[The end of life and deontology].
Since palliative care and euthanasia are very much in the news at the moment, there is a need to remind the medical profession of the rules of ethics dealing with the topic.
Biomedical subjects
Publications and source records attributed to J Marin.
Since palliative care and euthanasia are very much in the news at the moment, there is a need to remind the medical profession of the rules of ethics dealing with the topic.
The kinetics of 99mTc-Trimethyl-Br-IDA blood clearance was analysed in the rat 24 h after warm ischaemia and reperfusion of the liver. There were changes in the elimination of 99mTc-Trimethyl-Br-IDA depending on the length of the ischaemic period and the dose given. Statistically significant differences were found between the various periods of ischaemia when higher doses of the radionuclide were utilised. At lower doses, the clearance was not capable to discriminate between control rats and rats submitted to 45 min of ischaemia, but it did discriminate more severe degrees of ischaemic liver injury. Instead, galactose elimination capacity discriminated between ischaemic and control rats, but not between 45 and 90 min or between 90 and 120 min of ischaemia. Alanine aminotransferase was able to discriminate between control and ischaemic rats and between 45 and 90 min of ischaemia, but not between 90 and 120 min of ischaemia. The response of 99mTc-Trimethyl-Br-IDA clearance under extreme conditions of ischaemia and reperfusion is consistent and opens a possible window for the application of this test in the quantification of liver function in severely damaged livers and in decision making and prognosis in liver disease.
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OBJECTIVE: To compare a blind manual bedside method for placing feeding tubes into the small bowel vs. a sonographic bedside technique in critically ill patients. DESIGN: Prospective study with a random sample. SETTING: Multidisciplinary intensive care unit in a tertiary care university hospital. PATIENTS: Thirty-five adult patients. All patients were hemodynamically stable, mechanically ventilated, and required a nasoenteric tube placement for short-term enteral feeding due to impaired gastric emptying. INTERVENTIONS: A well-known, blind, manual, bedside method for postpyloric tube placement was always attempted first in all cases. The technique was considered successful when a postpyloric location of the tip of the tube was achieved as shown by abdominal roentgenogram. However, if after 30 mins we failed to enter the small bowel, a radiologist attempted a sonographic bedside technique for postpyloric tube insertion. Finally, when the feeding tube was in place, before starting enteral nutrition, a nasogastric tube was inserted into the stomach. MEASUREMENTS AND MAIN RESULTS: The blind manual method was successful in nine (25.7%) of the 35 patients and the final location of these feeding tubes was the proximal jejunum. The average time for placement of the feeding tubes with this manual technique was 13.9 +/- 7.4 mins (range 5 to 30). The sonographic technique was successful in 22 (84.6%) of the remaining patients and the final location of the feeding tubes was three (11%) tubes in the second portion of the duodenum, eight (31%) tubes in the third portion of the duodenum, and 11 (42%) tubes in the proximal jejunum. The average time for placement with the sonographic technique was 18.3 +/- 8.2 mins (range 5 to 35). The pyloric outlet was sonographically akinetic or severely hypokinetic in 13 patients, and in four of them, we were unable to achieve postpyloric tube placement. In these four patients, the tubes were subsequently placed by endoscopy. CONCLUSIONS: The sonographic bedside technique for placing feeding tubes into the small bowel in critically III patients has a success rate of 84.6% (confidence interval 71% to 98%) after the failure of the blind bedside manual method, proving that the former is significantly more successful. This sonographic technique facilitates the insertion of the tubes in patients who cannot be moved and in those patients with severe impairment of the peristaltic activity of the stomach.
In Belgium, the "Conseil de l'Ordre des Médecins", responsible for the the respect of ethical and professional rules receive many complaints about drafting and managing of medical certificates; the author describes the basic regulations.
Our study was carried out on 70 patients with invasive squamous carcinoma of the uterine cervix (CC) or invasive adenocarcinoma of the uterine cervix at all stages, admitted to the University Department of Gynecology and/or to the Institute of Oncology in Ljubljana. The patients were not selected by age. A questionnaire on known risk factors in CC was filled in for each of the 70 patients, and two tumor smears were taken for the determination of human papilloma viruses (HPV) 16 and 18 by means of in situ hybridization and polymerase chain reaction (PCR). Each patient also had the serum level of vitamin A determined. The results of our study revealed a correlation between HPV 16 or 18 infection (60:40) and CC. When analysing some already known risk factors, no statistically significant difference could be established for any of the factors studied, except for the age at first birth.
