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Multiorgan failure and hypermetabolism


The normal body response to injury is now well-known and has a number of cardiovascular factors, particularly tachycardia, increased contractility and cardiac output, increased oxygen consumption under the influence the secretion of catecholamines. Neuroendocrine response also includes the secretion of catecholamines natural, that of cortisol, antidiuretic hormone, the growth hormone, glucagon and insulin. Coagulation is as well activated (activation of the complement system and fibrinolytic systems). Such a response is a physiological after an assault. The maximum response is usually obtained 2-5 days after the initial insult, and then decreases bit by bit from the 7th to 10th day. Gradually reducing the total-body water takes place by a cover of diuresis with decreasing temperature and decrease of the tachycardia. In the absence of clinical signs, should be particularly vigilant because the perpetuation of this inflammatory response, may intervene.

Indeed, a number of patients maintained beyond the 10th day, whatever the organic forms of assistance offered (artificial ventilation, etc.) tachycardia, tachypnea, fever and a hyper metabolic state. This behavior is particularly common after trauma or severe infections, or following a cardiac arrest when resuscitation maneuvers were inadequate or relatively late in their occurrence. The inflammatory response is then accompanied in most cases, respiratory failure within 24 to 72 hours after the initial event. The target lung in these situations "pure" (trauma or infection) is usually the first attack. The term "ALI" in Anglo-Saxon, that is to say, Acute Lung Injury, corresponding to an acute lung includes pathophysiological conditions ranging from mild impairment in respiratory distress syndrome of the (ARDS), first described by Ashbaugh in 1967. Today, most authors agree to consider that there is a continuum between the ALI and ARDS without that one can speak of an all-or-nothing phenomenon. It seems cons rather be a phenomenon gradually evolving from a simple pathophysiologic abnormality not clinically detectable until reaching very serious life-threatening ARDS.

Acute lung injury most often begins with an alteration of the pulmonary capillary endothelium. These cellular phenomena are due to a complex interaction involving platelets, neutrophils, endothelial cells, all mediated by numerous mediators, most prominently cytokines such as TNF, interleukin 1, interleukin 6, and interleukin-8, promoting the expression of adhesion molecules on endothelial cells. The catalytic activation of polynuclear leads to the production of proteases and oxygen-free radicals. Achieving the endothelial cell which follows, leading to an increased permeability of the alveolar-capillary membrane while allowing the passage of plasma water in the alveoli, the inflammatory cells and maintaining their own account the phenomenon interstitial and alveolar inflammation. This fluid influx and cell explain the discrepancies noted on the radiograph, and abnormal PaO 2 / FIO 2.

These pathological changes are indeed the cause of a disorder reports overall ventilation / perfusion leading to hypoxemia, decreased lung compliance. Unfortunately, these pulmonary pathophysiological changes occurring at a time when oxygen demand is increased, requiring a minute ventilation of 15 to 20 L · minimum -1, which asks the patient is unable to respond spontaneously, which led to the need use of mechanical ventilation.

If mortality from ARDS is only 50%, most often death occurs in a context not only hypoxemia, but develops gradually multiorgan dysfunction syndrome related to a secondary infection. The source of infection is most often represented by the lung, thus achieved.

After the onset of lung disease, two clinical evolutionary trends are usually recorded. The first type of evolution, which is the most common, is readily seen after trauma, burns or surgery. This evolution was described by Faist et al and Meakins as a two-stage evolution in which the first is represented by the lung and the second by the gradual development of SIRS, complicated then an encephalopathy, including hematological abnormality's leukopenia, DIC, and thrombocytopenia, gastrointestinal damage with gastrointestinal bleeding, abnormally prolonged ileus following abdominal surgery, pancreatitis or acalculous cholecystitis. There is parallel to a rapid deterioration of liver function and renal function and death usually occurs in an array of multiple organ failure between day 14 and day 21 after the assault on the body.

The second evolutionary scheme, rarely seen after trauma, but more readily stored in medical situation's assault (severe sepsis, septic shock or cardiogenic) is the development of a lung (ALI) and kidney but also almost concomitant liver, furthermore, a decrease in left ventricular contractile function, at best described by the association of hemodynamic measurements and transesophageal echocardiography. Death occurs usually a little faster around the 10th day, in an array of multiple organ failure very similar to the above-described scheme.

Along with this chronological description, and organ by organ multi-visceral disease, it is possible to record in all situations; metabolic activation is responsible for the increased demand and consumption of oxygen the body. This hypermetabolisms characteristic of all cases of SIRS, organ dysfunction or multiple organ failure is characterized, on the hemodynamic, a painting by hyperdynamic with tachycardia, increased cardiac output, fall in systemic vascular resistance and decreased arteriovenous difference.

These situations are often characterized by poor utilization of oxygen delivered to the tissue, either for reasons internal cellular mitochondrial, or for reasons of "shunt intraviscerale" performing infusion's luxury metabolically inefficient. The consequence of these phenomena is roughly appreciated by the elevation of blood lactate. Abnormalities of regional avascularization in this situation are probably largely the cause of changes in oxygen consumption calculated. However, other assumptions remain valid, such as adequacy of tissue perfusion and an inability to correct extract the tissue oxygen.

All in all, it is possible to record in this phase hyper metabolic syndrome of organ dysfunction, significant changes regarding the metabolism of carbohydrates. It seems that energy use glucose is decreased in parallel to a reduction in the activity of pyruvate dehydrogenase. Gluconeogenesis is strongly stimulated under the influence of catecholamines at the expense of amino acids, which explains the catabolism usually encountered in these patients. The final pathway of glucose metabolism is represented by hyperglycemia relatively insensitive to exogenous insulin. The elevation of serum lactate is directly related to the elevation of pyruvate, especially in all situations where there are perfusion abnormalities. Protein metabolism is also affected in all situations of SIRS and MODS. The amino acids then represent an important source of energy, they are from the catabolism of skeletal muscles and various organs. This situation hyper catabolism was thus described by the term auto-cannibalism. There is indeed, a total that increased protein catabolism, and this process is unfortunately slightly offset by the exogenous administration of amino acids.

In total, the catabolism of amino acids important carries a considerable production of urea. Parallel to the peripheral catabolism, there is an increase in hepatic protein synthesis, usually described by the term "Acute Phase Protein," however, this does not reach anabolism quantitatively the importance of catabolism, which can reach 15 to 20 g nitrogen per day. The exogenous administration of protein can promote the hepatic synthesis and provide a therapeutic target in either nutrition. Even so, when the worsening liver dysfunction, hepatic synthesis decreases significantly and most often associated with poor prognosis. Unlike situations of fasting, serum levels of ketone bodies are low in all situations of SIRS and MODS. The late stage of pre-mortem; organ dysfunction syndrome is usually accompanied by an increase in hepatic lipogenesis with a release of serum VLDL. Finally, triglyceride clearance decreases leading to an unpunctual stage of MODS, the appearance of hypertriglyceridemia. This situation of hypermetabolisms characteristic of organ dysfunction syndrome and multiple organ failure, are best described in patients subjected to therapeutic interventions and technical assistance to enable prolonged survival (mechanical ventilation, hemodialysis, hemofiltration, drug use and positive inotropic tonicardiaques). This metabolic pathway is a common often end after the assault. It differs significantly in its chronology according to two evolutionary trends that have been proposed.

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