Case 33 A 42-year-old woman was admitted to the emergency department. The patient’s family reported that she had suffered a sudden onset of very severe headache and nausea. The ambulance was called immediately. The emergency physician diagnosed drowsiness, confusion, and meningism. Shortly after hospital admission her vigilance progressively declined further, requiring intubation and mechanical ventilation (Glasgow Coma Scale 8). Seventeen years previously the patient had suffered from a mild subarachnoid hemorrhage (SAH) caused by a left-sided intradural internal carotid artery (ICA) aneurysm located at the junction of the posterior communicating artery (PCoA). Aneurysm clipping was done without complication at that time. No follow-up examinations were performed. The family history and medical history were otherwise unremarkable. Noncontrast cranial CT showed a diffuse bleeding in the subarachnoid space of >1 mm thickness without intraventricular or intracerebral clots (Fisher grade 3). The CT also revealed signs of increased intracranial pressure (ICP) (Fig. B33.1A). CT angiography (CTA) demonstrated a fusiform supraophthalmic left ICA aneurysm as the most probable source of bleeding (Fig. B33.1B). Digital subtraction angiography (DSA) confirmed the left ICA aneurysm (diameter 11 × 9.6 × 7.2 mm) at the junction of the PCoA with an irregular configuration as the source of the SAH (Fig. B33.2). Severe SAH grade IV according to the Hunt & Hess grading system (Hunt and Hess 1968) and grade III according to Fisher et al (1980) after rupture of a left-sided supraophthalmic ICA aneurysm treated surgically by clipping 17 years before. An external ventricular drainage was implanted immediately after the CT scan for continuous monitoring and management of ICP. Coil occlusion was performed the following day without complications. Afterwards the patient was transferred to the neurosurgical intensive care unit (ICU). A second CT on the same day showed no detectable changes (not shown). No macroangiopathic changes. Normal angle-corrected systolic flow velocities were detected in the left ICA (53 cm/s). The right ICA was not measurable due to a central venous catheter in the internal jugular vein (Fig. B33.3). All transcranial measurements, initially and during the follow-up examinations, were performed without angle correction. Normal flow velocities in the lower range were seen in the middle cerebral artery (MCA), anterior cerebral artery (ACA), and posterior cerebral artery (PCA) in their first and second segments as well as in the intracranial ICA. Normal flow velocities were also seen in both basal veins of Rosenthal (BVRs). On the left side the MCA/ICA ratio—using the M1 part of the MCA, the extracranial part of the ICA, and systolic flow velocities—was 1.3 and the MCA/BVR ratio was 5 (Figs. B33.4–B33.9). Normal extracranial and intracranial flow parameters without evidence of cerebral hyperperfusion or VS. Daily measurements showed normal flow velocities throughout the observational period. The highest systolic flow velocity seen in the left ICA was 82 cm/s on day 5 (not shown). Fig. B33.2 DSA on the day after admission. (A) Right selective ICA injection, posteroanterior view, showing normal vessel anatomy with a fetal-type PCA as a variant (arrowhead). Note the long course of the M1-MCA with the M2 segment starting at the curvature. (B) Left selective ICA injection, posteroanterior view, showing the reappearance of the once wrapped left C2/C1-ICA aneurysm (11 × 9.6 × 7.2 mm). No vasospasm is detectable at this time. Fig. B33.3 Extracranial duplex, longitudinal plane, left-sided ICA with normal flow velocity on day 2 (53/18 cm/s). Fig. B33.4 TCCS (transtemporal approach), left-sided insonation, axial midbrain plane, left-sided M1-MCA revealing normal flow velocities on day 2 (70/24 cm/s). Transcranial flow assessment showed peak systolic flow velocities more than doubling in the left M1-MCA (168 cm/s) and in the right M1- and M2-MCA (M1 152 cm/s, M2 130 cm/s) on day 5, while values were normal in all other basal cerebral arteries. Flow velocities in the BVRs remained unchanged (not shown). The left MCA/ICA ratio was 2, and the left MCA/BVR ratio was 12. No evidence of cerebral hyperperfusion. Mild VS in the left and right MCA on day 5, better indicated by the MCA/ BVR ratio than by the MCA/ICA ratio. Normal systolic flow velocity of 80 cm/s was seen in the left ICA (not shown). Further increase of systolic flow velocity in the left M1-and M2-MCA segments (M1 215 cm/s, M2 195 cm/s) as well as in the right M1- and M2- MCA segment (M1 170 cm/s, M2 140 cm/s). Slightly increased systolic flow velocities were also seen in both A1-ACAs (left 140 cm/s, right 126 cm/s). Systolic flow velocities in the left and right BVR were 17 cm/s and 13 cm/s, respectively (not shown). The left MCA/ICA ratio was 2.7. Both MCA/BVR ratios were 13. Fig. B33.6 TCCS (transtemporal approach), left-sided insonation, axial midbrain plane, left BVR revealing normal flow velocities on day 2 (flow velocity 14/10 cm/s). Fig. B33.7 TCCS (transtemporal approach), right-sided insonation, axial midbrain plane right-sided M1-MCA with normal flow velocities on day 2 (60/21 cm/s). Fig. B33.8 TCCS (transtemporal