A Pediatric Epidural Catheter Fracture Suspected to Be Caused by a Glue.

A 65-day-old baby boy underwent the Kasai procedure under general and epidural anesthesia. The epidural catheter was inserted between the T11 and T12 vertebrae under general anesthesia, and secured with sterile tape, ethyl-2-cyanoacrylate glue, and film. Intra- and postoperative epidural analgesia was effective and there was no leakage around the insertion site. On the third day post-surgery, we tried to remove the catheter but discovered it was fractured 67mm from the tip. During the ultrasound examination, we observed a hyper-echoic structure located between the laminae of T11/T12. The pediatric orthopedic surgeon recommended removing the catheter to avoid long-term neurological sequelae of leaving the catheter, such as infection, fibrosis, migration, and irritation of neural tissues. It was surgically removed uneventfully on postoperative day 4. We requested the manufacturer to inspect the cross-section of the catheter under a microscope. The cross-section showed that 20% of the area had undergone tearing due to traction, while the remaining 80% was cracked. We also requested the manufacturer simulation after that. The same catheter, fixed on the polyolefin resin plate instead of skin with the same tape and glue, was easily fractured after three days. It is suspected that using ethyl-2-cyanoacrylate glue caused the catheter to fracture. When using glue containing ethyl-2-cyanoacrylate for pediatric epidural catheter fixation, special care is advised.

Epidural space "ballooning" during local anaesthetic injection in infants and children: An ultrasound observational study.

BACKGROUND: Infants and children require a larger dose of a local anaesthetic (LA) to establish epidural analgesia than adults, but the reason for this remains unclear. We hypothesised that prominent ventro-dorsal expansion of the epidural space limits cranio-caudal spread of LA in infants. Accordingly, we studied the dimensions of the epidural space with real-time ultrasound (US) before and after epidural injection. METHODS: Ninety-six infants and children aged 0-12 years who underwent abdominal surgery under combined epidural and general anaesthesia were examined in this prospective observational study. Using a micro-convex probe, US recordings of the posterior epidural space were performed while a LA (0.5 ml kg-1 ) was infused at 0.54 ml s-1 . The width in the ventro-dorsal dimension (VDD) of the posterior epidural space before and after injection was recorded; the change in VDD was defined as "ballooning". Correlations between "ballooning" and patient age, body mass index, and volume and rate of LA administration were analysed. RESULTS: "Ballooning" correlated positively but weakly with age (R2  = 0.25; p < .001) and the infused LA volume (R2  = 0.32; p < .001). The "magnitude of ballooning" ("ballooning" per ml of injected LA) correlated negatively but weakly with age (R2  = 0.27; p < .001). CONCLUSIONS: "Magnitude of ballooning" of the epidural space become inconspicuous with growing during epidural injection. This effect may slow the cranio-caudal spread of LA and explain partially why larger volumes of LA are required to effect a block in children.

Anesthetic management of a 12-year-old child with Kagami-Ogata syndrome for pectus excavatum: a case report.

BACKGROUND: Kagami-Ogata syndrome (KOS) is due to abnormal gene expression in the 14q32.2 imprinted region. Laryngomalacia and bell-shaped thorax of children with KOS can affect airway management of general anesthesia. CASE PRESENTATION: A 12-year-old girl with KOS had a mechanical ventilation history and underwent pectus excavatum repair for cosmetic reasons. Although she had undergone invasive thoracic surgery under general and epidural anesthesia, her respiratory rate and tidal volume were stable with adequate pain control mainly through epidural analgesia at the end of the surgery. We examined her larynx by a bronchoscope. Then, we successfully extubated her after confirming the normal movement of her larynx. CONCLUSIONS: When patients with KOS undergo pectus excavatum repair, anesthesiologists should prevent postoperative respiratory failure by providing adequate postoperative analgesia. Evaluation of airway patency and respiratory pattern before extubation is critical.

Thoracoscopic repair of congenital diaphragmatic hernia with countermeasures against reported complications for safe outcomes comparable to laparotomy.

