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Acute Respiratory Distress Syndrome

Notes

Acute Respiratory Distress Syndrome

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Overview

Acute respiratory distress syndrome (ARDS) occurs when the alveoli fill with fluid, which impairs gas exchange.

Characterized by acute dyspnea, hypoxemia, and pulmonary infiltrates.

Can lead to reduced lung compliance, increased pulmonary dead space, increased risk of pneumothorax, and pulmonary hypertension.

ARDS has a mortality rate of approximately 40%.

Treatment for acute respiratory distress syndrome requires treatment of the underlying causes.

Mechanical ventilation restores airflow, but beware of potential complications, including: volutrauma (overdistention of the alveoli), alectectrauma (alveolar strain from repeated opening and closing), and, biotrauma (from migration of pro-inflammatory molecules and pathogens).

Treatment includes fluid management measures, such as diuretics, to reduce left atrial filling pressure; some also recommend the use of neuromuscular blockades.

Newborn respiratory distress syndrome (aka, infant respiratory distress syndrome, respiratory distress syndrome of the newborn) occurs when there is inadequate production of surfactant by premature lungs, leading to alveolar collapse; thus, treatment includes administration of synthetic surfactant and oxygen support. The risk of neonatal respiratory distress correlates with the degree of prematurity.

Pathophysiology

Exudative Phase: The initial response to injury, and occurs within the first 7 days after exposure.

To illustrate the early steps of this phase, we draw an alveolus with Type I alveolar epithelial cells, which are the sites of gas exchange, and, Type II alveolar epithelial cells, which secrete and recycle surfactant and are progenitors of Type I epithelial cells.

We draw a pulmonary capillary in close proximity.

Inflammation damages the capillary endothelium and alveolar epithelium, and increases the permeability of these layers. We show neutrophils and their pro-inflammatory cytokines, but be aware that other cells of the innate immune system also play a role in barrier injury.

Next, we re-draw the alveolus and capillary and show the breaks in their protective layers.

Protein-rich fluid, activated neutrophils, and other pro-inflammatory mediators and cellular debris pass through the barrier and fill the alveolus.

These infiltrating proinflammatory mediators damage the epithelial lining of the alveolus, leaving the basement membrane "denuded."

Furthermore, due to the loss of alveolar epithelial cells, surfactant production and fluid resorption is inhibited, which compounds fluid retention.

Hyaline membranes from along the denuded basement membranes; these are formed by accumulating cellular debris and fibrin.

The coagulation cascade is triggered by capillary endothelial damage, which leads to the formation of microthrombi in the vessels.

As a result of these pathological processes, gas exchange is inhibited, dead space is increased, pulmonary hypertension occurs, and lung compliance decreases.

Proliferative Phase: barrier repair and fluid resorption and occurs days 7-21 after exposure to pulmonary injury.

The alveolar epithelium and capillary endothelium barriers are re-established.
Thus, surfactant production and fluid reabsorption resume.
Epithelium sodium channels and aquaporins are inserted in the alveolar epithelium, and move fluids to the interstitium.

Macrophages and lymphocytes remove apoptotic and inflammatory mediators, thus reducing further harm to the epithelia.

As part of the healing and rebuilding process, fibroblasts and other interstitial cells proliferate to form a provisional extracellular matrix, which will eventually be removed by matrix metalloproteinases.

However, in some individuals, pro-inflammatory and fibrotic forces overwhelm the healing and clearance process.

Fibrotic Phase: Fibrosis
Extensive epithelial damage trigger over-proliferation and differentiation of fibroblasts and deposition of collagen, which leads to tissue fibrosis and destruction of the microvasculature.
Thus, pulmonary dysfunction continues.

Causes of ARDs

Direct and indirect causes of lung injury lead to acute respiratory distress.

The most common causes are pneumonia (direct) and sepsis (indirect)
– Account for more than half of all ARDS cases.

Additional Direct Causes:
– Aspiration of gastric contents
– Pulmonary contusion
– Near drowning
– Vaping.

Be aware that lung injury caused by vaping is sometimes called "EVALI" – "E-cigarette or Vaping Associated Lung Injury", and is particularly associated with vaping fluids containing Vitamin E acetate (Vitamin E acetate is used in THC vaping products).

Additional Indirect Causes:
– Trauma
– Repeated blood transfusion
– Pancreatitis
– Drug reactions or overdoses (ex: various narcotics, aspirin, tricyclic antidepressants).

Berlin Definition of Acute Respiratory Distress Syndrome

Establishes diagnostic criteria.

Onset of signs and symptoms must be within the last 7 days of known clinical insult, with new or worsening symptoms during the last week.

Chest X-ray or CT will show bilateral opacities consistent with pulmonary edema.

Respiratory failure cannot be otherwise fully explained by cardiac failure or fluid overload.

Presence of acute hypoxemia.
– Based on the ratio of the partial pressure of arterial oxygen (PaO2) to the fraction of inspired oxygen (FiO2) (assessed while the patient is on a ventilator with a positive-end expiratory pressure (PEEP) of 5 or greater cm H2O).
– Hypoxemia severity can be categorized as mild (201-300 mmHg); moderate (101-200 mmHg), or severe (100 mmHg or less).

Board Review

ARDS

Getting ready for boards? Review these concise, bulleted high yield reviews for your exam.

USMLE & COMLEX-USA

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Physician Assistant (PA)

Internal Medicine (ABIM)

References

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