الفهرس 
Pathophysiology of SepsisOnly 14 pages are availabe for public view
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Abstract
Sepsis is a clinical syndrome that complicates severe infection and is characterized by systemic inflammation and widespread tissue injury. In this syndrome, tissues remote from the original insult display the cardinal signs of inflammation, including vasodilatation, increased microvascular permeability, and leucocyte accumulation. Although inflammation is an essential host response, current believes regarding the onset and progression of sepsis center upon a ”dysregulation of the normal response”, with a massive and uncontrolled release of proinflammatory mediators creating a chain of events that leads to widespread tissue injury and frequently to death , Current pathophysiologic concepts of sepsis include Activation of coagulation, Impairment of anticoagulant mechanisms, so the coagulation system and anti-inflammatory cascade work in concert, with one potentiating the effects of the other.
A number of organ abnormalities may occur in septic shock. The lungs may develop low- pressure pulmonary oedema, or adult respiratory distress syndrome. Dissiminated intravascular coagulation may ocurr and carries a high mortality. Renal impairment & gastrointestinal dysfunction may occur secondary to regional ischemia, Central nervous system dysfunction is also common, cardiac muscle dysfunction causing myocardial depression, hepatic dysfunction, adrenal insufficiency, vasodilatation, disturbed oxygen consumption, delivery and disturbed peripheral metabolism.
Clinical signs of systemic inflammation such as changes in body temperature, leukocytosis, and tachycardia may therefore have an infectious or non-infectious etiology and are neither specific nor sensitive for sepsis. It is, thus, frequently difficult to distinguish patients with systemic infection from those who appear septic but have no evidence of infection. Bacteriologic evidence of infection also has drawbacks because it may not develop concurrently with clinical signs of sepsis, and a negative bacteriologic result does not exclude the presence of infection or sepsis. Since these common clinical and laboratory parameters lack sensitivity and specificity, others are needed to provide an early marker of the infectious etiology of a generalized inflammatory response and thus allow early diagnosis and the application of more specific therapeutic interventions.
A lot of markers help in diagnosis and prognosis of sepsis which include procalcitonin, polymorphnuclear elastase enzyme, cytokines, eosinophils, acute phase reactant proteins and Blood lactate level.
The basic treatment of sepsis involves control of infection by antibiotics and surgical intervention if required, fluid resuscitation by colloid and crystalloids, blood transfusion when required, vasopressor and inotropic therapy, administration of oxygen and ventilation and others.