Srp Ark Celok Lek
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Randomized Controlled Trial Comparative Study Clinical Trial
[Advantage of combined spinal, epidural and general anesthesia in comparison to general anesthesia in abdominal surgery].
Type and technique of anesthesia have an important effect on per operative surgical course. The aim of the study was prospective analyses of advantages of combined spinal, epidural and general anesthesia (CSEGA) versus general anesthesia (GA) in abdominal surgery according to: 1. operative course (haemodynamic stability of patients, quality of analgesia, undesirables effects), 2. postoperative course (quality of analgesia, unfavourable effects, temporary abode of patients in intensive care). Using prospective randomized double blind controlled study, we evaluated two groups of patients whom the same type of abdominal surgical intervention was planed and the only difference was the type of technique of anesthesia. ⋯ First group of patients spent less time in intensive care (three days) than second group (six days). Final subjective effect of analgesia, according to verbal descriptive scale (VDS) of pain was satisfying with 75% of patients of the first group and 15% of patients of the second group. According to results investigation, advantages of CSEDGA versus GA in abdominal surgery manifold: better hemodynamic stability and perfusion of operative region, decrease of single doses of opioid analgesics, local and general anesthetics followed by the decrease of their side effects, better intensity and longer duration of analgesia, improved total functional capability of patients.
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Tissue expose to excessive levels of circulating thyroid hormones results in thyrotoxicosis. In most cases, thyrotoxicosis is due to hyperactivity of the thyroid gland. Cardiovascular and myopathic manifestations are predominant clinical features in most hyperthyroid patients, aged 60 years and older. Some of patients have apathetic hyperthyroidism which presents with weight loss, small goiter, severe depression and without clinical features of increased sympathetic activity [3, 6]. About 50% of patients with cardiovascular manifestations have no evidence of underlying heart disease. Cardiac problems resolve when euthyroid state is established [3]. Three treatment modalities are available in hyperthyroidism, namely medicament therapy, surgery and radioactive iodine. Antithyroid drug therapy complications, can be mild such as rash, which is managed without cessation of therapy by antihistamines administration. On the other hand, very serious complications such as agranulocytosis, necessitate immediate discontinuation of the medication and appropriate treatment. Although extremely rear, it is life-threatening with highly variable recovery time. ⋯ Agranulocytosis is very rare but very serious complication of antithyroid drug therapy. It can be detected in about 0.1-1% patients during the first three months of treatment. Sudden appearance, heralded by sore throat and fever, prompt physicians to seek white blood cell and differential count [1-3]. Confirmation of diagnosis urges cessation of drug therapy and appropriate antibiotic treatment. Recently, it was reported that recombinant human granulocyte colony-stimulating factor (rhG-CSF) is to be effective in shortening the recovery time in the neutropenic patients undergoing chemotherapy and also in patients with other types of neutropenia [5]. Tamai at al. [7] confirmed positive outcome in 34 patients treated with rhG-CSF compared to corticosteroid treatment. Hematologic laboratory abnormalities disappear 7-10 days after session of therapy. Patients completely recover two to three weeks later. Fatal outcome was also described [1-5]. Thyroid hormones have profound effects on cardiovascular physiology, especially on heart rate, cardiac output and systemic vascular resistance. In patients with hyperthyroidism, cardiac output is much higher than in normal persons. This is the result of direct effect of thyroid hormones on cardiac muscle contractility, heart rate and decrease in systemic vascular resistance. Excessive thyroid hormone secretion increases cardiac Na-K-activated plasma membrane ATP-ase and sarcoplasmic reticulum Ca-activated ATP-ase with resultant in increase myocardial contractility [6, 9]. Sinus tachycardia is the most common rhythm disorder in hyperthyroidism, but paroxysmal tachycardia and atrial fibrillation are not rare. This can be explained by increased heart rate, cardiac output, blood volume, coronary artery flow and peripheral oxygen consumption in thyrotoxicosis [9]. Patients with coronary arteriosclerosis can develop angina pectoris during thyrotoxic stage, which can be explained by imbalance between cardiac demand and supply. Myocardial damage is often in thyrotoxic patients with chronic hart failure, together with myocardial infarction in patients without coronary disease [2,6]. Congestive heart failure and atrial fibrillation are relatively resistant to digitalis treatment because of high metabolic turn over of medication and excessive myocardial irritability in hyperthyroidism [6]. Cardiovascular and myopathic manifestations predominate in older hyperthyroid patients (over 60 years) and some of them can have only few symptoms of hyperthyroidism [1-3]. Thyrotoxic state characterized by