Acta neurochirurgica · 2020
Routine use of perfusion computed tomography for the detection of delayed cerebral ischemia in unconscious patients after aneurysmal subarachnoid hemorrhage.
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Ditz Claudia, Hartlieb Mathis, Neumann Alexander, Machner Björn, Schacht Hannes, Krajewski Kara L, Leppert Jan, Tronnier Volker M, Küchler Jan
Аннотация
BACKGROUND: Delayed cerebral ischemia (DCI) after aneurysmal subarachnoid hemorrhage (aSAH) is difficult to diagnose in unconscious patients, but it is essential for the prognosis. We analyzed the diagnostic value of routinely performed perfusion computed tomography (rPCT) to detect DCI-related hypoperfusion in this subgroup of patients.
METHODS: Retrospective analysis of unconscious aSAH patients who underwent rPCT according to a predefined protocol. We exclusively analyzed PCT examinations in patients who were clinically and functionally asymptomatic with regard to transcranial Doppler ultrasound (TCD) and invasive neuromonitoring at the time of the PCT examination. The perfusion maps were quantitatively evaluated to detect DCI-related hypoperfusion. Possible clinical risk factors for the occurrence of DCI-related hypoperfusion in rPCT imaging were analyzed by multivariate analyses.
RESULTS: One hundred thirty-six rPCTs were performed in 55 patients. New onset of DCI-related hypoperfusion was observed in 18% of rPCTs. The positive predictive value of rPCT to detect angiographic CVS was 0.80. Between examination days 6 and 10, the rate of DCI-related hypoperfusion was increased significantly (p < 0.05). After rPCT imaging with proof of DCI-related hypoperfusion, short-term follow-up showed secondary cerebral infarction (SCI) in 38%, compared with 5% for patients with normal perfusion on rPCT. The parameters "high risk phase (examination days 6-10)" and "new onset of DCI-related SCI" were significantly associated with the occurrence of DCI-related hypoperfusion in rPCT.
CONCLUSIONS: In unconscious and asymptomatic aSAH patients, rPCT identifies DCI-related hypoperfusion in a relevant number of examinations. However, despite timely endovascular rescue therapy, a significant proportion of secondary infarction still occurs in this subgroup.
METHODS: Retrospective analysis of unconscious aSAH patients who underwent rPCT according to a predefined protocol. We exclusively analyzed PCT examinations in patients who were clinically and functionally asymptomatic with regard to transcranial Doppler ultrasound (TCD) and invasive neuromonitoring at the time of the PCT examination. The perfusion maps were quantitatively evaluated to detect DCI-related hypoperfusion. Possible clinical risk factors for the occurrence of DCI-related hypoperfusion in rPCT imaging were analyzed by multivariate analyses.
RESULTS: One hundred thirty-six rPCTs were performed in 55 patients. New onset of DCI-related hypoperfusion was observed in 18% of rPCTs. The positive predictive value of rPCT to detect angiographic CVS was 0.80. Between examination days 6 and 10, the rate of DCI-related hypoperfusion was increased significantly (p < 0.05). After rPCT imaging with proof of DCI-related hypoperfusion, short-term follow-up showed secondary cerebral infarction (SCI) in 38%, compared with 5% for patients with normal perfusion on rPCT. The parameters "high risk phase (examination days 6-10)" and "new onset of DCI-related SCI" were significantly associated with the occurrence of DCI-related hypoperfusion in rPCT.
CONCLUSIONS: In unconscious and asymptomatic aSAH patients, rPCT identifies DCI-related hypoperfusion in a relevant number of examinations. However, despite timely endovascular rescue therapy, a significant proportion of secondary infarction still occurs in this subgroup.