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Retained foreign bodies after surgery
ASSOCIATION FOR ACADEMIC SURGERY AND SOCIETY OF UNIVERSITY SURGEONS—ABSTRACTS 169. RETAINED FOREIGN BODIES AFTER SURGERY. Heniford B, Lincourt A, Harrell A, Cristiano J, Sing R, Kercher K; Carolinas Medical Center Background: Medical errors during surgery are not well studied. To define risk factors associated with this type of error, we performed a case control analysis. Methods: We retrospectively reviewed medical records involving the ICD-9 code (998.4) for unintentional foreign object remaining in the body during surgery and incident reports gathered by the Department of Risk Management over a 10 year period from 1996 to 2005. Each case was then matched with three randomly selected controls (108 control patients total) that underwent the same type of operation during the same time period. Results: Thirty-six patients had retained foreign objects (42% sponges and 53% instruments). The abdominal cavity was most commonly involved (39%) followed by the thoracic cavity (22%) although no body cavity remained uninvolved. Eleven patients required readmission (33%), thirty patients required reoperation (83%), and there was no mortality. When compared to controls, patients with retained foreign objects were more likely to have had a longer operation (207 minutes vs. 164 minutes, p⫽0.006), a greater number of major surgical procedures at the same time (2.3 vs. 1.6, p⫽0.01) performed by multiple surgical teams (11% vs. 3%, p⫽0.05), and more likely to have had an incorrect instrument/ sponge count recorded (11% vs. 2%, p⫽0.03). In multivariate analysis, factors associated with a significantly higher risk of retained foreign objects were the total number of major procedures performed (OR 1.5, [95% CI, 1.1 – 2.1], p⫽0.02), and an incorrect count (OR 15.8, [95% CI, 1.2218.6], p⫽0.03). Conclusion: Retained foreign objects after surgery are associated with multiple major surgical procedures being performed at the same time and an incorrect instrument or sponge count. Identification of these risk factors using case-control analysis may influence operating room policy and reduce these types of errors.
TRAUMA/CRITICAL CARE III-Immunology and ischemia reperfusion 170. PROFOUND HYPOTHERMIA IS SUPERIOR TO ULTRAPROFOUND HYPOTHERMIA IN IMPROVING SURVIVAL IN A SWINE MODEL OF LETHAL HEMORRHAGE. H. B. Alam 1, P. Rhee 2, T. Lin 3, N. Ahuja 3, E. C. Ayuste 2, K. Honma 2, Z. Chen 2; 1Massachusetts General Hospital/ Harvard Medical School, Boston, MA, 2Uniformed Services University of the Health Sciences, Bethesda, MD, 3 Washington Hospital Center, Washington, DC. Rapid induction of profound hypothermia can provide valuable time for repair of complex injuries, and improve survival from uncontrolled lethal hemorrhage (ULH). We have previously demonstrated that profound hypothermia must be induced rapidly (2oC/min) and reversed gradually (0.5oC/minute) for best results. However, the optimal depth of hypothermia in the setting of ULH remains unknown. This experiment was designed to compare the impact of profound (15oC and 10oC) and ultra-profound (5oC) hypothermia on survival and organ functions in a swine model of complex vascular injuries. METHODS: ULH was induced in 32 swine (80-120 lbs) by creating an iliac artery and vein injury, followed 30 minutes later (simulating transport time) by laceration of the descending thoracic aorta. Through an emergency thoracotomy approach, a catheter was placed in the aorta, and cold organ preservation solution was infused using a roller pump to rapidly (2oC/minute) induce hypothermia. Vascular injuries were repaired during 60 minutes of induced asanguinous hypothermic arrest. The experimental groups were (n⫽8/group): 1)
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normothermic control, 2) profound hypothermia to 15oC, 3) to 10oC, and 4) ultraprofound hypothermia to 5oC. After repair of injuries, animals were re-warmed (0.5oC/min) on cardiopulmonary bypass, and whole blood was infused during this period. The animals were monitored for six weeks for neurologic deficits, cognitive function (learning), and organ dysfunction. Capacity to learn new skills was measured by the presenting the animals with color-coded boxes that contained food. Boxes were placed in changing locations, and only one of the boxes could be opened. Scoring system took into account the number of right and wrong attempts, time taken to open the right box, and number of sessions to master the task. In addition, an objective 75-point scale was used to determine neurologic function. RESULTS: All normothermic animals died, whereas 6-week survival rates for 15oC, 10oC and 5oC groups were 62.5%, 87.5% and 25% respectively (p⬍0.05: 1vs. 2&3 and 3 vs. 4). The surviving animals from 15 and 10oC groups were neurologically intact, displayed normal learning capacity, and had no long-term organ dysfunction. The survivors from 5oC group displayed markedly slower recovery and impaired cognitive functions. CONCLUSION: In a model of lethal injuries, rapid induction of profound hypothermia can prevent death. The depth of hypothermia influences survival, with the best outcome following induction of profound hypothermia to a core temperature of 10oC. 171. 