Residence in or travel to an area with local transmission of COVID-19, or close contact with a suspected or confirmed case in the 14 days prior to symptom onset.
May be difficult to distinguish clinically from bacterial pneumonia. In addition to fever, cough, and dyspnea, other common presenting symptoms include sore throat, myalgia, fatigue, and altered sense of taste and/or smell.
Patients with respiratory distress may have tachycardia, tachypnea, or cyanosis accompanying hypoxia.
Many patients with COVID-19 pneumonia meet the criteria for ARDS, but there is uncertainty about whether severe COVID-19 pneumonia is a distinct phenotype of ARDS.
Real-time reverse transcription polymerase chain reaction: positive for SARS-CoV-2 RNA.
It is not possible to differentiate COVID-19 from other causes of pneumonia on chest imaging.
A history of cardiac disease, acute myocardial ischemia or infarction, or a known low ejection fraction suggests cardiogenic pulmonary edema, as do an S3 and elevated neck veins on physical examination.
Heart failure is suggested on chest x-ray by an enlarged cardiac silhouette, a vascular pedicle width >70 mm, central infiltrates, and Kerley B lines.
Brain natriuretic peptide levels >500 picograms/mL also suggest cardiogenic edema.
An echocardiogram and measurement of the pulmonary artery occlusion pressure may be needed if the history and physical and lab tests do not rule out cardiogenic pulmonary edema.
A history of fever and cough with or without sputum production.
Patients may have pleuritic chest discomfort.
Severe pneumonia with bilateral infiltrates on chest x-ray meets the radiographic criteria for ARDS.
If patients do not have severe hypoxemia with their pneumonia (PaO₂/FiO₂ ≤300 or SpO₂/FiO₂ ≤315), they do not have ARDS.
Onset is usually subacute, over days to weeks.
Patients are previously healthy, with no related systemic illness.
Some authors have termed this disease idiopathic ARDS.
Meets all the clinical criteria for ARDS.
Best differentiated by history.
Associated with bleeding from the small vessels of the airways (capillaritis) and seen in many conditions, ranging from autoimmune to mitral valve diseases.
Almost always a reversible form of respiratory failure, once the underlying cause is known.
A syndrome of hypoxia with infiltrates on chest x-ray.
The hallmark is finding sequentially bloodier aliquots of fluid during serial bronchoalveolar lavage.
Serologic tests to look for autoimmune diseases may help differentiate it from ARDS.
Presents as a mild to severe pneumonia in previously healthy people.
Patients have an excellent response to intravenous corticosteroids.
The hallmark of this disease is increased numbers of eosinophils (upward of 50%) on bronchoalveolar lavage.
A pneumonitis after inhalation of an organic antigen.
Patients present with infiltrates and a pneumonia-like syndrome that is clinically indistinguishable from ARDS if severe.
Differentiated from ARDS by clinical history of an inhalational allergen, usually of avian origin.
Corticosteroids may be beneficial.
No differentiating investigations.
Acute pulmonary edema after removal of an upper airway obstruction, most commonly caused by laryngospasm.
Causes an acute respiratory failure often requiring mechanical ventilation with varying levels of positive end-expiratory pressure.
The keys to differentiation are the history of upper airway obstruction, postsurgical development, and the rapid resolution of symptoms.
No differentiating investigations.
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