Does admission body temperature predict mortality after acute stroke?
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Body Temperature↗
Biomedical subjects
Kiyoshi Takagi
Publications and source records attributed to Kiyoshi Takagi.
Natural hypothermia immediately after transient global cerebral ischemia induced by spontaneous subarachnoid hemorrhage.
OBJECT: Spontaneous subarachnoid hemorrhage (SAH) has an aspect of graded transient global cerebral ischemia. The purpose of the present study was the documentation of sequential changes in body temperature immediately after SAH-induced transient global cerebral ischemia in humans. METHODS: Patients admitted within 12 hours after the initial onset of SAH were examined retrospectively (426 patients). Patients with unruptured cerebral aneurysms served as a control group (73 patients). Body temperature measured at the axilla on admission was analyzed. The grade of SAH was established according to the Glasgow Coma Scale (GCS): Grade I, GCS Score 15; Grade II, GCS Score 11 to 14; Grade III, GCS Score 8 to 10; Grade IV, GCS Score 4 to 7; and Grade V, GCS Score 3. The mean body temperature of patients in the control group was 36.49 +/- 0.45 degrees C (mean +/- standard deviation). The mean body temperature of patients in the SAH group who had been admitted within 4 hours of onset for Grades I to V were significantly different (p < 0.001, analysis of variance [ANOVA]): 36.26 +/- 0.7 degrees C, 59 patients; 35.98 +/-0.85 degrees C, 73 patients; 35.52 +/- 0.79 degrees C, 25 patients; 35.9 +/- 1.09 degrees C, 108 patients; and 35.56 +/- 1.14 degrees C, 73 patients, respectively. These values were significantly lower than those in control volunteers, except for patients with Grade I SAH. The reduction in body temperature was unrelated to the location of the cerebral aneurysm and was not the product of circadian rhythm. The temperatures of patients in the SAH group who were admitted beyond 4 hours after onset for each grade were significantly different (p < 0.01, ANOVA): 36.8 +/- 0.91 degrees C, 36 patients; 36.74 +/- 0.68 degrees C, 31 patients; 36.73 +/- 0.38 degrees C, three patients; 37.41 +/- 1.37 degrees C, 17 patients; and 38.9 degrees C, one patient, respectively. These values were significantly higher than those in patients admitted within 4 hours of SAH onset for all grades except Grade V, and significantly higher than control values in patients with Grades I and IV SAH. CONCLUSIONS: These results indicate that body temperature falls and then rises immediately after the SAH-induced transient global cerebral ischemia without cardiac arrest in humans. The reduction in temperature may be a natural cerebral protection mechanism that is activated shortly after ischemic insult.
Adult↗
Biosimulation and visualization: effect of cerebrovascular geometry on hemodynamics.
Hemodynamics plays an important role in cardiovascular disorders, and the authors are applying numerical and experimental studies of cerebrovascular blood flow to the creation and rupture of cerebral aneurysms. In particular, this study aims to investigate the effects of cerebrovascular geometry on hemodynamics, such as flow pattern, wall shear stress distribution, and pressure. This report consists mainly of two parts: numerical study of blood flow in the artery extracted from computer tomography data, and numerical and experimental studies of a curved pipe model. The simulation was conducted by using a finite element method; the experiment was conducted by particle imaging velocimetry. Numerical and experimental results are compared and both show similar secondary flow behavior.
Blood Flow Velocity↗
Body temperature in acute stroke.
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Acetaminophen↗
[Body temperature in the super-acute phase of the cerebrovascular disorders: mainly focused on the subarachnoid hemorrhage].
BACKGROUNDS AND PURPOSE: Body temperature in the acute phase of cerebrovascular disorders(CVDs) may influence the outcome. However, the natural course of body temperature after CVDs has not yet been clarified. The purpose of this study was to elucidate the natural courses of body temperature after CVDs. PATIENTS AND METHODS: We retrospectively investigated 681 patients with CVDs(subarachnoid hemorrhage(SAH): 478, cerebral ischemia: 47, intracerebral hemorrhage(ICH): 156) who were admitted within 24 h after onset. The body temperature was measured with an electronic thermometer at the axilla on admission. The body temperatures of 73 patients with non-ruptured cerebral aneurysms on admission(admitted between 09:00 and 15:00) were used as normal control group. RESULTS: The body temperature in the control group was 36.49 +/- 0.45 degrees C. In comparison, the temperature in the SAH group was significantly lower(35.88 +/- 1.00 degrees C, n = 338, p < 0.001) when the patients were admitted within 4 h after onset, and significantly higher (36.80 +/- 0.85 degrees C, n = 140, p < 0.05) when they were admitted after 4 h and up to 24 h. There was a significant negative correlation between the severity of the SAH and body temperature within 4 h and a significant positive correlation beyond 4 h. Body temperature in the cerebral ishcemia group was significantly lower than in the control group(36.09 +/- 0.59 degrees C, n = 17, p < 0.05) when the patients were admitted within 2 h, but was close to that in the control group when they were admitted beyond 2 h and up to 24 h after onset (36.45 +/- 0.58 degrees C, n = 30). The falls of body temperature in the super-acute phase in the SAH and the cerebral ischemia groups were observed in patients admitted between 09:00 and 15:00. Although body temperature in the ICH group was slightly lower when the patients were admitted within 4 h and slightly higher when admitted beyond 4 h and up to 24 hours after onset, no significant differences were observed in comparison with the control group. In the super-acute phase of the cerebral ischemia and the ICH, body temperature tended to be lower in the patients with worse condition. CONCLUSION: This study clearly demonstrated that body temperatures in patients with CVDs changed rapidly within 24 h after onset. Body temperature in the SAH group within 4 h and that in the cerebral ischemia group within 2 h after onset was significantly lower than in the control group. These temperature falls were not the products of circadian rhythm. The temperature in the SAH group beyond 4 h and up to 24 h after onset rose significantly. Comparison with normal controls and consideration of the circadian rhythm are important when studying changes of body temperature in patients with CVDs.
Acute-Phase Reaction↗