT 60 mmHg
ARDS/ALI - LATE signs/symptoms
tachycardia, episodes of bradycardia
agitation
extreme dyspnea
respiratory and metabolic acidosis
crackles/wheezes
chest x-ray → whiteout/bilateral infiltrates
PaO2 on room air ABOUT 30 mmHg, refractory hypoxemia despite INCREASED FiO2
ARDS/ALI - TREATMENTs (pulmonary stabilization strategies)
intubation with mechanical ventilation
PEEP, usually 15 cm H2O or greater; monitor for barotrauma and decreased cardiac output; treat hypotension, but do NOT discontinue PEEP
NOTE: disconnection of the ventilator circuit and PEEP will result in alveolar derecruitment and hypoxemia that may not be readily corrected
limit plateau pressure to 30 cm H2O or less
limit tidal volume (Vt) to 5-6 mL/kg → “permissive hypercapnia” to prevent volutrauma
a low Vt will cause a rise in the PaCO2 and a drop in the pH; however, patients tend to tolerate a pH as low as 7.2
ARDS/ALI - TREATMENTS (cardiovascular strategies / other treatments)
cardiovascular stabilization (support BP (fluids, vasopressors, especially when ARDS is due to septic shock); monitor for arrhythmias
prone positioning (helps deliver blood flow to underperfused lung units, thereby improving ventilation/perfusion; keeps alveolar lung units open, thus improving gas exchange and preventing further injury (USE EXTREME CAUTION to avoid misplacement/loss of airway; prevent a pressure injury)
monitor acid-base balance
DVT/stress ulcer prophylaxis
analgesia/sedation
nutritional support
nitric oxide, prone positioning may provide improvement in oxygenation
coordinate interdisciplinary team - PT, OT, dietitian
prevent, identify organ failure
emotional support
monitor for complaications
NO STEROIDS!! (except for select patients with Covid-19 pneumonia)
ARDS/ALI - COMPLICATIONS
usually die from multiple organ dysfunction syndrome, as well as….
secondary infections
pulmonary embolus
ileus
skin breakdown
malnutrition
barotrauma → pneumothorax, subcutaneous emphysema