fatigue, apathy, extreme weakness, low-grade fever and sometimes congestive heart failure are designated as apathetic hyperthyroidism. Such patients have small goiters, mild tachycardia and often cool and dry skin with few eye signs [6]. Patients with subclinical hyperthyroidism are at increased risk for atrial fibrillation [9]. Unstable angina and non-Q myocardial infarction (non ST elevation) are acute manifestation of coronary artery disease. The acute coronary syndrome of unstable angina, non-Q myocardial infarction and Q-wave myocardial infarction have atherosclerotic lesions of the coronary arteries as a common pathogenic substrate. Erosions or ruptures of unstable atherosclerotic plaque triggered pathophysiologic processes, resulted in thrombus formation at the site of arterial injury. This leads to abrupt reduction or cessation through the affected vessel. Clinical manifestations of unstable angina and non-Q myocardial infarction are similar and diagnosis of non-Q myocardial infarction is made on the basis of elevated serum markers indicative of cardiac necrosis, detected in peripheral circulation. Acute coronary syndrome ranging from unstable angina to myocardial infarction an non-Q myocardial infarction represents increasingly severe manifestations of the same pathophysiologic processes [10,11]. In conclusion, these 62-year-old woman presented with apathetic form of recurrent hyperthyroidism associated with two serious complications, life-threatening agranulocytosis and acute coronary syndrome.
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Each fracture of long or pelvic bones as well as large contusions of subcutaneous fat tissue cause releasing of fat globules that rapidly penetrate into circulation through the ruptured veins of the injured tissue, and reach the lung circulation [1,2]. During the first phase, fat emboli block the functional lung circulation by their mechanical effect in capillaries producing so called isolated post-traumatic lung fat embolism [3]. The surface layer of a fat embolus, which is practically in liquid state, behaves as a membrane of very high density, i.e., as it is under high pressure which obstruct the blood stream [4] that is finally stopped at the level of lung blood vessels with diameter of approximately 20 mu [5]. This pathophysiological mechanism produces cor pulmonale acutum, with poor pathological findings [8]. Nowadays, the post-mortem diagnosis of lung fat embolism is based on microscopical examination of tissue specimens, usually prepared with special histological staining (Sudan III) [9]. The grading of fat embolism according to Sevitt's criteria is generally accepted [10]. Taking of slices from apicoventral areas of the lungs has been recommended [11]. With longer outliving period, the total number of fat emboli in the lung circulation gradually decreases, due to their disintegration and resorption. It has been stated that fat globules completely disappear about 4-6 weeks after injury, and that they should not be searched for microscopically in this post-traumatic phase [11]. ⋯ The analysis of our sample showed that the most severe grade of post-traumatic lung fat embolism (microscopical grade III according to Sevitt's criteria) was determined in older individuals, more severely injured, and with shorter outliving period. The severity of fat embolism depends neither on sex of the injured, nor on development of post-traumatic hypovolemic shock. The obtained results related to the influence of hypovolemic shock on severity of fat embolism should be accepted with a caution. Namely, sometimes there is an intention to simplify a procedure of creating of autopsy conclusion about the cause of death, so that loss of blood is not mentioned at all, in spite of fact that it could have been a concurrent cause of death, while in other cases exsanguination is designated as a sole cause of death, forgetting the possibility that fat embolism could have really been the immediate cause of death.
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One of the clinical manifestations of renovascular hypertension (RVH) may be a recurrent pulmonary oedema both in the absence or in the presence of systolic left ventricular dysfunction. This type of pulmonary oedema characterized as "flash" pulmonary oedema is ascribed to elevated angiotensin II concentrations with consequent hypertension as well as to volume overload resulting from decreased pressor natriuresis when there are significant stenoses of both or one renal arteries. The investigation included 30 patients with RVH treated by percutaneous transluminal angioplasty of the stenosed renal artery (PTRA) and/or stent implantation (PTR-ST) and 30 patients with surgical resection of the abdominal aortic aneurysm (AAA). ⋯ Pulmonary oedema occurred preoperatively in four out of 30 patients with abdominal aortic aneurysm in whom significant renal artery stenoses coexisted. Two patients died despite surgery, one patient is clinically stable and the medicament treatment of heart failure is inevitable in the fourth with a left ventricular aneurysm following myocardial infarction. The occurrence or recurrence of pulmonary oedema in the absence of other explanation should suggest the possibility of bilateral or unilateral renal artery stenosis requiring renal revascularization for blood pressure regulation as well as for elimination of other manifestations/complications.