Resuscitation Essay

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Fluid resuscitation of trauma patients in a state of hypovolemic shock has traditionally been assessed by clinical parameters, such as heart rate, blood pressure, central venous pressure and urine output. However, these endpoints of volume replacement could be misleading in patients with compensated shock. In addition, tissue hypoperfusion following vasoconstriction cannot be ruled out. An ideal marker of adequate resuscitation is one that accurately and reliably assesses resolution of tissue hypoxia and is predictive of patient mortality and outcome. In addition, it should provide this information in a timely fashion (within the first few hours) to prevent the adverse consequences of under-resuscitation and prolonged tissue hypoxia.
Normalization of the vital signs mentioned above has been used as endpoints of resuscitation. However, critical review of this practice has highlighted the inadequacy of relying solely upon vital
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Base deficit represents the number of mEq/L of additional base that must be added to a liter of blood to normalize the pH. A significant base deficit has been found to be a marker of mortality in many studies5-7. Normal values vary among institutions but tend to be greater than - 2mmol/L. In a study of non-head injury trauma patients, patients younger than 55 years, with a base deficit of ≥8 mmol/L predicted a 25% higher mortality than those with lower base deficit8. Furthermore, in hemorrhagic shock, changes in the base deficit often precede changes in other hemodynamic parameters9. While physiological response mechanisms can maintain blood pressure, urine output, and pH; hemorrhage causes early changes in both arterial and venous base deficit. Although base deficit is often used as an indirect measure of lactic acidosis, it can also be elevated in situations such as diabetic ketoacidosis, salicylate overdose, and renal

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