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.
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 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.
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