2 |
4 PREVENTION |
Upper airway obstruction (negative pressure pulmonary edema[5] )
Neurogenic causes[6] (seizures, head trauma, strangulation, electrocution).
2.3Other/unknown
Injury to the lung may also cause pulmonary oedema through injury to the vasculature and parenchyma of the lung. The acute lung injury-acute respiratory distress syndrome (ALI-ARDS) covers many of these causes, but they may include:
Inhalation of hot or toxic gases
Pulmonary contusion, i.e., high-energy trauma (e.g. X-Ray showing pulmonary oedema vehicle accidents)
Aspiration, e.g., gastric fluid
Reexpansion, i.e. post large volume
thoracocentesis, resolution |
of |
pneumothorax, |
post decortication, removal |
of |
endobronchial |
obstruction, e ectively a form of negative pressure pulmonary oedema.
Reperfusion injury, i.e. postpulmonary thromboendartectomy or lung transplantation
Immersion pulmonary edema[7][8]
Multiple blood transfusions
Severe infection or inflammation which may be local or systemic. This is the classical form of ALI- ARDS.
There are also a range of causes of pulmonary edema which are less well characterised and arguably represent specific instances of the broader classifications above.
Arteriovenous malformation
Hantavirus pulmonary syndrome
High altitude pulmonary edema (HAPE), probably a manifestation of neurogenic pulmonary edema[9][10]
Envenomation, such as with the venom of Atrax robustus[11]
Flash pulmonary edema
Swimming induced pulmonary edema
3 Diagnosis
There is no one single test for confirming that breathlessness is caused by pulmonary edema; indeed, in many cases, the cause of shortness of breath is probably multifactorial.
Low oxygen saturation and disturbed arterial blood gas readings support the proposed diagnosis by suggesting a pulmonary shunt. Chest X-ray will show fluid in the alveolar walls, Kerley B lines, increased vascular shadowing in a classical batwing peri-hilum pattern, upper lobe diversion (increased blood flow to the superior parts of the lung), and possibly pleural e usions. In contrast, patchy alveolar infiltrates are more typically associated with noncardiogenic edema[2]
Especially in the case of cardiogenic pulmonary edema, urgent echocardiography may strengthen the diagnosis by demonstrating impaired left ventricular function, high central venous pressures and high pulmonary artery pressures.
Blood tests are performed for electrolytes (sodium, potassium) and markers of renal function (creatinine, urea). Liver enzymes, inflammatory markers (usually C-reactive protein) and a complete blood count as well as coagulation studies (PT, aPTT) are also typically requested. B-type natriuretic peptide (BNP) is available in many hospitals, sometimes even as a point-of-care test. Low levels of BNP (<100 pg/ml) suggest a cardiac cause is unlikely.[2]
4 Prevention
In those with underlying heart disease, e ective control of congestive symptoms prevents pulmonary edema.