[Accidental skin burns by fire of an antiseptic agent ignition by the spark of electric cautery].

Surgical fire is a rare complication during the operative period. But, it is a severe complication when it occurs. There are antiseptic agents with strong inflammability used for skin preparation. We report accidental skin burns caused by the spark of electric cautery. The patient was a 29-year-old (50 kg, 158 cm, physical status ASA1) woman who underwent laparotomy for acute abdomen. Anesthesia was induced and tracheal intubation was performed without trouble. Anesthesia was maintained with oxygen, air, remifentanil and sevoflurane. The skin of the surgical site was sterilized with an alcoholic antiseptic containing chlorhexidine before the operation. Several minutes after the start of operation, a fire occurred on using the electric cautery. Immediately, fire was extinguished by hands. The cover cloth is peeled off and it was confirmed that the burn extended from the right thoracic region to the buttocks. After cooling, it became a burn of II to III degrees. Operation was restarted, and at the end, the patient was allowed to breathe spontaneously for 5 minutes and extubated afterwards. The disinfectant with alcoholic content has a strong inflammability. It is necessary to dry it enough before using cautery.

[Assessment of sublingual PCO2 during selective cerebral perfusion].

We monitored sublingual tissue PCO2 (PSLCO2) continuously with an ISFET (ion-sensitive field effect transistor) based PCO2 sensor during and after surgical treatment for descending aortic aneurysm. Using femoro-femoral bypass and a beating heart technique, distal end of aneurysm was clamped and then selective cerebral perfusion was performed into the left subclavian and left common carotid arteries. Aneurysmectomy and reconstructive surgery were carried out with proximal end of the left common carotid artery being clamped. Upon starting selective cerebral perfusion, PSLCO2 increased abnormally. PSLCO2 increased from 38 mmHg just after induction of anesthesia to the maximum value of 87 mmHg during selective cerebral perfusion. Three hours after arriving in the intensive care unit, the patient developed convulsion and anisocoria and the computed tomography showed cerebral infraction. Since the blood flow to the tongue is fed through the internal and external carotid arteries, the increase in PSLCO2 is supposed to be caused by the decrease of blood flow to the tongue during selective cerebral perfusion. The monitoring of PSLCO2 may be a useful method to estimate the brain blood flow during selective cerebral perfusion.

[Successful anesthetic management of three patients with cardiac dysfunction for non-cardiac surgery using olprinone hydrochloride].

Non-cardiac surgery presents significant risks to patients with cardiac dysfunction. The relative safety of different anesthetic techniques has been studied without mentioning any clear indication. The depression of myocardial contractility by anesthetic agents limits their use in patients with cardiac dysfunction, especially for induction of anesthesia. We used olprinone hydrochloride perioperatively in the anesthetic management of three patients. In all cases, anesthetic induction, intraoperative course and the postoperative period proceeded uneventfully. We consider that perioperative use of continuous olprinone hydrochloride infusion may be suitable for patients with cardiac dysfunction for non-cardiac surgery.

Involvement of spinal tyrosine kinase in inflammatory and N-methyl-D-aspartate-induced hyperalgesia in rats.

Phosphorylation of a subunit of N-methyl-D-aspartate (NMDA) receptor by protein tyrosine kinase (PTK) Src or Trk is known to enhance its channel activity. We examined whether a spinally administered selective PTK inhibitor, lavendustin A, which has high affinity for Src and Trk tyrosine kinases, could influence the development and maintenance of inflammatory hyperalgesia or NMDA-induced hyperalgesia. Inflammation was induced by injection of a mixture of carrageenan and kaolin into the tail base of rats. In another group of rats, hyperalgesia was induced by intrathecal administration of NMDA. Intrathecal administration of lavendustin A (1.0 microg) or NMDA receptor antagonist, (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cycloheptane-5,10-iminemaleate, MK-801 (3.0 microg) before injection of a mixture of carrageenan and kaolin or after the development of inflammation inhibited carrageenan-kaolin-induced mechanical hyperalgesia. Intrathecal injection of 1.0 microg NMDA produced thermal and mechanical hyperalgesia. Co-administration of 1.0 microg lavendustin A with NMDA significantly reduced the duration of spontaneous pain behaviour and inhibited NMDA-induced hyperalgesia. Lavendustin A itself did not cause any sedation, motor impairment or analgesia. Our results suggest that inhibition of PTK could be therapeutically effective as an analgesic in some NMDA receptor-mediated hyperalgesic states.