Characteristics and prognostic value of acute catecholamine surge in patients with aneurysmal subarachnoid hemorrhage

Abstract

The present findings suggest that sympathetic activation in patients in the acute phase of SAH reflects the severity of SAH, and is closely related to the development of delayed vasospasm, leading to the subsequent immune response and inflammatory reactions. Strategies for suppressing catecholamine at the hyper-acute phase may contribute to vasospasm prevention and improve patient outcome.

Hypophosphatemia after nontraumatic intracranial hemorrhage

“…In our study the difference in total maximum SOFA scores between hypophosphatemic and normophosphatemic patients was caused by higher SOFA cardiovascular scores in hypophosphatemic patients. This finding supports the theory of endogenous and exogenous catecholamine‐induced hypophosphatemia, because in addition to the mean arterial pressure level, the main factor in SOFA cardiovascular scoring is the need for vasopressors (epinephrine or norepinephrine) and/or inotropic agents (dobutamine) An apparent discrepancy was, however, that there were no differences in the cumulative dose of norepinephrine at day 1 and in the proportion of norepinephrine dependency between hypophosphatemic and normophosphatemic patients. However, in this study chronic hypertension was more common in patients with hypophosphatemia, and in the light of one case report it has been speculated that in patients with mild essential hypertension serum phosphate is inversely related to sympathetic tone and increased plasma epinephrine …”

The spontaneous arterial blood pressure rise after aneurysmal subarachnoid hemorrhage – A biphasic phenomenon

“…One study found an early peak of epinephrine, norepinephrine, and dopamine, which seems to correlate with the severity of SAH (Hunt and Kosnik grade), the development of delayed VS, and poor clinical outcome [14]. However, methodological flaws such as the time point and the source of blood samples weakens the validity of this study.…”

“…Other studies analyzed parameters of sympathetic activation without analyzing BP alterations after aSAH [4,14]. One study found an early peak of epinephrine, norepinephrine, and dopamine, which seems to correlate with the severity of SAH (Hunt and Kosnik grade), the development of delayed VS, and poor clinical outcome [14].…”

Temporal Profiles of Cerebral Perfusion Pressure After Subarachnoid Hemorrhage

“…(Ogura et al, 2012) In addition, most subjects were managed using induced hypervolemia and vasopressors with the goal of inducing hypertension after aneurysm treatment and preventing vasospasm. We retrospectively and indirectly evaluated intravascular volume using central venous pressure (CVP) as a surrogate measure (Figure 5).…”