Patient 6 was a 71-year-old male pedestrian struck by a vehicle with reported field GCS = 14. The patient was intubated for airway compromise, and arrived at the trauma center with presentation GCS = 3T5. His primary survey revealed polytrauma with gross limb deformities and signs of craniofacial injury. A Focused Assessment with Sonography for Trauma examination was negative; CT of the head revealed diffuse traumatic SAH and a small falcine subdural hematoma. He was found to have coagulopathy by admission laboratory evaluation. After resuscitation and correction of coagulopathy, the patient was admitted to neurocritical care and an ICP monitor was placed. Repeat cranial imaging demonstrated worsening bifrontal contusions and an enlarging left temporal contusion. The patient's neurologic examination declined to GCS = 3T despite aggressive medical management for refractory ICP. A family discussion was held on day 2, at which time a DNR-CC order was activated. The patient was terminally extubated. The end-of-life recordings are shown in Figure C.
Patient 7 was a 57-year-old male who was found at the base of a stairway. The patient neurologically deteriorated in the field, with decline in the GCS from 13 to 8, was intubated in the emergency department, and was admitted to the neuroscience intensive care unit. CT scans showed hemorrhagic contusions, subdural hematoma, and traumatic SAH. ICP, ptiO2, and rCBF probes, and intraparenchymal depth electrodes were placed in the right frontal lobe and continuous scalp DC/AC-EEG was monitored using Ag/AgCl-electrodes. Five SDs were observed on day 2, and elevated ICP at >40mmHg became intractable despite administration of muscle relaxants, pentobarbital, and 3% saline. Per discussions with family, a DNR-CC order was placed on day 5 and the patient was terminally extubated. Approximately 10 minutes thereafter, a slow, homogeneous DC shift was observed on intraparenchymal DC/AC-ECoG and scalp DC/AC-EEG electrodes in synchrony with the decline in oxygen saturation and PtiO2, a final ICP spike, and declining cerebral perfusion and respiratory arrest. Nonspreading depression was observed across intraparenchymal and scalp electrodes during the falling phase of ptiO2. Asystole for 20 seconds began 3 minutes later, only 13 seconds before the start of terminal SD (Fig ).