What Causes Pulmonary Edema?

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Patient Presentation
A 9-month-old, previously healthy, male came to clinic for followup 2 days after being discharged from the pediatric intensive care unit (PICU). He had been diagnosed with croup as an outpatient in clinic and started on dexamethasone. That night he worsened and was taken to the emergency room and was admitted to the PICU because of respiratory distress. His physical examination at admission had a respiratory rate of 64 breaths/minutes, heart rate of 110 beats/minute, normal blood pressure and temperature and an oxygen saturation of 86-88% on room air. His weight was decreased by 560 grams from a recent previous weight. His capillary refill was 2-3 seconds and his lips were slightly dry. He had marked tracheal tugging, nasal flaring, intercostal retractions and abdominal breathing. He was not cyanotic. He had coughing and stridor. HEENT had rhinorrhea. Lungs had rales but no rhonchi. The laboratory evaluation had a respiratory swab that was positive for parainfluenza virus, a blood gas with hypoxemia and no hypercapnia, and a chest radiograph with diffuse interstitial markings.

The diagnosis of acute respiratory distress with pulmonary edema due to parainfluenza virus was made. Over the next 2 days the patient’s clinical course showed that he did not require mechanical ventilation but did require continuous positive airway pressure and supplemental oxygen up to 40%. He was slowly weaned off support and was transferred to the floor where he continued to receive intravenous fluids until he was able to maintain his hydration. He was discharged after 4 days.

The pertinent physical exam today showed a wary infant with normal vital signs and oxygen saturation of 94-97%. Weight was back to normal.
He had rhinorrhea and no stridor but did have a hoarse cry. His lungs had no adventitial breath sounds. The patient’s clinical course showed that he had been improving since discharge, and had no obvious respiratory or hydration problems at the time. He was also scheduled to follow-up with pulmonary medicine in 2 weeks.

Discussion
Pulmonary edema is a potentially life threatening condition due to accumulation of excess fluid in the alveolar spaces and walls of the lung.
Patients show increased respiratory effort or distress (e.g. tachypnea, dyspnea or difficulty talking, use of excessory muscles, nasal flaring, tracheal tugging, etc.) and clinicians should beware signs of tiring (e.g. bradypnea and decreased effort) as the patient may be failing. Patients may have rales or rhonchi on pulmonary examination, and pallor or color changes may be noted. Blood gas analysis shows evidence of hypoxemia and often hypercapnia depending on the severity and underlying cause.

As with most diseases and problems, treating the underlying cause is fundamental. In addition, ventilatory management (including potential ventilatory pressure) to maintain adequate gas exchange is key. Providing supplemental oxygen is primary for most situations. Newborns with ductal dependent lesions, and hyperoxia-induced pulmonary vasodilatation would be a two of exceptions. Oxygen should be administered in the least invasive and comfortable manner that supplies the necessary oxygen. Other methods to potentially improve gas exchange can include emptying the stomach or elevating the head of the bed or placing the patient in another position (e.g. prone).

An overview of croup can be found here.

Learning Point
Pulmonary edema is usually divided into two types: cardiogenic pulmonary edema, or non-cardiogenic pulmonary edema. Cardiogenic pulmonary edema is due to increased hypostatic pressure in the pulmonary circulation. Noncardiogenic pulmonary edema is caused by some type of lung injury which causes increased pulmonary vascular permeability with resultant increase in pulmonary vascular permeability and accumulating fluid.

