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Objective: To test the hypothesis that antibiotics leading to greater endotoxin release are associated with greater mortality in septic trauma patients. Design: Post hoc analysis of data from a previously conducted prospective, randomized, multicenter study designed to evaluate the efficacy of interferon gamma in preventing infection and death in trauma patients. Setting: Nine level I trauma centers. Patients: Severely injured trauma patients at high risk for sepsis. Eighty percent (N=334) of the enrolled patients developed some manifestation of gram-negative sepsis, defined by the administration of gram-negative specific antibiotics. Main Outcome Measures: The in-hospital mortality rate of patients who received penicillin-binding protein 3/tumor necrosis factor (PBP3/TNF)–specific antibiotics associated with the greatest degree of endotoxin release and TNF production (PBP3/TNF group, n=78: aztreonam. ceftazidime, and cefotaxime sodium) was compared with that of patients not receiving these agents (non-PBP3/TNF group, n=256). Results: Mortality in the PBP3/TNF group (17%) was higher than in the non-PBP3/TNF group (8%, P=.02). The two groups were similar in their mean (±SD) Injury Severity Scores (34±9), ages (31 ± 12 years), and initial degree of bacterial contamination. Conclusions: Antibiotics that are associated with greater release of endotoxin and production of TNF are also associated with greater mortality in septic trauma patients. Decisions regarding antibiotic administration may need to consider the endotoxin-releasing properties of antibiotics in addition to their antibacterial sensitivity spectrum. Prospective studies of the effect of endotoxin-releasing properties of antibiotics on mortality are warranted. (Arch Surg. 1995;130:1234-1241)

Although the laser has been demonstrated to vaporize coronary artery plaque, there is little information about its ability to resect or vaporize the range of plaques present in peripheral vessels. This study attempts to determine the ability of the argon laser to resect all grades of atherosclerotic plaque, the risk of perforation during plaque resection, the effects on surrounding arteries, and the effect of different transmission media (air, saline solution, and blood) on the delivery of laser energy to the vessel. Seventy-five adult human cadaveric aortic specimens with a range of atherosclerosis from grossly normal artery to extensive calcification with ulceration were exposed to variable energy densities (200 to greater than 20,000 J/cm2) within 48 hours of harvesting. Specimens were examined grossly for the visual effects of laser and microscopically after preparation with hematoxylin-eosin, trichrome, and/or Verhoeff's elastin stains. Our results indicate that normal arteries and noncalcified plaques absorb laser energy and are vaporized. As the atherosclerosis becomes more complex with calcification, calcified regions are not vaporized and cannot be resected. In normal arteries and noncalcified plaque, perforation times were less than 5 seconds. Where palpable calcification was present in atherosclerotic lesions, average perforation time was doubled. In some vessels areas of calcification prevented wall perforation, but areas of subintimal hemorrhage perforated rapidly because of the selective absorption of laser energy by the red color of hemorrhagic tissue. These results remain the same when saline solution is used as a transmission media, although the amount of energy required to achieve the effects is increased.(ABSTRACT TRUNCATED AT 250 WORDS)

Laser energy applied to the vascular system was first reported in 1963 by McGuff and associates. Nearly 20 years later, much attention has been devoted in the media to laser applications in the treatment of atherosclerosis in the coronary circulation. While less attention has been directed toward laser applications for the treatment of peripheral vascular disease, peripheral vascular applications are now the major emphasis for clinical investigation of laser energy in the cardiovascular system. This report reviews the current status of clinical investigation and clinical/research issues facing workers studying laser applications in the peripheral vascular tree.Laser energy applied to the vascular system was first reported in 1963 by McGuff and associates. Nearly 20 years later, much attention has been devoted in the media to laser applications in the treatment of atherosclerosis in the coronary circulation. While less attention has been directed toward laser applications for the treatment of peripheral vascular disease, peripheral vascular applications are now the major emphasis for clinical investigation of laser energy in the cardiovascular system. This report reviews the current status of clinical investigation and clinical/research issues facing workers studying laser applications in the peripheral vascular tree.

