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Biomedical subjects

B Turinetto

Publications and source records attributed to B Turinetto.

At least 19 recordsLinked to original sources
PubMed2000

Delayed treatment of isthmic aortic rupture.

Traumatic rupture of the thoracic aorta is a life-threatening injury with a high mortality, and is difficult to manage in polytraumatized patients. Between 1980 and 1998, 50 patients were admitted to our Department with acute traumatic aortic rupture (TAR). The site of lesion was usually isthmic (86% of patients). From 1980 to 1992, 21 patients (Group I) underwent emergency surgical repair; from 1992 to January 1998, 29 patients (Group II) underwent intensive medical treatment, except one who was haemodynamically unstable and died 8h after the trauma from a massive haemothorax before an emergency thoracotomy could be attempted. The aortic rupture was followed up by MRI or CT scan. Twenty-one patients in Group II underwent aortic repair an average of 8.6 months after the injury. In two patients the operation was expedited because of an enlarging aortic aneurysm. In Group I the postoperative mortality was 19%, three patients developed postoperative paraplegia and one acute renal failure. In Group II there were no postoperative deaths and no major complications.

Adult↗
PubMed1998

Surgical indications and timing of repair of traumatic ruptures of the thoracic aorta.

BACKGROUND: The outcome of patients with acute traumatic rupture of the thoracic aorta after motor vehicle accidents is strongly conditioned by injuries to other districts. The timing of repair is controversial when the patients arrive alive to the hospital. METHODS: A series of 42 patients with acute traumatic rupture of the thoracic aorta observed between January 1980 and June 1996 was divided into two groups: group I underwent immediate repair (21 patients) and in group II operation was performed after intensive medical treatment and management of the associated lesions and monitoring of the aortic tear. RESULTS: The mortality in group I patients was 19% and the morbidity was more significant than in group II where no deaths were reported and complications were minor. CONCLUSIONS: Patients with acute traumatic rupture of the thoracic aorta may have a better fighting chance if aortic operation is postponed to the most favorable moment after undergoing life-sustaining measures and management of the major associated lesions. Needless to say, evolution should be closely monitored by computed tomographic scans and magnetic resonance imaging.

Accidents, Traffic↗
PubMed1993

[Role of transesophageal echography in the diagnosis of aortic dissection and in therapy programming].

The diagnostic accuracy of transesophageal echocardiography and its relevance on the decision making process were evaluated in 80 patients with suspected aortic dissection during a 37-month period. The diagnosis was proven by aortography and/or magnetic resonance and/or computerized tomography and/or surgery and/or autopsy in each case. Transesophageal echocardiography had no serious complication. A correct diagnosis of aortic dissection was made in 39 of 40 patients (sensitivity, 97.5%; specificity, 100%) and the type of dissection was correctly demonstrated in each case. Thrombi in the false lumen were detected in 16 patients. The primary entry site was correctly identified in 33 patients (85%). Aortic regurgitation was detected in 25 cases (severe in 9) and pericardial effusion in 14 (with tamponade in 2). Transesophageal echocardiography was more accurate than aortography in the diagnosis of noncommunicating intramural dissection (2 cases) and identified more precisely the retrograde extension of the dissection in DeBakey type III patients (4 cases). In 9 cases surgical indication was based on clinical data and transesophageal echocardiography alone. We conclude that transesophageal echocardiography allows a bedside, safe and accurate diagnosis of aortic dissection. In the majority of the patients it provides the minimal diagnostic information necessary to the therapeutical decision making.

Acute Disease↗
PubMed1993

Effect of glutathione monoethyl ester on glutathione level and cardiac energetics in reperfused pig heart.

The GSH level in myocardial tissue represents an important defense mechanism against oxygen toxicity. Since the ischemia-induced depletion of GSH might favour the cytotoxicity of oxygen-derived free radicals produced during reperfusion, we assessed the effects of the GSH donor, glutathione monoethylester, in anaesthetized pigs subjected to 90 minutes of coronary occlusion followed by 30 minutes reperfusion. The drug was infused intracoronarily at a dose of 1 mg/ml (0.5 ml/min) throughout the experimental period. After coronary occlusion and reperfusion, we found a decrease in GSH, ADP, ATP and phosphocreatine levels in reperfused compared with non-ischemic tissue. Less evident were the differences in mitochondrial function, there being only a reduction in the reperfused tissue of the respiratory control index and state 3 respiration values when pyruvate was used as substrate. The infusion with glutathione monoethylester decreased the depletion of tissue GSH and improved the GSH/GSSG ratio, particularly in the non-ischemic tissue. Moreover, the drug decreased the mitochondrial dysfunction at the level of pyruvate utilization and partially prevented the fall in ATP in the reperfused tissue. This study confirms a possible protective effect of glutathione monoethylester in the prevention of reperfusion-induced myocardial damage.

