الفهرس 
Incidence, Terminology and Pathophysiology of Sepsis SyndromeOnly 14 pages are availabe for public view
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Abstract
Sepsis syndrome is a complex condition that occurs as a result of the systemic manifestation of infection. It is associated with high mortality and morbidity risks for critically ill patients. Predisposing factors of sepsis include severe dysfunction of the immune system, the possibility of a prolonged hospitalization, invasive diagnostic and therapeutic procedures and burns. The source of infection is usually endogenous. Infections of the chest, abdomen, genitourinary system and primary blood stream cause more than 80% of sepsis. Septic shock is sepsis with hypotension despite adequate fluid resuscitation, This concept of staging system for sepsis based on four separate characteristics ( predisposition, infection, response and organ dysfunction).
The sepsis syndrome is recognized clinically by the presence of 2 or more of the following: pyrexia or hypothermia, tachycardia, respiratory rate greater than 20 breaths per minute or a PaCO2 in arterial gases less than 32 mmHg and white blood cell (WBC) count greater than 12,000 cells/μL, less than 4000 cells/μL or greater than 10% band forms.
Severe sepsis and septic shock are the end result of complex interactions between infecting organisms and several elements of the host response and reflect a primarily inappropriate response by the host to a microbial pathogenic insult. The key term that describes the pathophysiologic events in septic shock at any point in time is the ‘‘mismatch’’ of the host response to the intensity of the pathogenic stimuli ultimately leading to organ injury or dysfunction with or without hypotension. This mismatch results in, amongst other derangements, an immune profile that could be predominantly proinflammatory (systemic inflammatory response syndrome), mixed (mixed antagonistic response syndrome) or predominantly anti-inflammatory (compensatory anti-inflammatory syndrome). The nature of the interactions between the microbial pathogen and the host is complex and at the tissues results in excessive inflammation or immunosuppression, abnormal coagulation and blood flow and microcirculatory dysfunction leading to organ injury and cell death.HES solutions are artificial colloid solutions that are modified natural polysaccharides with volume-expansion properties. They are increasingly being used for the prevention and treatment of hypovolemia in numerous clinical situations, such as surgical, trauma, burn and intensive-care patients. HES is a nonionic starch derivative and can be sub-classified according to average molecular weight, molar substitution, concentration, C2/C6 ratio and maximum daily dose. The rationale for their clinical use is that they are low-cost colloids that are highly effective for increasing intravascular volume for sustained periods, believed to have anti-inflammatory properties as well as other desirable characteristics, such as having a smaller impact on tissue edema compared to commonly used crystalloids.
HES solutions are not localized to the circulatory system and are known to deposit in the skin, liver, muscle, spleen, endothelial cells and kidneys of patients who receive these products. The adverse effects depend on the volume and molecular weight of the hydroxyethyl starch preparations, the elimination depends on molar substitution degree, molecules smaller than the renal threshold are readily excreted in the urine while a small part of the larger ones are metabolized by plasma α–amylase before those degradation products are renally excreted. HES has remained detectable in plasma 4 months after infusion. HES can be used to treat patients with low blood volume caused by acute blood loss where treatment with a crystalloid infusion solution alone is not sufficient. Potential risks should be minimised by using HES solutions for no more than 24 hours and monitoring the kidney function of patients for at least 90 days. The (EMA-PRAC) informed that hydroxyl ethyl starch solutions are associated with increased mortality and kidney injury in patients with sepsis and increased risk of kidney injury in critically ill patients.
HES solutions are contraindicated in severe coagulopathy, Blood coagulation parameters should be monitored carefully in case of repeated administration. Large HES molecules interfere with fibrinogen, coagulation factor VIII and von Willebrand factor. In patients with renal insufficiency cumulative urinary excretion, even in the presence of severe non-anuric renal failure, is higher for hydroxyethyl starch130/0.4 than values published for older hydroxyethyl starch specifications. Hydroxyethyl starch 130/0.4 may be given to patients with severe renal impairment as long as urine flow is preserved.
Goal-directed therapy provides a straight forward approach to hemodynamic management in septic patients. The surviving sepsis campaign guidelines outline evidence-based recommendations for targeting treatment of patients at risk of developing severe sepsis and shock and aimed at providing resuscitation for sepsis-induced hypoperfusion and enhancing perfusion, antibiotic administration to infection, cultures to identify the source of infection, mechanical ventilation to optimize oxygenation and source control to contain the infection. The guidelines also advocate for the use of evidence –treatment practice for critically ill patients including glucose control, steroid use for adrenal insufficiency, prophylaxis measures for deep vein thrombosis, stress ulcer prevention, use of recombinant human activated protein C for patients with evidence of early organ system dysfunction , sedation , analgaesia and blood product administration as indicated.
The SSC and the institute for healthcare improvement have introduced a new concept called “treatment bundles” for the management of severe sepsis and septic shock, the two bundles that were developed were the six-hours resuscitation bundle and a 24-hours subacute care bundle. The six-hours bundle is comprised of three components, early identification, early antibiotics and cultures and early goal-directed therapy. EGDT may be initiated when hypotension is not resolved after adequate intra venous fluid (IVF) administration or in patients with a serum lactate elevation (≥4mmol/L) regardless of blood pressure.