© Borgis - New Medicine 3/2005, s. 45-52
Charalambos Iliadis1, Dimitris J. Apostolopoulos2, Costas Giannakenas2, Tryfon Spyridonidis2, Greta Wozniak3, Panagiotis Georgoulias3, Fotis Tzirtzidis1, Theodoros Maraziotis1, Pavlos J. Vassilakos2
The value of 99mTc-ECD SPECT early after the onset of subarachnoid hemorrhage in predicting symptomatic vasospasm and clinical outcome
1Neurosurgery Clinic, General Hospital of Larissa, Larissa, Greece
2Department of Nuclear Medicine, University Hospital of Patras, Patras, Greece
3Department of Nuclear Medicine, University Hospital of Larissa, Larissa, Greece
Aim: Investigating the prognostic value of brain perfusion SPECT, within the first few days after Subarachnoid Haemorrhage (SAH) and predicting subsequent development of symptomatic vasospasm and the clinical outcome were aims of the study.
Material and method: Forty-two patients with SAH, aged 17-80 years, in a relatively good clinical condition (Hunt and Hess grade12) underwent a 99mTc-ethyl cysteinate dimer (ECD) SPECT, 0-5 days after hospital admission. The perfusion was measured semi-quantitatively using symmetrical regions of interest, automatically drawn over cortical and subcortical structures on consecutive transverse slices. A summed perfusion defect score (SPDS) was used to quantify the brain perfusion. Vasospasm was assumed in patients presenting deterioration of consciousness, increase in body temperature or newly developed neurological deficit at least 3 days after SAH, or at least 48 hours after surgery, that could not be explained otherwise. The outcome was assessed six months after SAH and graded according to the Glasgow outcome scale (GOS).
Results: Twenty-seven patients had abnormal SPECT studies. Perfusion abnormalities were associated with CT findings, but not with patients´ neurological status on admission. Fifteen patients developed clinical vasospasm from day 4 to 13 post SAH, 19 had an uncomplicated course, while in an additional 8 cases the presence of other confounding factors rendered the diagnosis of vasospasm uncertain. SPDS differed significantly between groups with and without symptomatic vasospasm. All patients with vasospasm had abnormal SPECT studies on admission (100% Negative Predictive Value-NPV), while the Positive Predictive Value (PPV) was 75%. Similarly, regarding the clinical outcome 6 months after SAH, among other known predictor variables, SPECT showed the highest NPV (93.3%) for a favourable outcome (GOS 4 or 5). However, its PPV was only 52%.
Conclusion: The implementation of brain perfusion SPECT-ECD early after SAH seems to provide important prognostic information. A normal study is highly predictive of an uncomplicated clinical course and of a favourable outcome. An abnormal SPECT is accompanied with a reasonable PPV for subsequent symptomatic vasospasm, but with a low PPV regarding the clinical outcome.
Subarachnoid hemorrhage (SAH), usually caused by a ruptured berry aneurysm, accounts for only 3% of all strokes, but for 5% of stroke deaths and for more than one quarter of potential life years lost through stroke (1). Surgical occlusion (clipping) or endovascular packing (coiling) of the aneurysm prevents rebleeding in most cases, although the impact of early intervention on the final outcome has not been proven (2). Postoperative vasospasm remains a major complication, producing ischaemic deficits and accounting for a significant morbidity after subarachnoid hemorrhage (3). Vasospasm presents in some 40% to 70% of all cases and is symptomatic in 17% to 40% of patients (4). It almost never occurs before day 3 from SAH, has maximal incidence on days 6-8, and rarely occurs (5) after day 17. The disorder is clinically characterized by confusion or decreased consciousness with focal neurological deficit. Prophylactic use of nimodipine has been shown to prevent ischaemic consequences of vasospasm and to improve clinical outcome (6). When vasospasm develops, haemodilution, hypertension, and hypervolemia (the triple H) therapy is generally used (7). Other therapeutic strategies, such as a local intra-arterial infusion of papaverine and a balloon angioplasty are also available (8). In order to be effective, therapy must be implemented early in the course of vasospasm – a fact that underscores the importance of early diagnosis.
Intra-arterial angiography can establish vasospasm by direct demonstration of narrowing of the arterial lumen, but it is invasive and carries a small but not negligible risk for transient or permanent neurological complications (9). A number of non-invasive methods are available today and their use depends on local preferences, availability and expertise. Techniques for the manifestation of arterial spasm include Transcranial Doppler sonography (10), MR angiography (11), and spiral CT angiography (12). The effect of vasospasm on cerebral parenchyma (or regional cerebral blood flow disturbances) can be assessed by xenon-enhanced CT (13), diffusion weighted MRI (14) and positron emission tomography (15).
Single-photon emission computed tomography (SPECT) by either (1, 2, 3) I-N-isopropyl-p-iodoamphetamine (IMP), or 99mTc-hexamethyl-propylene amine oxime (HMPAO) or 99mTc-Ethyl-Cysteinate Dimer (ECD) has also been used by various investigators for the diagnosis of delayed cerebral ischemia following SAH (16, 17, 18-31). In these studies SPECT has been considered a useful technique for the evaluation of SAH and cerebral vasospasm. However, the usefulness of early SPECT findings for the prediction of clinical cerebral vasospasm and the prognosis of the clinical outcome has been addressed by only a few studies (16, 18, 22, 25, 29). In the present study, 99mTc-ECD SPECT was performed within the first few days from the onset of SAH in order to determine its prognostic value.
