J Neurosurg 144:995–1002, 2026
This report examines the physiological consequences of commonly used neurosurgical irrigation fluids, highlighting effects on synaptic transmission, vascular responses, spreading depolarization, and long-term cellular toxicity. Preclinical brain-slice and animal models demonstrate that normal saline, lactated Ringer’s, and PlasmaLyte can impair neuronal function, alter electrolytes and pH, and worsen recovery compared with artificial cerebrospinal fluid (aCSF).
Clinical observations and preliminary trials mirror experimental findings: aCSF associates with improved postoperative neurophysiology, reduced chronic subdural hematoma recurrence, and better outcomes after aneurysm surgery. The authors advocate prioritizing physiologically matched irrigation solutions and propose targeted clinical trials to evaluate aCSF or electrolyte-optimized fluids across neurosurgical and ICU applications.
Risk premise Nonphysiological neurosurgical irrigation solutions may be an underrecognized contributor to impaired neurological recovery and potentially long-term impairment.
High-volume exposure Irrigation volumes commonly exceed 1 L intraoperatively, and ICU intraventricular irrigation around 60 mL/hr can total ~1.5 L/day for multiple days—large relative to ~125 mL total CSF volume and ~500 mL/day CSF production.
Composition mismatch Commonly available fluids (normal saline, lactated Ringer’s, PlasmaLyte) are roughly iso-osmolar to CSF but differ substantially from CSF in pH and key ions/metabolites (e.g., NS lacks bicarbonate, Ca²⁺, Mg²⁺ and is acidic; LR lacks Mg²⁺ and is acidic).
Synaptic suppression (NS) Superfusion with normal saline rapidly abolishes excitatory postsynaptic potentials; adding Ca²⁺ only partially restores activity, implying multiple missing factors beyond Ca²⁺.
Mechanisms (pH/Mg²⁺ effects) Low pH in NS and LR can depress AMPA/NMDA receptor currents, while LR’s lack of Mg²⁺ can cause transient hyperexcitability followed by loss of synaptic transmission with continued exposure.
Spreading depolarization vulnerability After a spreading depolarization, tissue recovers fully in aCSF but shows profound, persistent suppression of synaptic transmission in LR (even with glucose/oxygen supplementation), with LR also prolonging the depolarization signal.
Preclinical harms In animal and cell models, NS and LR are associated with worse edema/cellular damage than aCSF, and ventriculocisternal NS infusion in rats caused seizures, death, and cortical/CA1 cell death not seen with aCSF.
Clinical signals favor aCSF In endoscopic and other neurosurgical contexts, NS irrigation has been linked to CSF acidification and decreases in glucose/calcium, and comparative studies/meta-analyses report better outcomes with aCSF (e.g., reduced chronic subdural hematoma recurrence; improved early recovery after aneurysm clipping; faster BAEP recovery in microvascular decompression).
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