ARDS/Pulm effusion Flashcards
Acute Respiratory Distress Syndrome (ARDS)
general
Life-threatening diffuse inflammatory form of lung injury
Characterized by bilateral lung infiltrates and progressive hypoxemia without cardiac failure
The underlying mechanism of ARDS is capillary endothelial injury and diffuse alveolar damage (DAD)
Epidemiology:
Most common cause of non-cardiogenic pulmonary edema
~190,000 cases of ARDS in the United States each year
~22% of patients who are mechanically ventilated meet the criteria for ARDS
Mortality rate: 9-20%
(you give supplemental O2 and they stay hypozic and desat) (can;t be related to cardio
ARDS
Etiology
Direct lung injury
Results from clinical disorders that affect the lungs either directly or indirectly
Direct lung injury:
Bacterial and viral pneumonia
Aspiration of gastric contents
Pulmonary contusion
Near-drowning incidents
Toxic inhalation injury
Lung transplant
ARDS
Etiology
Indirect lung injury
Indirect lung injury:
Sepsis (most common cause)
Severe trauma with prolonged hypovolemic shock
Drug overdoses
Bone marrow transplantation
Post-cardiopulmonary bypass
Massive blood transfusion
Pancreatitis
Fat or amniotic fluid embolism
ARDS
Patho - 1
EXUDATIVE
(the worst phase)
Occurs in 3 phases – exudative, proliferative, fibrotic
Exudative: 6-72 hours after the eliciting factor
Initial injury (cytokines) causing damage to pneumocytes and pulmonary endothelium → disrupted barriers between capillaries and airspaces (leaky)
Inflammatory reaction is initiated with endothelial cells secreting pro-inflammatory molecules and expressing adhesion molecules on their surface
Immune cells (neutrophils – 1st to arrive) stick and then migrate into the alveoli → neutrophils will release proteases and reactive oxygen molecules, and more cytokines to perpetuate the cycle
Edema fluid, protein, and cellular debris flood the airspaces
Disruption of surfactant → ↑ surface tension → airspace collapse, ventilation-perfusion mismatch, right-to-left shunting of venous blood leading to pulmonary hypertension
ARDS
what kind of shunting do we see?
Right to left.
deoxygenated blood getting back into circulation leading to hypoxia
ARDS
Patho - 2
Proliferative
Beginning stages of lung repair
Alveolar epithelial cells begin proliferating along the alveolar basement membranes
Macrophages clean up cellular debris and attract and activate fibroblasts
New pulmonary surfactant is produced
ARDS
Patho - 3
Fibrotic
Abnormal deposition of collagen in the alveolar ducts and interstitial membranes by fibroblasts
Lung scarring; “stiff” lungs → restrictive lung disease
Stiff lungs – poor lung compliance, reduced diffuse capacity, microvascular occlusion
ARDS
Expected vitals
Mild dyspnea → respiratory distress/failure
Vitals
Tachypnea
Tachycardia
Fever may/may not be present
Hypoxemia despite supplemental oxygen
ARDS
PE findings
Physical exam
Diffuse crackles (rales)
Worse at the bases
Labored breathing
Retractions
Restlessness and/or anxious
Cyanosis
Altered level of consciousness
Exam findingsNOTconsistent with ARDS: new or changed murmur, S3 or S4 gallop, jugular venous distension (JVD), lower extremity pitting edema
ARDS
Dx (4)
Berlin diagnostic criteria of ARDS:
- Acute onset (within 1 week)
- Diffuse bilateral infiltrates on chest x-ray or CT scan
- No evidence of heart failure or fluid overload
- Partial pressure of O2/fraction of inspired O2(PaO2/FiO2) < 300 mmHg:
Mild ARDS:201–300 mm Hg
Moderate ARDS: 101–200 mm Hg
Severe ARDS: ≤ 100 mm Hg
if you have JVD, pulm edema, cardiomegaly,pedal edema its HF not ARDS
CXR Day 1
70-year-old female admitted with acute respiratory failure, fever (38ºC) and dyspnea. She was tachypneic (30 bpm), with lymphopenia and low oxygen saturation (SpO2 85%, PAFI<250). Covid-19 positive.
