Therapeutic hypothermia remains a promising treatment for patients with severe traumatic brain injury (TBI). Multiple animal studies have suggested that hypothermia is neuroprotective after TBI, but clinical trials have been inconclusive. Systemic hypothermia, the method used in almost all major clinical trials, is limited by the time to target temperature, the depth of hypothermia, and complications, problems that may be solved by selective brain cooling. We evaluated the effects on brain temperature of a cooling device called the ChillerPad,™ which is applied to the dura in a non-human primate TBI model using controlled cortical impact (CCI). The cortical surface was rapidly cooled to approximately 15°C and maintained at that level for 24 h, followed by rewarming over about 10 h. Brain temperatures fell to 34-35°C at a depth of 15 mm at the cortical gray/white matter interface, and to 28-32°C at 10 mm deep. Intracranial pressure was mildly elevated (8-12 mm Hg) after cooling and rewarming, likely due to TBI. Other physiological variables were unchanged. Cooling was rapidly diminished at points distant from the cooling pad. The ChillerPad may be useful for highly localized cooling of the brain in circumstances in which a craniotomy is clinically indicated. However, because of the delay required by the craniotomy, other methods that are more readily available for inducing hypothermia may be used as a bridge between the time of injury to placement of the ChillerPad.
Acetylcholine plays an important role as a neurotransmitter in the central nervous system with involvement in both sleep and arousal. Dexmedetomidine, midazolam, and propofol are widely used for sedation of patients in intensive care medicine. In this study, we have examined the effect of continuous administration of dexmedetomidine, midazolam, and propofol on acetylcholine release in the rat cerebral cortex, using an in vivo microdialysis technique. Following infusion of a control solution, male Wistar rats (n = 6/group) were administered dexmedetomidine at 0.3 μg/kg/min, midazolam at 20 mg/kg/h, or propofol at 50 mg/kg/h over a 2-h period. Using a brain microdialysis method, extracellular acetylcholine concentrations were measured up to 2 h after administration of each agent at 15-min intervals. In the midazolam group, acetylcholine levels were significantly reduced with midazolam infusion, remaining low even after the drug was stopped. In the propofol group, acetylcholine levels were significantly decreased during propofol infusion, but returned to control levels once the infusion was stopped. Dexmedetomidine administration decreased acetylcholine release, but this finding was not statistically significant. From this study, midazolam and propofol but not dexmedetomidine significantly suppressed acetylcholine release in the cerebral cortex at sedative doses. Even though the righting reflex recovered almost the same after the cessation of drug administration, midazolam suppressed acetylcholine release longer than propofol.
Takotsubo cardiomyopathy is an acute syndrome involving apical ballooning and consequent dysfunction of the left ventricle. Most cases of left ventricular dysfunction resolve within 1 month. We present the case of a 40-year-old woman who developed severe heart failure caused by takotsubo cardiomyopathy with severe left ventricular dysfunction during the perinatal period. Because of the presence of multiple myomas, she was scheduled to undergo a cesarean section under general anesthesia. However, after induction of general anesthesia, she had to be awakened because of the presence of a difficult airway. Because she exhibited insufficient oxygenation, she was transferred to the emergency center. Upon hospital admission, she expectorated large amounts of pink sputum, indicating severe pulmonary edema. Cesarean section was performed immediately. Echocardiography revealed severe left ventricular dysfunction. Full recovery of cardiac function required almost 1 month, after which she was discharged from the hospital without further complications. This is the first reported case of takotsubo cardiomyopathy induced by a failed intubation during a scheduled cesarean section. Takotsubo cardiomyopathy usually shows a good prognosis, but if this myopathy develops during the perinatal period, it can worsen because of excessive preload following the termination of fetoplacental circulation.
To deal with an arterial bleeding from the chest wall after a blunt chest injury, embolization of the bleeding arteries can be a valuable therapeutic option, which is less invasive than a thoracotomy. However, its results are variable, being highly operator-dependent. In the present case, we performed successful emergency embolization of the 4th and 5th intercostal arteries for persistent hemorrhage following blunt trauma to the chest. Several days after the first embolization, secondary embolization was required for treating a pseudoaneurysm that was formed in the 5th intercostal artery. Although the mechanisms underlying pseudoaneurysm formation are not clearly understood, its rupture is potentially fatal. Therefore, it is essential to carefully follow-up patients who experience blunt chest injury to avoid this serious complication.
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