The mining industry in Serbia has an important place in the country's economic development. Bearing in mind that the number of injuries that occur in the mining industry is unacceptably high, occupational safety and health is a challenge that existing and future mines will have to deal with. Studying injuries in mining, it was noticed that injuries requiring an absence from work for more than three days (especially fatal ones) are diametrically different in relation to the cause and manner of events related to injuries for which an absence from work is not necessary. In this research, authors focused on injuries that were characterized as ones requiring an absence from work. The statistical analysis of work-related injuries in mining is presented, as well as analysis of the direct causes of injuries, which are described as unsafe conduct of employees, unsafe conduct of company's management and/or unsafe working environment. In relation to classification of causes of injuries, a recommendation on what needs to be changed in order to remedy this situation in Serbia is given.
Febrile conditions of unidentified origin are still unknown in modern medicine despite the development of diagnostic procedures. There are various agents of long-term temperature encompassing numerous infectious or non-infectious diseases.
The aim of this study was to determine if there was a statistically significant difference in the values of proinflammatory cytokines (IL-1, TNFα, IL-6) in patients who meet the criteria for febrile conditions of unidentified origin, between the group of infectious, malignant, rheumatic, “other” diseases and undiagnosed patients.
The study was conducted in the Immunology laboratory of the Center for Molecular Medicine and Stem Cells Research of the Faculty of Medical Sciences in Kragujevac. Blood samples were taken from patients tested at the Clinic for Infectious Diseases, of the Clinical Center of Kragujevac, in the period from 2014 to 2016. The study included 70 patients.
The measured values of the level of TNFα showed significantly higher values in a group of malignant diseases than in the group of infectious diseases, while the values of IL-1 and IL-6 did not show statistical significance.
TNFα can improve diagnosing in case of patients with an unknown febrile condition, which can shorten the length of the hospital stay and reduce the volume of performance of diagnostic procedures.
Gastrointestinal complications are common among patients on peritoneal dialysis. Risk factors for the development of gastrointestinal complications in this patient population include: toxic effects of uremic toxins, frequent use of nonsteroidal anti-inflammatory drugs, Helicobacter pylori infection, angiodysplasia, increased intra-abdominal pressure, use of bioincompatible solution for peritoneal dialysis, increased glucose in solutions for peritoneal dialysis, secondary hyperparathyroidism (hypercalcemia), a disorder of lipid metabolism (hypertriglyceridemia), and the duration of peritoneal dialysis treatment. The most important non-infectious gastrointestinal complications in patients on peritoneal dialysis are: gastrointestinal bleeding, herniation and leaking of the dialysate from the abdomen (increased intra-abdominal pressure), impaired lung function (intra-abdominal hypertension), acute pancreatitis, and encapsulating sclerosis of the peritoneum. Intra-abdominal hypertension is defined as IAP ≥ 12 mmHg. Pouring the peritoneal dialysis solution leads to increased intra-abdominal pressure, which results in the development of hernias, pleuro-peritoneal dialysate leakage (hydrothorax), and restrictive pulmonary dysfunction. Risk factors for the development of acute pancreatitis in this patient population include: uraemia, secondary hyperparathyroidism with hypercalcemia, hypertriglyceridemia, features of the peritoneal dialysis solution (osmolarity, acidity, glucose, chemical irritation, and calcium in the solution for peritoneal dialysis lead to “local hypercalcemia”), toxic substances from the dialysate, the bags and tubing, and peritonitis and treatment of peritonitis with antibiotics and anticoagulants. Encapsulating sclerosis of the peritoneum is rare and is the most serious complication of long-term peritoneal dialysis. It is characterized by thickening of the peritoneum, including cancer, and signs and symptoms of obstructive ileus. Diagnosis is based on clinical, laboratory and radiological parameters. Encapsulating sclerosis of the peritoneum can be indicated by an AR-CA-125 concentration of less than 33 U/min and a concentration of AR-IL-6 greater than 350 pg/min in the effluent of patients with ultrafiltration weakness. Treatment consists of stopping peritoneal dialysis, using anti-inflammatory (corticosteroids) and anticicatricial drugs (tamoxifen), while surgical treatment includes enterolysis and adhesiolysis.
Prevalence of cognitive disorders is high in maintenance hemodialysis patients. Montreal cognitive assessment (MoCA) is used for detecting and evaluation of cognitive disorder degree in this patient population. In examined patient population, only 5 (12.5%) of them had normal cognitive function (MoCA ≥26). Mild cognitive impairment (MoCA 18-26) was found in 65.9% (29) patients, while moderate cognitive disorder (MoCA 10-17) was detected in 6 (21.6%) patients. Major cognitive disorder wasn’t detected in examined population. Statistically signifi cant correlation was not established between laboratory parameters and overall MoCA score. Statistically signifi cant correlation, however, was established between MoCA item that evaluates space and time orientation and intermediate secondary hyperparathyroidism and space and time orientation and severe secondary hyperparathyroidism. Hemodynamic instability during hemodialysis and silent ischemia of the brain are increasing risk of appearance of cognitive disorders in maintenance hemodialysis patients.
