Neurogenic pulmonary edema

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

Historical Perspective

• [Disease name] was first discovered by [scientist name], a [nationality + occupation], in [year] during/following [event].
• In [year], [gene] mutations were first identified in the pathogenesis of [disease name].
• In [year], the first [discovery] was developed by [scientist] to treat/diagnose [disease name].

Pathophysiology

• Pulmonary edema may develop in the setting of a sudden neurologic event. Neurogenic pulmonary edema usually appears within minutes to hours after cerebral injury.
• Neurogenic pulmonary edema 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
  • Infections
• The pathogenetic factors for the onset of neurogenic pulmonary edema include:
  • 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.
• 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.

Differentiating neurogenic pulmonary edema from other Diseases

• Neurogenic pulmonary edema must be differentiated from other diseases with same symptoms, include:
  • 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.

Epidemiology and Demographics

• The incidence of neurogenic pulmonary edema is approximately 2000 to 42900 per 100,000 individuals in patients with subarachnoid hemorrhage.
• The incidence of neurogenic pulmonary edema is approximately 20000 per 100,000 individuals in patients with traumatic brain injury.

Age

• Patients of all age groups may develop [disease name].

• [Disease name] is more commonly observed among patients aged [age range] years old.
• [Disease name] is more commonly observed among [elderly patients/young patients/children].

Gender

• [Disease name] affects men and women equally.

• [Gender 1] are more commonly affected with [disease name] than [gender 2].
• The [gender 1] to [Gender 2] ratio is approximately [number > 1] to 1.

Race

• There is no racial predilection for [disease name].

• [Disease name] usually affects individuals of the [race 1] race.
• [Race 2] individuals are less likely to develop [disease name].

Risk Factors

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

Natural History, Complications and Prognosis

• Misdiagnosis and inappropriate treatment may worsen cerebral damage because of hypoxemia or reduced cerebral perfusion pressure.
• 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.

Diagnosis

Symptoms

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

Physical Examination

• 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

Laboratory Findings

Arterial blood gas test:

• 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

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

Treatment

Medical Therapy

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

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

Surgery

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

Prevention

• Treating the underlying neurologic disease is the only way of preventing the recurrence of pulmonary edema.