[Intraoperative crisis and surgical Apgar score].

Intraoperative crisis is an inevitable event to anesthesiologists. The crisis requires effective and coordinated management once it happened but it is difficult to manage the crises properly under extreme stressful situation. Recently, it is reported that the use of surgical crisis checklists is associated with significant improvement in the management of operating-room crises in a high-fidelity simulation study. Careful preoperative evaluation, proper intraoperative management and using intraoperative crisis checklists will be needed for safer perioperative care in the future. Postoperative complication is a serious public health problem. It reduces the quality of life of patients and raises medical cost. Careful management of surgical patients is required according to their postoperative condition for preventing postoperative complications. A 10-point surgical Apgar score, calculated from intraoperative estimated blood loss, lowest mean arterial pressure, and lowest heart rate, is a simple and available scoring system for predicting postoperative complications. It undoubtedly predicts higher than average risk of postoperative complications and death within 30 days of surgery. Surgical Apgar score is a bridge between proper intraoperative and postoperative care. Anesthesiologists should make effort to reduce the postoperative complication and this score is a tool for it.

Suppression of stretch reflex activity after spinal or systemic treatment with AMPA receptor antagonist NGX424 in rats with developed baclofen tolerance.

BACKGROUND AND PURPOSE: Baclofen (a GABA(B) receptor agonist) is the most commonly used anti-spasticity agent in clinical practice. While effective when administered spinally or systemically, the development of progressive tolerance represents a serious limitation for its long-term use. The goal of the present study was to characterize the treatment potency after intrathecal or systemic treatment with the selective AMPA receptor antagonist NGX424 on stretch reflex activity (SRA) and background muscle activity (BMA) in rats with developed baclofen tolerance. EXPERIMENTAL APPROACH: Animals were exposed to 10 min of spinal ischaemia to induce an increase in BMA and SRA. Selected animals were implanted with an intrathecal PE-5 catheter and infused intrathecally with baclofen (1 µg·h⁻¹ ) for 14 days. Before and after baclofen infusion, changes in BMA and SRA were measured at 2 day intervals. After development of baclofen tolerance, the animals were injected intrathecally (1 µg) or subcutaneously (3, 6 or 12 mg·kg⁻¹) with NGX424, and changes in BMA and SRA were measured. KEY RESULTS: Intrathecal or systemic delivery of NGX424 significantly suppressed the BMA and SRA in baclofen-tolerant animals. This effect was dose dependent. The magnitude of BMA and SRA suppression seen after 1 µg (intrathecal) or 12 mg·kg ⁻¹ (s.c.) of NGX424 injection was similar to that seen during the first 5 days of baclofen infusion. CONCLUSIONS AND IMPLICATIONS These data demonstrate that the use of NGX424 can represent an effective therapy to modulate chronic spasticity in patients who are refractory or tolerant to baclofen treatment.

The Rheb-mTOR pathway is upregulated in reactive astrocytes of the injured spinal cord.

Astrocytes in the CNS respond to tissue damage by becoming reactive. They migrate, undergo hypertrophy, and form a glial scar that inhibits axon regeneration. Therefore, limiting astrocytic responses represents a potential therapeutic strategy to improve functional recovery. It was recently shown that the epidermal growth factor (EGF) receptor is upregulated in astrocytes after injury and promotes their transformation into reactive astrocytes. Furthermore, EGF receptor inhibitors were shown to enhance axon regeneration in the injured optic nerve and promote recovery after spinal cord injury. However, the signaling pathways involved were not elucidated. Here we show that in cultures of adult spinal cord astrocytes EGF activates the mTOR pathway, a key regulator of astrocyte physiology. This occurs through Akt-mediated phosphorylation of the GTPase-activating protein Tuberin, which inhibits Tuberin's ability to inactivate the small GTPase Rheb. Indeed, we found that Rheb is required for EGF-dependent mTOR activation in spinal cord astrocytes, whereas the Ras-MAP kinase pathway does not appear to be involved. Moreover, astrocyte growth and EGF-dependent chemoattraction were inhibited by the mTOR-selective drug rapamycin. We also detected elevated levels of activated EGF receptor and mTOR signaling in reactive astrocytes in vivo in an ischemic model of spinal cord injury. Furthermore, increased Rheb expression likely contributes to mTOR activation in the injured spinal cord. Interestingly, injured rats treated with rapamycin showed reduced signs of reactive gliosis, suggesting that rapamycin could be used to harness astrocytic responses in the damaged nervous system to promote an environment more permissive to axon regeneration.

