Eiichi Goto

The assessment of three methods to verify tracheal tube placement in the emergency setting

We studied prospectively the reliability of clinical methods, end-tidal carbon dioxide (ETCO(2)) detection, and the esophageal detector device (EDD) for verifying tracheal intubation in 137 adult patients in the emergency department. Immediately after intubation, the tracheal tube position was tested by the EDD and ETCO(2) monitor, followed by auscultation of the chest. The views obtained at laryngoscopy were classified according to the Cormack grade. Of the 13 esophageal intubations that occurred, one false-positive result occurred in the EDD test and auscultation. In the non-cardiac arrest patients (n=56), auscultation, the ETCO(2), and EDD test correctly identified 89.3, 98.2*, and 94.6%* of tracheal intubations, respectively (*, P<0.05 vs. the cardiac arrest patients). In the cardiac arrest patients (n=81), auscultation, the ETCO(2), and the EDD tests correctly identified 92.6**, 67.9, and 75.3% of tracheal intubations, respectively (**, P<0.05 vs. EDD and ETCO(2)). The frequencies of Cormack grade 1 or 2 were 83.9% in the non-cardiac arrest, and 95.1% in the cardiac arrest patients. In conclusion, the ETCO(2) monitor is the most reliable method for verifying tracheal intubation in non-cardiac arrest patients. During cardiac arrest and cardiopulmonary resuscitation, however, negative results by the ETCO(2) or the EDD are not uncommon, and clinical methods are superior to the use of these devices.

The efficacy of esophageal detector devices in verifying tracheal tube placement: a randomized cross-over study of out-of-hospital cardiac arrest patients.

We performed this prospective study to evaluate the efficacy of esophageal detector devices (EDDs), both the bulb and the syringe-type, to indicate positioning of endotracheal tubes (ETTs) in out-of-hospital cardiac arrest patients. Forty-eight adult patients with out-of-hospital cardiac arrest were enrolled. Immediately after tracheal intubation and ETT cuff inflation in the emergency department, the patients were allocated randomly to two cross-over groups. In Group 1 (n = 24), patients underwent a bulb test and a syringe test in sequence. In Group 2 (n = 24), patients underwent a syringe test and a bulb test in sequence. End-tidal carbon dioxide (ETCO2) was also monitored. In 56 attempts at tracheal intubation, the bulb, the syringe, and ETCO2 indicated all eight esophageal intubations. In 48 tracheal intubations, the bulb test correctly indicated 34 tracheal intubations (sensitivity, 70.8%). The syringe test identified 35 tracheal intubations (sensitivity, 72.9%). The results of both tests agreed in 33 tracheal intubations. ETCO2 was detected in 31 tracheal intubations (sensitivity, 64.6%). No statistical difference was found among the tests. EDDs were less sensitive in detecting tracheal intubation for out-of-hospital cardiac arrest patients. Therefore, proper clinical judgment in conjunction with these devices should be used to confirm ETT placement in these difficult situations. Implications The esophageal detector device (EDD) failed to confirm endotracheal tube (ETT) placement in more than 25% of tracheal intubations in this study. One must not rely too heavily on the results of the EDD alone, and proper clinical judgment in conjunction with all available modalities should be used to confirm ETT placement in out-of-hospital cardiac arrest patients.

Accuracy and Reliability of the Self-inflating Bulb to Verify Tracheal Intubation in Out-of-hospital Cardiac Arrest Patients

BackgroundTo determine the sensitivity and specificity of the self-inflating bulb (SIB) to verify tracheal intubation in out-of-hospital cardiac arrest patients. MethodsSixty-five consecutive adult patients with out-of-hospital cardiac arrest were enrolled. Patients were provided chest compression and ventilation by either bag–valve–mask or the esophageal tracheal double-lumen airway by ambulance crews when they arrived at the authors’ department. Immediately after intubation in the emergency department, the endotracheal tube position was tested by the SIB and end-tidal carbon dioxide (ETco2) monitor using an infrared carbon dioxide analyzer. We observed the SIB reinflating for 10 s, and full reinflation within 4 s was defined as a positive result (tracheal intubation). ResultsFive esophageal intubations occurred, and the SIB correctly identified all esophageal intubations. Of the 65 tracheal intubations, the SIB correctly identified 47 tubes placed in the trachea (72.3%). Delayed but full reinflation occurred in one tracheal intubation during the 10-s observation period. Fifteen tracheal intubations had incomplete reinflation during the observation period, and two tracheal intubations did not achieve any reinflation. Thirty-nine tracheal intubations were identified by ETco2 (60%). When the SIB test is combined with the ETco2 detection, 59 tracheal intubations were identified with a 90.8% sensitivity. ConclusionsThe authors found a high incidence of false-negative results of the SIB in out-of-hospital cardiac arrest patients. Because no single test for verifying endotracheal tube position is reliable, all available modalities should be tested and used in conjunction with proper clinical judgment to verify tracheal intubation in cases of out-of-hospital cardiac arrest.

