Abstract • In the last ten years anaerobic organisms have emerged as the major infecting agent in surgical patients. While these groups of organisms including Bacteroides fragilis, clostridia, and anaerobic cocci persist, there has, in addition, developed In the last few years a virulent group of nosocomial infections, and modern management of sepsis is primarily directed at gram-negative and anaerobic infections, which include nosocomial infections, for example, those caused by the Serratia group. Much has been learned about control of infections from the patient who has sustained thermal injury. While topical water-soluble antibiotics have been a remarkable advance in the care of the burn patient, systemic and subeschar antibiotics have proved essential in the management of severe burn injury. There is increasing evidence that there is remarkable interference with host defense mechanisms in patients who have sustained burns or significant trauma or intraabdominal infection. The patient sustaining nonthermal traumatic injury also sustains reduction in host resistance. Because of this and the additional initial contamination, in the traumatized patient antibiotic therapy should be started early and as a therapeutic measure. Newer localization techniques, including sonography and computed axial tomography scanning, have helped localize abdominal infections early. Specific antimicrobial therapy may thus be begun as an adjunct to the surgical therapy of intra-abdominal infection. (Arch Intern Med 1982;142:2012-2022) References 1. Krizek T: Biology of surgical infection. Infect Dis Semin , 1977, pp 3-7. 2. Curreri PW, Marvin JA: Current therapy of the burned patient. Univ Washington Med 1975;4:16-24. 3. Warden JD, Mason AD Jr, Pruitt BA Jr: Evaluation of leukocyte chemotaxis in vitro in thermally injured patients. J Clin Invest 1974;54: 1001-1004.Crossref 4. Grogan JB: Suppressed in vitro chemotaxis of burn neutrophils. J Trauma 1976;16:985-988.Crossref 5. Fikrig SM, Karl SC, Suntharalingam L: Neutrophil chemotaxis in patients with burns. Ann Surg 1977;186:746-748.Crossref 6. Alexander JW: Serum and leukocyte lysosomal enzymes. Arch Surg 1967;95:482-491.Crossref 7. Munster AM, Hoagland HC, Pruitt BA: The effect of thermal injury on serum immunoglobulins. Ann Surg 1970;172:965-969.Crossref 8. Daniels JC, Larson DL, Abston S, et al: Serum protein profiles in thermal burns: I. Serum electrophoretic patterns, immunoglobulins and transport protein. J Trauma 1974;14:137-152.Crossref 9. Davis JM, Dineen P, Gallin JI: Neutrophil degranulation and abnormal chemotaxis after thermal injury. J Immunol 1980;127:1467-1471. 10. Altman LC, Furukawa CT, Klebanoff SJ: Depressed mononuclear chemotaxis in thermally injured patients. J Immunol 1977;119:199-205. 11. Warden GC, Mason AD, Pruitt BA Jr: Suppression of leukocyte chemotaxis in vitro by chemotherapeutic agents used in the management of thermal injuries. Ann Surg 1975;181:363-369.Crossref 12. Dineen P, Shires GT: Tetracyclines in abdominal trauma and abdominal infections. Bull NY Acad Med 1978;54:177-195. 13. Altemeier WA: Manual of Control of Infection in Surgical Patients: American College of Surgeons. Philadelphia, JB Lippincott Co, 1976. 14. Dineen P: Infections following crushing or gross impact , in Hoeprich PD (ed): Infectious Diseases , ed 2. Hagerstown, Md, Harper & Row Publishers Inc, 1977, chap 147. 15. Shires GT: Principles in management of hemorrhagic shock , in Shires GT (ed): Care of the Trauma Patient , ed 2. New York, McGraw-Hill Book Co, 1979, chap 1. 16. Dineen P: Gas gangrene , in Hoeprich PD (ed): Infectious Diseases , ed 2. Hagerstown, Md, Harper & Row Publishers Inc, 1977, chap 149. 17. Bennett J: Tetanus , in Hoeprich PD (ed): Infectious Diseases , ed 2. Hagerstown, Md, Harper & Row Publishers Inc, 1977, chap 120.
Archives of Internal Medicine – American Medical Association
Published: Oct 25, 1982