Acute damage to the kidney is a serious complication in patients in intensive care units. The causes of acute kidney damage in these patients may be prerenal, renal and postrenal. Sepsis is the most common cause of the development of acute kidney damage in intensive care units. For the definition and classification of acute kidney damage in clinical practice, the RIFLE, AKIN and KDIGO classifications are used. There is a complex link between acute kidney damage and other organs. Acute kidney damage is induced by complex pathophysiological mechanisms that cause acute damage and functional disorders of the heart (acute heart failure, acute coronary syndrome and cardiac arrhythmias), brain (whole body cramps, ischaemic stroke and coma), lung (acute damage to the lung and acute respiratory distress syndrome) and liver (hypoxic hepatitis and acute hepatic insufficiency). New biomarkers, colour Doppler ultrasound diagnosis and kidney biopsy have significant roles in the diagnosis of acute kidney damage. Prevention of the development of acute kidney damage in intensive care units includes maintaining an adequate haemodynamic status in patients and avoiding nephrotoxic drugs and agents (radiocontrast agents). The complications of acute kidney damage (hyperkalaemia, metabolic acidosis, hypervolaemia and azotaemia) are treated with medications, intravenous solutions, and therapies for renal function replacement. Absolute indications for acute haemodialysis include resistant hyperkalaemia, severe metabolic acidosis, resistant hypervolaemia and complications of high azotaemia. In the absence of an absolute indication, dialysis is indicated for patients in intensive care units at stage 3 of the AKIN/KDIGO classification and in some patients with stage 2. Intermittent haemodialysis is applied for haemodynamically stable patients with severe hyperkalaemia and hypervolaemia. In patients who are haemodynamically unstable and have liver insufficiency or brain damage, continuous modalities of treatment for renal replacement are indicated.
Prevalence of cognitive disorders is high in maintenance hemodialysis patients. Montreal cognitive assessment (MoCA) is used for detecting and evaluation of cognitive disorder degree in this patient population. In examined patient population, only 5 (12.5%) of them had normal cognitive function (MoCA ≥26). Mild cognitive impairment (MoCA 18-26) was found in 65.9% (29) patients, while moderate cognitive disorder (MoCA 10-17) was detected in 6 (21.6%) patients. Major cognitive disorder wasn’t detected in examined population. Statistically significant correlation was not established between laboratory parameters and overall MoCA score. Statistically significant correlation, however, was established between MoCA item that evaluates space and time orientation and intermediate secondary hyperparathyroidism and space and time orientation and severe secondary hyperparathyroidism. Hemodynamic instability during hemodialysis and silent ischemia of the brain are increasing risk of appearance of cognitive disorders in maintenance hemodialysis patients.
Cardiorenal Syndrome Type 1 (CRS-1) is defined as an acute worsening of heart function leading to acute kidney injury and/or dysfunction. It is an important cause of hospitalization which affects the diagnosis as well as the prognosis and treatment of patients. The purpose of this paper is to analyze causes that lead to the development of cardiorenal syndrome type 1 and its clinical consequences, as well as to emphasize the clinical importance of its early detection. The clinical studies and professional papers dealing with etiopathogenesis, diagnosis and treatment of cardiorenal syndrome type 1, have been analyzed. The most important role in the occurrence of cardio renal syndrome type 1 is played by hemodynamic mechanisms, activation of neurohumoral systems, inflammation and imbalance between the production of reactive oxygen species (ROS) and nitric oxide (NO). Diagnosis of cardiorenal syndrome type 1 involves biomarkers of acute renal injury among which the most important are: neutrophil gelatinaseassociated lipocalin (NGAL), cystatin C, kidney injury molecule 1 (KIM-1), liver-type fatty acid binding protein (L-FABP), IL-18 and the values of nitrogen compounds in serum. In addition to a pharmacological therapy, various modalities of extracorporeal ultrafiltration are applied in treatment of CRS-1, particularly if there is resistance to the use of diuretic therapy. As opposed to the experimental models, in clinical practice acute renal injury is often diagnosed late so that the measures taken do not give the expected results and the protective role shown in experimental conditions do not give the same results. For all these reasons, it is necessary to analyze the pathophysiology of renal impairment in cardiorenal syndrome as well as detect early indicators of kidney injury that could have clinical benefit and positive impact on reducing the cost of treatment.
