Abstract
<title>Abstract</title> <p> Background/Objective: Maintaining acid-base balance within the central nervous system (CNS) is essential for neuronal homeostasis. Disruptions in this balance can result in respiratory disturbances, elevated intracranial pressure, or coma. These disturbances can occur concurrently with stroke, or CNS infection. However, they are augmented by various neurosurgical procedures involving CSF manipulation, either through direct ventricular irrigation during endoscopic neurosurgical procedures or by CSF exchange technologies. The IRRAflow active cerebrospinal fluid (CSF) exchange system (IRRA <italic>flow</italic> ) manages acid-base balance changes in the ventricular system through continuous irrigation with fluids and medications and removal of endogenous CSF. We describe a novel clinical syndrome of iatrogenic metabolic acidosis and respiratory compensation in response to exogenous fluid introduction in the ventricular fluid system using IRRAflow. The syndrome was previously seen with endoscopic neurosurgical procedures that require irrigation with normal saline. We also recommend fluid alternatives for more effective use of the IRRAflow system or different endoscopic procedure and increased awareness of CSF derangements. Methods We describe 2 cases involving patients with subarachnoid hemorrhage who developed a syndromic response characterized by tachypnea, conjunctival hyperemia, encephalopathy, and fluctuating language deficits due to continuous 0.9% normal saline irrigation. Results Both patients exhibited reproducible symptoms that persisted despite stable neuroimaging until normal saline was replaced with lactated Ringer solution, after which clinical parameters normalized within 3 hours. We named this condition <italic>SALT-CRAMD syndrome</italic> (saline acidosis leading to tachypnea, central respiratory alkalosis, and metabolic derangements). Pathophysiologic analysis based on the literature suggests that normal saline induced central hyperchloremia and dilutional acidosis, leading to heightened chemoreceptor activation in the medulla oblongata, triggering excessive respiratory drive and compensatory hypocapnia. Conclusion Awareness of SALT-CRAMD syndrome is crucial for understanding the profound pathophysiologic concepts of CSF dynamics, whether induced during treatment with active CSF exchange, endoscopic neurosurgical procedures, stroke, or CNS infections. </p>