Posthemorrhagic Hydrocephalus in Patients with Subarachnoid Hemorrhage Occurs Independently of CSF Osmolality

• Published in: International journal of molecular sciences Vol. 24; no. 14; p. 11476
• Main Authors: Lolansen, Sara Diana, Rostgaard, Nina, Capion, Tenna, Norager, Nicolas H., Olsen, Markus Harboe, Juhler, Marianne, Mathiesen, Tiit Illimar, MacAulay, Nanna
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 14.07.2023; MDPI
• Subjects: Cerebrospinal Fluid Shunts - adverse effects; Electrolytes; Glucose; Hemorrhage; Hospitalization; Humans; Hydrocephalus; Hydrocephalus - etiology; Neurosurgical Procedures - adverse effects; Patients; Stroke; Stroke (Disease); Subarachnoid hemorrhage; Subarachnoid Hemorrhage - complications; Weaning; Denmark; posthemorrhagic hydrocephalus; osmolality; subarachnoid hemorrhage; cerebrospinal fluid
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms241411476

The molecular mechanisms underlying the development of posthemorrhagic hydrocephalus (PHH) remain incompletely understood. As the disease pathogenesis often cannot be attributed to visible cerebrospinal fluid (CSF) drainage obstructions, we here aimed to elucidate whether elevated CSF osmolality following subarachnoid hemorrhage (SAH) could potentiate the formation of ventricular fluid, and thereby contribute to the pathological CSF accumulation observed in PHH. The CSF osmolality was determined in 32 patients with acute SAH after external ventricular drainage (EVD) placement and again upon EVD removal and compared with the CSF osmolality from 14 healthy control subjects undergoing vascular clipping of an unruptured aneurism. However, we found no evidence of elevated CSF osmolality or electrolyte concentration in patients with SAH when compared to that of healthy control subjects. We detected no difference in CSF osmolality and electrolyte content in patients with successful EVD weaning versus those that were shunted due to PHH. Taken together, elevated CSF osmolality does not appear to underlie the development of PHH following SAH. The pathological CSF accumulation observed in this patient group must thus instead be attributed to other pathological alterations associated with the abnormal presence of blood within the CSF compartments following SAH.