The hypothalamic-pituitary-thyroid axis in preterm infants; changes in the first 24 hours of postnatal life

The purpose of this study was to measure serum T4, free T4, TSH, T3, rT3, T4 sulfate, and thyroxine binding globulin at four time points within the first 24 h of life (cord and 1, 7, and 24 h) in infants between 24 and 34 wk gestation. The infants were subdivided into gestational age groups: 24-27 wk (n = 22); 28-30 wk (n = 26); and 31-34 wk (n = 24). The TSH surge in the first hour of postnatal life was markedly attenuated in infants of 24-27 wk gestation [8 compared with 20 (28-30 wk) and 23 mU/liter (31-34 wk)]. T4 levels in the most immature group declined over the first 24 h, whereas levels increased in the more mature groups [mean cord and 24-h levels: 65 and 59 (NS) vs. 70 and 84 (P < 0.002) vs. 98 and 125 (NS) nmol/liter]. Free T4 and T3 showed only small, transient increases in the most immature group and progressively larger and sustained increases in the other gestational groups. rT3 and T4 sulfate levels in cord serum were higher in the most immature infants, and in all groups levels decreased initially and then variably increased. The features of a severely attenuated or failed hypothalamic-pituitary-thyroid response to delivery critically define this 24- to 27-wk group as distinct from more mature preterm infants.     

The variability of the heart rate in the first 24 hours after fibrinolytic therapy in acute myocardial infarct]

AIM OF THE STUDY: The role of heart rate variability changes in the appraisal of reperfusion after fibrinolytic therapy in acute myocardial infarction is still controversial. The aim of this study was to analyze the influence of reperfusion and infarct site on heart rate variability within 24 hours after infarction. PATIENTS AND METHODS: We studied 45 patients with a mean age = 56.3 +/- 12.4 years, 25 with anterior infarction and 20 with inferior infarction. The reperfusion was defined by the simultaneous presence of three classic noninvasive criteria (fast relief of pain, fast regression of ST segment elevation and early peak of CK). We studied heart rate variability parameters in time-domain and frequency-domain on a 24-hour Holter ECG started at the same time as fibrinolytic therapy. RESULTS: Thirty-three patients showed reperfusion. We did not find significant differences in the several parameters of heart rate variability between patients with reperfusion and patients without reperfusion, but the patients with anterior wall infarction showed a significant reduction in SDNN in comparison with patients with inferior wall infarction (84 +/- 28 ms vs 102 +/- 30 ms; p = 0.05). pNN50 (5.3 +/- 7.2 ms vs 10.5 +/- 9.8 ms; p = 0.04), LF (618 +/- 591 ms2 vs 1374 +/- 1761 ms2; p = 0.05) and TP (1415 +/- 1199 ms2/Hz vs 3015 +/- 4243 ms2/Hz). CONCLUSION: These data suggest a relationship between infarct severity and sympathetic activation and/or reduction of vagal modulation, but a potential beneficial effect of reperfusion on autonomic nervous system alterations was not evident in the first day of acute myocardial infarction.     

Pathophysiology and treatment of haemodynamic instability in acute pulmonary embolism: the pivotal role of pulmonary vasoconstriction

Acute massive pulmonary embolism has a high mortality rate. Fatal haemodynamic deterioration is caused by an acute increase in pulmonary vascular resistance. Traditionally, the degree of mechanical obstruction of the pulmonary vasculature by the embolic thrombus is considered to be the major determinant of this increase in right ventricular afterload. However, there is evidence to suggest that another factor plays an important role, since there is a marked discrepancy between the haemodynamic manifestations of acute pulmonary embolism and the degree of mechanical obstruction. Historic studies indicate that this discrepancy is largely explained by pulmonary vasoconstriction caused by vasoactive mediators, released mainly by activated platelets. Thromboxane-A(2) and serotonin are probably the two most important pulmonary vasoconstrictors in this context. Antagonising their effects dramatically increases tolerance to experimental pulmonary embolism in animals. In humans, this concept should eventually find its way into clinical practice. In the future, acute massive pulmonary embolism could be treated with antagonists to pulmonary vasoconstrictors, or with direct pulmonary vasodilators.     

