Introduction
Pulmonary edema (PE) is characterized by the accumulation of fluid in the parenchyma and air spaces of the lungs. Most often PE is associated with respiratory failure and impaired gas exchange. Globally, PE is known to be characterized by two major factors, the first is associated with the injury of the lung parenchyma which is termed as non-cardiogenic pulmonary edema. The second is associated with the failure of the left ventricle of the heart to release blood from the pulmonary circulation within the system and is termed as cardiogenic pulmonary edema (Glaus, Schellenberg , and Lang. 2010). The major cause of PE in most cases is heart failure and other cardiovascular diseases. Researchers and healthcare professionals have considered history of lung disease, vascular disorders, and a prior history of PE itself as major risk factors for PE. However, PE may also be caused due to high altitude exposure, illicit drug use, trauma, lung damage, drowning, and major injury. Based on current evidence, PE maybe caused due to pneumonia, kidney failure, hypertension, pancreatitis, sepsis, and r obstructed heart valves (Glaus, Schellenberg , and Lang. 2010).
Classification of pulmonary edema
Based on current evidence and the aetiology of PE, it is broadly classified as cardiogenic and non-cardiogenic PE (Alwi. 2010). (a) Cardiogenic: Caused to due increased in wedge pressure as a result of inefficient blood escape from the pulmonary circulation. Mainly due to fluid overload, ventricular failure, and arrhythmias (Alwi. 2010). It is also associated with hypertensive crisis and elevation of wedge pressure due to load on the left ventricle (Alwi. 2010). (b) Non-cardiogenic: It is mainly characterized by negative pulmonary pressure which is associated with upper airway obstruction. This phenomenon may cause the rupture of capillaries and alveoli. It is also known to be linked with acute respiratory distress syndrome. This type of PE is also caused by seizures and head trauma (Alwi. 2010).
Incidence and Prevalence
Based on current evidence, the prevalence of Negative-pressure pulmonary edema (NPPE) is nearly 0.1%. The incidence of NPPE is reported to be approximately 11%. Most patients who receive anaesthesia suffer from negative pressure pulmonary edema. Furthermore, only 1 in 1000 patients are known to suffer from PE globally. More than 500 thousand people die due to PE in the US with an estimated growth of 25% annually owing to increased CVD.
Pathophysiology: The pathophysiology of edema is mainly localized or systemic. In PE, edema can be due to impaired venous drainage or inflammation. The other aetiology for PE is characterized by the right heart failure or nephrotic syndrome. There are many forms of PE and the generalized form is known as anasarca. Based on the accumulation of fluid and transudate, there are 3 places where fluid can be accumulated: (a) Peritoneal cavity: ascites (b) Pleural cavity: hydrothorax and (c) Pericardial cavity: hydropericardium. Some of the common pathophysiological characteristics observed are pulmonary infections and hypersensitivity reactions, thickened alveolar walls (Figure 1), acute distention of capillaries (Figure 1), accumulation of fluid (transudate) in the alveolar lumen, distention of interstitial edema, and replacement of air with unwanted liquid. (Figure 2)
Epidemiology: More than 1/3rd of patients with status epilepticus are known to have NPE. Based on current evidence, more than 50% of patients with head injury, severe or blunt head impact have PE. Most patients who are reported to the emergency room with subarachnoid haemorrhage account for 71% of PE. Furthermore, PE is known to complicate conditions of intercerebral and subarachnoid haemorrhage. More than 60% of these patients would have recurrence of PE even after treatment due to individual factors (Chioncel. Et al. 2010).
Signs and Symptoms: PE is associated with breathlessness and fatigues. Some of the common symptoms of PE include excessive sweating, coughing blood, wheezing, abnormal heart rate, breathing difficulty, leg swelling, and decreased alertness (Alwi. 2010).Severe symptoms of PE may also include shock, organ death (due to lack of oxygen), and respiratory failure. Chronic symptoms of PE include sudden weight gain, shortness of breath, and difficulty in breathing accompanied with anxiety and tiredness (Alwi. 2010).
