Peripheral nerve conduction abnormalities precede morphological alterations in an experimental rat model of sepsis.

PURPOSE: The pathological mechanisms of critical illness polyneuropathy (CIP), an acute neuromuscular disorder, remain unknown. In this study, we evaluated nerve and vascular properties that might account for electrophysiological abnormalities, including reduced nerve conduction amplitude, in the early phase of CIP. METHODS: Rats were administered intravenous saline (C-group; n = 31) or lipopolysaccharide (3 mg/kg/day; L-group; n = 30) for 48 h. Subsequently, tracheotomy was performed and sciatic nerves exposed bilaterally. A catheter was inserted into the left internal carotid artery to measure the mean arterial pressure (MAP). Nerve conduction velocity (NCV), nerve blood flow (NBF), evoked amplitudes, chronaxie, rheobase, and the absolute refractory period (ARP) were measured from the sciatic nerves. Degeneration, myelination, and neutrophil infiltration were examined in the sciatic nerves using histology and electron microscopy. RESULTS: The NBF (C-group 25 ± 3 ml/100 g/min, L-group 13 ± 3 ml/100 g/min, p < 0.001) was lower in the L-group, but the MAP was similar between groups (C-group 119 ± 17 mmHg, L-group 115 ± 18 mmHg, p = 0.773). LPS also caused a severe reduction in amplitude (C-group 0.9 ± 0.2 mV, L-group 0.2 ± 0.1 mV, p < 0.001), while latency and NCV were not affected. Of note, response amplitudes partially recovered with an increase in stimulus intensity. LPS treatment increased the rheobase and decreased the chronaxie (rheobase: C vs L-group; 0.35 ± 0.07 vs 1.29 ± 0.66 mA, p < 0.001; chronaxie 171 ± 24 vs 42 ± 20 µs, p < 0.001), while ARP was unchanged. No primary axonal degeneration or inflammatory infiltration was observed. CONCLUSIONS: Our findings suggest that primary electrophysiological deterioration is due to threshold alterations rather than morphological alterations after 48 h of LPS treatment.

Thrombomodulin improves maternal and fetal conditions in an experimental pre-eclampsia rat model.

AIM: The aim of this study was to investigate whether the consecutive administration of recombinant thrombomodulin (r-TM) for 4 days improves maternal and fetal conditions and physiological outcomes in an N'-nitro-L-arginine-methyl ester hydrochloride-induced and low-dose endotoxin-induced pre-eclampsia (PE). METHODS: r-TM or saline was administrated i.v. to normal pregnant and experimental PE rats for 4 days. The maternal condition, vascular endothelial growth factor receptor-1 (VEGFR-1), fetal conditions, uteroplacental blood flow (UPBF), and oxygenation in the placenta and fetal brain was evaluated on gestational day 21. RESULTS: Significant increases in the mean arterial blood pressure, VEGFR-1 values and fetal death rate were observed in PE rats compared with control rats, while maternal and fetal bodyweight and fetal brain weight were substantially lower. Hypoperfusion and hypo-oxygenation in both the placenta and fetal brain tissues occurred in PE rats. Although r-TM failed to improve hypertension and affect the differences in maternal bodyweight between the groups, r-TM significantly improved hypoperfusion and fetal and maternal conditions, including VEGFR-1 values (6.5 ± 4.0 vs 2.2 ± 2.7 ng/mL, PE vs PE with r-TM, respectively; P < 0.05). Although not significant, a decrease in the fetal death rate was observed in PE rats administrated r-TM (36.1 ± 17.6% vs 25.0 ± 23.8%, P = 0.077). CONCLUSION: The severe reductions in the UPBF and the placental oxygenation imply that regional hypoperfusion occurs in association with systemic mean arterial pressure. r-TM may be a candidate medical treatment for PE complications.

[Unexpectedly complicated laryngoscopy caused by a massive mandibular tori].

Here, we report a case of an unexpectedly complicated laryngoscopy caused by massive mandibular tori. A 64-year-old man with mitral regurgitation and aortic regurgitation was scheduled for a double valve replacement. Thyromental distance and the Mallampati score were used as predictive factors of difficult intubation, and both factors were within the normal range. Anesthesia with controlled ventilation was started with fentanyl, propofol and vecuronium. After the attainment of full muscle relaxation, an experienced anesthesiologist performed direct laryngoscopy. It was not possible to intubate the patient under direct laryngoscopy because of massive mandibular tori which had not been detected prior to induction. Following the failure of direct laryngoscopy, a McCoy laryngoscope and a gum elastic bougie were deployed to improve vision. Intubation with a 7.5 mm tube was successful at the third attempt. We hope our experience will serve as a reminder to clinicians that mandibular tori, although benign and without subjective symptoms, could have significant effects upon direct laryngoscopy by compromising the line of vision. Preoperative oral evaluation is critical and aggressive treatment should be considered.

[Case of laparoscopic cholecystectomy in a patient with glucose-6-dehydrogenase deficiency].

We report management of anesthesia in a patient suffering from glucose-6-phosphate dehydrogenase (G6PD) deficiency, a condition that induces acute hemolysis when associated with surgical stress and infection, or following the application of oxidant drugs. A 5 year-old-male patient, suffering from G6PD deficiency was scheduled for laparoscopic cholecystectomy. The patient had exhibited signs of hemolysis during the course of various infections and after ingesting fava beans (favism). Anesthesia was induced with midazolam and vecuronium and maintained with nitrous oxide in oxygen and sevoflurane. There was no hemolytic change during the perioperative period. It was clear that this combination of drugs provided safe anesthesia for the G6PD patient in the present study. The most important considerations for patients with G6PD deficiency is firstly, the avoidance of oxidative stress, which can be caused by a variety of different conditions, and secondly, the use of anti-oxidative anesthetic drugs.

[Two cases of intraoperative cerebral hemorrhage caused by undiagnosed metastatic brain tumors].

The authors report two cases of intraoperative cerebral hemorrhage caused by metastatic brain tumors. Delayed recovery from general anesthesia and neurological deficit were found in these patients. Brain CT in case 1 showed bilateral subdural hemorrhage and parenchymal massive hemorrhage in case 2. It is thought that the causes of hemorrhage are due to the changes in morphology of vessels, deterioration in cerebral circulatory regulated system, and increased intracranial pressure caused by tumors. Since the incidence of metastatic brain tumor has increased with prolonged survival time induced by progress in cancer therapy, preoperative brain examination and careful attention to vital signs during anesthesia are needed.