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 2 was a 56-year-old woman with aSAH. ICP increased up to 25mmHg despite EVD, artificial ventilation, and analgosedation. She became hemodynamically unstable and required intravenous noradrenaline at a rate of 0.56 µg/kg/min. ECoG and LDF displayed 5 SDs, which induced spreading depressions of activity, spreading ischemias of up to 190-second duration (Fig A), and spreading suppressions of low-frequency vascular fluctuations. Spreading ischemia concurred with disturbed autoregulation similar to a previous report. Accordingly, ptiO2 seemed to follow the fluctuations of mean arterial pressure (MAP). The PTDDD was 102.3 minutes and occurred on day 1.\nIn addition to a large intracerebral hemorrhage (ICH) in the right temporal lobe, magnetic resonance imaging (MRI) on day 1 revealed large infarcts in the territories of both anterior cerebral arteries, the right MCA, and both posterior cerebral arteries, as well as lacunar infarcts in right thalamus and pons. On day 2, a family discussion was held and a DNR-CC order was activated. The patient was terminally extubated. Figure B shows the nonspreading depression of activity during the falling phase of ptiO2. A very slow, homogeneous DC positivity started simultaneously with the drop in ptiO2. Superimposed on this DC positivity, the terminal SD then started at electrode 3.