Neurogenic Pulmonary Edema Treatment & Management

Updated: Nov 11, 2020
  • Author: Tej K Naik, MD; Chief Editor: Zab Mosenifar, MD, FACP, FCCP  more...
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Approach Considerations

The initial focus of neurogenic pulmonary edema (NPE) treatment is control of the underlying neurologic insult and associated complications, which may include surgical options. Surgical management is directed at the neurologic insult (eg, intracerebral hemorrhage, subdural hematoma) because NPE has no direct surgical treatment.

Neurological insults severe enough to cause NPE always warrant admission to hospital. Most patients require close cardiac monitoring, requiring initial admission to a monitored bed. A telemetry unit or step-down unit bed may suffice for less severe cases. Intensive care admission may be required if patients develop increasingly severe hypoxemia or respiratory distress, or if invasive monitoring is required.

Patients with NPE generally have multiple comorbidities that dictate the setting in which they are receiving care. Transfer between levels of acute care (ie, ICU to transitional care units, and subsequently to general medical/surgical ward) is influenced by a variety of factors. The most important of these is likely the underlying neurological insult that led to the development of pulmonary edema. Once this is managed and stabilized, further transitions between level of care are dictated by clinical circumstances. These include an ongoing need for mechanical ventilation, hemodynamic parameters, and the need for regular neurologic monitoring.


Medical Care

General supportive care for neurogenic pulmonary edema (NPE) includes supplemental oxygen to correct hypoxemia. Mechanical ventilation may be necessary, either noninvasive with a face mask or via an endotracheal tube. [29] The goals of mechanical ventilation are to assure adequate oxygenation and ventilation and to prevent iatrogenic lung injury. To avoid excessively high inflation pressures, tidal volumes between 5 and 6 mL/kg or predicted body weight are used.

With the use of low inflation volumes, positive end-expiratory pressure (PEEP) is added to prevent compression atelectasis. The peak inspiratory (plateau) pressure should be kept below 30-35 cm water, and eucapnia should be maintained to avoid further increases in intracranial pressure. High levels of PEEP may be required to treat severe hypoxemia. Caution is advised, however, because PEEP can inhibit cerebral venous return and increase intracranial hypertension.

Diuretic therapy may reduce lung water by decreasing capillary hydrostatic pressure and increasing colloid osmotic pressure, but the strategies to reduce lung water are not uniformly successful. The use of diuretics to minimize or reduce fluid overload seems a more reasonable approach, but adequate cardiac output and cerebral perfusion pressure must be maintained.

The goal of management in respiratory failure is to achieve an adequate level of oxygenation in the vital organs. Swan-Ganz catheterization may be helpful in guiding fluid and hemodynamic management, particularly if diuretics are used.

To maintain adequate tissue oxygenation, sufficient cardiac output (cardiac index >2.2 L/min/m2) and hemoglobin (>10 g/L) are required to ensure optimal oxygen delivery. Because cardiac output depends on cardiac filling pressures (central venous pressure and wedge pressure), meticulous monitoring of intravascular volume is mandatory. See the Cardiac Output calculator.


Pharmacological agents are not used routinely in the treatment of neurogenic pulmonary edema (NPE). Several agents, such as alpha-adrenergic antagonists, beta-adrenergic blockers, dobutamine, and chlorpromazine, have been advocated, but assessment of their effectiveness is difficult because NPE is usually a self-limited condition that resolves spontaneously.

Alpha-adrenergic antagonists (eg, phentolamine) can prevent NPE or hasten its resolution in experimental models. However, no human trials have established the safety and efficacy of these agents. These agents may be used to treat concomitant systemic hypertension, if present, but care must be taken to avoid significant hypotension that can diminish cerebral perfusion. [30, 31]

Beta-adrenergic agonists, in theory, are used to counteract the alpha-adrenergic–induced increase in systemic vascular resistance by increased inotropic effect with reflex-mediated decrease in afterload. Some studies have used dobutamine and shown a distinct improvement in myocardial function in patients with NPE. [32, 33] A more recent study looked at patients with NPE who were taking lower doses of dopamine (< 6 mcg/min/kg) and showed this to be a reasonable alternative to dobutamine. Recommendations against using higher doses of dopamine have also been published, given the possible effects on increased afterload.



Consultations may include the following:

  • Critical care medicine specialist or intensivist for ongoing intensive care

  • Neurosurgeon and/or neurologist for evaluation and management of any underlying precipitating event

  • Interventional radiologist for some specific neurologic vascular issues