9/15- Acute Respiratory Distress Syndrome (ARDS) Flashcards
What is seen here?
Characteristic of ARDS???
Case)
- 32 yo obese but healthy female
- Presented with 3 days high fever, dry cough, and worsening SOB
- Admitted -> rapid flu test positive; oseltamivir started
- More hypoxic -> required intubation and mechanical ventilation
- Additional antibiotics added
- Required increasing support from mechanical ventilator to achieve adequate oxygenation
- Required sedation and neuromuscular block
…
What is ARDS?
What are some micro-anatomical features?
Diffuse injury to the alveolo-capillary membranes from direct and indirect causes
- Sloughing of epithelial layer
- Endothelial cell injury
- Denuded basement membrane
- Flooding of alveolus with protein rich fluid and cellular debris and leukocytes
What are hallmarks of ARDS?
- Non- cardiogenic pulmonary edema
- Hypoxemia, hypercarbia
- Respiratory failure, frequently requiring mechanical ventilation
What are some disorders associated with development of ARDS (direct and indirect)?
Direct
- Gastric aspiration
- Pneumonia
- Less commonly: inhalation injury, pulmonary contusion, fat emboli, near drowning, reperfusion injury, amniotic fluid embolism
Indirect
- Sepsis
- Multiple trauma
- Less common: acute pancreatitis, transfusion related (TRALI), DIC, burns, head injury, drug overdose, cardiopulmonary bypass
Etiology of ARDS
Pneumonia + Sepsis + Aspiration accounts for 75% of all cases
- Pneumonia (40%)
- Sepsis (22%)
- Aspiration (15%)
- Trauma (8%)
- Transfusion (5%)
Review: what forces are at play in entry of fluid into lungs from vasculature?
Starling forces
- Balance between hydrostatic pressure and osmotic pressure
More leak when:
- Higher hydrostatic pressure
- Lower osmotic pressure
What are the different situations which may lead to edema/differences in the resulting fluid?
Cardiogenic pulmonary edema
- High L atrial pressure
- Transudate (edema fluid/plasma protein ratio is < 0.5)
Non-cardiogenic edema (increased permeability)
- Exudate (edema fluid/plasma protein ratio > 0.5)
What is the histopathology: DAD?
Exudative (7 days)
- Hyaline membranes
- (injury to type I pneumocytes and alveolar capillary membrane -> increased permeability)
Proliferative (7-21 days)
- Type II pneumocyte hyperplasia
- Prominent interstitial inflammation
Fibrotic (>21 days, starts early)
- Fibrosis of alveolar ducts and interstitium -> bullae and cyst formation
- Fibrosis of vascular intima -> vascular obstruction
Pathophysiology (in regards to alveolar epithelium)?
Physiological results?
Alveolar epithelium
- Loss of tight junction and sloughing
- Leakage of protein rich fluid into alveolar space
- Loss of surfactant and increased surface tension -> atelectasis
- Impaired hypoxic vasoconstriction
Results in:
- Low V/Q (acts like shunt; can’t oxygenate)
- Increased work of breathing
Pathophysiology (in regards to endothelial cell)? Physiological results?
Endothelial cell injury
- Increased permeability
- Neutrophils, red cells, protein rich fluid into interstitial then alveolar spaces
- Formation of microthrombi
- Increased pulmonary vascular resistance
Results in: acts like dead space (can’t ventilate -> CO2 increase)
Radiographic pattern of DAD/ARDS?
CXR: bilateral infiltrates
- Maybe diffuse or patchy
CT chest:
- Heterogeneous and patchy involvement
- More prominent in dependent regions (lower lobes)
- Ground glass or consolidative pattern
What is seen here?
Nonspecific findings in chest CT of pt with DAD/ARDS
Principles of treatment?
- Recognize and treat the cause
- Lung protective ventilation
- Conservative fluid strategy
- Supportive care
- Prevent complications
- Nutritional support
What may be involved in “treating the cause” of ARDS?
