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a
Department of Neurology, Rudolf Magnus Institute of Neuroscience, and b Julius Center for Health Sciences and
Key Words creased slightly in both groups (difference 3 mm/h; 95% CI:
Subarachnoid hemorrhage Ischemia Platelets 15 to 20). None of the determinants at baseline predicted
Leukocytes the development of DCI. An increased risk of poor outcome
predicted by a high initial leukocyte count (OR 2.5; 95% CI:
1.15.7) decreased after adjustment for clinical variables (OR
Abstract 2.1; 95% CI: 0.85.5). Conclusion: Counts of platelets and leu-
Background and Purpose: A proinflammatory prothrom- kocytes disproportionally increase during the occurrence of
botic state may increase the risk of delayed cerebral ischemia DCI after aneurysmal SAH. Drugs with anti-thrombotic or
(DCI) after aneurysmal subarachnoid hemorrhage (SAH). We anti-inflammatory properties should be studied for preven-
studied the relationship of levels of leukocytes, platelets, C- tion and treatment of DCI. Copyright 2010 S. Karger AG, Basel
reactive protein (CRP), and erythrocyte sedimentation rate
(ESR) with the development of DCI and with clinical outcome
in patients with aneurysmal SAH. Methods: In 125 patients
admitted within 72 h after aneurysmal SAH, we dichoto- Introduction
mized initial blood levels at their median values and investi-
gated the prediction of DCI with Cox proportional hazard In patients who survive the initial hours after aneurys-
analysis and of poor clinical outcome with logistic regression mal subarachnoid hemorrhage (SAH) and in whom the
analysis. We also analyzed concentrations before and after aneurysm is secured, delayed cerebral ischemia (DCI) is
onset of DCI with the paired-samples t test and compared a frequent neurological complication, and an important
changes with those in patients without DCI. Results: During contributor to death or poor functional outcome. The
the development of DCI (unrelated to treatment), patients pathogenesis of DCI is still incompletely understood. Va-
had a larger increase in counts of platelets (difference 49 ! sospasm is partly responsible for its development, but
109/l; 95% CI: 298) and leukocytes (difference 2.6 ! 109/l; since 30% of patients with DCI have no detectable vaso-
95% CI: 0.45.0) than patients without DCI during the same spasm [1], other factors must also be involved [2]. Char-
period. CRP increased during DCI and decreased in patients acterization of predictors of DCI and poor outcome may
without DCI (difference 14 mg/l; 95% CI: 29 to 58). ESR in- improve the identification of patients with an increased
Excluded
n = 10 perimesencephalic
hemorrhage
n = 8 no detectable aneurysm
n = 1 cerebral ischemia before
admission
Analysis of
n = 106
outcome
Excluded
Analysis of
n = 91
ischemic events
n = 14 unrelated to treatment
n = 13 <24 h after operation
n = 6 <24 h after coiling
28 to 12. The difference between patients with DCI un- was 2.5 (95% CI 1.15.7) (table 3). In the multivariable
related to treatment and control patients without treat- analysis, a non-significant trend remained with an OR of
ment was 14 mg/l (95% CI 29 to 58). During DCI, ESR 2.1 (95% CI 0.85.5). The other markers did not predict
increased by 31 mm/h (95% CI 1250) in the entire group poor outcome.
of patients with DCI of any cause and by 11 mm/h (95%
CI 5.9 to 29) in the subgroup of patients with DCI unre-
lated to treatment. In the entire control group, ESR in- Discussion
creased by 22 mm/h (95% CI 1429) and in the subgroup
of controls without intervention by 42 mm/h (95% CI 26 The main findings of the present study were increases
58). There was no relevant difference between patients in both platelet and leukocyte counts during the develop-
with and without DCI. ment of DCI which were significantly larger than in pa-
After exclusion of patients with an infection at the tients without DCI at the same period after onset of an-
time of the blood samples we used for the analysis of DCI, eurysmal SAH. This disproportionate increase in platelet
all results remained essentially the same. count during the development of DCI has not been re-
ported previously. Our findings suggest that a prothrom-
Clinical Outcome botic and proinflammatory condition is involved in the
The crude OR for poor outcome in patients with an development of DCI. In a previous study in this same pa-
initial leukocyte count above the median (13.6 ! 109/l) tient population, we found an increase in sP-selectin dur-
Fig ures in parentheses contain percentages or ranges. WFNS = World Federation of Neurological Surgeons Scale [5].