Anticoagulants in the treatment of severe pulmonary embolism. A prospective study

This prospective study was designed to obtain information on the fate of patients with severe pulmonary embolism who received anticoagulants as first-line treatment, in order to identify those in whom other treatments available might be expected to reduce mortality or sequelae. Thirty-seven patients selected as they showed evidence of acute cor pulmonale entered the study. Seven of them (18.9 p. 100) died in hospital, and these were patients whose age (p = 0.004), degree of pulmonary obstruction (p = 0.008) and serum lactate dehydrogenase level (p = 0.001) were significantly higher than those of the other patients. The mean values of these parameters (64 years, 72 p. 100 and 450 IU/l respectively) made it possible to select patients with a high risk of death. At the end of the follow-up period (25 +/- 12 months) only 2 patients complained of moderate dyspnoea, in contrast with the high incidence (17/18 patients) of paraclinical abnormalities observed 3 months after the initial accident. We conclude that clinical trials comparing other treatments with the one we used would be useful if their objective was to reduce mortality in high risk patients. On the other hand, it seems impossible to demonstrate a functional improvement: we found our treatment satisfactory and its results independent of the abnormalities observed on the 3rd month.     

Early discharge of patients with pulmonary embolism: a two-phase observational study.

The aim of the present study was to assess whether patients with pulmonary embolism (PE) could be managed as outpatients after early discharge from hospital using low molecular weight heparin instead of remaining as in-patients until effective oral anticoagulation was achieved. Phase 1 of the study identified criteria for the safe discharge of selected patients; phase 2 treated a cohort of low-risk patients with PE as outpatients with tinzaparin using existing deep venous thrombosis services. In phase 1, 127 (56.4%) of 225 patients were considered unsuitable for outpatient management. Reasons included: admission for another medical reason; additional monitoring or requirement for oxygen; bleeding disorders; previous PE/further PE while on warfarin; co-existing major deep venous thrombosis; likelihood of poor compliance; significant immobility; and pregnancy. In phase 2, 157 patients with PE received outpatient anticoagulation therapy. There were no deaths, bleeding or recurrent thromboembolic events during acute treatment with low molecular weight heparin. The median (range) length of hospital stay was 1.0 (1-4) day, with a median saving of 5.0 (1-42) bed-days per patient. Patients were highly satisfied with outpatient management; 144 (96.6%) indicated that they would prefer treatment as outpatients for a subsequent pulmonary embolism. Early discharge and outpatient management of pulmonary embolism appears safe and acceptable in selected low-risk patients, and can be implemented using existing outpatient deep venous thrombosis services.     

Acute massive pulmonary embolism. Clinical and haemodynamic findings in 23 patients studied by cardiac catheterization and pulmonary arteriography

Twenty-three patients are reported in whom a diagnosis of acute massive pulmonary embolism was confirmed by pulmonary arteriography. All patients had a history of less than 48 hours' duration and only two had previous cardiorespiratory disease. In such patients the haemodynamic abnormalities determined at catheterization are due to pulmonary embolism as an isolated disturbance. These abnormalities include an only moderate degree of pulmonary hypertension (PA systolic pressure 38.4+/-6.8 mm. Hg), right ventricular ;failure' (RVED 11.5+/-4.9 mm. Hg), arterial oxygen desaturation (86.4+/-11.2%) and a wide arteriovenous oxygen difference (8.1+/-1.8 ml./100 ml.), and low cardiac output. These haemodynamic abnormalities find their expression in the presentation and the clinical, electrocardiographic, and radiological findings which are described.     

Deep venous thrombosis and the risk of pulmonary embolism. A systematic study.

The influence of several diseases and clinical conditions on the presence of pulmonary embolism (PE) in a large series of patients with deep venous thrombosis (DVT) in the lower extremities was analyzed prospectively. Lung scan findings from a series of 434 consecutive patients with DVT (with and without symptoms of PE) were studied and then correlated to five clinical variables: age, sex, elapsed time since clinical symptoms had appeared in the leg to diagnosis, degree of proximity of venous thrombus, and the presence or not of several risk factors that could have predisposed to thrombus development. According to scintigraphic findings, 164 patients were considered to have PE (asymptomatic in 76 of them), while 200 patients were classified as having only DVT. Lung scan was considered to be indeterminate for PE in 70 patients, and they were not included in the study. No differences were found in terms of age, sex, interval of time elapsed since onset of symptoms to diagnosis, or in the degree of proximity of the thrombus. However, several differences between groups were found when comparing the presence or absence of several predisposing factors for thrombosis: DVT developing in immobilized patients was associated with a significantly lower incidence of PE as compared with nonimmobilized patients (p = 0.005). Conversely, patients with a history of venous thromboembolism (VTE) had a significantly higher rate of embolism (31/51 vs 133/313; p = 0.01). On logistic regression analysis, a history of VTE showed a statistically significant association with more than a twofold higher risk of having PE for patients with such an antecedent. Our findings suggest that different pathophysiologic pathways could perhaps explain differences in embolic potential.     