We report two cases of acute myeloid leukemia (M1 and M5B subtypes) with a similar translocation, t(3;11)(q21;q13). We discuss the involvement of these breakpoints in acute leukemia and their putative clinical implications.
Cytogenetic data of 41 patients diagnosed with multiple myeloma (MM) are reported. In all samples, cytogenetic studies were made of short-term and B-cell-stimulated culture: 20 cases (48.8%) showed chromosome abnormalities; 14 karyotypes were hypo- or pseudodiploid, and six were hyperdiploid. The most frequent numerical changes affected chromosomes 7, 11, 5 (gains), 14, 20, and Y (losses). Chromosome structural rearrangements of 22q were noted in six patients. Other and recurrent cytogenetic abnormalities were changes involving chromosomes 1, 14, and 17. A significant relation was observed between presence of chromosome abnormalities and the following hematologic parameters: clinical stage III (p = 0.0212), bone marrow (BM) plasma cell infiltration greater than 30% (p = 0.0379), presence of bone lesions (p = 0.0051), and beta 2-microglobulin levels greater than 4,000 md/dl (p = 0.0194).
Previous studies from several laboratories have established that adenovirus is a common cause of severe childhood bronchiolitis. The observation that children with an established history of bronchiolitis subsequently developed unremitting airways obstruction even after adequate steroid therapy led us to postulate that this bronchial obstruction might be due to persistence of an adenoviral infection. This hypothesis was tested by performing bronchoalveolar lavage (BAL) on a group of 34 children with a mean age of 5 yr (range, 14 mo to 14 yr) who showed an unfavorable response to standard corticosteroid and bronchodilator therapy. Analysis of cytospin preparations of BAL fluid at the light-microscopic level, using a monoclonal antibody to detect adenoviral antigens, demonstrated that capsid protein was present in 31 of 34 (94%) of the children examined. Limited repeat studies within 1 yr showed 6 of 8 (75%) were positive twice when tested on two occasions, and that three were positive in all occasions when sampled three times. Cultures of the BAL fluid were also positive for adenovirus in six of six cultures performed, indicating that the virus was in some cases replicating. Similar studies of control patients without persistent asthma showed no evidence of adenovirus. We conclude that persistent and/or latent adenoviral infection may contribute to the pathogenesis of childhood asthma in which there is an unfavorable response to steroid and bronchodilatation therapy.
The modifications of systemic hemodynamics, oxygen transport and tissular oxygenation in mechanically-ventilated critical ARF (acute respiratory failure) patients, after the correction of its hypocapnia by addition of dead space (VD) are determined. The prospective and randomized study was carried out in a multidisciplinary ICU. Fifteen ARF patients were studied within the first 48 hours of evolution. All the patients were intubated and mechanically ventilated. Three stages were delimited: I) 30 min after the beginning of anesthesia; II) 30 min after adding 30 cm of VD; III) 30 min after replacing the previous VD with a VD of 60 cm. Similar steady states had been reached when the measurements were taken. Ventilation parameters and FiO2 were kept stable. In stage I the patients presented a pure respiratory alkalosis and, with respect to hemodynamics, a hyperdynamic situation. In stage II the acid-base balance was normalized with a continuation of the hyperdynamic situation and an increase in mixed venous oxygen tension and saturation (PvO2 and SvO2) (p < 0.001). Stage III was characterized by a pure hypercapnic acidosis and an increase in capillary wedge pressure (CWP) (p < 0.05), right atrial pressure (RAP) (p < 0.001) and cardiac output (Qt) (p < 0.001); simultaneously, the systemic vascular resistances (SVR) decreased (p < 0.01), the PvO2, SvO2 and oxygen delivery (DO2) increased (p < 0.001); oxygen utilization coefficient (OUC) decreased (p < 0.01). The results suggest that the variations in PvO2 and SvO2 are a direct consequence of the modifications in blood flow.(ABSTRACT TRUNCATED AT 250 WORDS)
