Hemodynamic Instability of Patient With Spontaneous Subarachnoid Hemorrhage

Spontaneous subarachnoid hemorrhage (sSAH) is one of the most severe neurological conditions. The hemodynamic instability due to endogenous catecholamine response and inflammatory patterns influences the risk of an unfavorable outcome and the development of clinical implications such as neurological and non-neurological issues. Serum levels of highly specific cardiac troponin (cTNI), natriuretic peptides (NT-ProBNP), S100 beta protein, neuron-specific enolase (NSE), glial fibrillary acidic protein (GFAP), ubiquitin carboxy-terminal hydrolase (UCH-L1), soluble Tumor Necrosis Factor Receptor-2 (sST2), and soluble urokinase plasminogen activator receptor (suPAR), as well as urinary levels of epinephrine and norepinephrine, can be measured as biomarkers in sSAH to explore the systemic response to the stress of bleeding. However, not all sSAH cases equally develop this endogenous cascade responsible for neurological and systemic events. There is no clear validation of threshold levels of endogenous factors applicable in clinical practice to define hemodynamic instability that has only a neurological or multi-organ impact post-SAH.

Inclusion criteria

• Patients with spontaneous subarachnoid hemorrhage, including those with perimesencephalic subarachnoid hemorrhage and aneurysmal subarachnoid hemorrhage.
• Adult patients.
• Confirmed presence of spontaneous subarachnoid hemorrhage through neuroimaging.
• Obtained informed consent for specific study biomarkers

Exclusion criteria

• Age <18 years.
• Post-traumatic subarachnoid hemorrhage.