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A series of new tantalum complexes containing the κ 3 O,S,O-type alkoxide ligand from 2,2′-thiodiethanol (tdgolH 2 ) have been synthesized and characterized. The complexes [TaCp*Cl 2 {[O(CH 2 ) 2 ] 2 S-κ 3 O,S,O}] (1) and [TaCp*Me 2 {[O(CH 2 ) 2 ] 2 Sκ 3 O,S,O}] (2) were prepared by reaction of 2,2′-thiodiethanol with [TaCp*X 4 ] (X = Cl, Me). The tantalum dihydride complex [TaCp*H 2 {[O(CH 2 ) 2 ] 2 S-κ 3 O,S,O}] (3) and its analogue containing the 2,2′-thiobis(6-tert-octylphenolate) ligand (4) were synthesized by reaction of the respective dichlorides with 2 equiv of NaBHEt 3 . In addition, [TaCp*Me(TfO){[O(CH 2 ) 2 ] 2 S-κ 3 O,S,O}] (5) and [TaCp*(TfO) 2 {[O-(CH 2 ) 2 ] 2 S-κ 3 O,S,O}] (6; TfO = F 3 COSO 2 − ) were synthesized by reaction of 2 with 1 and 2 equiv of triflic acid, respectively. The reactivity of this family of complexes with nucleophiles was also studied and, as a result, three azatantalacyclopropane complexes (7−9) and the carbene [TaCp*{C(Me)N(H)xylyl-κ 1 C}(OH){[O(CH 2 ) 2 ] 2 S-κ 3 O,S,O}] (10) were characterized. The single-crystal structures of 1 and 6 were determined by Xray diffraction methods.

Poisoning by smoke is the main cause of morbidity and mortality in fires. Smoke is a mixture of carbonaceous particles suspended in hot air and toxic gases. Of these, carbon monoxide (CO) and primarily hydrocyanic acid (CNH), are those that provoke tissue anoxia. The clinical manifestations of smoke poisoning are variables. Some of the potential manifestations could be: eye irritation, sore throat, laryngeal stridor, dysphagia, carbonaceous sputum, cough, dyspnea, laryngospasm, bronchospasm, coronary syndrome, coma, hypoxemia, lactic acidosis, cyanosis and death. In the assessment of these patients the presence of soot in the nose, mouth or sputum suggests serious poisoning. Lactate levels higher than 10mmol/L indicates levels of cyanide major than 40micromole/L. The pulse co-oximetry has assumed an important step forward for the diagnosis, appraisal and monitoring of these patients. In the treatment it will be essential to assess the need of an early intubation. The administration of oxygen to the 100% will be essential. As an antidote to the cyanide, the first-choice is the hydroxocobalamin. Its administration has to be early. Its administration criteria are: patient who has inhaled smoke (remnants of soot in the mouth, pharynx or sputum) and has neurological disorder (confusion, coma, agitation, seizures) and also presents one of the following circumstances: bradypnea, respiratory arrest, cardiorespiratory arrest, shock, hypotension, lactate ≥8mmol/L or lactic acidosis. Logically, the rest of the management will be conventional depending on symptoms or complications.

Hypokalemia in opiate overdose is an event concerning which no previous references have been made. Twenty-four addicts to parenteral drugs without recent withdrawal, admitted consecutively to the emergency room of University Hospital of Salamanca, were studied. All patients had the clinical criteria of acute opiate intoxication (acute alteration of mental status, respiration of 12 or less per minute, miotic pupils); the questionnaire study, conducted after recovery, confirmed the diagnosis of intravenous heroin overdose, which nine cases coexisted with intravenous cocaine administration. No other psychodepressant drugs, such as benzodiazepines, alcohol, or barbiturates, were associated. All the subjects were treated with the opiate antagonist naloxone, given at an initial dose of 0.4 mg intravenously; this was repeated after 3-10 minutes if no response occurred. No supplements of potassium were added. Blood samples were obtained from all subjects before naloxone administration. Values are expressed as means_+ SE. Pair-wise comparisons were analyzed using the Wilcoxon or Mann-Whitney tests for paired or unpaired observations, respectively.The mean plasma potassium concentration of all patients at admission was 3.43 +0.12 mmol/1 (range 2.30-5.10 mmol/1); 14 patients (58.3%) were hypokalemic (K+< 3.5 mmol/1). Arterial blood gases and the acid-base balance measured at admission showed a decrease in both pH (7.20_+0.04) and bicarbonate (22.40 _+ 2.11 mmol/1), with hypoxemia (pO2 = 56.4 ± 3.35 mmHg) and hypercapnia (pCO2 = 57.2_+ 4.42 mmHg). There was a relationship between the level of consciousness and kalemia: the deep coma patients (n= 17) had plasma potassium concentrations that were significantly lower than patients with obnubilation, but who responded to painful stimuli (n=7; 3.21_+0.11 mmol/1 vs 4.01 _+ 0.28 mmol/1, P <0.01); also, significantly lower plasma potassium concentrations were observed in the patients who needed more than 0.8 mg naloxone for recovery of consciousness than those who needed lower doses of the antagonist (2.95_+0.16 mmol/1 vs 3.60_+0.42 mmol/1, P<0.02). Plasma potassium concentrations were higher in combined heroin and cocaine overdose than in heroin overdose alone. In six patients it was possible to determine plasma potassium concentrations just after recovery of consciousness after naloxone administration, showing a decrease of kalemia with respect to its values at admission (Fig. 1); spontaneous normalization -without potassium supplements of kalemia in these patients was verified 4-6 h after recovery from the overdose episode.Experimental studies have shown a dissociation of the sympathetic nervous system and adrenal medullary responses fol-lowing sympathoadrenal stimulus in acute hypoxia [2] and after the administration of naloxone to rats chronically treated with morphine [1]. The hypokalemiant action of epinephrine due to stimulation of 132-adrenergic receptors and the hyperkalemiant action of norepinephrine (cz-adrenergic stimulus) [3]. These observations led us to hypothesize t...

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1–4% of all visits to emergency rooms are due to adverse drug events (ADEs), but data about preventability and cost due to preventable ADEs in this setting are limited. OBJECTIVE: To determine the incidence of ADEs associated with emergency department (ED) visits and subsequent hospital admissions; to assess their preventability and to estimate the costs of preventable ADEs to our institution, a 750 bed university tertiary care center. METHODS: All patients who visited the ED from October 1995 to March 1996 were prospectively‐evaluated. Recorded data included: medical and medication history, laboratory data, serum drug concentrations, ED procedures, intervention therapy, and characteristics and outcome of ADEs. Patients admitted as a result of the ADE were followed to collect information of invasive and non invasive procedures, therapy, length of stay, and intensive care. Preventable ADEs were analyzed to identify the associated factors. A cost analysis was performed. RESULTS: From a total of 33,975 visits to the ED, 766 (2.25%) were due to ADEs. A total of 336 (43.9%) ADEs were assessed as preventable; these resulted in 121 hospital admissions, 1,575 stays, 121 ICU days, and 15 deaths. Inappropiate dose prescribed and inadequate monitoring of drug therapy accounted for 46% and 31% of preventable ADEs; 17% preventable ADEs were due to automedication. The estimated hospital annual cost for all ADEs was $1.42 million and for preventable ADEs was almost $1 million. CONCLUSIONS: Many ADES seen in ED patients are preventable and contribute substantially to hospital costs. At a time when much emphasis is put on the limitation of health expenses, here is a domain where expense‐cutting could probably be done reasonably easily, while increasing quality of care.