BACKGROUND: Thoracoscopic repair is the preferred treatment for congenital diaphragmatic hernia (CDH); however, several complications, including visceral injury, hypercapnia, and a high incidence of recurrence, have been reported. The purpose of this study was to evaluate the efficacy of countermeasures against these complications at ensuring safe thoracoscopic repair. METHODS: Between January 2000 and December 2014, 40 patients with Bochdalek-type CDH were treated. Of these, 24 patients met the defined criteria for this study, 8 of whom underwent thoracoscopic repair beginning in January 2010 (TS group) and 16 underwent laparotomy before December 2009 (LT group). Perioperative variables and postoperative complications were compared between the groups. Countermeasures against adverse events in the TS group included an endoscopic surgical spacer to prevent visceral injury, intrapulmonary percussive ventilation to avoid hypercapnia, pausing CO2 insufflation to reduce tension during the repair, and prioritizing patch repair in cases of strong tension at the defect. RESULTS: Primary closure was performed in 4 of 8 cases in the TS and 11 of 16 cases in the LT group. There was no visceral injury or conversion to laparotomy in the TS group. The mean operative duration was significantly longer (212 vs. 115 min, respectively, p = 0.0001), and the mean blood loss was significantly less in the TS than in the LT group (1.0 vs. 10.1 mL, respectively, p = 0.01). The intraoperative minimum arterial pH and maximum pCO2 were similar between the groups. All patients survived, and none experienced recurrence. CONCLUSIONS: Our countermeasures to complications of thoracoscopic repair may contribute to safe outcomes equivalent to those of laparotomy in patients meeting our criteria.

Effects of dibutyryl cyclic adenosine monophosphate on hypercapnic depression of diaphragmatic contractility in pentobarbital-anesthetized dogs.

BACKGROUND: Hypercapnia is associated with diaphragm muscle dysfunction that causes a reduction of diaphragmatic force generated for a constant elective myographic activity. No published data are available concerning hypercapnic depression of diaphragmatic contractility during dibutyryl cyclic adenosine monophospate (DBcAMP) administration. OBJECTIVE: The aim of this study was to assess the effects of DBcAMP on hypercapnic depression of diaphragmatic contractility in pentobarbital-anesthetized dogs. METHODS: This experimental study was conducted from July to December 2008 at the Department of Anesthesiology, Institute of Clinical Medicine, University of Tsukuba, Tsukuba, Japan. Adult (aged >5 years) mongrel dogs weighing 10 to 15 kg were randomly divided into 3 equal groups. Hypercapnia (80-90 mm Hg) was induced with 10% carbon dioxide added to the inspired gas. When hypercapnia was established, group 1 was infused with low-dose DBcAMP (0.05 mg/kg/min); group 2 was infused with high-dose DBcAMP (0.2 mg/kg/min); and group 3 received placebo (saline). Study drug was administered intravenously for 60 minutes. Diaphragmatic contractility was assessed by transdiaphragmatic pressure (Pdi) at baseline, induction of hypercapnia, and study drug administration. RESULTS: Twenty-one dogs were divided into 3 groups of 7. There were no significant differences observed at baseline. In the presence of hypercapnia, Pdi (mean [SD], cm H2O) at low- (20-Hz) and high-frequency (100-Hz) stimulation was significantly decreased from baseline in each group (all, P = 0.001). In groups 1 and 2, Pdi at both stimuli was significantly increased during DBcAMP administration compared with hypercapnia-induced values (group 1: 20-Hz, 13.5 [2.2] vs 15.0 [2.4], respectively, P = 0.001, 100-Hz, 21.2 [1.6] vs 22.5 [1.6], P = 0.001; group 2: 20-Hz, 13.7 [1.4] vs 19.2 [1.7], P = 0.001, 100-Hz, 21.0 [2.4] vs 27.2 [2.5], P = 0.001). The Pdi at both stimuli during DBcAMP administration was significantly higher in group 2 than in group 1 (20-Hz, 19.2 [1.7] vs 15.0 [2.4], P = 0.001, 100-Hz, 27.2 [2.5] vs 22.5 [1.6], P = 0.003). In group 3, Pdi did not significantly change in regard to either stimulus from hypercapnia-induced values. CONCLUSION: DBcAMP, in a dose-dependent manner, was associated with improved hypercapnic depression of diaphragmatic contractility in these pentobarbital-anesthetized dogs.