she died on day 4
ARDS
CXray
Chest X-ray:
ARDS: bilateral pulmonary infiltrates
Finding more consistent with bacterial pneumonia: consolidation
Findings more consistent with cardiogenic pulmonary edema:
Pulmonary venous congestion
Cardiomegaly
Pleural effusion
ARDS
ARDS
Labs
Labs
BNP levels < 100 pg/mL favors ARDS
Arterial blood gas (ABG):
Hypoxemia
Additional testing to determine the underlying cause (example: lipase for possible pancreatitis)
ARDS
Tx
Patients are managed in the ICU
Correct the underlying cause
Supplemental oxygen:
Most patients require a high FiO2 (> 50%)
Delivered via high-flow nasal cannula, nonrebreather face mask, or by intubation (mechanical ventilation)
Failure of oxygen saturation improvement > 90% - suspect right-to-left shunting of blood
Mechanical ventilation:
If oxygen saturation is < 90% on high-flow oxygen
High PEEP
Low tidal volume (6 mL/mg)– most critical factor in reducing mortality rates
Prone positioning improves oxygenation
Fluid management is difficult
Large volume to maintain blood pressure
Fluid restriction to reduce left atrial filling pressure and improve oxygenation
Diuretics can facilitate fluid restriction/removal
Patients will require high PEEP (positive-end expiratory pressure) to keep the alveoli from collapsing
ARDS
Prognosis and RF
Serious condition that is usually associated with high mortality and morbidity
Risk factors forestimating the prognosis in a patient with ARDS:
Advanced age
Direct lung injuries result in twice the number of mortalities
Preexisting organ dysfunction from chronic diseases:
Chronic liver disease
CKD
Immunosuppression
The majority ofpatientsrecover most of their lung function over several months
PE
Pleural Fluid
Forces (hydrostatic and osmotic pressures) responsible for producing pleural fluid within the capillary bed of theparietal pleura
Pleural fluid is absorbed bylymphvessels in the diaphragmatic and mediastinal surfaces of theparietal pleura; ultimately drains into the right atrium
The normal mean rate of production andabsorptionof the pleural fluid is 0.2 mL/kg/hour
The entire volume of pleural fluid normally turns over within 1 hour
How does pleural effusion form?
Formation of a pleural effusion results from:
Overproduction of pleural fluid OR
Inability of the lymphatic system to remove fluid as it is produced
Pleural Effusion
general
Exudative vs transudative
Excessive accumulation of fluid within the pleural cavity (between the parietal and visceral pleura)
Classified as exudative or transudative based on Light’s criteria
Exudative
Caused by inflammation and ↑ capillary permeability
Fluid rich in protein and LDH in the pleural space
Transudative
Caused by a combination of ↑ hydrostatic pressure in the vasculature and ↓ oncotic pressure in the plasma
P effusion
etiology
transudate vs exudate
Transudate:
Examples:
Heart failure (HF)- 90% of cases
Livercirrhosis
Hypoalbuminemia
Nephrotic syndrome
Exudate:
Examples:
Pneumonia
Empyema
Tuberculosis (TB)
Malignancy(most commonly a primary lung cancer)
Connective tissuediseases
Pancreatitis
Asbestos
Post-cardiac injury syndrome
pulm effusion
Pulm embolism
THis is the only cause that will give you both transudative and exudative
Pulmonary embolism
Transudative effusion
Obstruction of the pulmonary circulation → ↑ hydrostatic pressure
Exudative effusion
Release of vasoactive mediators from platelet-rich clots → ↑ capillary permeability
pulm effusion
Symptoms
May be asymptomatic
Symptoms
Dyspnea(most common)
Pleuritic chestpain
Indication of pleuralinflammation
Worsens with deep inspiration or cough
Fever
Cough- can have wityh both types.
Pulm effusion
PE Findings
inspection palpation and percussion
Inspection:
An asymmetrical chest expansion (reduced expansion on the side of the effusion)
Fullness ofintercostal spaces(can’t see until its big)
Palpation:
↓ or absenttactile fremitus
Tracheal deviation
Tracheais shifted to the opposite side of the effusion
Percussion:
Effusion >300 mL, chest examination will also be notable for dullness topercussion
The upper border dullness follows a laterally ascending curve apexing at themidaxillary line(Ellis–Damoiseau line)
fremitus increases with consolidation/pneumonia
Pulm effusion
PE findings
auscultation
Auscultation:
↓ or inaudible breath sounds over the effusion
Bronchial breath sounds, bronchophony, and egophony:
Heard over the lung parts directly above the effusion
Pleural friction rub synchronous with respiration
Pulm effusion
Determining the Etiology
Look for associated symptoms and physical examination findings that may clue you in:
Fever, chills, productive cough → pneumonia
Unintentional weight loss, early satiety, loss of appetite, constant chest pain → malignancy
Night sweats, hemoptysis, and travel to endemic area → tuberculosis
Weight gain, orthopnea, peripheral edema, jugular venous distention → congestive heart failure
Occupational exposure to asbestos → mesothelioma
Joint pain with or without effusion and/or skin rash → connective tissue disease
“If you are effusing in TWO, think AUTOIMMUNE”
Pulm effusion
CXray
Chestx-ray
Best initial test to determine the presence of an effusion
Minimum of 200 mL of fluid to obliterate the costophrenic angle
Findings
Abnormal blunting of costophrenic angles
Fluid within horizontal or oblique fissures
Effusions may demonstrate a meniscus
Massive effusions
Complete opacification of a hemithorax
Tracheal deviationaway from the affected side
Mediastinal shift
PA CXR showing bilateral pleural effusions:
Blunting of the costophrenic angle (particularly on the right)
Meniscus on the left
MOST of the time bilat effusion is CHF but take Hx into account could be other things.