Laser therapy for arteriosclerosis: current reviewDavid J. Dries, Marc E. Pollock and John EugeneDepartment of Surgery, University of California, Irvine101 City Drive South, Orange, California 92668IntroductionShortly after the ruby laser was introduced, in 1959, a study for the use of this rubylaser for the in -vitro dissolution of arteriosclerotic plaque was performed.) With subse-quent advances in laser technology and with refined delivery techniques, laser applicationsto the treatment of arteriosclerosis in the coronary arteries and peripheral vascular sys-tem is a reality. This report reviews the disease process, arteriosclerosis, and the ef-forts towards laser treatment of this disease. We conclude with a review of the technicalbarriers to the routine application of laser energy in arteriosclerotic cardiovasculardisease and the progress being made to overcome these obstacles.ArteriosclerosisCardiovascular diseases remain the chief cause of death in Western society and have beenthe focus of research and treatment efforts for decades.2 Arteriosclerosis is the majorcause of stroke and myocardial infarction implicated in most deaths due to cardiovasculardisease. The earliest sign, the fatty streak, is a flat lipid -rich lesion containingmacrophages and smooth muscle cells. These primary changes of arteriosclerosis may befound as early as childhood. Progression of fatty streaks to the next lesion, the fibrousplaque, has been demonstrated in serial studies of coronary arteries in children growing toyoung adulthood. Fibrous plaques contain increased smooth muscle cells with variousamounts of intracellular and extracellular lipid surrounded by a connective tissue matrixand fibrous cap. Deeper portions of these lesions may contain necrotic debris, crystals ofcholesterol and calcium. Progressive accumulation of calcium and other debris along withhemorrhage into the substance of a plaque marks evolution from advanced to complex arterio-sclerosis and the replicative capability of plaque cells is diminished in comparison tonormal endothelial cells of the arterial wall.Several factors appear to be at work in the development of plaques. The initial injuryappears to involve the endothelium. Chemical injury to the endothelium (as can occur withhypercholesterolemia) may allow adherence of platelets and subsequent involvement of bloodborne monocytes with growth factor release from various cell types causing smooth muscleproliferation and macrophage accumulation characteristic of early atherosclerosis. Directstimulation of endothelium as can occur with hypertension, diabetes mellitus or cigarettesmoking may also induce smooth muscle accumulation with subsequent plaque formation. Me-chanical injury causing segmental removal of endothelium is another way to allow plateletand monocyte accumulation with subsequent plaque formation at the site of injury.The clinical presentation of arteriosclerotic lesions has been reviewed by DeBakey andcoworkers in over 13,000 patients treated over a 35 year period.3 They noted that occlusivedisease due to arteriosclerosis could be classified according to anatomic distribution intoone of five patterns: (1) the coronary arterial bed, (2) the major branches of the aortic

The laser has been used diagnostically and therapeutically in many clinical disciplines. Until recently, cardiac surgery has found little advantage for the use of light energy compared to conventional techniques. Early studies, however, show promise in utilizing the laser as an instrument for increased precision of tissue ablation and for access to areas percutaneously that were previously approached through the open chest.The laser has been used diagnostically and therapeutically in many clinical disciplines. Until recently, cardiac surgery has found little advantage for the use of light energy compared to conventional techniques. Early studies, however, show promise in utilizing the laser as an instrument for increased precision of tissue ablation and for access to areas percutaneously that were previously approached through the open chest.

Background Ventilated patients with asymmetry of lung or chest wall mechanics may be vulnerable to differing lung stresses or strains dependent on body position. Our purpose was to examine transpulmonary pressure (PTP) and end-expiratory lung volume (functional residual capacity (FRC)) during body positioning changes in an animal model under the influence of positive end-expiratory pressure (PEEP) or experimental pleural effusion (PLEF). Methods Fourteen deeply anesthetized swine were studied including tracheostomy, thoracostomy, and esophageal catheter placement. Animals were ventilated at VT = 10 ml/kg, frequency of 15, I/E = 1:2, and FIO2 = 0.5. The animals were randomized to supine, prone, right lateral, left lateral, and semi-Fowler positions with a PEEP of 1 cm H2O (PEEP1) or a PEEP of 10 cm H2O (PEEP10) applied. Experimental PLEF was generated by 10 ml/kg saline instilled into either pleural space. PTP and FRC were determined in each condition. Results No significant differences in FRC were found among the four horizontal positions. Compared to horizontal positioning, semi-Fowler's increased FRC (p

Lung injury resulting from inhalation of smoke or chemical products of combustion continues to be associated with significant morbidity and mortality. Combined with cutaneous burns, inhalation injury increases fluid resuscitation requirements, incidence of pulmonary complications and overall mortality of thermal injury. While many products and techniques have been developed to manage cutaneous thermal trauma, relatively few diagnosis-specific therapeutic options have been identified for patients with inhalation injury. Several factors explain slower progress for improvement in management of patients with inhalation injury. Inhalation injury is a more complex clinical problem. Burned cutaneous tissue may be excised and replaced with skin grafts. Injured pulmonary tissue must be protected from secondary injury due to resuscitation, mechanical ventilation and infection while host repair mechanisms receive appropriate support. Many of the consequences of smoke inhalation result from an inflammatory response involving mediators whose number and role remain incompletely understood despite improved tools for processing of clinical material. Improvements in mortality from inhalation injury are mostly due to widespread improvements in critical care rather than focused interventions for smoke inhalation. Morbidity associated with inhalation injury is produced by heat exposure and inhaled toxins. Management of toxin exposure in smoke inhalation remains controversial, particularly as related to carbon monoxide and cyanide. Hyperbaric oxygen treatment has been evaluated in multiple trials to manage neurologic sequelae of carbon monoxide exposure. Unfortunately, data to date do not support application of hyperbaric oxygen in this population outside the context of clinical trials. Cyanide is another toxin produced by combustion of natural or synthetic materials. A number of antidote strategies have been evaluated to address tissue hypoxia associated with cyanide exposure. Data from European centers supports application of specific antidotes for cyanide toxicity. Consistent international support for this therapy is lacking. Even diagnostic criteria are not consistently applied though bronchoscopy is one diagnostic and therapeutic tool. Medical strategies under investigation for specific treatment of smoke inhalation include beta-agonists, pulmonary blood flow modifiers, anticoagulants and antiinflammatory strategies. Until the value of these and other approaches is confirmed, however, the clinical approach to inhalation injury is supportive.