الفهرس 
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Abstract
Shock is a state of acute cardiovascular or circulatory failure. Whether shock results from hemorrhage, sepsis, or cardiac failure, mortality rates exceed 20%. Shock results from the widespread failure of the circulatory system to oxygenate and nourish the body tissues adequately. At the cellular level, shock alters mitochondrial energy transfer and evokes the production and accumulation of toxic chemicals. Shock occurs in approximately 2% of all hospitalized infants, children, and adults in developed countries, and the mortality rate varies substantially depending on the etiology and clinical circumstances. Of patients who do not survive, most do not die in the acute hypotensive phase of shock, but rather as a result of associated complications and multiple-organ dysfunction syndrome (MODS). The pathophysiologic mechanisms that can result in shock are divided into 4 separate (but potentially overlapping) categories: (1) hypovolemic, (2) distributive, (3) cardiogenic, and (4) obstructive. Shock is a clinical diagnosis based on a thorough history and physical examination. In cases of suspected septic shock, an infectious etiology should be sought through culture of clinically appropriate specimens and prompt initiation of empirical antimicrobial therapy. Patients presenting to the the Emergency Department in a state of shock frequently have no obvious cause. Rapid recognition of shock requires the integration of information from the immediate history and physical examina-tion and is strongly supported by the presence of a worsening base deficit or lactic acidosis. Early recognition and prompt intervention are extremely important in the management of all forms of shock. Baseline mortality is much lower in pediatric shock than in adult shock, and further improvements in mortality are associated with early interventions. The initial assessment and treatment of the pediatric shock patient should include stabilization of airway, breathing, and circulation as established by the American Heart Association’s pediatric advanced life support and neonatal advanced life support guidelines. Depending on the severity of shock, further airway intervention, including intubation and mechanical ventilation, may be necessary to lessen the work of breathing and decrease the body’s overall metabolic demands. Given the predominance of sepsis and hypovolemia as the most common causes of shock in the pediatric population, most therapeutic regimens are based on guidelines established in these settings. Immediately following establishment of intravenous (IV) or intraosseous access, aggressive, early goal-directed therapy should be initiated unless there are significant concerns for cardiogenic shock as an underlying pathophysiology. Rapid IV administration of 20 mL/kg isotonic fluid should be initiated in an attempt to reverse the shock state. This bolus should be repeated quickly up to 60-80 mL/kg; it is not unusual for severely affected patients to require this volume within the 1st hr of treatment. Rapid fluid resuscitation totaling 60-80 mL/kg or more is associated with improved survival without an increased incidence of pulmonary edema. Another line for management of shock is the use of vasopressor therapy. The primary goal of vasopressor support is to increase cardiac output and oxygen delivery to vital organs when crystalloid resus¬citation alone is inadequate. Epinephrine is typically used as a continuous infusion (0.02–0.5 μg/kg/min) for severe sustained hypotension and as a bolus (0.01 mg/kg, maximum dose = 1 mg) for bradycardia, asystole, or pulseless arrest. There are, however, clinical conditions that may benefit from smaller doses of bolus epinephrine. For example, brief periods of hypotension during medical procedures, intermittent hemodynamic instability, and augmentation of low blood pressure in a prearrest condition. While a resuscitation dose of epinephrine would be inappropriate (as it would cause an unacceptable large increase in blood pressure and heart rate, a smaller dose may be particularly useful. Low-dose bolus vasopressors have been used for decades by anesthesiologists to prevent postreperfusion injury after solid organ transplant, control cerebral oxygenation during anesthesia and manage acute hypotension during spinal surgery. The use of bolus dose phenylephrine has been described in the emergency department setting to augment blood pressure during periods of hypotension surrounding intubation. The specific aim of this study is to characterize current practice (use of fluid boluses only) and the combined use of low-dose epinephrine boluses (≤ 5 μg/kg/dose) added with the fluid boluses. The study included 120 pediatric patient aged 1 month and 18 years old admitted to PICU of Asyut university children hospital with different medical and surgical conditions leading to an acute hypotensive episode. The study showed marked increase in blood pressure with the added epinephrine bolus with lower mortality rate in those patients in relation to patients receiving fluid bolus only. However, the duration of hospital stay remained the same in both patients which show that epinephrine has no long term effect on those patients.