Pulm effusion
Pulm effusion
Lateral decubitus films
Lateral decubitus films
Most sensitive
Can detect effusions with a minimum of 50 mL
Look at the distance between the chest wall and top of the fluid level
Diagnostic thoracentesis should be performed on all patients that have pleural fluid ≥ 10 mm (1 cm) of thickness on imaging and that is new or of uncertain etiology
**Determine if the effusion is:
Fluid layering (free-flowing) → transudative effusion
Loculated → exudative effusion**
Pulm effusion
Pleural Fluid Analysis
Sample of pleural fluid by performing a diagnostic thoracentesis
Pleural fluid should be sent for:
Cultures and microscopy
Bacteria
Acid-fast bacilli
Fungi
Cytology
Cell count with differential
pH
Lactate dehydrogenase (LDH)
Total protein
Albumin
Glucose
Additional investigations include(based on clinical suspicion):
Amylase→pancreatitis,esophageal rupture
Triglycerides→ chylothorax
Rheumatoid factorand antinuclear antibodies→ autoimmune disorders
Acid-fast bacillismear and adenosinedeaminase (ADA) →TB
Pleural effusion
Lights criteria
Exudative pleural effusion with any one of the following characteristics:
Pleural fluid protein/serum protein ratio > 0.5
Pleural fluid LDH/serum LDH ratio > 0.6
Pleural fluid LDH > 2/3 of the upper limit of normal for serum
Transudative pleural effusions meet none of the above characteristics
Pulm effusion
Tx
Initial management for symptomatic patients
Assessairway, breathing, andcirculation
Providesupplemental oxygen
Urgent drainage if:
Severe respiratory distress orrespiratory failure
Evidence ofobstructive shock
Interventions
Therapeutic thoracentesis
1-1.5 L per treatment
Chesttube placement(tube thoracostomy)
Indwelling pleural catheter
Management of symptoms and the underlying cause
NSAIDs or other analgesics for pleuritic pain
pulm effusion
Complications(4)
pulm effusion
Thoracentesis
Performed using ultrasound to allow for visualization of anatomical structures
Needle is inserted above the rib to avoid damage to the intercostal vein, artery, and nerve
Procedural risks:
Pneumothorax
Vascular injury →hemothorax
Re-expansionpulmonary edema
Special Forms of Pleural Effusion
Parapneumonic effusion (effusion around an infection)
Uncomplicated vs complicated
Parapneumonic effusion (effusion around an infection)
Exudative, neutrophilic pleural fluid associated withpneumonia
Classification:
Uncomplicated
No bacterial invasion of thepleura
Will resolve with management of thepneumonia
Complicated
Bacterial invasion of thepleura
Bacteriaare rapidly cleared from thepleural space→ cultures are usually negative
parapleural effusion
Empyema
Empyema
Bacterial infection of thepleura
Pleural fluid will be thick, viscous, and opaque (pus)
Require surgical drainage with a thoracostomy or chest tube PLUS antibiotics
pulm effusion
special pulm effusion
Chylothorax
Chylothorax
Lymphatic fluid in the pleural cavity due to impaired drainage
Etiology:
Trauma
Surgery
Malignancy
Congenital anomalies
Pleural fluid
Cloudy and milky-appearing fluid
Exudate
High concentration of triglycerides and chylomicrons
Lymphocytic predominance
special pulm effusions
Hemothorax
Hemothorax
Accumulation of blood in the pleural cavity
Etiology:
Trauma
Malignancy
Coagulopathy
Connective tissue disease
Pleural fluid:
Frank blood (pleural fluid hematocrit > 50% peripheral hematocrit)
Exudate
pulm effusion
when is thoracentesis not required?
Thoracentesis not required:
Heart failure with symmetric pleural effusions and no chest pain or fever
Diuresis can be tried, and thoracentesis avoided unless effusions persist for≥3 days
