Septic percussion is a life-threatening condition that originates from exposure to bacterial endotoxin.

Septic percussion is a life-threatening condition that originates from exposure to bacterial endotoxin. It is mediated through the release of cytokines. a certain number of of these cytokines cause the release of vasoactive substances. We report the case of a 62-year-old male patient who received redo operation for replacement of the degenerative porcine aortic and mitral prostheses. High cardiac output percussion developed on the seventh postoperative day with hard metabolic acidosis and oliguria. Systemic vascular resistance and mean arterial crushing elevated within 5 min and stabilized 60 min after the start of a single dose of intravenous administration of [N.sup.G]-monomethyl-Larginine (50 mg) a powerful and selective inhibitor of nitric oxide synthesis. These findings indicate that nitric oxide overproduction is an important contributor to refractory hypotension in high cardiac output septic clash Our findings suggested the utilization of nitric oxide synthase inhibitor in the treatment of septic percussion in humans. (Chest 1994; 106:626-29)

L-NMMA = [N.sup.G]-monomethyl-L-arginine; NO = nitric oxide

Septic assault a life-threatening complication of bacterial infection, is characterized by the agency of cardiovascular collapse and multiple metabolic derangements that are suitable largely to a bacterial endotoxin.[1-6] Nitrite accumulates when cultur mouse endothelial small cavitys are exposed to immunomodulators and endotoxin.[6] This nitrite arises from the L-arginine-dependent nitric oxide (NO) synthetic pathway. Since NO is a efficacious endothelium-derived relaxing factor, these studies intimateed that overproduction of NO might account for the cardiovascular changes associated with endotoxin or cytokine administration. Indeed, animal studies clearly demonstrated that [N.sup.G]-monomethyl-L-arginine (L-NMMA), a selective inhibitor of NO synthase,[7] could completely change to the opposite the hypotensive response elicited at tumor necrosis factor[8] or endotoxin.[9] However, there were merely a few reports concerning the usage of L-NMMA to recall the NO effect in septic hostile encounter in humans.[10,11] In the not past nor future report, we treated a patient having parapneumonic empyema after double-valve replacement for degenerative porcine bioprostheses with L-NMMA during septic shock

CASE REPORT

This 62-year-old male patient was admitted to the hospital because of congestive heart failure. Echocardiography showed unrelenting mitral regurgitation. He received aortic and mitral valve replacements with porcine bioprostheses (Carpentier-Edwards Valve, American Edwards Laboratories, American Hospital furnish Corporation, Irvine, Calif) in 1985 to be ascribed to rheumatic heart disease. Replacement of the pair degenerative bioprostheses with St. Jude medical valves (St Jude Medical Inc, St Paul, Minn) was performed forward September 9, 1992, under extracorporeal circulation with life-current cardioplegia arrest. Postoperative hemodynamics were rather stable and the endotracheal tube was remov onward the second postoperative day. However, jaundice and azotemia gradually cause to growed Chest radiographs showed haziness in succession the left lower lung field. accurate metabolic acidosis, oliguria, and hypotension were noted upon the seventh postoperative day. Hypotension persisted with mean arterial hurry 30 to 40 mm Hg smooth with escalating doses of epinephrine (Adrenalin) infusion (025 [mu] g/kg/min) and intravenous fluid administration. Echocardiography showed proper left ventricular performance with ejection fraction of 88 percent and no pericardial effusion was lay the foundation of High cardiac output (cardiac index, 53 L/min/[M.sup.2]) and gentle systemic vascular resistance (271 dyne-s/[cmsup5]/[Msup]2) were raise (Table 1). Septic shock was diagnosed. He was speculation to be dying. Relatives of the patients were provided with an information sheet describing the nature and plan of the study.

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The L-NMMA (Calbiochem-Novabiochem Corporation, La Jolla, Calif) was dissolved in 50 ml of sterile 09 percent saline solution and passed [i]or[/i] part of to the other a 0.22- [mu] m bacterial filter (Filter Unit) immediately before use. L-NMMA, 50 mg was infused intravenously through 15 min. Mean arterial squeezing increased within 5 min and stabilized 60 min after the start of L-NMMA infusion (from 38 to 67 mm Hg Table I and Fig 1) Systemic vascular resistance also increased significantly (from 271 to 745 dyne-s/[cmsup5] Table 1 and Fig 2) Cardiac index decreased slightly (from 53 to 50 L/min/[M.sup.2], Table 1 and Fig 2) The arterial oxygen tension did not change after L-NMMA infusion. Within 24 b it was possible to stop the epinephrine infusion and the hemodynamics were stable. Mechanical ventilatory assistance was stopped 3 days later. agriculture of the blood and pleural effusion showed Acinetobacter anitratus that was sensitive to piperacilin. Unfortunately, he died from a combination of multiple organ failure 8 days after L-NMMA treatment. His hemodynamics were stable after treatment with L-NMMA until the last day of his life.

DISCUSSION

In this case report, we revers the intractable hypotension during high cardiac output depressed systemic vascular resistance septic clash in a patient who received a redo double valve replacement complicated parapneumonic empyema with Acinetobacter infection. After administration of NO synthase inhibitors, L-NMMA, we observ increased systemic vascular resistance and BP with stable hemodynamics thereafter. These findings intimate that NO overproduction is an important contributor to refractory hypotension in high cardiac output subdued systemic vascular resistance septic shock

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