Dose-related effects of olprinone on hypercapnia-Induced impairment of diaphragmatic contractility in pentobarbital-anesthetized dogs.

BACKGROUND: In a previous study, olprinone was found to be more effective than milrinone in improving hypercapnic depression of diaphragmatic contractility in dogs. OBJECTIVE: The purpose of this experimental study was to assess the doserelated effects of olprinone on hypercapnia-induced impairment of diaphragmatic contractility. METHODS: This study was conducted at the Department of Anesthesiology, Institute of Clinical Medicine, University of Tsukuba, Tsukuba, Japan. Hypercapnia (partial pressure of carbon dioxide [C02] in arterial blood 80-90 mm Hg) was induced in pentobarbital-anesthetized dogs by adding 10% C02 to their inspired gas. When hypercapnia was established, the dogs were randomly assigned to 1 of 4 groups: (all dogs were administered a bolus dose of olprinone 10 mg/kg) group 1 was maintained with olprinone 0.1 µg/kg · min(-1); group 2 was maintained with olprinone 0.3 µg/kg · min(-1); group 3 was maintained with olprinone 0.5 µg/kg min(-1); and group 4 received no study drug. The study drug was administered IV for 60 minutes. Diaphragmatic contractility was assessed by transdiaphragmatic pressure (Pdi). The study investigator was not blinded to treatment assignment. RESULTS: Twenty-four healthy adult mongrel dogs were used in the study; 6 dogs were assigned to each treatment group. In the presence of hypercapnia in each group, Pdi (mean [SD], cm H2O) at low-frequency (20-Hz) and high-frequency (100-Hz) stimulation significantly decreased from baseline (all, P = 0.001). During study drug administration in groups 1, 2, and 3, Pdi at both stimuli levels increased significantly from hypercapnia-induced values (all, P = 0.001); in group 4, Pdi to each stimulus did not change significantly from hypercapnia-induced values. There was a significant correlation between olprinone dose and Pdi at both stimuli (all, P = 0.001). The regression equations were: Pdi at 20-Hz stimulation (cm H2O) = 24.97 × olprinone dose (µg/kg · min(-1)) + 13.54 (r = 0.887; n = 24) and Pdi at 100-Hz stimulation (cm H2O) = 29.18 × olprinone dose (µg/kg · min(-1)) + 20.55 (r = 0.911; n = 24). CONCLUSION: Olprinone was associated with a dose-dependent improvement of hypercapnia-induced impairment of diaphragmatic contractility in these pentobarbital-anesthetized dogs.

The effects of different dobutamine infusion rates on hypercapnic depression of diaphragmatic contractility in pentobarbital-anesthetized dogs.

BACKGROUND: Previously, we demonstrated that dobutamine was more effective than dopamine for the improvement of diaphragmatic contractility during hypercapnia. Here, we studied the effects of different dobutamine infusion rates on hypercapnic depression of diaphragmatic contractility in pentobarbital-anesthetized dogs. METHODS: Animals were divided into four groups of six each. In each group, hypercapnia (80-90 mm Hg) was produced by adding 10% CO2 to inspired gas. When hypercapnia was established, group Dob 0 received no study drug; group Dob 5 was induced with dobutamine 5 microg x kg(-1) x min(-1); group Dob 10 was induced with dobutamine 10 microg x kg(-1) x min(-1); group Dob 15 was induced with dobutamine 15 microg x kg(-1) x min(-1). Study drugs were administered IV for 60 min. Diaphragmatic contractility was assessed by measurement of transdiaphragmatic pressure (Pdi). RESULTS: In the presence of hypercapnia, in each group, Pdi at low-frequency (20 Hz) and high-frequency (100 Hz) stimulation decreased from baseline (P < 0.05). In group Dob 0, Pdi to each stimulus did not change from hypercapnia-induced values. In groups Dob 5, Dob 10 and Dob 15, during the study drug administration, Pdi at both stimuli increased from hypercapnia-induced values (P < 0.05). There was a significant positive correlation between dobutamine infusion rates and Pdi at both stimuli (P = 0.0001). CONCLUSION: Dobutamine effectively improves hypercapnic depression of diaphragmatic contractility in an infusion rate-dependent manner in pentobarbital-anesthetized dogs.