Material and method
Forty-two consecutive patients (19 men and 23 women) with SAH, admitted to the neurosurgery clinic of our hospitals between February 1998 and December 2002, were included in the study (Table 1). Their age ranged from 17 to 80 years (mean 57.2 ±11.9, median 58). Inclusion criteria were: a) SAH proven by CT examination which occurred within 24 hours from admission, b) age between 17 and 80 years, c) a good clinical condition (Glasgow Coma Score = 12, Hunt and Hess grade
Table 1. Patient characteristics, risk factors, DSA findings, SPECT findings, kind of treatment, clinical course and a 6-month outcome.
|Patient No||Sex||Age||H&H grade||GCS on admission||CT (Fisher grade)||DSA (Site of the aneurysm)||SPECT score (SPDS)||SPECT grade||Treatment||Clinical Vasospasm (clinical findings)||Outcome (GOS)|
|1||M||17||I||14||2||neg||12||2||conservative||Yes (confusion, visual impairment)||5|
|2||M||40||III||13||3||pos (ACA)||17||3||surg clip ? VPS||Yes (right VII cranial nerve palsy)||4|
|4||F||59||II||14||2||pos (ACA)||1||1||surg clip||No ||5|
|5||F||74||I||15||3||pos (PCA L+MCA R)||14||2||surg clip||Yes (confusion, left hemiparesis)||1|
|7||M||80||III||14||4||pos (ACA)||15||2||endov coil||Yes (confusion, left hemiparesis)||1|
|10||F||69||II||14||2||neg||17||3||conservative||Yes (confusion, dysarthria, visual impairment)||5|
|11||M||72||II||14||3||pos (MCA L)||10||2||surg clip||No||1|
|13||M||45||II||13||3||pos (MCA L)||12||2||surg clip||Uncertain||5|
|15||M||55||II||14||2||pos (BA)||11||2||endov coil ? surg clip||Yes (confusion, left leg hypokinesis)||3|
|18||F||71||II||15||2||pos (ACA)||12||2||surg clip ? VPS||Yes (left cranial nerve III palsy)||3|
|19||M||60||I||15||2||pos (ACA)||5||1||surg clip||No||5|
|21||F||57||II||14||2||pos (IC)||14||2||endov coil||No||5|
|22||M||47||III||12||3||pos (ACA)||16||2||surg clip||Yes (drowsiness, confusion)||1|
|23||F||56||II||14||2||neg||13||2||conservative||Yes (headache, drowsiness, left leg hypokinesis)||5|
|24||M||41||II||15||2||pos (ACA)||10||2||surg clip||No||4|
|25||F||53||II||14||3||pos (MCA R)||14||2||surg clip||Yes (confusion, left hypokinesis)||3|
|29||M||53||II||13||2||pos (MCA R)||15||2||endov coil||Yes (Confusion)||4|
|32||F||68||II||14||3||pos (MCA R)||13||2||surg clip||Yes (confusion, left hemiparesis)||4|
|33||M||69||II||14||4||pos (ACA)||19||3||conservative||Yes (aphasia, right hemiparesis)||1|
|34||F||64||II||14||3||pos (PCA L)||16||2||surg clip ? VPS||Yes (confusion, anisocoria)||3|
|37||F||49||III||14||4||pos (MCA R)||20||3||surg clip||Uncertain||4|
|38||F||65||I||14||3||pos (ACA)||19||3||surg clip ? VPS||Yes (Confusion)||3|
|42||F||60||III||13||3||pos (MCA R)||11||2||surg clip||Uncertain||4|
neg=negative, pos=positive, ACA=anterior communicating artery, PCA=posterior communicating artery, MCA R(L)=right (left) middle cerebral artery, BA=basilar artery, IC=internal carotid, surg=surgical, endov=endovascular, (r) = followed by, VPS=venticulo-peritoneal shunt.
Clinical and laboratory investigation
Patients had a routine laboratory work-up, which included repeated blood tests and CT examinations. The amount of blood in the subarachnoid space was graded according to the Fisher scale. Patients´ clinical condition on admission was graded according to the Hunt and Hess scale (H&H) and the Glasgow Coma Score (GCS) (Table 1). Neurological status was carefully assessed daily during hospitalization. Digital subtraction arteriography was performed within the first 2 days from admission for the majority of patients, or later (after day 14), if a patient´s clinical condition did not permit. If DSA failed to reveal an aneurysm, the second DSA was performed 1-2 days before hospital discharge. Surgical clipping of the aneurysm demonstrated by the first or by the second DSA was a standard therapeutic procedure (Table 1). In 4 occasions endovascular treatment (coiling) was undertaken. Vasospasm was assumed on clinical basis if deterioration of consciousness, increase in body temperature or new neurological deficit developed at least 3 days after SAH that could not be explained by electrolyte or metabolic disturbances, hydrocephalus or re-bleeding. When a new neurological deficit occurred after surgery, it was attributed to vasospasm only if it was detected 48 hours or more after craniotomy, and if it could not be explained otherwise. The patients developing severe hydrocephalus acutely after SAH or post-operatively were treated with ventricular-peritoneal shunting. The outcome was assessed at 6 months after SAH and was graded according to the Glasgow outcome scale (GOS) (Table 1).
SPECT perfusion imaging
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