UNLABELLED Meningococcal disease is the most significant cause of morbidity and mortality even in the most developed socio-economic surroundings. Meningococcal sepsis and meningitis are caused by Neisseria meningitidis (NM), which is surrounded by polysaharide capsule, which is the main factor of virulence. THE GOAL OF THE WORK was to confirm the frequency and characteristics of meningococcal disease as well as the justification of introducing vaccination. Through retrospective analysis of the history of the disease, a total of 87 patients with meningococcal sepsis hospitalized at the hospital for infectious in Tuzla in the period 1995 to 2004. diseases were included. Out of 87 hospitalized patients, 34 patients (39%) had meningococcal sepsis, meningococcal sepsis and meningitis had 50 patients (57.6%), and only 3 patients (3.4%) had only meningitis. The diseases most frequently appears in males, 54 patients (62.0%), and in females, 33 patients (38.0%). The largest number of diseased is in the period 0-12 months, 39 patients (44.8%), and then in the period from 13-24 months, 19 diseased (21.8%), from 3-6 years of age 12 patients (13.8%), after sixth year of age meningococcal disease appears in a smaller percent. The youngest patient was 3 and a half months old, and the oldest was 23 years old. Diagnosis was established based on the history of the disease, clinical examination, lab researches, biochemical and bacteriological search of liquid. Etiological cause was proved through liquor culture in 24 cases (27.5%), hemoculture in two cases (2.29%). Death was the result in eight cases (9.1%), one patient (1.1%) resulted in the amputation of a finger, and the rest of 78 patient (89.6%) are cured without sequel. Patients are treated with the Penicillin G, Ampicillin, and in a case of the resistance, were treated with cephalospores of third generation. CONCLUSION the meningococcal disease, and especially its form of Waterhause-Friderichsen syndrome represents a hard disease which in 50% of cases has a death as the result.

Neurologic complications after severe brain injuries are the result of primary injuries in the moment of impact and secondary injuries which evolve over the minutes and days later. According to statistics, secondary injuries were documented in about 90 percent of patients who died after traumatic brain injury. Low oxygen delivery in hypotension, hypoxia, oedema, intracranial hypertension or changes in cerebral blood flow all account for development of secondary injuries. Primary injuries are more or less complete, but secondary injuries could be prevented with adequate therapy. Understanding mechanisms of secondary injuries could help identify potentially beneficial therapies. Important elements of therapy are: head position, normoglycemia, osmotherapy, normal body temperature, optimal blood pressure, adequate oxygenation. barbiturate therapy. Neutral head and neck position is recommended to prevent intracranial hypertension. Hyperglycemia with less ATP leads to ishaemic acidosis, hypoglycemia enhances decomposition of phospholipids and release of fat acids, what makes the celulare damage worse. Normocapnia is recommended and adequate oxygenation (PaO2 higher than 90%). To prevent dehydration and electrolyte imbalance, serum electrolytes should be examined every 4-6 h as well as osmolarity. Moderate therapeutic hypothermia could be of benefit, and maintaining of optimal blood pressure (MAP above 90 mmHg), especiallz in the first period after injury. As thez have a lot of adverse effects, barbiturates are recommended only when conventional therapies show no effect. Patients should be hydrated well before induction of barbiturates. In organized trauma centers and with adequate intensive care the mortality from traumatic brain injury decreased from 50% in 1970, to about 30% nowdays.

CO2 pneumoperitoneum is an insuflication of CO2 into abdominal cavity in order to enable visulation of organs, and easier manipulation with instruments during laparoscopic surgery. Pressure that is being used is between 12 to 20 mmHg, but it is usually 14 mmHG, and it is higher than a pressure in the port system, which is between 7 to 10 mmHG. This causes changes in activity of AST, ALT and bilirubin during the laparoscopic surgery. In this research we have had two groups of 30 patients that had laparoscopic holecystectomy (researched group) and laparoscopic (control group) surgical technique. We have had compared values of activity for AST, ALT and bilirubin before and after the surgeries (after 6, 24, 48 and 72 hours). We concluded that changes of activity for AST, ALT and bilirubin during laparoscopic surgery are more outstanding with higher degree of significance than what happened during laparotomic surgery. Changes are of transitory nature and after 72 hours they return to the preoperative values.

Malnutrition is very common in critically ill patients. According to the available data, a high percentage of patients (30-60%) suffers from some degree of malnutrition, and in 10-15% of patients malnutrition can be very severe. Patient's nutritional status usually worsens during hospitalization. In malnutrition, the functions of all organ systems change. Surgical treatment is a stress for the body, which leads to the predominant catabolic response with accelerated decomposition of the non-fat tissue, resulting in enhanced gluconeogenesis and negative nitrogen balance, which further compromise body's vital functions. Due to such physiological effects, malnutrition is followed by increased number of complications of the underlying disease, higher mortality rate, prolonged hospitalization and increased treatment costs. Malnutrition is common in clinical practice, so at the time of the admission, all patients should be checked for signs of malnutrition. After noticing the presence of the increased risk, it is necessary to make a plan for preoperative nutritional support, in order to prepare the patient optimally for the surgical procedure. It is also necessary to check the factors which might lead to further worsening of the nutritional status of the patient. With adequate screening and therapy, it is possible to improve patients' general condition and the outcome, as well as to reduce the percentage of complications, mortality rate and treatment costs.

