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convalescent phase of pertussis
After 2-4 weeks
• Coughing episodes become less frequent and less severe
• Can last 1-3 months
Severe dyspnea of rapid onset + hypoxemia + diffuse pulmonary infiltrates =
respiratory failure
Common causes of ARDS
Pneumonia and sepsis (~40-60%)
• Aspiration of gastric contents, trauma, multiple transfusions, drug overdose
• Trauma like pulmonary contusion, multiple bone fractures, chest wall trauma/flail chest
Increased risks of ARDS
• Multiple comorbidities
• Older age
• Chronic alcohol abuse
• Metabolic acidosis
• Pancreatitis
• Severity of critical illness
three phases of ARDS
exudative, proliferative, and fibrotic
Elaborate on the exudative phase of ARDS
first 7 days of illness after exposure and onset of respiratory symptoms
exudative phase symptoms
Dyspnea, tachypnea, increased work of breathing->respiratory fatigue->respiratory failure
- Severe hypoxemia +/- hypercapnia
CXR findings of exudative phase
opacities consistent with pulmonary edema involving ≥ 75% of lung fields
Elaborate on proliferative phase of ARDS
-day 7 to day 21
-Most patients extubated during this phase
Elaborate on fibrotic phase
• Some patients require long-term MV support and/or supplemental oxygen
• Extensive alveolar-duct and interstitial fibrosis
• Intimal fibroproliferation in the pulmonary microcirculation -> progressive vascular occlusion and pulmonary hypertension
Treatment of ARDS
1) Recognition and treatment of underlying medical and surgical disorders
(2) Minimization of unnecessary procedures and their complications
(3) Standardized "bundled care" approaches for ICU patients
(4) Prompt recognition of nosocomial infections (5) Provision of adequate nutrition
Mechanical ventilation can aggravate lung injury...What are the two principal mechanisms
“Volutrauma” from repeated alveolar overdistention from excess tidal volume
“Atelectrauma” from recurrent alveolar collapse
Manage vent settings carefully
When managing patients with mechanical ventilation what position do we put them in and what are some risks
Prone Positioning
• Improves arterial oxygenation and reduces mortality
• Risks-> accidental endotracheal extubation, loss of central venous catheters, orthopedic injury
how and why do we do fluid management
Aggressive attempts to reduce left atrial filling pressures with fluid restriction and diuretics
• Limited hypotension and hypoperfusion of critical organs like Kidneys
Prognosis of ARDS
Mortality 34.9% - 46.1%
• Most patients regain nearly normal lung function
• Exercise limitation and decreased physical quality of life commonyears later despite normal PFT's
Respiratory Distress Syndrome in the Newborn was formerly also known as what
hyaline membrane disease
what is primary cause of Respiratory Distress Syndrome in the Newborn
deficiency of pulmonary surfactant in an immature lung
Patho process of Respiratory Distress Syndrome in the Newborn
Surfactant deficiency--> alveolar collapse--> low lung compliance and volume--> ventilation and perfusion mismatch--> hypoxemia
what babies are increased risk of this
decreased gestational age (premature babies)
diagnosis of Respiratory Distress Syndrome in the Newborn
Clinical findings of a preterm infant with progressive respiratory failure shortly afterbirth + characteristic chest imaging
• CXR->low lung volume + diffuse reticulogranular ground glass appearance with air bronchograms
signs of respiratory distress in newborn
Tachypnea, nasal flaring, expiratory grunting, cyanosis, and intercostal, subcostal, and subxiphoid retractions
• Decreased breath sounds, pallor, and diminished perfusion
clinical course of Respiratory Distress Syndrome in the Newborn
Progresses over the first 48 to 72 hours with increased respiratory distress
• Begins to resolve after 72 hours
• Resolution of symptoms by one week of age
Management of Respiratory Distress Syndrome in the Newborn
-Antenatal corticosteroid therapy in high-risk pregnant individuals
-Initial respiratory support (noninvasive)
-Surfactant
- Supportive care
what does the supportive care of Respiratory Distress Syndrome in the Newborn
• Maintenance of thermal neutral environment
• Optimal fluid balance with avoidance of fluid overload
• Maintenance of adequate perfusion
• Caffeine therapy for neonates with clinically significant apnea and in all extremely preterm infants (GA <28 weeks)
• Early nutrition
Indications for mechanical ventilation
Decrease the work of breathing and reverse life-threatening hypoxemia and respiratory acidosis
May be used as an adjunct to other forms of therapy
types of mechanical ventilation
Noninvasive ventilation (NIV)
invasive ventilation (MV) (or conventional mechanical)
What does noninvasive ventilation consist of
-Tight-fitting face mask or nasal mask
-Bilevel positive airway pressure ventilation
downsides of noninvasive ventilation
-patient intolerance
-Limited success in patients with acute hypoxemic respiratory failure
when is noninvasive ventilation used
COPD exacerbations and respiratory acidosis
When is conventional MV implemented
once a cuffed tube is inserted into the trachea
T or F 25-30% of MV patients will require prolonged MV (>21 days)
False
5-13%
Elaborate on tracheostomy
• More comfortable
• Requires less sedation
• More secure airway
• May also reduce weaning time
When is tracheostomy indicated
indicated if a patient needs MV for > 10-14 days
complications of tacheostomy
Bleeding, cardiopulmonary arrest, hypoxia, structural damage, pneumothorax, pneumomediastinum, wound infection
Bacterial Infectious Disorders
not a question just like to separate my quizlets
What is pneumonia
Infection of the pulmonary parenchyma
4 types of pneumonia
Community-acquired (CAP)
hospital-acquired (HAP)
ventilator-associated (VAP)
Healthcare-associated (HCAP)
what is HCAP pneumonia?