Acetylcholine (ACh, 1-50 microM) and carbachol (1-10 microM) concentration-dependently enhanced the electrically evoked tritium overflow in guinea pig carotid arteries preincubated with [3H]norepinephrine (NE). However, lower concentrations of ACh and carbachol (0.05 and 0.1 microM) slightly reduced this overflow. Phentolamine (1 microM) potentiated the inhibitory and reduced the facilitatory effects of ACh, whereas hexamethonium (300 microM) did not modify either effect. Several muscarinic receptor antagonists shifted both ACh effects to the right. The order of potencies (apparent pKb values) was, for the facilitatory effect, atropine (10.14) > pirenzepine (8.66) > p-fluoro-hexahydrosila-difenidol (p-F-HHSiD) (6.82) > or = to methoctramine (6.33), and the order for the inhibitory effect in the presence of phenotolamine was atropine (10.00) > methoctramine (7.86) > or = to AF-DX 116 (7.70) > pirenzepine (6.72) > p-F-HHSiD (6.00). ACh (0.01-10 microM) induced endothelium-dependent vasodilatation in perfused segments of guinea pig carotid arteries, and this effect was competitively inhibited by the above-mentioned muscarinic receptor antagonists. The order of potencies (pA2 values) was atropine (9.96) > p-F-HHSiD (8.05) > pirenzepine (7.64) > methoctramine (6.83). These results suggest that the noradrenergic nerve endings in guinea pig carotid arteries possess M2 inhibitory and M1 facilitatory muscarinic receptors that modulate NE release, and the endothelial cells possess M3 muscarinic receptors that mediate ACh-induced vasodilatation.
Between 1983 and 1990 the authors treated 193 patients with laryngo-tracheal stenoses of diverse etiology. In 119 cases the stenoses was in the trachea. In 36 the stenoses extended to the subglottic region and in 1 case the carina was involved. The surgical procedure used in the tracheal stenosis was resection of the stenotic segment followed by end to end anastomosis. In most cases up to 6 cm of trachea could be resected. Two patients required a silastic prosthesis because the length of the stenotic area, 9 and 11 cm. The patient with the carinal involvement was treated by the insertion of a long Montgomery T tube. When the lesion included the subglottic area a partial resection of the cricoid cartilage and the damaged trachea was used. Associated surgical procedures had to be performed in order to close tracheo-esophageal fistulas, 2 cases, fixation of one of the vocal cords, 9 cases. Tracheal stenoses were cured in 90% of the cases with one surgical procedure, when the stenoses extended to the subglottic region, the cure rate was only 88.6%.
Lung function and bronchial response to methacholine were studied in 47 young adults who had had childhood asthma, and after a period of 14-21 years, showed a different clinical evolution. At present, these subjects have been classified in four clinical groups: asymptomatic, rhinitic, asthmatic only due to exercise, and asthmatic. The same study was performed in 23 healthy individuals without personal histories of respiratory or allergic pathology. We found low spirometric basal values in both the asthmatic group (FEV1 and FEF25-75) and in the group with asthmatic responses to exercise (FEF25-75). No significant differences were found among asymptomatic, rhinitic, and control groups. While airway hyperreactivity was observed in patients who still had asthma, the bronchial response to methacholine in asymptomatic and rhinitic groups was not different from the control group. We conclude that both lung function and bronchial response to methacholine in most of the adults who had asthma in infancy and had been without asthmatic symptoms for many years are similar to those observed in the general population.
