Neurogenic pulmonary edema

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1], Associate Editor(s)-in-Chief: Shaghayegh Habibi, M.D.[2]

Neurogenic pulmonary edema usually appears within minutes to hours after a cerebral injury. It is an acute life-threatening complication associated with many forms of central nervous system injury, such as brain or spinal cord hemorrhage, trauma, tumors, epilepsy and infections. The pathogenetic factors for the its onset include increased intracranial pressure and severe over-activation of the sympathetic nervous system. Neurogenic pulmonary edema must be differentiated from other diseases with same symptoms, include aspiration pneumonia, cardiogenic pulmonary edema, angioedema and asthma attack. NPE is characterized by dyspnea, bilateral basal pulmonary crackles and the other signs and symptoms of pulmonary edema, in the absence of cardiac failure. Arterial blood gas test shows hypoxemia, hypercapnia and acidosis. In treatment of neurogenic pulmonary edema, the main principle is supportive treatment and decreasing intracranial pressure as in acute respiratory distress syndrome.

• In 1908, W. T. Shanahan noted acute pulmonary edema as an adverse effect of epileptic seizures.
• During WWI, francois Moutier noted the sudden onset of pulmonary edema among soldiers shot in the head.^[1][2]
• In the Vietnam War, alveolar edema and hemorrhage seen in the lungs of soldiers dying after isolated bullet head wounds.^[3]

• Pulmonary edema may develop in the setting of a sudden neurologic event. Neurogenic pulmonary edema usually appears within minutes to hours after cerebral injury.^[4][5]
• Neurogenic pulmonary edema is an acute life-threatening complication associated with many forms of central nervous system injury, such as:^[5]
  • Brain or spinal cord hemorrhage
  • Trauma
  • Tumors
  • Epilepsy
  • Infections
• The pathogenetic factors for the onset of neurogenic pulmonary edema include:^[6]
  • Increased intracranial pressure
  • Severe over-activation of the sympathetic nervous system
• Neurogenic pulmonary edema may develop as a result of activation of specific CNS trigger zones in the brainstem, leading to a rapid sympathetic discharge, rise in systemic blood pressure, baroreflex-induced bradycardia, and enhanced venous return. These cause pulmonary vascular congestion characterized by interstitial edema, intra-alveolar accumulation of transudate and hemorrhages.^[7]
• The initiating mechanism may be a marked, although brief, generalized vasoconstriction, followed by a shift of blood from the peripheral vascular bed to the pulmonary vascular bed.^[8]

• Neurogenic pulmonary edema must be differentiated from other diseases with same symptoms, include:^[9]
  • Aspiration pneumonia
  • Cardiogenic pulmonary edema (such as acute heart failure and pericardial tamponade)
  • Angioedema
  • Anaphylaxis
  • Asthma attack
  • Atelectasis
  • Bronchitis
  • COPD exacerbation
  • Pneumonia

• For more information about differential diagnosis of pulmonary edema click here.

• The incidence of neurogenic pulmonary edema is approximately 2000 to 42900 per 100,000 individuals in patients with subarachnoid hemorrhage.^[10][11]
• The incidence of neurogenic pulmonary edema is approximately 20000 per 100,000 individuals in patients with traumatic brain injury.^[12]
• Age, gender, race and other epidemiologic and demographic features are based on underlying neurologic problem. Overall pulmonary edema commonly affects individuals older than 65 years of age.

• Severe brain damage represents a risk factor for developing neurogenic pulmonary edema, which include:^[13]
  • Cerebral hemorrhage
  • Subarachnoid hemorrhage
  • Head injuries
  • Seizures

• Misdiagnosis and inappropriate treatment may worsen cerebral damage because of hypoxemia or reduced cerebral perfusion pressure.^[13]
• Common complications of neurogenic pulmonary edema are based on underlying neurological damage and pulmonary edema (include electrolyte disturbance, leg and/or abdominal swelling and respiratory arrest).
• Prognosis is generally poor and the associated mortality rate is high, but surviving patients usually recover very quickly.^[14][15]

• NPE is characterized by dyspnea, bilateral basal pulmonary crackles and the other signs and symptoms of pulmonary edema, in the absence of cardiac failure.^[16]
• For more information about symptoms in pulmonary edema click here.

• Patients with neurogenic pulmonary edema usually appear:
  • Anxious
  • Decrease in level of consciousness
• Physical examination is remarkable for the signs of underlying neurologic damage and pulmonary edema, include:
  • Wheezing
  • Prolonged expiratory phase
  • Retraction of intercostal muscle
  • Use of accessory muscles of respiration
  • Nasal flaring
  • Tachypnea
  • Bradycardia
  • High systemic blood pressure

• Hypoxia:
  • Oxygen saturation < 90%
  • PaO2 < 60 mm Hg

• Hypercapnia:
  • CO2 > 45–55 mm Hg

• Acidosis:
  • PH < 7.35 nEq/liter
  • Early findings of pulmonary edema may be respiratory alkalosis because of hyperventilation

• Imaging findings are remarkable for the pulmonary edema and underlying neurologic damage.
• For more information about imaging findings in pulmonary edema click here.

• In treatment of neurogenic pulmonary edema, the main principle is supportive treatment and decreasing intracranial pressure as in acute respiratory distress syndrome.^[17]

• For more information about medical therapy in pulmonary edema click here.

• The mainstay of treatment for pulmonary edema is medical therapy. Surgery may be reserved for underlying neurological damage.

• Treating the underlying neurologic disease is the only way of preventing the recurrence of pulmonary edema.^[18]

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