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Items 1 - 4 of 4 |
One page. |
Critical drug overdoses and emergency medical services: where should we put our efforts?
Perez A.
Publication Types:
PMID: 15576533 [PubMed - in process]
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Use of vasopressin in a canine model of severe verapamil poisoning: a preliminary descriptive study.
Sztajnkrycer MD, Bond GR, Johnson SB, Weaver AL.
Department of Emergency Medicine, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA. sztajnkrycer.matthew@mayo.edu
OBJECTIVES: The purpose of this preliminary study was to evaluate the effect of arginine vasopressin (AVP) administration in a model of shock induced by calcium channel antagonist overdose and to determine endogenous serum AVP concentrations in calcium channel antagonist-induced shock. METHODS: This was a controlled, randomized laboratory investigation based on a previously described canine model of verapamil toxicity. After induction of verapamil toxicity, animals in both the control and the experimental groups (n = 6 each) received a continuous infusion of verapamil. Experimental animals received an escalating dose of AVP, while control animals received an equal volume of 0.9% saline infusion. The hemodynamic end point was return of mean arterial pressure (MAP) to within 20% of baseline. Surviving animals were killed after 60 minutes. RESULTS: In the treatment group, administration of low-dose AVP (4 mU/kg/min) resulted in further declines in cardiac index and heart rate. No significant change was noted in MAP with low-dose AVP. A slight increase in MAP was noted with both escalating doses of AVP and equivalent volumes of normal saline. By the end of the 60-minute antidote/saline phase, the MAPs of the saline control group and the AVP experimental group were similar. The primary hemodynamic end point was not achieved in either the AVP or the saline control arm. Mean baseline serum AVP concentration in control animals was 5.8 pg/mL, increasing to 225 pg/mL during the toxicity phase. CONCLUSIONS: In an animal model of verapamil-induced shock, endogenous AVP levels increased nearly 40-fold compared with baseline levels. Escalating doses of exogenous AVP worsened cardiac index and failed to return MAP to within 20% of baseline.
PMID: 15576513 [PubMed - in process]
Oral arsenic trioxide poisoning and secondary hazard from gastric content.
Kinoshita H, Hirose Y, Tanaka T, Yamazaki Y.
Niigata City General Hospital, Niigata, Japan. kinosita@hosp.niigata.niigata.jp
In a suicide attempt, a 54-year-old man ingested arsenic trioxide. Gastric lavage was performed, but most of the poison remained as a mass in his stomach. A total gastrectomy was also performed to avoid intestinal perforation and arsenic poisoning. After the operation, he developed ventricular fibrillation. At one point, his circulation recovered spontaneously, but he later died from refractory circulatory failure. Many medical staff members were exposed to fumes from the patient's stomach. Some of the staff were diagnosed with corneal erosion or laryngitis. Because arsenic trioxide reacts with acid to produce arsine, the symptoms experienced by medical staff are directly attributable to arsine produced as a result of the reaction of arsenic trioxide with gastric acid. This case highlights the need for the introduction of protective measures to safeguard medical staff from exposure to arsine gas during the treatment of patients poisoned from ingested arsenic trioxide.
PMID: 15573038 [PubMed - in process]
Severe salicylate poisoning treated conservatively.
Basavarajaiah S, Sigston P, Budack K.
Department of General Medicine, Kent and Sussex Hospital, Tunbridge Wells TN4 9AT, UK. drsandy270478@yahoo.co.uk
PMID: 15574860 [PubMed - in process]
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