ARDS 

Case:

            45 y.o. white female with a PMH of mycoses fungoides (cutaneous T-cell lymphoma) s/p autologous BMT (complicated by thrombocytopenia) 39 days prior to admission.  Pt presented to ER with persistent epistaxis on day #38 s/p BMT, and was admitted to the hospital.  The next morning, the patient was found to be tachypneic and cyanotic.  Pulse ox showed 02 sats of 35-40%.  Pt was placed on 100% O2 non-rebreather facemask before transfer to MICU.  PT has no h/o pulmonary disease, and respiratory status was normal the day before.  PT subsequently was intubated for hypoxemic respiratory failure. 

Radiological findings: 

            CXR (11/20) -- day of transfer -- diffuse bilateral alveolar infiltrates, air bronchograms, Costophrenic angles delineated, L heart border not seen, R heart border visible, not well delineated, difficult to assess heart size.

            CXR (11/20) -- post intubation -- diffuse, bilateral infiltrates, air bronchograms, no visible heart, no diaphragmatic border, ET tube 5 cm from carina (3-5 cm = well positioned).

            CXR  (11/24) -- marked improvement -- bilateral infiltrates, R heart border, R diaphragm better defined than 11/20, L heart border and L diaphragm not well visualized, ET tube 5-6 cm from carina. 

Definition of ARDS:

ARDS (acute respiratory distress syndrome) refers to the severe end of the spectrum of “acute lung injury”. 

Acute lung injury is characterized by three clinical features: 

-Widespread, bilateral radiographic infiltrates 

-A ratio of partial pressure of arterial oxygen to the fraction of inspired oxygen (PaO2/FiO2) less than or equal to 300 mm Hg. 

-No clinical evidence for an elevated left atrial pressure.  Pulmonary capillary wedge pressure of 18 mm Hg or less.  

For a diagnosis of ARDS to be made, the second criteria above requires a PaO2 to FiO2

ratio of 200 mm Hg or less. 

Etiology: (to date, more than 60 causes of ARDS have been identified.)

-Sepsis (most common)

-Aspiration of gastric contents

-Infectious pneumonia

-Trauma

-Near-drowning

-Massive/multiple blood transfusions

-Drugs

-Lung and bone marrow transplantation

-Head injury

-Lung contusion

Multiple other causes as well 

Pathophysiology:

            Clinical signs and symptoms of ARDS occurs primarily as a result of inflammatory injury to the alveoli causing diffuse alveolar damage.  Pro-inflammatory cytokines and neutrophils accumulate in the lungs in response to a variety of precipitants.  Eventually the capillary endothelium and alveolar epithelium are damaged, resulting in an accumulation of bloody, proteinaceous edematous fluid in the alveoli. This causes impaired gas exchange, impaired lung compliance, and pulmonary hypertension. 

Classic Clinical Presentation:

Initially, the patient will present with clinical features that reflect the precipitant of ARDS.  For example, if sepsis is the cause of ARDS, the patient may appear febrile and hypotensive.  As the patient’s disease progresses to include ARDS, usually this is marked by severe hypoxia, dyspnea, tachypnea, stiff lungs, and diffuse radiographic infiltrates.  Pulmonary dysfunction typically develops within 24 to 48 hours.  Patients can also complain of chest pain and a dry cough.  Mechanical ventilation is almost always required. Physical exam may reveal tachycardia, trachypnea, diffuse rales, rhonchi, and wheezes. ABG usually show an acute respiratory alkalosis, an elevated alveolar-arterial oxygen gradient, and severe hypoxemia reflecting a right to left shunt. 

Radiographic findings: 

The chest X-ray usually shows diffuse, fluffy alveolar infiltrates in all lung zones with prominent air bronchograms.  Although this finding is sometimes seen in patients without ARDS.  For instance, patients with CHF may have similar chest X-ray findings.  ARDS is favored over CHF when there is an absence of radiographic findings that are characteristic of CHF, such as cardiomegally, pulmonary venous congestion, and Kerley B lines.  To be sure that the patient’s symptoms are from ARDS and not CHF, one can check the pressure of the left side of the heart by measuring the pulmonary wedge pressure.  A left ventricular pressure of less than 18 would suggest that the pulmonary edema is not do to a back-up of blood from the left heart causing orthostatic pulmonary edema.  By the same token, an elevated wedge pressure does not exclude the possibility of ARDS, because it is estimated that 20% of patients with ARDS have concomitant left ventricular dysfunction. 

Complications:

Complications of ARDS are usually from mechanical ventilation and include:

pneumothorax, subcutaneous emphysema, pneumomediastinum, interstitial emphysema, and air embolism.   

Prognosis:

Mortality 35-40%, with most patients dying of from the underlying cause of ARDS.

Long term survivors of ARDS often show only mild abnormalities in pulmonary function and are usually asymptomatic.