Causes of pulmonary edema include:

  • Acute respiratory distress syndrome (ARDS) is a common reason for pulmonary edema and “is a rapidly progressive noncardiogenic pulmonary edema that initially manifests as dyspnea, tachypnea and hypoxemia, and then quickly evolves into respiratory failure.”
    A diagnosis of ARDS in pediatric patients:

    • Occurs within 7 days of insult
    • The respiratory failure is not fully explained by cardiac failure or fluid overload
    • New pulmonary infiltrates consistent with parenchymal disease
    • Specific oxygenation levels need to be required depending on if the patient is mechanically ventilated and if there is other concomitant problems such as chronic lung disease, or heart disease (e.g. cyanotic congenital heart disease or left ventricular dysfunction).
  • Cardiac
    • Congenital heart disease
    • Congestive heart disease/ Left ventricular failure
    • Pulmonary venous obstruction
  • Infection
    • Pneumonia
    • Croup
    • Epiglottitis
  • Pulmonary
    • Airway obstruction
    • Reexpansion after pneumothorax, effusion, atelectesis, tumor, surgery, etc.
      Reexpansion pulmonary edema is not very common but occurs after rapid reexpansion of the lung after a few days of collapse.
  • Trauma
    • Burns
    • Chest
    • Inhalation
    • Neurogenic due to increased intracranial pressure. Neurogenic pulmonary edema can be hard to differentiate from cardiogenic pulmonary edema.
      The pathophysiology is not well understood but is thought to begin with increased intracranial pressure leading to increased catecholamines and sympathetic storm, which then leads to systemic vasoconstriction and accumulating blood in the pulmonary system. Increased blood leads to pulmonary hypertension, increased capillary permeability and thereby pulmonary edema.
    • Single or multiple organ system
  • Miscellaneous
    • Acute mountain sickness
    • Heroin overdose
    • Transfusion reaction
    • Perinatal lung disease

Questions for Further Discussion
1. What are causes of respiratory failure? A review can be found here
2. What are indications for using dexamethasone? A review can be found here
3. What are normal blood gas values?
4. What is the difference between stridor and stertor? A review can be found here

Related Cases

To Learn More
To view pediatric review articles on this topic from the past year check PubMed.

Evidence-based medicine information on this topic can be found at SearchingPediatrics.com and the Cochrane Database of Systematic Reviews.

Information prescriptions for patients can be found at MedlinePlus for these topics: Throat Disorders and Lung Diseases.

To view current news articles on this topic check Google News.

To view images related to this topic check Google Images.

To view videos related to this topic check YouTube Videos.

Kira S. Reexpansion pulmonary edema: review of pediatric cases. Paediatr Anaesth. 2014;24(3):249-256. doi:10.1111/pan.12283

Khemani RG, Smith LS, Zimmerman JJ, Erickson S, Group for the PALICC. Pediatric Acute Respiratory Distress Syndrome: Definition, Incidence, and Epidemiology: Proceedings From the Pediatric Acute Lung Injury Consensus Conference. Pediatr Crit Care Med. 2015;16(5_suppl):S23. doi:10.1097/PCC.0000000000000432

Hirsch AW, Nagler J. Reexpansion Pulmonary Edema in Pediatrics. Pediatr Emerg Care. 2018;34(3):216-220. doi:10.1097/PEC.0000000000001435

Simma L, Neuhaus TJ. Common diagnosis at an unusual age – pulmonary oedema in a toddler. BMJ Case Rep. Published online October 21, 2018:bcr-2018-225389. doi:10.1136/bcr-2018-225389

Saguil A, Fargo MV. Acute Respiratory Distress Syndrome: Diagnosis and Management. Am Fam Physician. 2020;101(12):730-738.

Lo-Cao E, Hall S, Parsell R, Dandie G, Fahlström A. Neurogenic pulmonary edema. Am J Emerg Med. 2021;45:678.e3-678.e5. doi:10.1016/j.ajem.2020.11.052

Saguil A, Fargo MV. Acute Respiratory Distress Syndrome: Diagnosis and Management. Am Fam Physician. 2020;101(12):730-738.

Malek R, Soufi S. Pulmonary Edema. In: StatPearls. StatPearls Publishing; 2022. Accessed February 6, 2023. http://www.ncbi.nlm.nih.gov/books/NBK557611/

Author
Donna M. D’Alessandro, MD
Professor of Pediatrics, University of Iowa

Published