Reconsideration of Neurogenic Pulmonary Edema as Source of Metastatic Cerebral Abscess Following Subarachnoid Hemorrhages: A Preliminary Study

Abstract

Background: Subarachnoid hemorrhage (SAH) may be a cause of neurogenic pulmonary edema (NPE). It is well known that lymphatic fluid draining by thoracic duct to lungs consists of many dangerous metabolites, degraded tissue particles, and microbiologic pathogens. However, not enough studies have investigated whether NPE causes septicemia or not. In this study, we retrospectively examined our experimental materials to determine whether there is a meaningful relationship between NPE and cerebral abscess formation. Methods: Forty-two rabbits were divided into 3 groups: Control (n = 5), SHAM (n = 7), and SAH (n = 30) with severe neurogenic lung edema detected in rabbits. The SHAM and SAH groups received 1 mL saline and 1 mL autologous arterial blood into the Sylvian cisterna, respectively. Weight, heartbeat, respiration rate, and blood pressure were recorded by routinely using monitoring devices. All multilevel lungs and brain tissue microsections were examined by stereologic and Cavalier methods. For statistical analysis, NPE criteria and the numbers of abscess or abscess resembling cores in the brains were estimated in all groups and compared. The Mann Whitney-U test was used to analyze the results statistically. Results: All rabbits were around 4 years old; body weight was between 3.94 and 4.5 kg; normal heart rhythm rate was found between 251 ± 39/minutes and 281 ± 30/minutes; and respiration rate was between 24 ± 5/minutes and 36 ± 7/minutes. Histopathologic examinations showed that abscess formations frequently spread in middle cerebral arterial territories of all animals in the NPE-detected rabbits. While average abscess numbers were estimated as 3 ± 1 in 7 animals (n = 7; P < 0.005) in severe NPE-detected rabbits, only 1 ± 1 abscess core was detected in a less severe NPE that developed in 3 (n = 3; P < 0.05) animals. The vasospasm index values of pulmonary arteries (PAs) of all animals were 1.233 ± 0.065 in the control group; 1.567 ± 0.0430 in the SHAM group, and 2.890 ± 0.0453 in the SAH group (P < 0.05). Conclusions: This experimental study showed that NPE is a relatively common pathology following experimental SAH in rabbits. The NPE is frequently complicated with brain abscess as shown in this study. The pathophysiologic mechanism was concluded, as NPE may be responsible for cerebral abscess development via bacteria/cytotoxic particles conveyed by thoracic duct to lungs and transferred from the ruptured alveoli-capillary membrane to the brain by way of systemic circulation. © 2018 Elsevier Inc.