1 Graded according to the Hijdra method (maximum score = 30) [6]; our median = 22.
ing the development of DCI [8]. At that time, we conclud- mented platelet function may be involved in the
ed that the increased levels of sP-selectin were most prob- pathogenesis of cerebral infarction after aneurysmal SAH
ably derived from platelets. The findings of the present [10, 11]. Patients who developed DCI showed the highest
study are in line with that conclusion. thromboxane release [11]. Nimodipine treatment has been
Platelet function has previously been implicated in the shown to increase platelet count and to decrease platelet
pathogenesis of DCI after SAH. One study reported evi- thromboxane B2 release [12]. Since all patients in our study
dence of platelet activation 4 days after the initial hemor- received nimodipine, irrespective of the development of
rhage only in the patients who developed symptomatic va- DCI, this cannot explain the difference in changes in
sospasm [9]. Two other studies also proposed that aug- platelet count between patients with or without DCI. Yet
Platelets, !109/l
All 27 247868 291894 46 14 to 76 49 239860 281873 42 25 to 59 4 35 to 29
No intervention 11 264872 357864 93 34 to 153 36 237859 281880 44 23 to 65 49 1.6 to 98*
Intervention 16 235865 246885 11 16 to 39 13 245867 281853 36 1.9 to 69 25 17 to 65
Leukocytes, !109/l
All 29 12.483.8 13.283.7 0.8 0.7 to 2.3 55 13.384.2 12.383.8 1.0 1.8 to 0.2 1.8 3.3 to 0.3**
No intervention 11 13.483.2 15.283.4 1.8 1.1 to 4.8 40 13.183.9 12.384.0 0.8 1.8 to 0.2 2.6 5.0 to 0.4**
Intervention 18 11.784.0 11.983.4 0.2 1.6 to 1.9 15 13.785.3 12.283.5 1.5 3.0 to 0.1 1.7 3.9 to 0.7
CRP, mg/l
All 29 51884 85893 34 8 to 59 55 58883 74896 16 8 to 38 18 54 to 18
No intervention 11 54867 60847 6 40 to 53 40 64888 56885 8 28 to 12 14 58 to 29
Intervention 18 49894 998111 50 20 to 81 15 43867 1208111 77 19 to 136 27 33 to 87
ESR, mm/h
All 11 31826 62828 31 12 to 50 39 24818 46828 22 14 to 29 9 27 to 6.8
No intervention 6 40832 51833 11 5.9 to 29 29 26819 40825 14 6.8 to 21 3 15 to 20
Intervention 5 21812 75817 54 30 to 79 10 21818 63829 42 26 to 58 12 38 to 13
Marker available in a total of n patients; numbers are <106 if initial laboratory values within 72 h
after subarachnoid hemorrhage are missing.
1Platelets adjusted for WFNS (World Federation of Neurological Surgeons Scale) grade at admis-
sion, loss of consciousness at the time of aneurysm rupture, signs of acute ischemia at the time of
aneurysm rupture, amount of cisternal blood, and sex.
Leukocytes adjusted for loss of consciousness at the time of aneurysm rupture, signs of acute isch-
emia at the time of aneurysm rupture, age, WFNS grade at admission, and amount of cisternal blood.
CRP adjusted for loss of consciousness at the time of aneurysm rupture, WFNS grade at admis-
sion, amount of ventricular blood, and signs of acute ischemia at the time of aneurysm rupture.
ESR adjusted for amount of ventricular blood, amount of intracisternal blood, age, loss of con-
sciousness at the time of aneurysm rupture, and sex.
another study found a more severe early decrease in plate- was not related to the time of onset of the symptoms, or
let count in patients with symptomatic vasospasm com- by mixing patients with and patients without an operation
pared with those without [13]. This inconsistency between during the period of sampling in that study.
the findings from this study and those in our patients may The mechanism behind the increased platelet count is
be explained by the timing of the measurements which unknown. Reactive thrombocytosis occurs after major