POS-525 INTEREST OF MANNITOL IN INTRACRANIAL HYPERTENSION DURING HEMODIALYSIS IN A PATIENT WITH ACUTE BRAIN INJURY: A CASE REPORT

Abstract

Hemodialysis (HD) Patients with acute brain injury are at increased risk of dialysis disequilibrium syndrome (DDS). This is due to the added risk of increased intracranial pressure (ICP) during or following dialysis. We present here a case of severe intracranial hypertension due to post traumatic subdural hematoma in a long-term HD patient, improved by continuous mannitol infusions during HD sessions. A 37-year-old Caucasian woman, in HD during five years, had a car accident in january 2021 with initial loss of consciousness, vomiting, severe headache and a Glasgow score of 14/15. Cerebral CT showed frontal hemorrhagic contusions, a right temporal subdural hematoma, subarachnoid hemorrhage, a non-displaced fracture of the sagittal/frontal bones and severe cerebral edema (figure 1). The patient was transferred to the neurosurgical department for medical management and monitoring. No emergency surgery was needed. On day 4, during her first hemodialysis session post brain injury, the patient presented neurological deterioration, severe headache and vomiting. Her blood pressure was of 143/63, heart rate recorded at 76 and oxygen saturation was stable at 100%. On suspicion of cerebral edema, the session was stopped. CT revealed exacerbation of cerebral edema, with no change in lesions or hemorrhage. Similar problems were encountered on the following session. We tried a test dose of Mannitol 20%: 50ml over 5minutes after start of hemodialysis. Neurologic signs disappeared and the patient was stable. Slow Continous mannitol infusion at a dose of 0,2g/kg body weight was undergone during 3-hours HD session with blood pressure and heart rate monitoring. No complications and no clinical significant changes were observed, except a mild elevation of blood pressure(174/95) controlled by mannitol infusion rate reduction. On day 8, the patient received slower dose of Mannitol 20% : 0,2g/kg body weight over 3.5hours of hemodialysis with 50ml infused over 20min and the remaining 60ml over 3 hours. Repeated blood tests showed no hypernatremia. From day 10 and onwards, the patient was able to tolerate hemodialysis with similar settings. On day 20, a further CT scan showed improvement in cerebral edema and temporal hematoma. we began administrating smaller doses of Mannitol ( 0,1g/kg body weight). On day 28, Mannitol was discontinued, as neurological functions were stable and control cerebral CT showed almost total resorption of the hemmorage and a marked edema reduction (figure 2). This case highlights the inherent risks associated with hemodialysis in patients with acute brain injury. The patient in question was likely predisposed to DDS due to cerebral edema after traumatic subdural hemmorage. In high-risk patients, we suggest the infusion of hypertonic solutions such as mannitol during dialysis. It seems to be well tolerated and may allow correction of ICP and optimisation of hemodialysis sessions. However, the risk of hypertensive crisis and hypernatremia should be considered.