American College of Radiography (ACR) Recommendations: Based on the report and guidelines stated by the ACR, prevention and improved diagnosis are the forefront of PE treatment and management. The ACR recommends lung ultrasound and chest x-ray as first-line diagnostic modalities followed by computed topography (CT) for detailed assessment of the lung abnormalities. First-line treatment for PE includes artificial ventilation or breathing assistance followed by medications such as diuretics and anti-hypertensives. ACR does not promote the use of narcotics such as morphine for PE. (ACR, 2015).
Diagnosis (Imaging): The first-line of diagnosis for PE is chest x-ray which determines the presence of fluid accumulation or any other abnormalities which would exclude the existence of any other diseases. Pulse oximetry is a conventional method to assess the oxygen content of the blood. This would help in partial analysis of PE. Electrocardiogram (ECG). Is utilized to assess the function of heart through non-invasive means. Echocardiogram helps in the diagnosis of any health problems such as fluid accumulation, heart valve problems, congenital heart defects, and abnormal motions of ventricular walls.
Imaging modalities: Some of the most widely used diagnostic modalities for PE include chest radiography, lung ultrasound, and thoracic computed tomography (Cardinale, et al. 2014). All imaging modalities have been useful in the accurate and faster diagnosis of PE with minimal safety issues involved. Hydrostatic pulmonary edema is mainly diagnosed with the help of radiographic findings. Pulmonary congestion and vertical reverberation artefact (B-lines) in PE are rectified with lung ultrasound (Cardinale, et al. 2014).
Advantages/disadvantages of available imaging techniques: In comparison to lung ultrasound and chest radiography, the computed tomography (CT) has been associated with major disadvantages due to its high costs and minimal use in emergency situations. Most researchers also claim that CT has relevant high radiation exposure which may relate to safety issue for patients (Martindale, Noble, & Liteplo. 2013). Vascular opacity redistribution and interstitial edema may not be studied with the help of chest x-rays and may require lung ultrasound coupled with other radiographic examinations. This can be considered as a major disadvantage of chest x-rays for PE examination and diagnosis. (Martindale, Noble, & Liteplo. 2013). The major advantage of the lung ultrasound is that it detects B-lines. However, the low specificity of this modality is considered as a majoe disadvantage. However, a recent study identified that lung ultrasound is better than chest radiography for the diagnosis of PE (Martindale, Noble, & Liteplo. 2013).
Appearance of the pathology using various imaging techniques: Pulmonary edema with small pleural effusions can be identified with the help of chest x-ray (Figure 4[a]) (Sureka, Bansal, & Arora, 2015).Chest x-rays help in the assessment of various abnormalities within the lungs and heart. Researchers have also observed a unique bat or butterfly shaped edema in the lungs with the help of lung ultrasound. (Figure 4[c]) (Sureka, Bansal, & Arora, 2015). Lung ultrasound remains the most preferred and effective imaging modality for the diagnosis of PE. Computed tomography may also help in the assessment of PE by evaluating contrast images of eddema within the lungs. (Figure 4. [b]) (Sureka, Bansal, & Arora, 2015).
Treatment: aspiration (fluid is sucked from the lungs using a tube inserted down the throat) diuretics (medication used to remove fluid from the body), heart medications to control your pulse and relieve pressure, and surgery (opening the chest and removing the fluid). Some cases of pulmonary edema may need treatment with mechanical ventilation.
Prognosis: The treatment and management of PE is dependent on the severity and other individual factors of PE. Healthcare professionals recommended early treatment of PE to prevent complications and life-threatening situations. The condition is dependent on extrinsic and intrinsic factors that may influence the progression of the disease. In rare and severe cases, patients may also require artificial ventilation for breathing for an extended time. The management of PE is correlated with the cause of the disease. High altitude PE is not severe and can be managed with the help of medications. However, chronic conditions of PE should be treated efficiently and based on current evidence. PE can also be prevented if proper care is taken of the individual at risk of developing PE.
