Management objectives (TableB) include source control of the infectious process, by antibiotic therapy and drainage where appropriate, and ensuring that O 2 delivery is supported to match the typically elevated tissue metabolic needs.
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Table 8 Therapeutic management of the hypotensive patient with sepsis
Early localization and eradication of the inflammatory focus underlying the septic state is vital. Empirical antibiotic therapy is commenced after obtaining appropriate cultures. Although no clinical trial has revealed the optimal regimen in septic shock, a conservative approach includes a third-generation cephalosporin plus an aminoglycoside. If history and clinical examination suggest an anaerobic infection, then metronidazole or clindamycin should be added. Antibiotic therapy must be changed according to the susceptibility of specific organisms found by culture and sensitivity testing.
Initial therapy in sepsis also follows basic principles of resuscitation. Hypotension is often associated with hypovolemia and therefore may respond well to fluid therapy. Early red blood cell transfusion may be considered to maintain a hemoglobin of 100 to 130 g/l. Infusion of red cells stored for more than 15 days may produce splanchnic ischemia. Since vascular reactivity and myocardial contractility are impaired in sepsis, a- and b-agonists may be considered in the early treatment of circulatory compromise.
After restoring normotension, therapy is directed at optimizing O 2 delivery to the tissues as this syndrome is a distributive disorder and a 'normal' blood pressure alone does not ensure adequacy of nutritive organ blood flow. Septic patients have elevated metabolic needs and an O 2 extraction deficit; therefore high normal levels of O 2 delivery (> 600 ml/min/m2) are considered beneficial. However, there is considerable controversy about the concept of augmenting O 2 delivery to 'supranormal' values (cardiac index above 4.5 l/min/m2); there is no clear evidence that this improves patient outcome. Consequently, O 2 delivery may be supported towards a level thought to be appropriate for the patient's metabolic needs withot compromising organ function (e.g. increased myocardial O 2 consumption due to excessive doses of inotrope). This level of delivery may often be higher in a young patient than in an elderly patient with pre-existent cardiovascular morbidity. If the pulmonary artery wedge pressure is low, fluids may be beneficial; if it is high, vasodilators such as nitroglycerine may improve cardiac output.
A decrease in arterial lactate may be taken as a sign of response to therapy, since elevated arterial lactates have been associated with decreased survival from sepsis. The mixed venous oxygen saturation is maintained above 50 per cent to avoid the onset of regional O 2 debts in the face of a decreased ability of the tissues to extract O2. Acidosis resulting in an arterial pH of less than 7.2 may indicate ongoing anaerobic metabolism.
At present it is only possible to offer supportive treatment for septic-specific lesions such as circulatory failure or impaired cellular O 2 utilization. New strategies currently under investigation, such as therapies directed at scavenging oxygen radicals, endotoxin, or other mediators of inflammation, may provide additional benefit. Refractory hypotension
Beyond the consideration of more invasive therapeutic strategies, refractory hypotension should always lead to a re-evaluation of the diagnosis. In patients with trauma, pneumothorax or pericardial obstruction frequently remain unrecognized in the first few hours after the incident, but they may prevent (often concomitant to aggravation of the process) restoration of circulatory function. Addison's disease may lead to unresponsiveness of the circulation to standard therapies of hypotension and requires corticosteroid therapy.
Finally, the hypotensive condition may have caused organ failure (single or multiple), thus initiating further pathological processes such as gut ischemia, ischemia of the brain, or secondary myocardial depression, all of which are followed by additional circulatory failure.
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