- Control sepsis (find source, anti-microbial therapy, drainage of abscess, surgery)
- Manage trauma (surgical or not)
How is mechanical ventilation used in ARDS cases (Broadly/Mechanics)
MECHANICS
Used to take over the work of breathing
- Blood flow can be redirected to vital organs
- Allow adequate level of sedation and neuromuscular block
Application of positive pressure to improve oxygenation (up to certain limits)
Adjust ventilation to optimize acid base status (up to certain limits)
What is the principle of protective ventilation?
LUNG PROTECTIVE VENTILATION
- Use of lower tidal volumes (6ml/kg based on IBW)
- Limit airway pressures (plateau pressure
What are the goals of ventilation (measurements)?
GOALS
- Oxygenation: PaO2 55-80 mHg or SpO2 88-95%
- Lowest FIO2 and PEEP
What is PEEP? How does it affect certain lung volumes/functions?
PEEP = positive end expiratory pressure
- Increases FRC
- Decrease alveolar edema
- Recruitment of collapsed alveoli
- Avoid repetitive opening and closing of alveoli
(Gas exchange can occur to blood flow even during exhalation)
What should avoided/minimized in mechanical ventilation?
- Avoid lung overdistention
- Minimize O2 toxicity (keep FiO2 under 60%)
What are adverse effects of mechanical ventilation?
Increased intrathoracic pressure can decrease venous return
- Decreased cardiac output
- Hypotension - Increased intracranial pressure*
- Decreased perfusion to visceral organs
*(especially in head trauma pts with cephalic edema, may be better to raise FiO2 than pressure)
Barotrauma
- Pneumothorax
- Pneumomediastinum
Ventilator induced lung injury
Need for sedation
Decreased mobility
Describe conservative fluid management in ARDS cases
- Clinical trials have shown decreased duration of mechanical ventilation – 2.5 days
- Use of diuretics and close monitoring of fluid balance
- Limited by hypotension and tissue hypoperfusion (kidney insufficiency, increased lactic acid)
What are the evidence-based recommendations for ARDS therapies?
What are supportive measures of ARDS?
- Hemodynamic support (keep BP high)
- Sedation and pain control
- Prophylaxis for DVT, stress ulcer bleeding
- Prevent aspiration and nosocomial infection
- Nutritional support
- Early mobilization and physical therapy
- Treat co-morbidities: DM, HTN, heart failure, delirium
Prognosis and Outcome of ARDS?
- Timeline
- Factors for increased mortality
- Etiology (and what cause -> highest mortality)
Death
- < 72 hrs: underlying cause
- > 72 hrs: multi-organ failure
Risk factors for increased mortality
- Advanced age > 75 yo
- Sepsis and age > 60 yo
- Pre-existing organ dysfunction: liver cirrhosis, chronic kidney disease, alcohol abuse, immunosuppression
Etiology:
- Direct causes > indirect causes
- Sepsis as a cause carries highest mortality
Characteristics of ARDS survivor
- Lung function
- Impairments
- Psychiatric
- Overall health
- Work
Recovery of nearly normal lung function
- Maximum recovery in 6 months
- 1/3 have nearly normal spirometry and diffusing capacity
- Extent of recovery is related to severity of lung injury
Physical impairment – low exercise tolerance
Cognitive impairment
Psychiatric morbidity
- Depression and PTSD
Reduced health related quality of life
Less than half return to work
Summary
- ARDS is caused by injury to the integrity of the alveolar-capillary membrane that allows protein rich fluid to escape from the pulmonary capillaries
- There is cascade of inflammation and repair
- Management of ARDS is treatment of the underlying cause and supportive care
- Mortality is decreasing but post-ARDS survivors have significant impairment and disability
Clinical course of ARDS
Hemodynamic support
- Vasopressors; arterial blood pressure monitoring
- IV fluids; bicarbonate for the severe acidosis
Mechanical ventilation
- Increased PEEP
- Low tidal volume
- Sedation
Look for cause
- Elevated amylase -?pancreatitis
- MSSA bronchial fluid
Treat DKA
Nutritional support
