Neurogenic Pulmonary Edema

Introduction

Pulmonary edema is characterized by an accumulation of fluid in the air spaces and interstitium of the lung. It may be due to intrinsic pathology of the lung or due to systemic factors. Hence, pulmonary edema has been traditionally classified into cardiogenic and noncardiogenic causes. Cardiogenic pulmonary edema ensues due to acute left ventricular failure, following a variety of insults like myocardial infarction. Noncardiogenic pulmonary edema may be caused by acute lung injury or adult respiratory distress syndrome (ARDS). Cardiogenic pulmonary edema is caused by increased pulmonary hydrostatic pressure, secondary to elevated pulmonary venous pressure.

Neurogenic Pulmonary Edema (NPE)

Neurogenic pulmonary edema (NPE), a relatively rare form of pulmonary edema, follows central nervous system (CNS) insult. It is caused by an increase in pulmonary interstitial and alveolar fluid. It has the potential to increase the secondary injury to the brain and can often be fatal. A number of CNS insults like subarachnoid hemorrhage (SAH), traumatic brain injury (TBI), cervical spinal cord injury (SCI), and intracerebral hemorrhage are associated with NPE.

Epidemiology

The exact number of NPE incidences is not clear, as most of the data are derived from case reports or studied with a few patients or with different diagnostic criteria. The reported incidences of NPE range from 2% to 42% in patients with SAH. The SAH patients with NPE have higher mortality approaching 10%. Increasing age, delay in surgery, and clinical and radiological presentations (poor-grade SAH) were associated with higher incidences of NPE. In TBI patients, reports of development of NPE is as high as 20%. In a large autopsy series by Rogers et al., the incidence of NPE was 32% in TBI patients who died at the scene, and it increased to 96% within 96 h following TBI. The incidence of NPE following status epilepticus is not clear. However, it is estimated that nearly one-third of patients with status epilepticus develop NPE.

Pathophysiology of NPE

The pathophysiology of NPE following CNS insult is poorly understood. The common finding in these cases is the severity of the CNS insult and sudden increases in intracranial pressure (ICP). The raised ICP level in these patients correlates with extravascular lung water (EVLW) and occurrence of NPE ( Figure 1 ). There are two probable mechanisms by which NPE develops following CNS injury:

• 1.

  Damages to the neurons directly or indirectly affects the pulmonary vascular bed, leading to increased permeability and hence pulmonary edema.

• 2.

  Overstimulation of the vasomotor center inflicts changes in autonomic function.

The sudden increase in ICP leads to neuronal compression or damage, which follows an intense activation of the CNS. The increased secretion of catecholamines lead to systemic vasoconstriction and shift of blood from systemic to pulmonary circulation. This, in association with increased pulmonary vascular permeability, increases EVLW and NPE.