Acute Respiratory Distress Syndrome
last authored: July 2011, David LaPierre
last reviewed:
Introduction
Acute Respiratory Distress Syndrome (ARDS) is characterized by abrupt, diffuse lung injury leading to severe hypoxia and pulmonary infiltration across lung fields.
Also known as shock lung or wet lung, it is the most severe type of acute lung injury.
ARDS affects approximately 40-75 people/100,000 anually.
The Case of Henry P.
Henry is a 48 year-old man who is admitted to the hospital with pneumonia. Three hours later, his shortness of breath becomes significantly worse, to the point he is unable to talk.
- how would you diagnose ARDS?
- what might be causing it?
- how do you treat Henry?
Causes and Risk Factors
ARDS has many causes:
- lung infection (most common)
- sepsis and other causes of shock
- gastric aspiration
- lung contusion
- trauma and injury: fractures and fat emboli, burns, radiation
- oxygen toxicity
- smoke inhalation
- heroin/methodone overdose
- ASA
- barabiturates
- paraquat
- multiple blood transfusions
- near drowning
- disseminated intravascular coagulation
- pancreatitis
- uremia
- cardiopulmonary bypass
- hypersensitivitry reactions
- idiopathic ARDS (also known as acute interstitial pneumonia)
- eclampsia
Pathophysiology
ARDS results from diffuse alveolar capillary damage. During the first phase, alveolar flooding with protein-rich exudate leads to loss of diffusion capacity and profound hypoxia. The infiltate also contains inflammatory cells, leading to diffuse alveolar damage. Type I cells are destroyed, and the basement membrane lies naked.
During the second, organizing phase, over the next 3-10 days, fibrosing alveolitis involves alveolar collapse, fibroblast proliferation, and formation of hyaline membranes. This leads to continued hypoxia, decreased compliance, and increased dead space. Diffuse tissue destruction is not easily repaired, and fibrotic scarring results.
Molecular mediators of ARDS include:
- IL-1 and TNF, which recruit neutrophils and lead to transcription of NF-kB-mediated genes
- complement and coagulation pathways
- platelet-activating factor
- free radicals
- lipoxygenase pathways
- proteases
- nitric oxide
- endotoxin
- cyclooxygenase pathways
Resolution may take 6-12 months.
Signs and Symptoms
- history
- physical exam
History
ARDS is characterized by the rapid onset of severe, life-threatening respiratory insufficiency (dyspnea and tachypnea).
History should focus on the precipitating event.
A history of heart disease is rare.
Physical Exam
The patient may be lethargic, with decreased level of consciousness.
Skin may be moist and cyanotic.
Tachypnea and tachycardia may be present.
Pulses are hyperdynamic.
In keeping with an absence of heart failure, JVP is not normally elevated, and edema is normally absent.
Investigations
- lab investigations
- diagnostic imaging
Lab Investigations
Initial investigations should include:
- arterial blood gases showing severe arterial hypoxemia and decreased PaO2, with a PaO2/FiO2 ratio less than 200, refractory to oxygen therapy.
Follow-up labs should focus on:
- ABGs
- multisystem failure: CBC, electrolytes, liver enzymes, renal function tests
Diagnostic Imaging
ECG can shouw sinus tachycardia, as well as non-specific ST-T wave changes.
Chest radiographs are intially normal but soon show diffuse alveolar infiltration and bilateral opacities. As this can mimic heart failure, clinical correlates are also required for diagnosis. Specific findings include:
- normal heart size
- small lung volumes
- bilateral haziness (ground glass appearance)
- air bronchograms: bronchi are visible outside the heart shadow due to consolidation
Pulmonary arterial wedge pressure (surrogate for left atrial pressure) is <18 mmHg, suggesting no clinical evidence of left heart failure.
Chest CT can reveal diffuse, bilateral infiltrate and bullae.
Differential Diagnosis
The differential diagnosis of ARDS includes other causes of respiratory distress and failure, listed here.
Treatments
Patients with ARDS are normally cared for in the ICU.
Initial stabilization should focus on oxygenation and fluid status, with monitoring of blood pressure, heart rate, and oxygen saturation.
The underlying cause is addressed as quickly as possible. The patient may benefit from the prone position (why?)
Mechanical ventilation via intubation is frequently required. Lower tidal volumes are used, with positive end expiratory pressure (PEEP) to keep the airways open.
Fluid recuscitation should be used to attempt to restore perfusion while avoiding fluid overload. Crystalloids are most frequently used, though packed RBCs can be added to increase oxygenation. Monitor metabolic acid-base function and renal function to assess perfusion. If fluid recuscitation is unsuccessful, inotropic support can be given, including inotropic drugs such as dopamine or dobutamine to maintain cardiac output, as well as vasopressor drugs such as phenylephrine or norepinephrine.
Treatments that have unclear benefit include:
- corticosteroids
- antioxidants
- pulmonary surfactant
- activated protein C
Once stable, daily labs and chext imaging should be carried out. A Swan-Ganz catheter can assist in monitoring oxygen delivery.
Ongoing care includes:
- adequate sedation during ventilation
- DVT prophylaxis
- GI prophylaxis, with suctioning
- skin, eye, and mouth care
- nutritional support
Consequences and Course
Depending on care available, mortality rate is 40-60%.
Complications can include:
- respiratory acidosis
- oxygen toxicity
- mechanical trauma from ventilator
- superinfection
- multiple organ failure
- death
- permanent lung disease: dyspnea, cough
Resources and References
www.ARDS.net.org
Cataletto M. Respiratory Distress Syndrome, Acute. In: 5-Minute Clincal Consult, 2011. Ed: Domino FJ.
Piantadosi CA and Schwartz DA. 2004. The acute respiratory distress syndrome. Ann Intern Med 141:460-70.
Wheeler AP, Bernard GR. 2007. Acute lung injury and the acute respiratory distress syndrome, a clinical review. Lancet. 369:1553-64.
Topic Development
authors:
reviewers:
 |