Thrombotic thrombocytopenic purpura (TTP) is a clinical syndrome that manifests with thrombocytopenia, microangiopathic haemolytic anaemia and symptoms and signs of kidney and brain damage, but it rarely involves other organs. The main pathophysiological cause of TTP is diminished metalloproteinase ADAMTS13 activity; the main function of ADAMTS13 is to degrade large multimers of the von Willebrand factor. Diminished activity of ADAMTS13 is caused either by a genetic mutation in the gene that codes ADAMTS13 (congenital TTP) or by antibodies that block ADAMTS13 enzyme activity or accelerate the degradation of ADAMTS13 (acquired TTP). Clinically, TTP presents most frequently with signs and symptoms of brain and kidney damage with concomitant haemorrhagic syndrome. TTP is suspected when a patient presents with a low platelet count, microangiopathic haemolytic anaemia (negative Coombs tests, low haptoglobine concentration, increased serum concentration of indirect bilirubin and lactate dehydrogenase, increased number of schysocytes in peripheral blood) and the typical clinical presentation. A definitive diagnose can be made only by measuring the ADAMTS13 activity. The differential diagnosis in such cases includes both typical and atypical haemolytic uremic syndrome, disseminated intravascular coagulation, HELLP syndrome in pregnant women and other thrombotic microangiopathies. The first line therapy for TTP is plasma exchange. In patients with acquired TTP, in addition to plasma exchange, immunosuppressive medications are used (corticosteroids and rituximab). In patients with hereditary TTP, the administration of fresh frozen plasma is sometimes required.
Secondary hypertension occurs in 5-10% of cases in the patient population with primary hypertension. The most common forms of secondary hypertension are as follows: parenchymal renal disease (renoparenchymal hypertension), renal artery stenosis (renovascular hypertension), adrenal gland adenoma (primary hyperaldosteronism), a tumour of the adrenal gland marrow (pheochromocytoma) and adenoma of adrenal and pituitary glands (Cushing’s syndrome). In patients with a typical clinical picture of secondary hypertension, the appropriate diagnostic tests should be conducted based on the suspected form of secondary hypertension. Determining a diagnosis of secondary hypertension is gradual. First, the appropriate screening tests are performed. If the screening test is positive, then additional tests to confirm the forms of secondary hypertension are conducted. Once a diagnosis of the appropriate form of secondary hypertension is confirmed, tests to distinguish causes and laterality tests to determine the precise localisation of the pathological process are applied to evaluate the response to therapy. Analysing the results of endocrine diagnostic tests provides an accurate diagnosis and selection of optimal therapeutic procedures.
Cardiovascular diseases are the leading cause of death in patients who undergo regular hemodialysis. Oxidative stress is a non-traditional risk factor for the development of cardiovascular diseases in this population of patients. It is defined as tissue damage caused by balance disturbance between the formation of free radicals and the function of protective antioxidative systems. The superoxide anion and hydrogen peroxide are precursors in the formation of stronger oxidants, such as: hydroxyl radical, peroxynitrite and hypochloric acid. Superoxide dismutase is the first line of antioxidant protection while catalase, glutathione peroxidase, trace elements, vitamin C, vitamin E, N-acetylcysteine and coenzyme Q10 also have a significant antioxidative role. Hemo-dialysis is itself a trigger for the increased formation of oxygen free radicals. The two main pathophysiological mechanisms of the increased formation of free oxygen radicals during the hemo-dialysis session are: bionicompatibility of the dialysis membrane and the presence of endotoxins in the hemodialysis solution. The measurement of myeloperoxidase concentration in a patient’s serum during hemodialysis is an indicator of the severity of oxidative stress induced by the dialysis membrane (an indicator of the biocompatibility of the dialysis membrane). The main clinical consequences of oxidative stress include: atherosclerosis, erythropoietin resistance, malnutrition and amyloidosis associated with hemodialysis. The evaluation of oxidative stress in patients undergoing hemodialysis is performed by measuring the concentration of lipid peroxidation products (malonyldialdehyde, 4-hydroxynonenal, TBARS, F2-isoprostane, oxLDL), protein oxidation (AOPP), protein gelling (AGE), and oxidation of nucleic acids (8-OHdG). The antioxidant treatment strategy consists of replenishing vitamin C, vitamin E, selenium, N-acetylcysteine and coenzyme Q10. On-line hemodialysis, a biocompatible vitamin E-coated dialysis membrane, an ultra-pure solution for hemodialysis, prevent oxidative stress, reduce the rate of cardiovascular morbidity and mortality and improve life quality of patients treated with regular hemodialysis.