case_images: PMC10720614_01
case_images: (A) Refractory status epilepticus treatment timeline. cEEG, continuous electroencephalography. Shows a detailed timeline from the patient's first seizure to the initiation of cEEG monitoring to burst-suppression. Triangles connotate boluses or loads, and lines connotate continuous infusions. The patient received loads of IV levetiracetam, IV lorazepam, and IV midazolam, and underwent endotracheal intubation for airway protection. Following intubation, IV midazolam and IV propofol infusions were initiated and up-titrated for suspicion of ongoing non-convulsive status epilepticus (NCSE). Upon initiation of cEEG monitoring, right temporal lateralized periodic discharges (LPDs) and right temporal focal seizures were seen, prompting an increase in the rate of midazolam infusion with additional IV loads of valproate, levetiracetam, and ketamine, to achieve burst suppression. (B) ICP, CPP, MAP, and serum sodium trends along with the titration of sedatives, hyperosmolar therapies, and neuromuscular blocker infusions. ICP, intracranial pressure; CPP, cerebral perfusion pressure; MAP, mean arterial pressure. Triangles connotate boluses, and lines connotate continuous infusions. ICP monitoring was initiated on the second day of hospitalization after the onset of clinical DI and radiographic diffuse cerebral edema. Propofol, versed, and ketamine infusions were already running to maintain burst suppression for RSE. The initial ICP readings between 25-28 mmHg were treated with a mannitol bolus. A subsequent ICP peak of 50 mmHg was treated with hyperventilation, an increase in the propofol infusion rate, a mannitol and hypertonic saline bolus, followed by a hypertonic saline infusion. Ketamine infusion was discontinued due to a concern of possibly contributing to intracranial hypertension, but after multidisciplinary rounds on the next day, it was restarted. Shortly thereafter, the patient's ICP went up to 46 mmHg, for which the patient received another mannitol bolus which resulted in a transient ICP reduction before another ICP crisis to 32-34 mmHg. These subsequent ICP surges were treated with two mannitol boluses in conjunction with the initiation and rapid up-titration of cisatracurium infusion. ICP was transiently reduced, but became sustained at 40-70 mm Hg, despite an increase in the rate of cisatracurium, a hypertonic saline bolus, and continuation of all previous therapies.
case_images: fneur-14-1284098-g002.jpg
case_images: PMC10720614_01_fneur-14-1284098-g002.jpg
case_images: fig2
case_images: Figure 2A depicts a detailed timeline from the patient's first seizure to the initiation of cEEG monitoring to burst-suppression. Detailed pharmacological treatments are shown graphically, along with physiological trends of ICP, mean arterial pressure (MAP), and cerebral perfusion pressure (CPP) in Figure 2B.
case_images: Magnetic resonance imaging (MRI) brain fluid-attenuated inversion recovery (FLAIR) sequences. (A) MRI brain FLAIR sequence that demonstrates bright T2/FLAIR signal, suggesting diffuse grey matter edema which could indicate hypoxic-ischemic brain injury. (B) Repeat MRI brain FLAIR sequence a month later, showing near complete resolution of prior abnormalities and expected extra-cranial herniation of brain through the craniectomy sites.
case_images: fneur-14-1284098-g003.jpg
case_images: PMC10720614_01_fneur-14-1284098-g003.jpg
case_images: fig3
case_images: A repeat MRI brain almost a month after the first MRI showed complete resolution of the previously noted radiographic abnormalities (Figure 3).