Effects of milrinone and olprinone on hypercapnic depression of diaphragmatic contractility in pentobarbital-anesthetized dogs.

UNLABELLED: Abstract. BACKGROUND: Hypercapnia is associated with diaphragm muscle dysfunction that is a reduction of diaphragmatic force generated for stable electric myographic activity. OBJECTIVE: The purpose of this study was to test the effects of milrinone and olprinone on decreased diaphragmatic contractility induced by hypercapnia in pentobarbital-anesthetized dogs. METHODS: This experimental study was conducted at the Department of Anesthesiology, University of Tsukuba, Institute of Clinical Medicine, Tsukuba, Japan. Hypercapnia (partial pressure of carbon dioxide [CO2] in arterial blood 80-90 mm Hg) was induced by adding 10% CO2 to the inspired gas. When hypercapnia was established, group 1 received no study drug, group 2 was infused with milrinone (50 g/kg initial dose plus 0.5 g/kg · min(-1) thereafter), and group 3 was infused with olprinone (10 g/kg initial dose plus 0.3 g/kg · min(-1) thereafter). Diaphragmatic contractility was assessed by transdiaphragmatic pressure (Pdi). RESULTS: Twenty-four, healthy, adult mongrel dogs were used in the study; 8 dogs were assigned to each treatment group. In the presence of hypercapnia, in each group, Pdi (mean [SD], cm-H2O) at low-frequency (20 Hz) and highfrequency (100 Hz) stimulation significantly decreased from baseline (group 1: 20 Hz, 15.1 [2.4] vs 13.3 [2.7]; 100 Hz, 23.1 [2.7] vs 20.6 [2.5], both, P = 0.001; group 2: 20 Hz, 15.2 [2.0] vs 13.2 [2.5]; 100 Hz, 23.0 [2.5] vs 20.5 [2.5], both, P = 0.001; group 3: 20 Hz, 15.0 [2.2] vs 13.2 [2.1]; 100 Hz, 23.0 [2.5] vs 20.5 [2.7], both, P = 0.001). In group 1, the change in Pdi with regard to each stimulus was not significant when compared with the hypercapnia-induced values. In groups 2 and 3, during study-drug administration, Pdi increased significantly in response to both stimuli compared with hypercapnia-induced values (group 2: 20 Hz, 13.2 [2.5] vs 18.8 [2.2]; 100 Hz, 20.5 [2.5] vs 27.7 [2.3], both, P = 0.001; group 3: 20 Hz, 13.2 [2.1] vs 22.3 [3.5]; 100 Hz, 20.5 [2.7] vs 30.8 [2.2], both, P = 0.001). The increase in Pdi with both stimuli was significantly greater in group 3 than in group 2 (20 Hz, 22.3 [3.5] vs 18.8 [2.2], P = 0.035; 100 Hz, 30.8 [2.2] vs 27.7 [2.3], P = 0.046). CONCLUSIONS: The results of this experimental study of the effects of milrinone and olprinone on hypercapnic depression of diaphragmatic contractility in these pentobarbital-anesthetized dogs suggest that olprinone and milrinone significantly improved diaphragm muscle dysfunction induced by hypercapnia. The effects of olprinone were significantly greater than those of milrinone. Further studies are needed to determine the optimal dose of the study drugs.

The recovery profile of reduced diaphragmatic contractility induced by propofol in dogs.

