Pulmonary Edema

Overview

Definition

Pulmonary edema is the accumulation of excess fluid within the lung parenchyma and alveoli.

Epidemiology

• Approximately 80,000 cases per 100,000 people with congestive heart failure
• Men > women
• More often seen in the elderly or critically ill

Etiology

Pulmonary edema is classified based on the underlying etiology.

• Cardiogenic pulmonary edema:
  • Decompensated congestive heart failure:
    • Dietary indiscretion
    • Medication noncompliance
    • Worsening cardiac function
  • Acute coronary syndrome (ACS)
  • Hypertensive emergency
  • Arrhythmia
  • Acute mechanical cause (e.g., valvular disorder)
• Noncardiogenic pulmonary edema:
  • ARDS
  • Transfusion-related acute lung injury (TRALI)
  • Fluid overload related to renal failure
  • High-altitude exposure
  • Severe infection
  • Inhalation injury
  • Aspiration
  • Near drowning
  • Anaphylaxis
  • Lung reexpansion (e.g., after large-volume thoracentesis)
  • Medications and drugs
  • Neurogenic
    • Epileptic seizures
    • Traumatic brain injury
    • Intracranial hemorrhage

Pathophysiology

Starling forces

Starling forces explain how fluid moves from the blood into extravascular spaces, which leads to pulmonary edema. 

• Hydrostatic pressure:
  • Capillary hydrostatic pressure pushes fluid out of the capillary.
  • Interstitial hydrostatic pressure pushes fluid into the capillary.
• Oncotic pressure:
  • Plasma colloid osmotic pressure pulls fluid into the capillary.
  • Interstitial fluid colloid osmotic pressure pulls fluid out of the capillary.

Cardiogenic pulmonary edema

• Poor cardiac output → ↑ atrial pressure
• ↑ Pulmonary venous pressure
• ↑ Pulmonary capillary pressure
• Fluid moves into the interstitial spaces.
• ↑ Pressure in the interstitial spaces
• Fluid moves into the alveoli.
• ↓ Oxygen diffusion capacity → hypoxia and symptoms

Noncardiogenic pulmonary edema

Depending on the etiology, the cause of noncardiogenic pulmonary edema may be due to any of the following:

• ↑ Permeability of pulmonary capillaries
• ↑ Pulmonary vascular pressure
• Imbalance between hydrostatic and oncotic pressure

Clinical Presentation

Symptoms

• Increasing dyspnea (particularly with exertion)
• Respiratory distress
• Orthopnea
• Paroxysmal nocturnal dyspnea
• Cough:
  • Nonproductive
  • Frothy sputum
  • Blood tinged

Physical exam

Common findings for pulmonary edema:

• Tachypnea
• Tachycardia
• Hypoxia
• Crackles

Findings suggestive of a cardiogenic cause:

• Jugular venous distension
• Cardiac gallop
• Hepatojugular reflux
• Diaphoresis
• Lower extremity edema
• Weight gain

Diagnosis

Chest X-ray

The presence of pulmonary edema can be quickly seen on a chest X-ray. Subtle differences may be present depending on the etiology.

Cardiogenic pulmonary edema:

• Distribution of opacities: 
  • Perihilar (batwing appearance)
  • Diffuse (central and peripheral)
• Lung volume may be ↓
• Associated findings:
  • Prominent vessels; particularly in the upper chest (cephalization)
  • Kerley B lines:
    • Thin, linear pulmonary opacities near the chest wall 
    • Caused by interstitial edema and ↑ lymphatic drainage
  • Cardiomegaly
  • Pleural effusions

Noncardiogenic pulmonary edema:

• Distribution of opacities can vary:
  • Generally more peripheral
  • Batwing appearance may also be seen.
• Air bronchograms may be present.
• Normal or ↑ lung volume
• No cardiomegaly

Supporting workup

Tests can be used to determine the underlying etiology and to rule out a cardiac cause.

Laboratory evaluation:

• ↑ Troponin → ACS
• ↑ Creatinine → renal failure
• ↑ WBC → possible sepsis or pneumonia
• BNP is usually:
  • Normal in noncardiogenic pulmonary edema
  • ↑ In heart failure

Imaging:

• ECG:
  • ST-segment changes → ACS
  • Cardiac arrhythmia
• Echocardiogram:
  • Evaluate the left ventricular ejection fraction (LVEF) → ↓ in left heart failure
  • Assess for other cardiac abnormalities:
    • Cardiac tamponade
    • Valvular disease
    • Wall motion abnormalities → often seen in ACS

Management

Management of acute pulmonary edema is focused on counteracting the compromised physiologic mechanisms and treating the underlying cause.

• Always assess the patient’s airway, breathing, and circulation on arrival.
• Sit the patient up:
  • If hemodynamically stable
  • May provide some improvement in symptoms
• Provide oxygen support:
  • Nasal cannula for mild and uncomplicated hypoxia
  • Face mask for more moderate hypoxia
  • Noninvasive positive pressure ventilation for more severe hypoxia or increased effort to breathe:
    • ↑ Lung recruitment to improve gas exchange
    • Positive pressure to open the alveoli and prevent collapse due to fluid
    • Options: continuous positive airway pressure (CPAP) or bilevel positive airway pressure (BiPAP)
  • Mechanically ventilate those who fail the above options, are obtunded, or are in severe respiratory failure.
• Nitroglycerin:
  • Use in cardiogenic pulmonary edema for preload reduction.
  • Dilates blood vessels which ↓ pressure on the lungs
  • Monitor for hypotension.
• Diuretics:
  • ↑ Urination (removes fluid from the cardiovascular system)
  • May not be of benefit in some noncardiogenic etiologies
• Identify and treat the underlying condition.

Prognosis

• Depends on the underlying etiology
• Patients with cardiogenic pulmonary edema can quickly improve within a matter of minutes to an hour with rapid action.
• Patients with noncardiogenic pulmonary edema often take longer to improve.

Complications

• Endotracheal intubation and mechanical ventilation
• Multiorgan failure
• Respiratory and cardiac arrest

Differential Diagnosis

• Pneumonia: infection of the lung parenchyma most often caused by a bacteria or virus. Patients present with fever, dyspnea, and a productive cough. Chest X-ray findings usually show lobar consolidation; however, multifocal infiltrates can be seen in some cases. Management usually involves empiric antibiotics, which can be tailored if the causative organism is identified. Antivirals are used in cases where a viral cause is suspected.
• Pneumoconiosis: an occupational disease resulting from inhalation of inorganic particles into the lungs. Pneumoconiosis can cause chronic inflammation and fibrosis. Patients will have progressive dyspnea and dry cough. Chest X-ray findings can vary depending on the causative particle but may include ground-glass opacities, calcifications, lung nodules, and pleural irregularities. Management is mainly symptomatic.
• Interstitial lung disease: a group of conditions causing progressive fibrosis of the lungs. Patients may be asymptomatic or have a gradual onset of dyspnea and cough. Chest X-ray findings can vary from the infiltrate pattern to the location within the lungs, depending on the etiology. CT and biopsy may be needed for the diagnosis. Management depends on the etiology but can include steroids and immunosuppressive therapies.
• Diffuse alveolar hemorrhage: pulmonary hemorrhage due to damage to the pulmonary vessels. Etiologies can include systemic vasculitides, pulmonary infections, toxic exposures, and coagulation disorders. Patients may present with dyspnea, hemoptysis, or respiratory failure. A chest X-ray will show diffuse alveolar infiltrates. Bronchoscopy confirms the diagnosis. Management includes respiratory support while the underlying cause is determined and treated.