approach), right-sided insonation, axial midbrain plane right-sided A1-ACA with normal flow velocities on day 2 (52/20 cm/s). Fig. B33.9 TCCS (transtemporal approach), right-sided insonation, axial midbrain plane, right BVR with normal flow velocities on day 2 (flow velocity 12/10 cm/s). No evidence of cerebral hyperperfusion. Positive MCA/ ICA ratio, now also indicating VS in the left M1- and M2- MCA. Both MCA/BVR ratios still indicated VS in both MCAs. The marked increased flow velocities in both ACAs were also considered as signs of VS. No ischemic infarcts or signs of herniation were seen (not shown). Fig. B33.11 Extracranial duplex, longitudinal plane, left ICA with normal flow velocity on day 9 (55/23 cm/s). Fig. B33.12 TCCS (transtemporal approach), left-sided insonation, axial midbrain plane, left proximal M1-MCA segment with increased flow velocity on day 9 (flow velocity 274/125 cm/s). Fig. B33.13 TCCS (transtemporal approach), left-sided insonation, axial midbrain plane, left A1-ACA segment with increased flow velocity on day 9 (flow velocity 180/83 cm/s). As part of the clinical protocol a follow-up DSA was performed on day 9 which revealed moderate to severe bilateral VS mainly in the right distal M1-MCA and left A1-ACA, but also in the right proximal M1-MCA, A1-ACA, and C1-ICA and the left M1-MCA (Fig. B33.10). On the same day duplex sonography showed normal systolic flow velocities in the left (55 cm/s) and right (47 cm/s) ICA (Fig. B33.11). Transcranial color-coded duplex sonography (TCCS) revealed further increased systolic flow velocities in the left MCA (M1 274 cm/s, M2 196 cm/s) and the right MCA (M1 270 cm/s, M2 179 cm/s) as well as in both A1-ACA (right 216 cm/s, left 180 cm/s). Normal flow was seen in both PCAs. Systolic flow in the BVR remained almost unchanged on both sides (left 17 cm/s, right 11 cm/s). The MCA/ICA ratio was 5.0 on the left side and 5.7 on the right. The corresponding MCA/BVR ratio was 16 on the left side and 25 on the right (Figs. B33.12–B33.17). Fig. B33.15 TCCS (transtemporal approach), right-sided insonation, axial midbrain plane, right distal M1-MCA segment just before the curvature at a depth of 32 mm with increased flow velocity on day 9 (flow velocity 270/148 cm/s). Fig. B33.16 TCCS (transtemporal approach), right-sided insonation, axial midbrain plane, right A1-ACA segment with increased flow velocity on day 9 (flow velocity 216/95 cm/s). Fig. B33.17 TCCS (transtemporal approach), right-sided insonation, axial midbrain plane, right BVR with normal flow velocity on day 9 (flow velocity 11/9 cm/s). Severe VS in the MCA and ACA on both sides without evidence of cerebral hyperperfusion. No obvious changes of systolic flow velocities in both ICA ranging between 55 cm/s and 70 cm/s (not shown). TCCS was still performed daily. Flow velocities further increased in this period. The highest systolic flow velocities were measured in the right M1-MCA (351 cm/s) and at the junction to the M2-MCA (302 cm/s), in the left M1-MCA (386 cm/s) and M2-MCA (297 cm/s), and in the A1-ACA (right 230 cm/s, left 332 cm/s) on day 12. Flow velocities in the BVR ranged between 10 cm/s and 15 cm/s (Figs. B33.18–B33.23). The highest M1-MCA/ICA ratio was 5.9 on the left side and the highest M1-MCA/ BVR ratio was 24 on the right side. Continuing severe VS in both M1- and M2-MCAs and the A1-ACA. New ischemic infarcts in the left MCA territory with a mild space-occupying effect (Fig. B33.24). Fig. B33.19 TCCS (transtemporal approach), left-sided insonation, axial midbrain plane, left A1-ACA showing the highest flow velocity on day 12 (flow velocity 332/180 cm/s). Fig. B33.20 TCCS (transtemporal approach), left-sided insonation, axial midbrain plane, left BVR with almost unchanged flow velocity on day 12 (flow velocity 16/15 cm/s). Fig. B33.21 TCCS (transtemporal approach), right-sided insonation, axial midbrain plane, right M1-MCA just before its bifurcation showing the highest flow velocity on day 12 (flow velocity 362/205 cm/s). Fig. B33.22 TCCS (transtemporal approach), right-sided insonation, axial midbrain plane, right A1-ACA showing the highest flow velocity on day 12 (flow velocity 230/148 cm/s). Fig. B33.23 TCCS (transtemporal approach), right-sided insonation, axial midbrain plane, right BVR with normal flow velocity on day 12 (flow velocity 15/11 cm/s).
Subarachnoid Hemorrhage after Rupture of Left Supraophthalmic Internal Carotid Artery Aneurysm
Clinical Presentation
Initial Neuroradiologic Findings
Conventional Angiography
Diagnosis
Clinical Course (1)
Questions to Answer by Ultrasound Techniques
Initial Neurosonologic Findings (Day 2)
Extracranial Duplex Sonography
Transcranial Duplex Sonography
Conclusion
Neurosonologic Findings (Day 3 to Day 5)
Extracranial Duplex Sonography
Transcranial Duplex Sonography
Conclusion
Neurosonologic Findings (Day 6)
Extracranial Duplex Sonography
Transcranial Duplex Sonography
Conclusion
CT (Day 6)
Conventional Angiography (Day 9)
Neurosonologic Findings (Day 9)
Extracranial Duplex Sonography
Transcranial Duplex Sonography
Conclusion
Neurosonologic Findings (Day 10 to Day 17)
Extracranial Duplex Sonography
Transcranial Duplex Sonography
Conclusion
CT and CTA (Day 16)
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