Upper-extremity deep venous thrombosis and pulmonary embolism. A prospective study

We prospectively evaluated the prevalence of pulmonary embolism (PE) in 30 consecutive patients with proved deep venous thrombosis (DVT) of the upper extremity. Ten patients (seven male and three female; mean age, 43 years) had primary DVT, and 20 patients (14 male and six female; mean age, 52 years) had catheter-related DVT. Ventilation-perfusion lung scans were routinely performed at the time of hospital admission to all but one patient (one patient was critically ill, and he died four days after DVT diagnosis because of massive PE). Lung scan findings were normal in nine of ten patients with primary DVT, and they were indetermine in the remaining patient. By contrast, perfusion defects were considered highly suggestive of PE in four patients with catheter-related DVT; two patients had indeterminate lung scans, and 13 patients had normal scans. We conclude that PE is not a rare complication in upper extremity DVT, and that patients with catheter-related DVT seem to be at a higher risk.     

15例老年人肺动脉栓塞临床病理分析

目的分析尸检中６５岁以上老年人肺动脉栓塞（以下简称肺栓塞）的临床、病理资料，探讨老年人肺栓塞的特点及误诊原因。方法收集我院１９５１～１９９２年尸检１１１１例中老年人肺栓塞１５例，对照分析其临床、病理特点。结果男性１４例，女性１例，年龄６５～８２岁。误诊率８６．７％。原有基础病以冠心病、慢性阻塞性肺疾病（ＣＯＰＤ）、糖尿病为多。结论老年人肺栓塞病情重且复杂、临床表现不典型、各种疾病表现相互掩盖可能是误诊的主要原因     

The first 48 hours of investigation and intervention of an outbreak of legionellosis in the Netherlands

The Westfriese Flora is a one week flower show held every year in Bovenkarspel, in the north west of the Netherlands, with agricultural and consumer demonstrations on the same grounds. This year s show, held from 19 to 28 February, attracted 80 000 visito     

Time course of changes in intracellular K+, Na+, and pH of subendocardial Purkinje cells during the first 24 hours after coronary occlusion.

We investigated the basis for the alterations in the intracellular potassium and sodium activity occurring in subendocardial Purkinje fibers surviving in 24-hour infarcts by examining ion activities in these Purkinje fibers removed from infarcting hearts at earlier times. Specifically, we examined intracellular potassium activity, sodium activity, and pH at 1 and 3 hours after ligation of the left anterior descending coronary artery, and we correlated the changes in ion activity with changes in maximum diastolic potential. We tested various mechanistic hypotheses relating to how the ion activity changes develop and how they affect membrane potential. We found that intracellular sodium activity in tissue removed 1 hour after ligation was on average already maximally elevated by a factor of 2 over control (19.2 +/- 2.0 mM [mean +/- SEM] versus 9.4 +/- 0.4 mM). Potassium activity diminished progressively over the first 24 hours (from normal of 112.0 +/- 2.7 to 61.6 +/- 2.8 mM), although half of the decrease occurred during the first hour (to 86.8 +/- 4.1 mM). Intracellular pH did not change at either 1 or 3 hours. Whereas maximum diastolic potential depolarization exceeded the calculated depolarization of the potassium equilibrium potential by a factor of 2 in 24-hour infarcts, the depolarization at 1 and 3 hours could be more nearly attributed to the loss of potassium. The change in the dependence of maximum diastolic potential on potassium equilibrium potential may be due to changes in membrane conductance caused by ionic or biochemical factors. The changes in ion activity continuously develop during the first day after ligation and may be due to multiple factors and mechanisms.     

