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].

Classification

• [Disease name] may be classified according to [classification method] into [number] subtypes/groups:

• [group1]
• [group2]
• [group3]

• Other variants of [disease name] include [disease subtype 1], [disease subtype 2], and [disease subtype 3].

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.
• On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
• On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].

Differentiating [disease name] from other Diseases

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

Epidemiology and Demographics

• The prevalence of [disease name] is approximately [number or range] per 100,000 individuals worldwide.
• In [year], the incidence of [disease name] was estimated to be [number or range] cases per 100,000 individuals in [location].

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.
• Early clinical features include [manifestation 1], [manifestation 2], and [manifestation 3].
• If left untreated, [#%] of patients with [disease name] may progress to develop [manifestation 1], [manifestation 2], and [manifestation 3].
• Common complications of [disease name] include [complication 1], [complication 2], and [complication 3].
• 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

• There are no [imaging study] findings associated with [disease name].

• [Imaging study 1] is the imaging modality of choice for [disease name].
• On [imaging study 1], [disease name] is characterized by [finding 1], [finding 2], and [finding 3].
• [Imaging study 2] may demonstrate [finding 1], [finding 2], and [finding 3].

Other Diagnostic Studies

• [Disease name] may also be diagnosed using [diagnostic study name].
• Findings on [diagnostic study name] include [finding 1], [finding 2], and [finding 3].

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.

• The mainstay of therapy for [disease name] is [medical therapy 1] and [medical therapy 2].
• Response to [medical therapy 1] can be monitored with [test/physical finding/imaging] every [frequency/duration].

Prevention

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