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Neil A. Martin, Ravish V. Patwardhan, Michael J. Alexander, Cynthia Zane Africk, Jae Hong Lee, Ehud Shalmon, David A. Hovda and Donald P. Becker

✓ The extent and timing of posttraumatic cerebral hemodynamic disturbances have significant implications for the monitoring and treatment of patients with head injury. This prospective study of cerebral blood flow (CBF) (measured using 133Xe clearance) and transcranial Doppler (TCD) measurements in 125 patients with severe head trauma has defined three distinct hemodynamic phases during the first 2 weeks after injury. The phases are further characterized by measurements of cerebral arteriovenous oxygen difference (AVDO2) and cerebral metabolic rate of oxygen (CMRO2). Phase I (hypoperfusion phase) occurs on the day of injury (Day 0) and is defined by a low CBF15 calculated from cerebral clearance curves integrated to 15 minutes (mean CBF15 32.3 ± 2 ml/100 g/minute), normal middle cerebral artery (MCA) velocity (mean VMCA 56.7 ± 2.9 cm/second), normal hemispheric index ([HI], mean HI 1.67 ± 0.11), and normal AVDO2 (mean AVDO2 5.4 ± 0.5 vol%). The CMRO2 is approximately 50% of normal (mean CMRO2 1.77 ± 0.18 ml/100 g/minute) during this phase and remains depressed during the second and third phases. In Phase II (hyperemia phase, Days 1–3), CBF increases (46.8 ± 3 ml/100 g/minute), AVDO2 falls (3.8 ± 0.1 vol%), VMCA rises (86 ± 3.7 cm/second), and the HI remains less than 3 (2.41 ± 0.1). In Phase III (vasospasm phase, Days 4–15), there is a fall in CBF (35.7 ± 3.8 ml/100 g/minute), a further increase in VMCA (96.7 ± 6.3 cm/second), and a pronounced rise in the HI (2.87 ± 0.22).

This is the first study in which CBF, metabolic, and TCD measurements are combined to define the characteristics and time courses of, and to suggest etiological factors for, the distinct cerebral hemodynamic phases that occur after severe craniocerebral trauma. This research is consistent with and builds on the findings of previous investigations and may provide a useful temporal framework for the organization of existing knowledge regarding posttraumatic cerebrovascular and metabolic pathophysiology.

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Neil A. Martin, Ravish V. Patwardhan, Michael J. Alexander, Cynthia Zane Africk, Jae Hong Lee, Ehud Shalmon, David A. Hovda and Donald P. Becker

The extent and timing of posttraumatic cerebral hemodynamic disturbances have significant implications for the monitoring and treatment of patients with head injury. This prospective study of cerebral blood flow (CBF) (measured using 133Xe clearance) and transcranial Doppler (TCD) measurements in 125 patients with severe head trauma has defined three distinct hemodynamic phases during the first 2 weeks after injury. The phases are further characterized by measurements of cerebral arteriovenous oxygen difference (AVDO2) and cerebral metabolic rate of oxygen (CMRO2). Phase I (hypoperfusion phase) occurs on the day of injury (Day 0) and is defined by a low CBF15 calculated from cerebral clearance curves integrated to 15 minutes (mean CBF15 32.3 ± 2 ml/100 g/minute), normal middle cerebral artery (MCA) velocity (mean VMCA 56.7 ± 2.9 cm/second), normal hemispheric index (mean HI 1.67 ± 0.11), and normal AVDO2 (mean AVDO2 5.4 ± 0.5 vol%). The CMRO2 is approximately 50% of normal (mean CMRO2 1.77 ± 0.18 ml/100 g/minute) during this phase and remains depressed during the second and third phases. In Phase II (hyperemia phase, Days 1-3), CBF increases (46.8 ± 3 ml/100 g/minute), AVDO2 falls (3.8 ± 0.1 vol%), VMCA velocity rises (86 ± 3.7 cm/second), and the HI remains less than 3 (2.41 ± 0.1). In Phase III (vasospasm phase, Days 4-15), there is a fall in CBF (35.7 ± 3.8 ml/100 g/minute), a further increase in VMCA (96.7 ± 6.3 cm/second), and a pronounced rise in the HI (2.87 ± 0.22).

This is the first study in which CBF, metabolic, and TCD measurements are combined to define the characteristics and time courses of, and to suggest etiological factors for, the distinct cerebral hemodynamic phases that occur after severe craniocerebral trauma. This research is consistent with and builds on the findings of previous investigations and may provide a useful temporal framework for the organization of existing knowledge regarding posttraumatic cerebrovascular and metabolic pathophysiology.