cases of CAP caused by multi drug resistant (MDR) pathogens
most common bacteria with community acquire pneumonia
Strep Pneu
typical bacteria
S. pneumonia, H. influenza, S. aureus and gram-negativebacilli such as klebsiella pneumonia and pseudomonas aeruginosa
for the 50 thousandth time what are the atypical bacterias
mycoplasma pneumonia, chlamydia pneumonia, Legionella
respiratory viruses (influenza, parainfluenza, respiratorysyncytial virus)
what are atypicals associated with and what should it be treated with
-Resistant to all beta-lactam agents
-Must be treated with a macrolide, fluoroquinolone or a tetracycline
Aspiration leads to what type of bacteria and what is it seen with
Anaerobes
Alcohol or drug overdose, seizure disorder
Often complicated by abscess formation
___ pneumonia is a well-known complication of influenza infection
S. aureus
risk factors for CAP
alcoholism, asthma, immunosuppression, institutionalization, age >70
Clinical Manifestations of CAP
Fever, chills/sweats, cough, SOB, pleuritic chest pain, GI symptoms, fatigue, headache, myalgias
• Accessory muscle use, ↑/↓tactile fremitus, crackles, pleural friction rub
CXR for CAP
Results may suggest an etiologic involvement
Ex. upper lobe cavitary lesion TB
T or F Establishing a microbial etiology may or may not be necessary
true
Urinary antigen test is for what bacteria
Legionella and pneumococcal
Polymerase chain reaction is for what bacteria and what type of patients
-Legionella, mycoplasma pneumonia, chlamydia pneumonia, mycobacteria
-ICU admitted patients
CAP inpatients vs outpatient asessment tool
Pneumonia Severity Index (PSI)
• CURB-65 criteria• 0 = outpatient
• 1-2 = likely admission
• 3+ = likely ICU admission
initial therapy of CAP is ___
empiric
CURB-65 criteria
Confusion
Uremia (BUN > 19)
RR > 30
BP (SBP < 90 or DBP < 60)
Age > 65y.o.
Inpatient treatment for CAP
Inpatient treatment is typically IV
• Switch to oral treatment when patient can ingest the drugs, ishemodynamically stable, and is showing clinical improvement
• 5-day course is usually sufficient for otherwise uncomplicated CAP
Longer course of inpatient treatment is associated with what
Bacteremia, metastatic infection, or infection with a virulent pathogen (ex. P.aeruginosa or CA-MRSA)
CAP adjuvant treatment
Adequate hydration, oxygen therapy for hypoxemia, vasopressors, and assisted ventilation when necessary
• Steroids? Prednisone, Methylprednisolone
if failure to improve after 3 days of treatment suspect what
Noninfectious etiology, drug resistance, unsuspected pathogen
complications of CAP
Respiratory failure, shock and multiorgan failure, coagulopathy, exacerbation of comorbid illnesses, metastatic infection, lung abscess, and complicated pleural effusion
follow up for CAP
F/u CXR in 4-6 weeks
Pneumococcal vaccine
ventilator associated pneumonia is a common complication of
MV
Potential etiologic agents of VAP include
both MDR and non-MDR bacterial pathogens
Often institution-specific
VAP clinical manifestations
-Fever, leukocytosis, increase in respiratory secretions, pulmonaryconsolidation on physical examination, radiographic infiltrate
-Tachypnea, tachycardia, worsening oxygenation
what shoudl u do if you suspect VAP
Obtain diagnostic specimens and then begin treatment
t or f Most patients without risk factors for MDR infection can be treated with asingle agent
true
Lower incidence of atypical pathogens in VAP... what is the exception
Legionella
typical course length of VAP
7/8 days
with VAP treatment failure is not uncommon... what are some reasons for this
Inappropriate initial therapy, drug resistance, pneumonia due to a new superinfection, the presence of extra pulmonary infection, drug toxicity
complications of VAP
Prolongation of mechanical ventilation, pulmonary hemorrhage, bronchiectasis and parenchymal scarring leading to recurrent pneumonia, death
f/u of VAP
findings on CXR often worsen initially during treatment
• Clinical criteria is more helpful
prevention of VAP
• Avoid intubation or minimize its duration
• Minimizing microaspiration around the endotracheal tube cuff
• Minimize transportation of the patient outside the ICU for diagnostic tests or procedures