Conclusion
Pulmonary edema (PE) is characterized by the accumulation of fluid in the parenchyma and air spaces of the lungs. Most often PE is associated with respiratory failure and impaired gas exchange. (Alwi. 2010).Based on current evidence and the aetiology of PE, it is broadly classified as cardiogenic and non-cardiogenic PE (Figure 3). The non-cardiogenic PE is mainly characterized by negative pulmonary pressure which is associated with upper airway obstruction while cardiogenic PE is characterized by an increase in wedge pressure as a result of inefficient blood escape from the pulmonary circulation. (Figure 3). This paper provided an overview of pulmonary edema with respect to pathophysiology, epidemiology, diagnosis, and treatment modalities.
Future of disease research
Pulmonary edema remains one of the most prevailing respiratory disorders in the glob with majority of the cases in the US. Many new medications are under clinical trials for the management of PE. New novel drugs and formulations are in pipeline to improve the quality of life of patients with PE (Bajwa., & Kulshrestha. 2012).
Figure 1. Pathophysiology of Pulmonary Edema (Robbins and Cotran. 2015).
Figure 2. Pulmonary Edema (Magnified) (Robbins and Cotran. 2015).
Figure 3. Pathophysiology of Pulmonary Edema (Alwi. 2010).
(a) (b) (c)
(a) Pulmonary edema with small pleural effusions (both sides)
(b) Pulmonary edema on CT-scan (coronal MPR)
(c) Bat's wings of pulmonary oedema
Figure 4. Imaging modalities of PE by different imaging modalities (Sureka, Bansal, & Arora, 2015).
Figure 5. Normal Lung versus PE lung (Cardiogenic and non-cardiogenic) (Sureka, Bansal, & Arora, 2015).
References
Alwi I. (2010). Diagnosis and management of cardiogenic pulmonary edema. Acta Med
Indones. 2010 Jul;42(3):176-84.
ACR Manual on contrast. (2015). American Collgee of Radiography. Pdf file. Available at:
http://www.acr.org/~/media/37D84428BF1D4E1B9A3A2918DA9E27A3.pdf
Bajwa, S. S., & Kulshrestha, A. (2012). Diagnosis, Prevention and Management of
Postoperative Pulmonary Edema. Annals of Medical and Health Sciences Research, 2(2), 180–185. http://doi.org/10.4103/2141-9248.105668
Cardinale, L., Priola, A. M., Moretti, F., & Volpicelli, G. (2014). Effectiveness of chest
radiography, lung ultrasound and thoracic computed tomography in the diagnosis of congestive heart failure. World Journal of Radiology, 6(6), 230–237. http://doi.org/10.4329/wjr.v6.i6.230
Chioncel O, et al. (2010). Epidemiology, pathophysiology, and in-hospital management of
pulmonary edema: data from the Romanian Acute Heart Failure Syndromes registry. J Cardiovasc Med (Hagerstown). 2016 Feb;17(2):92-104.
Glaus T, Schellenberg S, Lang J. (2010). [Cardiogenic and non-cardiogenic pulmonary
edema: pathomechanisms and causes]. Schweiz Arch Tierheilkd. 2010 Jul;152(7):311-7. doi: 10.1024/0036-7281/a000073.
Martindale JL, Noble VE, Liteplo A. (2013). Diagnosing pulmonary edema: lung ultrasound
versus chest radiography. Eur J Emerg Med. 2013 Oct;20(5):356-60. doi: 10.1097/MEJ.0b013e32835c2b88.
Robbins and Cotran. (2015). Atlas of Pathology. Pulmonary pathology. Edema. 3E. Pdf file.
Available at: http://www.pathologyatlas.ro/pulmonary-edema-pathology.php
Sureka, B., Bansal, K., & Arora, A. (2015). Pulmonary edema − cardiogenic or
noncardiogenic? Journal of Family Medicine and Primary Care, 4(2), 290. http://doi.org/10.4103/2249-4863.154684