Propofol decreases contractility of the diaphragm, but no data are available for its effects on recovery. We studied the recovery profile of reduced diaphragmatic contractility induced by propofol in dogs. Animals were divided into 4 groups of 7 each. Group I, without fatigue, received only maintenance fluid; Group II, without fatigue, was infused with propofol; Group III, with fatigue, received no study drug; Group IV, with fatigue, was infused propofol. Propofol at an anesthetic dose (0.1 mg/kg initial dose plus 6.0 mg x kg(-1) x h(-1)) was administered for 60 min. In Groups III and IV, diaphragmatic fatigue was induced by intermittent supramaximal bilateral electrophrenic stimulation at 20-Hz for 30 min. We assessed diaphragmatic contractility by transdiaphragmatic pressure (Pdi). In group II, Pdi at low-frequency (20-Hz) stimulation decreased to less than baseline (P < 0.05), whereas there was no change in Pdi at high-frequency (100-Hz) stimulation. At 10 min after the end of propofol administration, Pdi at 20-Hz stimulation returned to baseline. When fatigue was established, in Groups III and IV, Pdi at 20-Hz stimulation decreased to less than baseline (P < 0.05), whereas Pdi at 100-Hz stimulation did not change. After administering propofol in Group IV, Pdi at 20-Hz stimulation decreased from fatigued values (P < 0.05). At 20 min after the end of propofol administration, Pdi at 20-Hz stimulation returned to fatigued values. We conclude that reduced contractility in nonfatigued and fatigued canine diaphragm induced by propofol recovers within 20 min after the cessation of administration.

Milrinone attenuates the negative inotropic effects of landiolol in halothane-anesthetized dogs.

BACKGROUND: Clinical use of high dose beta-blocker therapy is limited by excessive negative inotropic effects. Previous studies suggest that milrinone may be of utility in limiting the inotropic but not the chronotropic effects of beta blockers. We examined the hemodynamic effects of co-administration of a new potent selective beta(1) blocker, landiolol, and milrinone in halothane-anesthetized dogs. METHODS: Eighteen adult mongrel dogs were anesthetized with 1.2 MAC halothane. Hemodynamic measurements were made at baseline, 30 min after starting the milrinone (0.5 micro g x kg(-1) x min(-1)) or normal saline infusion (n = 9 in each), then 30 min after each change in the dose of landiolol infusion. The tested doses of landiolol were 10, 100, and 1000 micro g x kg(-1) x min(-1). RESULTS: Landiolol (>/= 10 micro g x kg(-1) x min(-1)) has significant and comparable negative chronotropic effects in both groups of dogs. While it also has significant negative inotropic effects in both groups, such effects are significantly attenuated in the dogs treated with milrinone. CONCLUSION: Milrinone is effective to attenuate the negative inotropic effects of landiolol in halothane-anesthetized dogs.

Midazolam-induced muscle dysfunction and its recovery in fatigued diaphragm in dogs.

Midazolam, widely used for sedation and anesthesia, decreases contractility in nonfatigued diaphragm; however, its effects on contractility in fatigued diaphragm that are implicated as a cause of respiratory failure have not been established. We therefore studied the effects of midazolam on diaphragm muscle function and recovery in fatigued diaphragm. Dogs were divided into three groups of eight each. In each group, diaphragmatic fatigue was induced by intermittent supramaximal bilateral electrophrenic stimulation at a frequency of 20-Hz stimulation for 30 min. When fatigue was established, Group I received no study drug; Group II was infused with a sedative dose (0.1 mg x kg(-1) x h(-1)) of midazolam; and Group III was infused with an anesthetic dose (0.5 mg x kg(-1) x h(-1)) of midazolam. We assessed diaphragm muscle function (contractility and electrical activity) by transdiaphragmatic pressure (Pdi) and integrated electrical activity of the diaphragm (Edi). In the presence of fatigue, Pdi at low-frequency (20-Hz) stimulation decreased from baseline values (P < 0.05), Pdi at high-frequency (100-Hz) stimulation did not change, and Edi to each stimulus did not change. With an infusion of midazolam, in Groups II and III, Pdi at both stimuli and Edi at 100-Hz stimulation decreased from fatigued values (P < 0.05). The decrease in Pdi and Edi was more in Group III than in Group II (P < 0.05). At 60 min after the cessation of midazolam administration, in Group II, Pdi and Edi recovered from midazolam-induced values (P < 0.05) and returned to fatigued values. In Group III, Pdi and Edi did not change from midazolam-induced values. We conclude that midazolam causes, in a dose-related manner, diaphragm muscle dysfunction in fatigued canine diaphragm and that at a sedative dose, but not at an anesthetic dose, midazolam does not delay its recovery.

