Neurogenic Pulmonary Edema - Pathophysiology, Etiology, Clinical Features, and Treatment

Introduction:

Neurogenic pulmonary edema is a complication of severe central nervous system injury. It is caused by an increase in pulmonary interstitial and alveolar fluid. Any acute central nervous system insult can result in pulmonary edema. The most common causes are cerebral hemorrhage, traumatic brain injury, subarachnoid hemorrhage, and seizures.

What Is the Pathophysiology of Neurogenic Pulmonary Edema?

• The medulla activates the sympathetic components of the autonomic nervous system.

• Bilateral lesions of the nuclei in the medulla induce pulmonary and systemic hypertension and pulmonary edema.

• Acute neurological crisis, associated with a marked increase in the intracranial pressure, stimulates the hypothalamus and the vasomotor centers of the medulla, which in turn initiates a massive autonomic discharge.

What Are the Mechanisms Involved in Edema Formation?

A central nervous system induces a dramatic change in the starling forces, which maintain the movement of fluid between capillaries and the interstitium. The two major causes are elevated intravascular pressure and pulmonary capillary leak. Both hemodynamic (cardiogenic) and non-hemodynamic (noncardiogenic) components are responsible for edema formation. Factors involved in edema formation are-

Changes in Capillary Hydrostatic Pressure:

• The changes in pulmonary vascular pressure are the most common starling forces to influence the formation of neurogenic pulmonary edema.

• An increase in left atrial pressure occurs due to the increase in sympathetic tone and venous return. The left ventricular function may decrease secondary to the direct effects of catecholamines and other mediators, as well as transient systemic hypertension.

• Pulmonary vasoconstriction occurs with sympathetic stimulation, which may increase the hydrostatic capillary pressure and produce pulmonary edema without affecting pulmonary capillary pressures.

Changes in Pulmonary Capillary Permeability:

• An increase in capillary permeability can result in neurogenic pulmonary edema without elevation of pulmonary capillary hydrostatic pressure because of inconsistency in causative hemodynamic alteration. But the report states that the alpha-adrenergic blockade can prevent neurogenic pulmonary edema.

• Norepinephrine, epinephrine, and the release of secondary mediators may directly increase pulmonary vascular permeability.

• A rapid increase in pulmonary vascular pressure due to pulmonary blood flow or pulmonary vasoconstriction may lead to pulmonary vascular injury.

What Is the Etiology of Neurogenic Pulmonary Edema?

Several factors contribute to the etiology of neurogenic pulmonary edema:

• Primarily any acute central nervous system injury can result in neurologic or pulmonary edema.

• The most common causes include subarachnoid hemorrhage, traumatic brain injury, cerebral hemorrhage, COVID-19, and seizures.

• The other etiological conditions involved are meningitis, spinal cord infarction, arteriovenous malformation, non-hemorrhagic stroke, and medication overdose.

What Are the Clinical Features of Neurogenic Pulmonary Edema?

Neurogenic pulmonary edema usually presents within minutes to hours after severe central nervous system insult. The symptoms are as follows:

• Dyspnea (shortness of breath).

• Bilateral basal pulmonary crackles.

• Absence of cardiac failure.

• Tachypnea (abnormally rapid breathing).

• Respiratory distress.

• Tachycardia (increased heart rate).

• Fever.

• Pulmonary edema occurs but with normal jugular venous pressure and with the absence of a cardiac gallop, which raises the possibility of a neurogenic cause.

What Are the Diagnostic Considerations?

• Neurogenic pulmonary edema tends to develop more rapidly than aspiration pneumonia. Aspiration frequently occurs in the state of altered consciousness.

• Though neurogenic pulmonary edema does not cause fever, the neurological insults that result in neurologic pulmonary edema may cause fever. It takes one to two weeks to resolve in case of aspiration pneumonia, whereas neurogenic pulmonary edema resolves within hours to several days.

Laboratory Findings:

• Elevated natriuretic peptides (A-type and B-type) are reported in patients with subarachnoid hemorrhage.

• Cardiac injury enzyme levels are elevated in patients with neurologic injuries, such as subarachnoid hemorrhage. The magnitude of elevation often correlates with the severity of the neurologic event and its effect on cardiac function.

Chest X-rays:

Chest radiographs show a bilateral alveolar filling process and a normal-sized heart. This may mimic congestive heart failure, with cephalization of blood flow. The distinguishing feature is that other features of heart failure, such as septal Kerley B lines (thin lines of 1 to 2 cm seen in the periphery of lungs), are not seen.

Other Tests:

• No specific cardiac tests confirm the diagnosis of this condition.

• Serial monitoring of cardiac function may demonstrate reduced left ventricular function resulting in neurogenic stress cardiomyopathy. Findings are regional wall motion abnormalities that extend beyond a single vascular bed.

• Echocardiographic findings may demonstrate a reduced ejection fraction and large areas of akinesis in relation to elevated serum troponin levels. Abnormal Q or QS waves and nonspecific ST or T wave changes are marked as predictors of neurogenic pulmonary edema associated with subarachnoid hemorrhage.

• Pulmonary artery wedge pressure may increase and reach higher levels.

• Hemodynamic measurements with right-sided heart catheterization are necessary to differentiate neurogenic pulmonary edema from cardiogenic pulmonary edema.

What Are the Treatment Approaches in Neurogenic Pulmonary Edema?

• The primary aim of treating neurogenic pulmonary edema is to control the underlying neurologic injury and associated complications. Most patients require close cardiac monitoring. Intensive care admission may be required if patients develop severe hypoxemia or if invasive monitoring is required.

• After the management of underlying neurological insult and stabilization, further transitions between the levels of care are carried out. These include the need for mechanical ventilation, neurologic monitoring, and the need for hemodynamic parameters to be maintained.

• Mechanical ventilation may be necessary either through a face mask or through an endotracheal tube.

• The aim of mechanical ventilation is to ensure adequate ventilation to prevent lung injury. To prevent high inflation pressures, tidal volumes between 5 to 6 mL per KG or predicted body weight are used.

• By using low inflation volumes, positive end-expiratory pressure (PEEP) is added to prevent compression atelectasis.

• High levels of positive end-expiratory pressure may be required to treat severe hypoxemia. Careful observation is required when using positive end-expiratory pressure because it can inhibit cerebral venous return and increase intracranial hypertension.

• The use of Diuretics to reduce fluid pressure seems effective, but adequate cardiac output and cerebral perfusion pressure should be maintained.

Drug Therapy:

• Several agents, such as alpha-adrenergic antagonists (used in treating high blood pressure), beta-adrenergic blockers (reduce blood pressure by blocking the effects of hormone adrenaline), Dobutamine, and Chlorpromazine, are recommended.

Conclusion:

Neurogenic pulmonary edema is well tolerated by patients, although some require ventilation support. It resolves within 48 to 72 hours in the majority of affected patients. The patient outcome is generally determined by the underlying neurological injury, which leads to neurogenic pulmonary edema unless significant respiratory complications develop.