Delayed response of transcranial myogenic motor-evoked potential monitoring to spinal cord ischemia during repair surgery for descending thoracic aortic aneurysm.

The efficacy of transcranial myogenic motor-evoked potential (tc-MEP) monitoring during thoracic aortic surgery has been the subject of some reports, because tc-MEP monitoring can rapidly reflect changes in spinal cord blood flow during thoracic aortic cross-clamping. In this article, we present a case in which delayed loss of tc-MEP signals was observed after cross-clamping of the descending thoracic aorta. We must be aware that tc-MEPs recorded from the lower extremities can fail to provide rapid detection of spinal cord ischemia in the upper thoracic level after cross-clamping of the descending thoracic aorta.

Intravenous infusion of dexmedetomidine can prevent the degeneration of spinal ventral neurons induced by intrathecal morphine after a noninjurious interval of spinal cord ischemia in rats.

BACKGROUND: In recent studies, we demonstrated that neuraxial morphine after noninjurious spinal cord ischemia in the rat could induce spastic paraplegia and degeneration of selective spinal ventral neurons. Our objective was to investigate the impact of dexmedetomidine infusion on the degeneration of spinal ventral neurons induced by intrathecal (IT) morphine after spinal cord ischemia. METHODS: Male Sprague-Dawley rats were given repetitive doses of IT morphine (40 microg x 2) at 1 and 5 h after a noninjurious interval (6 min) of spinal cord ischemia. The animals were assigned to one of the following four groups after the first IT injection (n = 8/group): Group S, IV infusion of saline (mL/h); Group Dex 0.1, dexmedetomidine (0.1 microg . kg(-1) x h(-1)); Group Dex 1, dexmedetomidine (1 microg x kg(-1) x h(-1)); Group Dex 3, dexmedetomidine (3 microg x kg(-1) x h(-1)). Follow-up evaluation included a sedation scale, the Motor Deficit Index to determine neurological dysfunction and histopathology of the spinal cord at 72 h of reperfusion. RESULTS: IV dexmedetomidine produced a dose-dependent increase in the sedation index. Repetitive IT morphine injection induced paraplegia and degeneration of the spinal ventral neurons. IV dexmedetomidine at a sedative dose in comparison with saline significantly attenuated neurological dysfunction and histopathological consequences. CONCLUSION: These data show that repetitive administration of IT morphine can induce paraplegia with degeneration of spinal ventral neurons, which can be attenuated by IV dexmedetomidine at a sedative dose. The use of dexmedetomidine may provide beneficial effects on neurological outcome after IT morphine after spinal cord ischemia in rats.

[Coma caused by hypermagnesemia in a pregnant woman complicated with HELLP syndrome].

This case report describes a pregnant woman with acute renal failure, caused by aggravation of HELLP syndrome, who developed coma induced by overdose of continuous magnesium sulfate administration for eclampsia. Before examination of serum concentration of magnesium, coma was suspected to be the result of brain vascular problem or brain infarction. Patient was treated in ICU and hemodialysis was started, and she recovered fully from abnormal neurological symptoms. This case illustrate that hypermagnesemia should be considered in the pregnant woman with coma at ER and ICU. Furthermore, the accurate information about the continuous administration of magnesium by previous clinician helped us to make correct diagnosis and to treat the patient successfully.