9 research outputs found

    Tension pneumothorax during peroral endoscopic myotomy for treatment of esophageal achalasia under general anesthesia

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    More and more endoscopically gastrointestinal procedures require anesthesiologists to perform general anesthesia, such as “peroral endoscopic myotomy”. Peroral endoscopic myotomy is a novel invasive treatment for the primary motility disorder of esophagus, called esophageal achalasia. Despite of its minimally invasive feature, there are still complications during the procedure which develop to critical conditions and threat patients’ lives. Herein we describe a case about tension pneumothorax subsequent to esophageal rupture during peroral endoscopic myotomy. The emergent management of the complication is stated in detail. The pivotal points of general anesthesia for patients undergoing peroral endoscopic myotomy are emphasized and discussed. Also, intraoperative and post-operative complications mentioned by literature are integrated. Resumo: Cada vez mais os procedimentos gastrointestinais feitos por endoscopia, tais como a miotomia endoscópica por via oral (MEVO), exigem anestesiologistas para administrar anestesia geral. A MEVO é um novo tratamento invasivo para o distúrbio de motilidade primária do esôfago, denominado acalasia esofágica (AE). Apesar de sua característica minimamente invasiva, existem complicações durante o procedimento que evoluem para condições críticas e de risco à vida. Descrevemos aqui um caso de pneumotórax de tensão após a ruptura do esôfago durante uma MEVO. O tratamento de emergência da complicação é relatado em detalhes. Os pontos cruciais da anestesia geral para pacientes submetidos à MEVO são enfatizados e discutidos. Além disso, as complicações mencionadas pela literatura nos períodos intraoperatório e pós-operatório são integradas. Keywords: Peroral endoscopic myotomy, Tension pneumothorax, Esophageal achalasia, General anesthesia, Palavras-chave: Miotomia endoscópica por via oral, Pneumotórax hipertensivo, Acalasia esofágica, Anestesia gera

    Tension pneumothorax during peroral endoscopic myotomy for treatment of esophageal achalasia under general anesthesia

    No full text
    Abstract More and more endoscopically gastrointestinal procedures require anesthesiologists to perform general anesthesia, such as "peroral endoscopic myotomy". Peroral endoscopic myotomy is a novel invasive treatment for the primary motility disorder of esophagus, called esophageal achalasia. Despite of its minimally invasive feature, there are still complications during the procedure which develop to critical conditions and threat patients’ lives. Herein we describe a case about tension pneumothorax subsequent to esophageal rupture during peroral endoscopic myotomy. The emergent management of the complication is stated in detail. The pivotal points of general anesthesia for patients undergoing peroral endoscopic myotomy are emphasized and discussed. Also, intraoperative and post-operative complications mentioned by literature are integrated

    Hypothermia but not NMDA receptor antagonism protects against stroke induced by distal middle cerebral arterial occlusion in mice.

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    Excitotoxicity mediated by the N-methyl-D-aspartate receptor (NMDAR) is believed to be a primary mechanism of neuronal injury following stroke. Thus, many drugs and therapeutic peptides were developed to inhibit either the NMDAR at the cell surface or its downstream intracellular death-signaling cascades. Nevertheless, the majority of focal ischemia studies concerning NMDAR antagonism were performed using the intraluminal suture-induced middle cerebral arterial occlusion (MCAO) model, which produces a large cortical and subcortical infarct leading to hypothalamic damage and fever in experimental animals. Here, we investigated whether NMDAR antagonism by drugs and therapeutic peptides was neuroprotective in a mouse model of distal MCAO (dMCAO), which produces a small cortical infarct sparing the hypothalamus and other subcortical structures. For establishment of this model, mice were subjected to dMCAO under normothermic conditions or body-temperature manipulations, and in the former case, their brains were collected at 3-72 h post-ischemia to follow the infarct development. These mice developed cortical infarction 6 h post-ischemia, which matured by 24-48 h post-ischemia. Consistent with the hypothesis that the delayed infarction in this model can be alleviated by neuroprotective interventions, hypothermia strongly protected the mouse brain against cerebral infarction in this model. To evaluate the therapeutic efficacy of NMDAR antagonism in this model, we treated the mice with MK801, Tat-NR2B9c, and L-JNKI-1 at doses that were neuroprotective in the MCAO model, and 30 min later, they were subjected to 120 min of dMCAO either in the awake state or under anesthesia with normothermic controls. Nevertheless, NMDAR antagonism, despite exerting pharmacological effects on mouse behavior, repeatedly failed to show neuroprotection against cerebral infarction in this model. The lack of efficacy of these treatments is reminiscent of the recurrent failure of NMDAR antagonism in clinical trials. While our data do not exclude the possibility that these treatments could be effective at a different dose or treatment regimen, they emphasize the need to test drug efficacy in different stroke models before optimal doses and treatment regimens can be selected for clinical trials

    Anesthesia-Induced Hypothermia Attenuates Early-Phase Blood-Brain Barrier Disruption but Not Infarct Volume following Cerebral Ischemia.

