Anesthesia and analgesia
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Anesthesia and analgesia · Mar 2004
Case ReportsLumbar epidural blood patch to treat a large, symptomatic postsurgical cerebrospinal fluid leak of 5 weeks duration in a 3-year-old.
A 3-yr-old with B-cell lymphoma presented with a 5-wk history of 400 mL/day cerebrospinal fluid (CSF) leak, which precluded chemotherapy, after placement of an Omaya reservoir and drain. Surgical repair was unsuccessful. Symptoms included irritability, failure to eat and noncommunication. After lumbar epidural blood patch with 7 mL the symptoms resolved immediately, allowing recommencement of chemotherapy. Epidural blood patch should be considered as possible early treatment for CSF leaks. ⋯ An epidural blood patch successfully treated a large cerebrospinal fluid leak of long duration in a 3-yr-old. Considering the distress of such a leak to the patient, staff, and parents, epidural blood patch may be considered as an early treatment option.
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Anesthesia and analgesia · Mar 2004
Effect of isoflurane on neuronal apoptosis in rats subjected to focal cerebral ischemia.
Although isoflurane can reduce ischemic neuronal injury after short postischemic recovery intervals, this neuroprotective efficacy is not sustained. Neuronal apoptosis can contribute to the gradual increase in infarct size after ischemia. This suggests that isoflurane, although capable of reducing early neuronal death, may not inhibit ischemia-induced apoptosis. We investigated the effects of isoflurane on markers of apoptosis in rats subjected to focal ischemia. Fasted Wistar-Kyoto rats were anesthetized with isoflurane and randomly allocated to awake (n = 40) or isoflurane (n = 40) groups. Animals in both groups were subjected to focal ischemia by filament occlusion of the middle cerebral artery for 70 min. Pericranial temperature was servo-controlled at 37 degrees C +/- 0.2 degrees C throughout the experiment. In the awake group, isoflurane was discontinued and the animals were allowed to awaken. In the isoflurane group, isoflurane anesthesia was maintained at 1.5 MAC (minimum alveolar anesthetic concentration). Animals were killed 7 h, 1 day, 4 days, or 7 days after reperfusion (n = 10/group/time point). The area of cerebral infarction was measured by image analysis in a hematoxylin and eosin stained section. In three adjacent sections, apoptotic neurons were identified by TUNEL staining and immunostaining for active caspase-9 and caspase-3. Infarct size was smaller in the isoflurane group than the awake group 7 h, 1 day, and 4 days after reperfusion (P < 0.05). However, this difference was absent 7 days after reperfusion. The number of apoptotic (TUNEL, caspase-3, and caspase-9 positive) cells 1 day after ischemia was significantly more in the awake versus isoflurane group. After a recovery period of 4 or 7 days, the number of apoptotic cells in the isoflurane group was more than in the awake group. After 7 days, the number of caspase-3 and -9 positive neurons was more in the isoflurane group (P < 0.05). The data indicate that isoflurane delays but does not prevent the development of cerebral infarction caused by ischemia. Isoflurane reduced the development of apoptosis early after ischemia but did not prevent it at later stages of postischemic recovery. ⋯ The effect of isoflurane on neuronal apoptosis was investigated in rats subjected to focal cerebral ischemia. In isoflurane-anesthetized animals, ischemia-induced apoptosis occurred during the later stages of postischemic recovery. Isoflurane did not inhibit postischemic neuronal apoptosis.