Asymptomatic and transitory electrocardiographic changes in the 24 hours following coronary transluminal angioplasty

Fifty patients underwent a 24-hour Holter system recording immediately after successful coronary angioplasty. Only those patients who had been "successfully" dilated and who, during the following 2 days, had remained totally symptomless and without changes in standard ECG were selected. Arrhythmias occurred in 18 patients: 12 had supraventricular arrhythmia, including 3 prolonged attacks of tachyarrhythmia due to atrial fibrillation; 6 had ventricular arrhythmia, with numerous extrasystoles in 5 cases and bursts of ventricular tachycardia in 1 case. Changes in ventricular repolarization were recorded as: (1) isolated T-wave modification (11 patients), and (2) ST-segment depression (11 patients) reaching or exceeding 2 mn in 5 cases and lasting from 4 to 33 minutes. These silent and transient electrical abnormalities were observed mostly during the 12 hours which followed transluminal angioplasty, and particularly after dilatation of the right coronary artery. The physiopathological mechanisms of these changes are uncertain, but their occurrence has no influence on mid-term results, i.e. the follow-up coronary arteriography at 6 months.     

肺栓塞的抗凝疗程和复发率分析

目的 探讨肺栓塞患者抗凝疗程和肺栓塞复发率的关系.方法 对2002-2009年我院诊治并好转出院的167例肺栓塞患者进行随访,分别观察存在临时危险因素的肺栓塞患者、特发性肺栓塞患者和持续存在危险因素的肺栓塞患者序贯口服华法林抗凝治疗的疗程、复发率和出血发生率,并分析复发率与年龄、性别的关系.结果 特发性肺栓塞患者的复发率高于存在临时危险因素的肺栓塞患者(P＜0.05).持续存在危险因素的肺栓塞患者口服抗凝疗程较其余两组长,但出血发生率也高于其余两组(P值均＜0.05).特发性肺栓塞患者男性复发率高于女性(P＜0.05).结论 肺栓塞患者序贯口服华法林抗凝疗程应采取个体化方案,在综合评价复发风险和出血风险后决定,使患者取得最佳的长期获益.

Abstract：

Objective To investigate the relationship between duration of anticoagulant therapy and recurrence rate in pulmonary embolism. Methods 167 patients with pulmonary embolism who were treated and improved in our hospital from 2002 to 2009 were followed up. The duration of anticoagulant therapy, recurrence rate and bleeding incidence were observed in patients with pulmonary embolism associated with temporary risk factors, patients with idiopathic pulmonary embolism and patients with pulmonary embolism associated with permanent risk factors. The relationship between recurrence rate and age, gender was analyzed. Results The recurrence rate in patients with idiopathic pulmonary embolism was higher than that in patients with pulmonary embolism associated with temporary risk factors ( P ＜0. 05). The duration of anticoagulant therapy in patients with pulmonary embolism associated with permanent risk factors was longer than that in other groups, but the risk of bleeding was also higher than that in other groups (all P ＜ 0. 05). The recurrence rate in male patients with idiopathic pulmonary embolism was higher than that in female patients ( P ＜0. 05). Conclusions For patients with pulmonary embolism,the duration of anticoagulant therapy must be individualized, is decided after the comprehensive evaluation of recurrence risk and bleeding risk,so that patients get the best long-term benefit.     

Changes in plasma vitamin levels in the first 48 hours after onset of acute myocardial infarction

To establish whether plasma vitamin measurements made after acute myocardial infarction (AMI) can be used in case-control studies of coronary artery disease, the short-term effect of AMI on plasma concentrations of 25-hydroxyvitamin D3, beta-carotene, vitamin E and retinol was investigated. Sequential measures of these vitamins were made during the first 48 hours after AMI in 13 patients admitted to the hospital within 4 hours after the onset of symptoms. Plasma levels of 25-hydroxyvitamin D did not change significantly during the first 12 hours after onset of symptoms. Beta-carotene levels increased significantly (p less than 0.05) during the first 12 hours and then decreased, whereas levels of vitamin E and retinol progressively decreased during the first 48 hours by 26 and 25%, respectively. These results suggest that, of these vitamins, only plasma measurements of 25-hydroxyvitamin D3 collected within 12 hours of onset of symptoms may provide reliable information for case-control studies of AMI.