Reconsideration of Neurogenic Pulmonary Oedema as a Source of Metastatic Cerebral Abscess Following Subarachnoid Hemorrhages: A Preliminary study

• Published in: World neurosurgery
• Main Authors: Gökyar, Ahmet, Aydın, Mehmet D, Özmen, Sevilay, Demirci, Elif, Marangoz, Abdullah H, Kuruoğlu, Enis, Çokluk, Cengiz
• Format: Journal Article
• Language: English
• Published: United States 20.04.2018
• Subjects: subarachnoid hemorrhage; Brain abscess; neurogenic pulmonary edema
• ISSN: 1878-8769

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 microbiological pathogens. However, there is no enough study which investigates if NPE cause septicemia or not. In this study, we retrospectively examined our experimental materials whether there is a meaningful relationship between the NPE and cerebral abscess formation. The 42 rabbits were divided into three Control group (n=5) and SHAM group (n=7), and SAH group (n=30) with severe neurogenic lung edema detected rabbits. The SHAM and SAH groups received 1 mL saline and 1 mL autologous arterial blood into the Sylvian cisterna, respectively. Weights, heartbeat and respiration rates and blood pressure values had been recorded along experiments by routinely using monitoring devices. All multilevel lungs and brain tissue micro sections were examined by Stereological and Cavalier methods: For statistical analysis, NPE criteria's and the numbers of abscess or abscess resembling cores in the brains were estimated in all groups and compared with each others. Mann Whitney-U test was used to analyze the results statistically. The documents of all rabbits are summarized as follows: All rabbits were around four years old age; body weight between 3.94 - 4.5 kilogram; the normal heart rhythm rate was found between 251±39/minutes - 281±30/minutes; respiration rate was between 24±5/minutes - 36±7/minutes. Histopathological examinations showed that the 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 seven animals (n=7; p<0.005) in severe NPE detected rabbits; only 1±1 abscess core was detected in a less severe NPE developed three (n=3; p < 0.05) animals. The vasospasm index (VSI) values of pulmonary arteries (PAs) of all animals were 1.233±0.065 in control group; 1.567±0.0430 in SHAM group and 2.890±0.0453 in SAH group. (p< 0, 05) CONCLUSIONS: This experimental study showed that the 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 pathophysiological mechanism was concluded, as The NPE may be responsible for cerebral abscess development via bacteria/cytotoxic particles conveyed by thoracic duct to lungs and them transferring from the ruptured alveoli-capillary membrane to the brain by way of systemic circulation.