Olprinone for the treatment, but not prevention, of fatigue-induced changes in guinea-pig diaphragmatic contractility.

UNLABELLED: Olprinone, a phosphodiesterase III inhibitor, improves the contractility in fatigued diaphragm in vivo, but no data are available for the treatment and prevention of fatigue-induced changes in vitro. We therefore examined the efficacy of Olprinone for the treatment and prevention of fatigue-induced changes in guinea-pig diaphragmatic contractility. The guinea-pig diaphragm strips were randomly allocated according to dose of Olprinone (0, 10(-6), 10(-5), and 10(-4) M) (n = 7 each) and were stimulated directly in an organ bath. Diaphragmatic contractility was measured by assessing twitch tension and force at 20-Hz and 100-Hz stimulation. Diaphragmatic fatigue was induced by generating rhythmic, repetitive contractions produced by 20-Hz stimulation for 5 min. In the first experiment, after the fatigue-producing period, Olprinone was administered to the organ bath for 5 min. In the second experiment, Olprinone was pretreated for 5 min, and then diaphragmatic fatigue was produced. In Experiment 1, after a fatigue-producing period, tetanic force to each stimulus decreased from baseline values (P < 0.05). Olprinone 10(-5)-10(-4) M caused an increase in force at both stimuli from fatigued values (P < 0.05). In Experiment 2, no change in tetanic force was observed by pretreatment with Olprinone (0-10(-4) M). After producing fatigue, tetanic force to each stimulus decreased from baseline values (P < 0.05). These results suggest that Olprinone 10(-5)-10(-4) M improves the fatigue-induced changes in guinea-pig diaphragmatic contractility and that pretreatment with Olprinone does not prevent diaphragmatic fatigability. IMPLICATIONS: Olprinone is effective for the treatment, but not prevention, of fatigue-induced changes in guinea-pig diaphragmatic contractility.

The effect of inhaled colforsin daropate on contractility of fatigued diaphragm in dogs.

UNLABELLED: We studied the effect of inhaled colforsin daropate, a water-soluble forskolin derivative, on the contractility of fatigued diaphragm in dogs. Animals were divided into 3 groups of 8. In each group, diaphragmatic fatigue was induced by intermittent supramaximal bilateral electrophrenic stimulation at a frequency of 20-Hz stimulation applied for 30 min. Immediately after the end of the fatigue-producing period, Group 1 received inhaled vehicle, Group 2 received inhaled colforsin daropate 0.1 mg/mL, and Group 3 received inhaled colforsin daropate 0.2 mg/mL. We assessed diaphragmatic contractility by transdiaphragmatic pressure (Pdi). After fatigue was produced, in each group, Pdi at low-frequency (20-Hz) stimulation decreased from baseline values (P < 0.05), and there was no change in Pdi at high-frequency (100-Hz) stimulation. In Groups 2 and 3, during colforsin daropate inhalation, Pdi at both stimuli increased from fatigued values (P < 0.05). The increase in Pdi was significantly larger in Group 3 than in Group 2. The integrated electrical activity of the diaphragm did not change in any group. We conclude that inhaled colforsin daropate causes an increase in contractility of fatigued canine diaphragm in a dose-related fashion. IMPLICATIONS: Diaphragmatic fatigue may contribute to the development of respiratory failure. Inhaled colforsin daropate improves, in a dose-dependent manner, the contractility of fatigued diaphragm in dogs.

Small dose of propofol for preventing nausea and vomiting after third molar extraction.