Trauma, surgery, burns and infection are accompanied with catabolic response which is characterized by enhanced protelysis, enhanced excretion of nitrogen, neoglucogenesis and resistance of peripheral tissues to insulin. This catabolic response is mediated through neural pathways and neuroendocrine axis. The purpose of this response is restoration of adequate perfusion and oxygenation and releasing of energy and substrates for the tissues, organs and systems which functions are essential for the survival. Metabolic response to injury and severe infection leads to decomposition of skeletal muscle proteins to amino acids, intensive liver gluconcogenesis from lactate, glycerol and alanin with enhanced oxidation of aminoacids. These substrates are necessary for synthesis of various mediators of protein or lipid nature, which are important for the defense and tissue regeneration. The changes result in negative balance of nitrogen, loss of body weight, and lower plasma concentration of all aminoacids. Patients who were unable to develop this hypercatabolic response have poor prognosis, and the patients with hypercatabolic response rapidly lose their body cell mass and without metabolic and nutritive support have more complications and higher mortality. Although neoglucogenesis, proteolysis and lipolysis are resistant to exogenous nutrients, metabolic support in critical illness improves the chances for survival until the healing of the disease. Casual therapy in such conditions is elimination of "stressors" which maintain abnormal endocrine and metabolic response. Adequate oxygenation, hemostasis, infection control and control of extracellular compartment expansion and low flows, are essential for the efficacy of nutritive support and that is the only way to convalescence and wound healing.

In last years there are still dilemmas about the starting of prompt resuscitation by volume restoring in haemorrhagic shock in penetrant, non-penetrant and vascular injuries. Will massive fluid administration before surgical control of bleeding, because of destroying the primary thromb, induce excessive bleeding and worse outcome, in regard to postponed resuscitation until the control of haemorrhage? What means that less fluid should be given, less than optimal, but in the quantity with which progressive circulatory shock will be avoided. According to some authors this should be followed in the treatment of non-penetrant injuries, what has been shown positive in animal models. There is also dilemma about the kind of fluid, crystalloids and what crystalloids, or colloids? Crystalloids are preferred, especially to Ringer lactat, except in the cases of traumatic brain injury when saline is better, because of mild hyperosmolarity. Hypertonic solutions 7.5% NaCl and 3% NaCl have advantages for prehospital resuscitation. As the advantages of colloids in regard to crystalloids were not proven, they should be used together with crystalloids, if the blood products are not available at the moment, and they should be given. It is considered that about 25% of overall colloid used is not justified. In the assessment of shock, i.e. tissue perfusion which is the most important parameter of shock, modern technologies measure systemic oxygenation SO2 as a balance of oxygen delivery DO2 and oxygen consumption DO2 and mixed venous blood PCO2. Noninvasive monitoring replaces invasive, and it can be even more precise and more accurate in parameter assessment. Sublingual capnography is new monitoring as indirect indicator of gut mucose perfusion and impedance monitoring which functions by means of measuring the changes of electrical impedance of thorax which are proportional to the pulse wave in aorta during systole and diastole.

Neurologic complications after severe brain injuries are the result of primary injuries in the moment of impact and secondary injuries which evolve over the minutes and days later. According to statistics, secondary injuries were documented in about 90 percent of patients who died after traumatic brain injury. Low oxygen delivery in hypotension, hypoxia, oedema, intracranial hypertension or changes in cerebral blood flow all account for development of secondary injuries. Primary injuries are more or less complete, but secondary injuries could be prevented with adequate therapy. Understanding mechanisms of secondary injuries could help identify potentially beneficial therapies. Important elements of therapy are: head position, normoglycemia, osmotherapy, normal body temperature, optimal blood pressure, adequate oxygenation, barbiturate therapy. Neutral head and neck position is recommended to prevent intracranial hypertension. Hyperglycemia with less ATP leads to ishaemic acidosis, hypoglycemia enhances decomposition of phospholipids and release of fat acids, what makes the cellular damage worse. Normocapnia is recommended and adequate oxygenation (PaO2 higher than 90%). To prevent dehydration and electrolyte imbalance, serum electrolytes should be examined every 4-6 h as well as osmolarity. Moderate therapeutic hypothermia could be of benefit, and maintaining of optimal blood pressure (MAP above 90 mmHg), especially in the first period after injury. As these have a lot of adverse effects, barbiturates are recommended only when conventional therapies show no effect. Patients should be hydrated well before induction of barbiturates. In organized trauma centers and with adequate intensive care the mortality from traumatic brain injury decreased from 50% in 1970, to about 30% now days.

In the treatment of the acute pancreatitis, the disease with high morbidity and mortality rate, the question is not how to treat the gland (which "eats" itself) but how to avoid deterioration of the vital functions of the organism. If intensive care is to be justified and evaluated, it is just this pathological condition. The classification on mild and severe form is generally accepted. Ranson s score and APACHE II score are used for the identification of the severe form of acute pancreatitis. Therapeutic guidelines for this disease are focused on: voluantibiotic therapy, pain relief and nutritional support. It is important to emphasize that regarding the caloric support, that in the severe form of the acute pancreatitis parenteral and enteral jejunal nutrition are needed.