Acute airway obstruction following placement of a subclavian Hickman catheter

The purpose of this case report is to describe the events, intervention, and aetiology which led to acute airway obstruction in an adult patient after the placement of a Hickman catheter. Airway obstruction secondary to superior vena cava obstruction occurred after placement of a subclavian vein Hickman catheter. This was felt to occur, in part, to a narrowed superior vena cava as evident by subclavian venography. It resulted in emergency oral tracheal intubation to relieve airway obstruction. Shortly after removal of the Hickman catheter, the signs of superior vena cava obstruction syndrome resolved and the patient was extubated without incidence. It is concluded that, although rare, the serious complication of acute airway obstruction can occur after placement of a Hickman catheter.     

Interceptive effect of Lapachol in rats

Lapachol is a naphtoquinone with therapeutic potential against Chagas disease and is also used as an antimalarial agent. To study the reproductive toxicity potential of Lapachol, pregnant Wistar rats were treated with 0.5 mL of distilled water (control group), 0.5 mL of hydroalcoholic solution (vehicle group), or 20 mg of Lapachol in 0.5 mL of hydroalcoholic solution (treated group) by oral gavage from the 8th to the 12th day of pregnancy. The following variables were observed: maternal body weight on days 1, 6, 15, and 21; food intake on days 2, 6, 15, and 21 of pregnancy. The number of live and dead fetuses and the sites of resorptions were counted. The ovaries were weighed and the corpora lutea were counted. Data were analyzed by ANOVA one-way Dunnett test and chi 2 test. Results showed that mothers were uneffected but there was 100% fetal/embryo mortality, indicative of a strong interceptive effect of Lapachol in rats.     

Defensive reactions are counteracted by midazolam and muscimol and elicited by activation of glutamate receptors in the inferior colliculus of rats

 The inferior colliculus is involved in conveying auditory information of an aversive nature to higher cortical structures. Gradual increases in the electrical stimulation of this structure produce progressive aversive responses from vigilance, through freezing, until escape. Recently, we have shown that microinjections of NMDA into the inferior colliculus mimic these aversive effects and that the neural substrates responsible for learned escape behavior in the inferior colliculus are regulated by GABA−benzodiazepine mechanisms. In the present study, we extend these observations showing that unlearned aversive responses are also depressed by muscimol and midazolam, both GABA-benzodiazepine agonists, and that microinjection of glutamate, an excitatory amino acid, into the inferior colliculus can trigger freezing responses. Electrical stimulation of the inferior colliculus of rats placed inside an open field allowed the determination of thresholds for the aversive responses, alertness, freezing and escape. Systemic administration (3 and 5.6 mg/kg) as well as microinjections into the inferior colliculus of the anxiolytic compound midazolam (10, 20 and 40 nmol) caused increases in threshold for these aversive responses. Similar results were obtained following microinjections of the GABA-A agonist muscimol (0.1, 1 and 5 nmol) into this brainstem structure. Microinjections of low doses of glutamate (5 nmol), presumed to activate mainly AMPA/kainate receptors, into the ventrolateral division of the central nucleus of the inferior colliculus of rats placed inside a circular arena induced aversive reactions, characterized by freezing responses. However, higher doses of glutamate caused no apparent effects. GDEE, an AMPA/kainate receptor antagonist, inhibited, whereas AP7, a NMDA receptor antagonist, did not influence these responses. It is suggested that GABA-benzodiazepine processes modulate the expression of defensive reactions in the inferior colliculus and that activation of fast-acting excitatory amino acid receptors in this midbrain region can trigger the initial steps of the defense reaction without eliciting the motor explosive behavior usually seen following the activation of NMDA receptors. Received: 13 May 1998 / Final version: 12 August 1998     

Differentiating the action of cataleptogenic bodies (author's transl)]

Responses to several drugs called cataleptogenic as shown in the "Catalepsy Testbattery", were analyzed for their trigger mechanism. The results lead to the conclusion that the neurophysiological mechanisms of neuroleptic drugs are based on an inhibition of the processing of afferences. Therefore the term "experimental catalepsy" seems to be applicable only to these drugs. On the contrary, opioid drugs induce a state of rigidity which even can be increased by manipulating the animal. These conclusions are verified by electromyographical studies. In our opinion this syndrome should not be called "catalepsy" but "opiate stiffness".     

Ruling out acute myocardial infarction. A prospective multicenter validation of a 12-hour strategy for patients at low risk

BACKGROUND. Although previous investigations have suggested that 24 hours is required to exclude acute myocardial infarction in patients who are admitted to a coronary care unit for the evaluation of acute chest pain, we hypothesized that a 12-hour period might be adequate for patients with a low probability of infarction at the time of admission. METHODS. Using a Bayesian model, we developed a strategy to identify candidates for a shorter period of observation from an analysis of a derivation set of 976 patients with acute chest pain who were admitted to three teaching and four community hospitals. In the derivation set, patients whose clinical characteristics in the emergency room predicted a low (less than or equal to 7 percent) probability of myocardial infarction had only a 0.4 percent risk of infarction if they had neither abnormal levels of cardiac enzymes nor recurrent ischemic pain during the first 12 hours of hospitalization. In an independent testing set of 2684 patients from the seven hospitals, 957 admitted patients (36 percent) were classified as candidates for this 12-hour period of observation according to a previously published multivariate algorithm. Few of these patients were actually transferred from a monitored setting at 12 hours. RESULTS. Of the 771 candidates for a 12-hour period of observation who did not have enzyme abnormalities or recurrent pain during the first 12 hours, 4 (0.5 percent) were subsequently found to have acute myocardial infarction, and only 3 (0.4 percent) died after primary cardiac arrests, all of which occurred three to five days after admission. Rates of other major cardiovascular complications were low in the patients who might have been transferred from the coronary care unit after 12 hours with this strategy. In patients with a higher initial risk of infarction, the standard strategy of 24-hour observation identified all but 11 of 739 acute myocardial infarctions (1 percent). CONCLUSIONS. Emergency room clinical data can be used to identify a large subgroup of patients for whom a 12-hour period of observation is normally sufficient to exclude acute myocardial infarction. Patient-specific evaluation and treatment can then proceed without the restrictions imposed by "rule-out" protocols for myocardial infarction.