Changes in Brain Tissue Oxygen During Endovascular Treatment of Cerebral Vasospasm

Fig. 1

Development of PtiO₂ in the left frontal lobe during endovascular intervention. Times for PTA in the left and right internal carotid artery and period of nimodipin administration are indicated

Case 2

A 54-year-old man developed a mild right-sided hemiparesis and confusion 6 days after SAH, and CT angiography revealed vasospasm bilaterally. Figure 2 shows the development of PtiO₂ in the left frontal lobe during anesthesia, verapamil infusion, and bilateral PTA. A decrease in MAP after anesthesia made the use of vasopressor agents (ephedrine and phenylephrine) necessary. After initiation of continuous phenylephrine infusion, PtiO₂ values decreased to near zero. No immediate effect of intraarterial verapamil was observed; the PtiO₂ rose to normal levels and even to values suggesting hyperperfusion (>80 mmHg) only after PTA. Angiography after the intervention showed resolution of the vasospasm.

Fig. 2

PtiO₂ values in the left frontal lobe during endovascular intervention. Times for anesthesia, vasopressor administration, intraarterial verapamil administration, and PTA are indicated

The increased PtiO₂ values obtained during intervention were not lasting. Within 24 h after intervention, PtiO₂ decreased to the level observed before the intervention and even below. Clinically, a dramatic worsening was observed after the intervention in this case. The mild paresis worsened to paralysis and the Glasgow Coma Scale (GCS) dropped from 14 to 6. CT scan revealed infarction in the left frontal lobe.

Case 3

Figure 3 shows PtiO₂ values during administration of vasopressor agents and intraarterial administration of nimopidin (2 mg in the ICA, bilaterally). A significant drop in PtiO₂ is observed after administration of vasopressor agents. After nimodipine administration, the PtiO₂ level rose to the preintervention level, but not above. No clinical improvement was seen after the intervention.

Fig. 3

PtiO₂ values in the left frontal lobe during endovascular intervention. Times for vasopressor administration and intraarterial nimodipin administration are indicated

Discussion

The above cases show that decreases in PtiO₂ values can be dramatically improved by mechanic/pharmacological dilation of the main cerebral arteries. However, no clinical improvement was seen in any of the cases. Several reasons can account for this. In Figs. 1 and 3, very low levels of PtiO₂ are seen during the intervention. In Fig. 1, the PtiO₂ level dropped to values below 2 mmHg for several minutes as the feeding artery was manipulated during PTA. No vasopressors were used in this case. In Fig. 3, a dramatic drop in PtiO₂ to near 0 mmHg was seen after initiation of vasopressor agents. The curves suggest that both manipulation of the arteries and the use of vasopressors in patients with cerebral vasospasm can cause ischemia, potentially leading to poorer outcome than without any intervention.

Only gold members can continue reading. Log In or Register to continue