Adenosine Diphosphate↗
PubMed1990

Changes in myocardial mitochondrial respiration after ligation of the coronary artery in pigs.

After ligation of the left coronary artery, porcine cardiac mitochondria were isolated by homogenizing the tissue and treating the myofibrillar pellet with nagarse. When compared with unligated controls, the ischemic myocardium showed decreases in phosphocreatine (to 41%), ATP (to 56%) and in the mitochondrial respiratory control index (to 69% and 78% as measured with glutamate and succinate respectively). No changes were found in the corresponding P/O ratios. Similar results were obtained upon separation of the mitochondria into two main fractions by a density gradient technique, though only one of these fractions showed a fall in succinate-supported respiration. The results suggest that ischemia decreases the NADH-dehydrogenase activity of cardiac mitochondria.

Adenosine Diphosphate↗
PubMed1990

[Post-infarction rupture of the interventricular septum. Evaluation of the main clinical parameters and postoperative survival].

We reviewed 16 patients with ventricular septal rupture complicating myocardial infarction who underwent surgical repair between January 1984 and August 1987. Nine of them had anterior acute myocardial infarction (56%) and 7 inferior acute myocardial infarction (44%). The overall surgical mortality was 43.8%; in the group of patients with early treatment (less than 15 days after acute myocardial infarction) the mortality was 55%, while in the group with later treatment (16-30 days) the mortality was 28% (p-NS). Survival was unrelated to preoperative evidence of shock, magnitude of the shunt or the extent of coronary artery disease. We found a better in-hospital survival in the group of patients with ventricular septal rupture complicating anterior acute myocardial infarction (77%) vs inferior acute myocardial infarction (28%) with statistical significance (p less than 0.05). After a follow-up ranging from 1 to 40 months (mean: 17 months), 78% of the in-hospital survivors were alive and they were all in NYHA class II-III. We conclude that the major determinant of in-hospital survival in our patients was the anatomical site of acute myocardial infarction. Furthermore, we believe that the surgical repair of the ventricular septal defect is helpful in modifying the negative outcome of such an acute myocardial infarction complication.

Aged↗
PubMed1987

[Atrial fibrillation in patients after aortocoronary bypass. Correlation with electrophysiologic properties evaluated intraoperatively].

An electrophysiologic study (EPS) has been performed before and after cardioplegia in 50 patients (pts) who underwent a coronary by-pass graft intervention (CBPG) in order to investigate the possible mechanism explaining the frequent episodes of paroxysmal atrial fibrillation (PAF) complicating the early follow-up and the possible role of the type of caval cannulation. Twenty-five pts underwent a separate caval cannulation and twenty-five only cannulation of the inferior vena cava. EPS has been performed before (34 degrees C) and after cardioplegia (37 degrees C). PAF complicated the 15 days early follow-up of 32% of the pts; 24% of the pts operated with 1 cannula and 40% of the operated with 2 cannulae respectively (N.S.). The pts with AF had an high percentage of splitting of the atrial signals during atrial premature stimulation (77% vs 5%, p less than 0.002) and a significant dispersion of the conduction times between high and low right atrium (36 +/- 21 vs vs 11 +/- 14 msec, p less than 0.002). In conclusion PAF has an high incidence in the early follow-up of CABG operation and occurs independently of the type of caval cannulation. The presence of a major dispersion of intra right atrial conduction together with an high incidence of fractionizing potentials already before cardioplegia in the pts with AF suggests that the atria with intrinsic conduction delays can be per se predisposed to develop atrial tachyarrhythmias during the early follow-up.

Atrial Fibrillation↗
PubMed1981

[Postoperative hypertension in the surgery of the large arteries].

High incidence of postoperative arterial hypertension, confined to the first 24-48 hours and independent of the preoperative pressure situation, has been noted in patients following vascular surgery. The phenomenon is more frequent in patients whose angiosclerotic symptomatology goes back more than 2 years, and in those in whom preoperative investigation showed high daily variability in measured values, always however within non-pathological limits. Analysis of possible intraoperative pathogenetic factors in postoperative hypertension reveals a significant relationship between this phenomenon and inhalatory anesthesia, particularly with fluothane and curarization with D-tubocurarine. Co-responsibility of respiratory factors, particularly hypercapnia, has never been documented by haemogasanalysis. As for the pathogenetic mechanisms responsible for this type of hypertension, measurement of urinary catecholamines has revealed a close relationship between the two phenomena. The same investigation, extended to a wider group of patients, showed that by comparison with patients submitted to balanced anaesthesia, those who had received inhalatory anaesthesia with fluothane show, with much greater frequency, increased urinary elimination of catecholamines during the operation and for 24-48 hours afterwards. Catecholaminic hyperincretion, more frequent in fluothane anaesthesia, thus seems to be an important pathogenetic factor in these hypertensive manifestations in which the angiosclerotic medium presumably acts as an amplifier.

Anesthesia↗