PURPOSE: The study goal was to evaluate the efficacy and safety of a small dose of propofol for the prevention of nausea and vomiting following third molar extraction. PATIENTS AND METHODS: In a prospective, randomized, double-blinded, placebo-controlled trial, 90 women received placebo or propofol at 2 different doses (0.25 mg/kg, 0.5 mg/kg) (n = 30 of each) intravenously at the end of surgery. A standard general anesthetic technique, including sevoflurane and nitrous oxide in oxygen, was employed throughout the surgical procedure. Emetic episodes and safety assessments were performed during 0 to 3 hours and 3 to 24 hours after after anesthesia. RESULTS: The rate of patients experiencing emesis-free (no nausea, retching, or vomiting) during 0 to 3 hours after anesthesia was 60% with placebo, 66% with propofol 0.25 mg/kg (P =.395), and 90% with propofol 0.5 mg/kg (P =.001); the corresponding rate during 3 to 24 hours after anesthesia was 60%, 63% (P = 0.5), and 87% (P =.02) (P values compared with placebo). No clinically serious adverse effects due to the study drug were observed in any group. CONCLUSIONS: Prophylactic therapy with a small dose (0.5 mg/kg) of propofol is effective for preventing postoperative nausea and vomiting in female patients undergoing general anesthesia for third molar extractions.

[Training of epidural anesthesia with pressure-guided method in pediatric patients].

Epidural anesthesia in pediatric patients has become popular, and some useful techniques have been introduced. We use the pressure-guided method to identify the epidural space. This method enables us to visualize, on the monitor, the pressure change as the needle advances. With this method, we, including even a new resident in anesthesia, can identify the epidural space objectively and safely. A pressure transducer with saline-filled tubing is connected to a Tuohy needle. As the needle advances, the pressure rises gradually. As soon as the needle enters the epidural space, the pressure suddenly decreases and synchronizes with the heart beats. In the first 10 months after I started working as a resident in anesthesia, I performed 16 pediatric epidural anesthesias successfully under the direction of the anesthetic specialist. I would like to emphasize that I was able to perform epidural anesthesia safely at the thoracic level (T 11 x 12) even in the newborn (body weight 3400 g). The pressure-guided method enables us, even a new resident, to accomplish epidural anesthesia at thoracic level in newborn.

Flumazenil recovers diaphragm muscle dysfunction caused by midazolam in dogs.

UNLABELLED: We studied the effects of flumazenil on diaphragm muscle dysfunction caused by midazolam in dogs. Animals were divided into three groups of eight each. In each group, anesthetic doses (0.1 mg/kg initial dose plus 0.5 mg. kg(-1). h(-1) maintenance dose) of midazolam were administered for 60 min. Immediately after the end of midazolam administration, Group 1 received no study drug; Group 2 was infused small-dose (0.004 mg. kg(-1). h(-1)) flumazenil; Group 3 was infused with large-dose (0.02 mg. kg(-1). h(-1)) flumazenil. We assessed diaphragm muscle function (contractility and electrical activity) by transdiaphragmatic pressure (Pdi) and integrated electrical activity of the diaphragm (Edi). After midazolam was administered in each group, Pdi at low-frequency (20-Hz) and high-frequency (100-Hz) stimulation decreased from baseline values (P < 0.05), and values of Edi at 100-Hz stimulation were less than those obtained during baseline (P < 0.05). In Group 1, Pdi and Edi to each stimulus did not change from midazolam-induced values. In Groups 2 and 3, with an infusion of flumazenil, Pdi at both stimuli and Edi at 100-Hz stimulation increased from midazolam-induced values (P < 0.05). The increase in Pdi and Edi was more in Group 3 than in Group 2 (P < 0.05). We conclude that flumazenil recovers the diaphragm muscle dysfunction (reduced contractility and inhibited electrical activity) caused by anesthetic doses of midazolam in dogs. IMPLICATIONS: In dogs, flumazenil recovers diaphragm muscle dysfunction (reduced contractility and inhibited electrical activity) caused by midazolam in a dose-related manner.