الفهرس 
Pathophysiology of sepsis in burned patientsOnly 14 pages are availabe for public view
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Abstract
Sepsis remains a critical and serious complication of a major burn injury with significant morbidity and mortality . Sepsis is widely recognized as a clinical syndrome resulting from systemic host response to infection . During inflammatory situations such as sepsis , significant alterations occur at multiple levels within both the coagulation system and the cells that regulate this system . The capillary endothelium becomes activated and transforms into a pro-thrombotic interface , which is critically involved in the cascade leading to multiple organ failure .
Thus interrupting this progression through early diagnosis and appropriate treatment is critical . Burn patients with sepsis should be examined immediately to determine the site and source of infection , including inspection of the entire burn wound surface . Quantitative cultures of burn wound tissue biopsy samples along with concomitant histological analysis are the preferred infection surveillance approach for burn wound .
Since these common clinical and laboratory parameters lack sensitivity and specificity , others are needed to provide early markers of a generalized inflammatory response and thus allow early diagnosis and the application of more specific therapeutic interventions , such as :- pro-calcitonin , IL-6 , which known as sepsis bio-markers .
Elevation of Pro-calcitonin serum concentration is associated with systemic infection . The normal range for serum PCT is less than 0.5 ng / mL . Mild elevations (0.5-2 ng/mL) are associated with viral infections , chronic inflammation . Sepsis , severe sepsis , and septic shock cause progressively higher elevations in serum PCT, even as high as 1,000 ng / mL .
Another commonly researched marker for sepsis is IL-6 , a pro-inflammatory cytokine that is released during the onset of an infection . IL-6 levels peak a few hours after inflammation begins and return to normal after a few days of successful immune response .
Once sepsis identified , treatment must be started as early as possible . Wide spectrum and timely anti-microbial treatment is curcial to improve patients out-come and reduce mortality rate .
When the pathogen is identified , anti-microbial therapy should be directed at the pathogen recovered on culture .
Fluid therapy should be initiated after adequate control of airway . Fluid resuscitation either by colloids or crystalloids , Volume replacement of ( 20- 40 ml / Kg) with isotonic solutions such as normal saline or ringers lactate can be safely given and repeated if necessary but still controversy continue about whether colloids or crystalloids are preferable .
Mechanical ventilation is often necessary to support the patient who has burn with inhalation injury . New strategies for mechanical ventilation include changes in traditional mechanical ventilation parameters such as the use of low-tidal-volume ventilation and high frequency ventilation .
The metabolic response to burn injury is similar to that of any physiological trauma . It results in systemic disturbances , including a major hormonal stress response and impaired immunity . In addition, there is a decrease in the normal endogenous activity of anabolic agents, such as human growth hormone and testosterone .
Nutrient requirements are markedly increased in the presence of the acute-phase response , and all patients with burns exceeding 20% TBSA should receive nutritional support . Because micro-nutrients play an essential role in metabolism and anti-oxidant defenses , a deficiency state is thought to amplify the already burn induced metabolic derangements and ongoing catabolism .
Vitamin - C plays an important role in collagen formation and anti-oxidant defenses in the immune system . The immune-enhancing diets/agents include arginine , glutamine , omega-3 fatty acids , and anti-oxidants such as tocopherol ( vitamin – E ) are recommended to improve outcome , and reduce mortality rate .