Methotrexate poisoning with acute hepatorenal dysfunction

A 17-year-old girl receiving high-dose methotrexate for the treatment of osteosarcoma developed complications of acute renal failure and liver dysfunction with a coagulation disorder. The methotrexate concentrations were quickly reduced from 600 μmol/L to 50 μmol/L by treatment with plasma exchange and hemodialysis at 72 hours after discontinuation of the drug. After this reduction, continuous hemodiafiltration was initiated to further lower the methotrexate concentrations because of the persistently high and then the actual rebound in the plasma concentrations after plasma exchange and hemodialysis treatment. Continuous hemodiafiltration was able to reduce the concentrations without any rebound, despite its low column clearance. The rebound in plasma methotrexate concentrations seems to be corrected by plasma methotrexate after plasma exchange and/or hemodialysis.

Activation of sensory neurons contributes to reduce spinal cord injury in rats

We previously demonstrated that activation of sensory neurons increases endothelial prostaglandin I(2) (PGI(2)) production by releasing calcitonin gene-related peptide (CGRP). Since PGI(2) reduces post-traumatic spinal cord injury (SCI) by inhibiting tumor necrosis factor (TNF) production, activation of sensory neurons in the spinal cord tissue may ameliorate spinal cord injury. This study examines these possibilities using rat models of compression trauma-induced SCI. Both SB366791, a specific vanilloid receptor antagonist, and CGRP (8-37), a CGRP receptor antagonist, significantly inhibited trauma-induced increases in spinal cord tissue 6-keto-PGF(1alpha) levels. SB366791, CGRP (8-37) and indomethacin (IM) enhanced increases in spinal cord tissue TNF levels at 2h after trauma and exacerbated motor disturbances. Administration of CGRP significantly reduced motor disturbances and inhibited increases in spinal cord tissue TNF levels through enhancement of increases in tissue levels of 6-keto-PGF(1alpha). These observations strongly suggest that activation of sensory neurons might ameliorate compression trauma-induced SCI, inhibiting TNF production through enhancement of endothelial PGI(2) production. Thus, although the spinal cord sensory neurons function as nociceptive neurons, they could also be critically involved in the cytoprotective system that attenuates SCI development and, thus, pharmacological stimulation of spinal cord sensory neurons might contribute to reduce spinal cord injury.

Possible involvement of central C–type natriuretic polypeptide receptor on water intake in spontaneously hypertensive rats, but not in normotensive Wistar-Kyoto rats

The present study was designed to examine the possible role of brain C-type natriuretic polypeptide receptor (GC-B) in spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto rats (WKY). The level of GC-B mRNA in various regions of the brain in both SHR and WKY was examined in the present study. The GC-B mRNA was unevenly distributed in rat brain, the transcript being expressed predominantly in the hypothalamus and cerebellum but comparatively at low level in the striatum and septum. However, the level in the septum was 3-fold higher in SHR than than in age-matched WKY, while no differences were observed in other regions of the brain. Intracerebroventricular administration of antisense oligonucleotide to GC-B mRNA inhibits the night-time water intake in SHR, but not in WKY. However, the daily food intake was not significantly altered by the injection of antisense oligonucleotide in both strains. These results demonstrate that the brain GC-B mRNA, particularly in septum, is increased in SHR and this increase may be closely related to the regulation of water-drinking behaviour in SHR.

POTENTIATION OF DIPSOGENIC ACTIONS BY CENTRALLY ADMINISTERED TYPE-C NATRIURETIC PEPTIDE IN SPONTANEOUSLY HYPERTENSIVE BUT NOT WISTAR-KYOTO RATS

1. The effects of type‐C natriuretic polypeptides (CNP) on the central dipsogenic and pressor responses to angiotensin II (AngII) were studied by the administration of agents into the lateral cerebral ventricle under conscious and unrestrained conditions in normotensive Wistar‐Kyoto (WKY) and spontaneously hypertensive rats (SHR).