The possible role of nitric oxide (NO) and other endothelial relaxant factors in the vasodilation induced by acetylcholine (ACh) in isolated segments of cat cerebral arteries was analyzed by using the following treatments: 1) the blockers of cyclo- and lipoxygenase, indomethacin and 5,8,11,14-eicosatetraynoic acid; 2) the NO inactivators, phenidone, hydroquinone and oxyhemoglobin; 3) the inhibitors of NO synthesis, NG-nitro-L-arginine methyl ester and NG-monomethyl-L-arginine; 4) the blockers of sodium pump activity, ouabain and K(+)-free medium; and 5) the antagonist of K+ channels, 4-aminopyridine (4-AP). A comparative study between the relaxant actions of exogenous NO and ACh was also performed. The most relevant results obtained were: 1) cat cerebral arteries are very sensitive to the endothelial effects of ACh, as well as to the exogenous NO; 2) ACh-induced endothelium-dependent dilatation is not affected by indomethacin and 4-AP, partially inhibited by 5,8,11,14-eicosatetraynoic acid, phenidone, hydroquinone, oxyhemoglobin and NG-nitro-L-arginine methyl ester and abolished by NG-monomethyl-L-arginine; 3) this latter effect is selectively antagonized by L-arginine, suggesting that the inhibition of NO synthase may be enough to abolish relaxation to ACh; and 4) sodium pump blockade abolished endothelial but not exogenous NO effects. From these results, we conclude that ACh-induced relaxation in these vessels can be entirely mediated by the release of endothelial NO. Although other endothelial factors cannot be discarded, their possible contribution to ACh-evoked relaxation is likely negligible.
A case of disseminated Scedosporium inflatum infection occurring in a neutropenic patient with acute myeloblastic leukemia is reported. Scedosporium inflatum was isolated from skin lesions, blood, urine and vitreous cultures. Amphotericin B treatment was ineffective in avoiding hematogenous spread. At autopsy, hyphae and ovoid conidia with truncate bases consistent with the morphology of Scedosporium inflatum were found in the lungs, kidneys, myocardium, liver, thyroid, spleen, lymph nodes, brain and the left eye. This is the first report of disseminated Scedosporium inflatum infection and the first time this organism has been isolated from a patient in Europe.
For a better understanding of low molecular weight heparin pharmacokinetics, 99m technetium labelled heparin and enoxaparin were injected intravenously to four normal volunteers, after approval by the Ethics Committee and preliminary animals studies. In vitro and in vivo, the labelled products proved to be stable and identical to the non-labelled drugs. Radioactivity curves in blood, organs and urines were similar for both products. Anti Xa plasma half-life was 3 times longer for enoxaparin than for heparin. Anti IIa plasma half-lives were similar. However, radioactivity persisted much longer than biological activities for both products. After chromatography, most of the radioactivity was bound to AT III, where an anti Xa activity peak was also detected. The anti Xa activity peak seen after adding AT III to plasma was much higher with heparin than with enoxaparin. In urine, biological activities, measured with AT III supplementation, were higher with enoxaparin than with heparin. These results suggest that phenomena other than biodistribution are responsible for the differences in pharmacokinetics observed between these two products. The two most likely explanations are differences in metabolism and/or a release of an endogenous factor.
The possible existence of a heterogeneous population of alpha 2-adrenoceptors (alpha 2A and alpha 2B, demonstrated by binding studies) in adrenergic nerve endings of cat and bovine cerebral arteries modulating noradrenaline release was investigated. Electrical field stimulation elicited an increase of tritium secretion from these vessels preincubated with (+/-)-[3H]noradrenaline, which was reduced by the alpha 2-agonists, clonidine (1 microM) and B-HT 920 (0.01 and 0.1 microM), in cat cerebral arteries but only by B-HT 920 in bovine cerebral arteries. This reduction was inhibited by the antagonist of the alpha 2B-subtype, prazosin, and the antagonists of alpha 2A- and alpha 2B-subtypes yohimbine and particularly rauwolscine. The effect of B-HT 920 was partially inhibited by clonidine in bovine, but not in cat cerebral arteries. In both types of arteries, prazosin, yohimbine and the alpha 1-agonist methoxamine (all at 1 microM) failed to modify the stimulated radioactivity liberation, whereas it was increased by 1 microM rauwolscine, and by yohimbine plus prazosin in cat cerebral arteries. The basal tritium release was enhanced by rauwolscine and prazosin in cat cerebral arteries but only by the latter in bovine cerebral arteries. These results suggest: (1) the existence of presynaptic alpha 2-adrenoceptors, mainly of the alpha 2B-subtype, in these vessels negatively modulating noradrenaline release, their activity being greater in cat than in bovine cerebral arteries, and (2) clonidine has no agonistic but a weak antagonistic action in the latter vessels.