how to Minimize microaspiration around the endotracheal tube cuff
-elevate the head of the bed (at least 30° above horizontal but preferably 45°)
-Specially modified endotracheal tubes
HAP in ___ patients is similar to VAP
non-intubated
In HAP there is a higher frequency of ____ pathogens
non-MDR
Allows monotherapy in a larger proportion of cases of HAP than of VAP
____ may be more common in HAP than VAP
anaerobes
Greater risk of macroaspiration
T or F in HAP there is Lower mortality rates and risk of antibiotic failure
true
Pneumonia accounts of __% of nosocomial infections
~24
Associated with more deaths than infections at any other body site
Mitigation strategies of pneumonia
• Frequent testing of readiness for extubation
• Remediation of risk factors in patient care
• E.g., minimizing aspiration-prone supine positioning
• Aseptic care of respirator equipment
• Noninvasive mechanical ventilation whenever feasible
What is a lung abscess?
Necrosis and cavitation of the lung following microbial infection
there can be single or multiple lung abscesses... usually marked by a single dominant one of what measurement
>2 cm in diameter
primary abscess is most common...how does this come about
• Aspiration• Often caused principally by anaerobic bacteria
• Occur in the absence of an underlying pulmonary or systemic condition
secondary abscess arise in what setting
underlying condition or a systemic process
Acute vs chronic lung abscess duration
Acute (<4-6 weeks in duration) or chronic (~40% of cases)
lung abscess is formed by colonization of what
Colonization of the gingival crevices by anaerobic bacteria or microaerophilicstreptococci
• Especially in patients with gingivitis and periodontal disease
primary abscess disease process
Anaerobic bacteria in the gingival crevices aspirated--> pneumonitis--> parenchymal necrosis and cavitation
secondary abscess can also arise from what
septic emboli
• Tricuspid valve endocarditis (often involving Staphylococcus aureus)
• Lemierre’s syndrome (classically involving Fusobacterium necrophorum
most common bacteria in lung abscess
Pseudomonas aeruginosa and other gram-negative rods most common
t or f obtaining culture of abscess is optional but you could do it
false
Obtaining culture is important
Lung Abscess Clinical Manifestations
Fevers, cough, sputum production, and chest pain
• Chronic and indolent presentations common with anaerobic lung abscesses
• Abscesses due to non-anaerobic organisms may present with a more fulminant course ( high quick fever, s.aureus)
Physical Exam Findings of lung abscess
Fevers, poor dentition/gingival disease, cavernous breath sounds
initial diagnostics for lung abscess
CXR initially but CT is better
primary abscess diagnostics
empirical therapy initiated, invasive diagnostics infrequently utilized
secondary abscess or empiric abx fail
sputum and blood cultures, serologic studies for opportunistic pathogens
• Bronchoscopy with bronchoalveolar lavage or protected brush specimen collection and/or CT-guided percutaneous needle aspiration
primary lung abcess treatment
1) Clindamycin OR•
(2) an IV β-lactam/β-lactamase combination, followed by amoxicillin-clavulanate
• Tx until abscess is cleared
• 3-4 weeks, up to 14 weeks
secondary abscess treatment
Tx directed at identified pathogen
t or f Abscess > 6-8cm is more likely to respond to antibiotic therapy without additional interventions
FALSE
Less likely to respond
complications of lung abscess
Persistent cystic changes (pneumatoceles) or bronchiectasis, recurrence of abscesses despite appropriate therapy, empyema, life-threatening hemoptysis, massive aspiration of lung abscess contents
prevention of lung abscess
Airway protection, oral hygiene, and minimized sedation with elevation of the head of the bed for patients at risk for aspiration
pneumococcal infections have to do with what bacteria
streptococcus pneumoniae
how do we prevent these pneumococcal infections
Routine childhood administration of pneumococcal polysaccharide-protein conjugate vaccine (PCV)
Not all pneumococcal serotypes are equally likely to cause disease
Pneumococcal Infections are transmitted by what
respiratory droplets