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    Blood-brain barrier (BBB) disruption is thought to facilitate the development of cerebral infarction after a stroke. In a typical stroke model (such as the one used in this study), the early phase of BBB disruption reaches a peak 6 h post-ischemia and largely recovers after 8-24 h, whereas the late phase of BBB disruption begins 48-58 h post-ischemia. Because cerebral infarct develops within 24 h after the onset of ischemia, and several therapeutic agents have been shown to reduce the infarct volume when administered at 6 h post-ischemia, we hypothesized that attenuating BBB disruption at its peak (6 h post-ischemia) can also decrease the infarct volume measured at 24 h. We used a mouse stroke model obtained by combining 120 min of distal middle cerebral arterial occlusion (dMCAo) with ipsilateral common carotid arterial occlusion (CCAo). This model produced the most reliable BBB disruption and cerebral infarction compared to other models characterized by a shorter duration of ischemia or obtained with dMCAO or CCAo alone. The BBB permeability was measured by quantifying Evans blue dye (EBD) extravasation, as this tracer has been shown to be more sensitive for the detection of early-phase BBB disruption compared to other intravascular tracers that are more appropriate for detecting late-phase BBB disruption. We showed that a 1 h-long treatment with isoflurane-anesthesia induced marked hypothermia and attenuated the peak of BBB disruption when administered 6 h after the onset of dMCAo/CCAo-induced ischemia. We also demonstrated that the inhibitory effect of isoflurane was hypothermia-dependent because the same treatment had no effect on ischemic BBB disruption when the mouse body temperature was maintained at 37°C. Importantly, inhibiting the peak of BBB disruption by hypothermia had no effect on the volume of brain infarct 24 h post-ischemia. In conclusion, inhibiting the peak of BBB disruption is not an effective neuroprotective strategy, especially in comparison to the inhibitors of the neuronal death signaling cascade; these, in fact, can attenuate the infarct volume measured at 24 h post-ischemia when administered at 6 h in our same stroke model

    Hypothermia induced by isoflurane-anesthesia had no effect on early infarct volume following distal middle cerebral arterial occlusion (dMCAo).

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    <p>To induce brain infarction, mice were subjected to 120 min of dMCAo coupled with ipsilateral common carotid arterial occlusion. At 4 h post-reperfusion (6 h after the onset of ischemia), hypothermia was induced by exposure to 1% or 2% isoflurane for 1 h. Control animals received 0% isoflurane in the same gas chamber and were normothermic. (<b>A</b>) Infarct area per coronal section was revealed by 2,3,5-triphenyltetrazolium chloride staining 24 h post-ischemia (n = 10 per group). Data are expressed as mean ± SEM. The x-axis indicates the location of the coronal section relative to the medial prefrontal cortex (mPFC). No significant difference was detected. (<b>B</b>) Infarct volume derived from (A); n = 10 per group. Data are expressed as mean ± SEM. n.s. indicates no significant difference.</p

    Early infarct volume and blood-brain barrier (BBB) disruption following distal middle cerebral arterial occlusion (dMCAo).

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    <p>Mice were subjected to 30 min or 120 min of cerebral ischemia induced by dMCAo with or without ipsilateral (ipsi-) or contralateral (contra-) common carotid arterial occlusion (CCAo). (<b>A</b>) Infarct volume was revealed by 2,3,5-triphenyltetrazolium chloride staining 24 h post-ischemia (n = 6 per group). Data are expressed as mean ± SEM, and *p<0.05 and ***p<0.001 indicate a significant infarct volume. (<b>B</b>) BBB permeability was determined by measuring Evans blue dye (EBD) extravasation 6 h post-ischemia (n = 3–5 per group). Data are expressed as mean ± SEM, and *p<0.05 indicates a significant difference compared to the contralateral hemisphere.</p

    Hypothermic but not normothermic isoflurane-anesthesia attenuates early blood-brain barrier (BBB) disruption following distal middle cerebral arterial occlusion (dMCAo).

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    <p>(<b>A</b>) Body temperature was measured continuously in mice using a rectal probe, and recorded at 0, 30, and 60 min after exposure to 1% or 2% isoflurane (n = 5 per group). Data are expressed as mean ± SEM, and ***p<0.001 indicates a significant change in body temperature over time. (<b>B</b>) To induce ischemic BBB disruption, the mice were subjected to 120 min of dMCAo coupled with ipsilateral common carotid arterial occlusion. At 4 h post-reperfusion (6 h after the onset of ischemia), the mice were placed for 1 h inside a gas chamber filled with 0%, 1%, or 2% isoflurane to induce hypothermia. The severity of BBB disruption was determined by comparing the concentrations of intravascular tracer Evans blue dye (EBD), injected 4 h post-reperfusion and quantified 1 h thereafter, extravasated into the left (control, non-ischemic) and the right (ischemic) hemisphere (n = 13–14 per group). Data are expressed as mean ± SEM. *p<0.05 and ***p<0.001 indicate a significant difference, whereas n.s. indicates no significant difference. (<b>C</b>) Same as (A), except that body temperature was maintained with a heating pad (n = 4 per group). (<b>D</b>) Same as (B), except that body temperature was maintained with a heating pad (n = 4–5 per group).</p
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