17-ESTRADIOL ADMINISTRATION FOLLOWING TRAUMA-HEMORRHAGE PREVENTS THE INCREASE IN KUPFFER CELL CYTOKINE RELEASE AND MAPK ACTIVATION PREDOMINANTLY VIA ESTROGEN RECEPTOR-␣. T. Suzuki, T. Shimizu, H. Yu, Y. Hsieh, M. A. Choudhry, K. I. Bland, I. H. Chaudry; University of Alabama at Birmingham, Birmingham, AL. Previous studies have shown that Kupffer cells (KC) are main source of circulating cytokines following trauma-hemorrhage (T-H) and 17-estradiol (E2) administration following T-H attenuates the elevation of plasma cytokine levels and KC cytokine production. Since studies indicate that ER-␣ is predominantly expressed in liver and plays a key role in E2-mediated salutary effects on hepatic function following T-H, we hypothesized that the salutary effects of E2 on KC cytokine production following T-H are mediated via ER-␣. Accordingly, we examined whether: 1) the salutary effects of E2 are mediated via estrogen receptor (ER)-␣ or ER-, and 2) MAPK play a role in mediating the salutary effects of E2. Male Sprague-Dawley rats underwent T-H (mean BP 40mmHg for 90min, then resuscitation). ER-␣ agonist propyl pyrazole triol (PPT) (5g/kg), ER- agonist diarylpropionitrile (DPN) (5g/kg), E2 (50g/kg) or vehicle (10% DMSO) was injected subcutaneously at the middle of resuscitation. At 24 hrs after T-H, KC were isolated and their release of IL-6, TNF-␣ and IL-10 in response to LPS (1g/ ml) was determined. In addition, the activation of MAPK (e.g., p38, ERK-1/2 and JNK) in KC was determined. One-way ANOVA and Tukey‘s test were used for analysis. Values are mean ⫾SEM of n ⫽ 5-6/group. As shown in the Figures below, IL-6, TNF-␣ and IL-10 release by KC increased following T-H, however, PPT or E2 administration significantly prevented the increase in KC cytokine production. Although the elevation of IL-6 and IL-10 production by KC was also attenuated by DPN treatment following T-H, KC capacity to produce these cytokines still remained significantly higher compared to sham. Moreover, PPT or E2 treatment prevented T-H-mediated activation of p38, ERK-1/2 and JNK in KC. However, DPN treatment had no significant effect on MAPK activation. Since ER-␣ agonist, PPT administration following T-H was more effective in attenuating the increases in KC cytokine production and the activation of MAPK in KC than ER- agonist DPN, it appears that the salutary effects of E2 on KC functions are mediated predominantly via ER-␣ and that these beneficial effects are likely mediated via an attenuation of MAPK activation following T-H.
TRAUMA/CRITICAL CARE III-Immunology and ischemia reperfusion 170. PROFOUND HYPOTHERMIA IS SUPERIOR TO ULTRAPROFOUND HYPOTHERMIA IN IMPROVING SURVIVAL IN A SWINE MODEL OF LETHAL HEMORRHAGE. H. B. Alam 1, P. Rhee 2, T. Lin 3, N. Ahuja 3, E. C. Ayuste 2, K. Honma 2, Z. Chen 2; 1Massachusetts General Hospital/ Harvard Medical School, Boston, MA, 2Uniformed Services University of the Health Sciences, Bethesda, MD, 3 Washington Hospital Center, Washington, DC. Rapid induction of profound hypothermia can provide valuable time for repair of complex injuries, and improve survival from uncontrolled lethal hemorrhage (ULH). We have previously demonstrated that profound hypothermia must be induced rapidly (2oC/min) and reversed gradually (0.5oC/minute) for best results. However, the optimal depth of hypothermia in the setting of ULH remains unknown. This experiment was designed to compare the impact of profound (15oC and 10oC) and ultra-profound (5oC) hypothermia on survival and organ functions in a swine model of complex vascular injuries. METHODS: ULH was induced in 32 swine (80-120 lbs) by creating an iliac artery and vein injury, followed 30 minutes later (simulating transport time) by laceration of the descending thoracic aorta. Through an emergency thoracotomy approach, a catheter was placed in the aorta, and cold organ preservation solution was infused using a roller pump to rapidly (2oC/minute) induce hypothermia. Vascular injuries were repaired during 60 minutes of induced asanguinous hypothermic arrest. The experimental groups were (n⫽8/group): 1)
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normothermic control, 2) profound hypothermia to 15oC, 3) to 10oC, and 4) ultraprofound hypothermia to 5oC. After repair of injuries, animals were re-warmed (0.5oC/min) on cardiopulmonary bypass, and whole blood was infused during this period. The animals were monitored for six weeks for neurologic deficits, cognitive function (learning), and organ dysfunction. Capacity to learn new skills was measured by the presenting the animals with color-coded boxes that contained food. Boxes were placed in changing locations, and only one of the boxes could be opened. Scoring system took into account the number of right and wrong attempts, time taken to open the right box, and number of sessions to master the task. In addition, an objective 75-point scale was used to determine neurologic function. RESULTS: All normothermic animals died, whereas 6-week survival rates for 15oC, 10oC and 5oC groups were 62.5%, 87.5% and 25% respectively (p⬍0.05: 1vs. 2&3 and 3 vs. 4). The surviving animals from 15 and 10oC groups were neurologically intact, displayed normal learning capacity, and had no long-term organ dysfunction. The survivors from 5oC group displayed markedly slower recovery and impaired cognitive functions. CONCLUSION: In a model of lethal injuries, rapid induction of profound hypothermia can prevent death. The depth of hypothermia influences survival, with the best outcome following induction of profound hypothermia to a core temperature of 10oC. 171. 17-ESTRADIOL ADMINISTRATION FOLLOWING TRAUMA-HEMORRHAGE PREVENTS THE INCREASE IN KUPFFER CELL CYTOKINE RELEASE AND MAPK ACTIVATION PREDOMINANTLY VIA ESTROGEN RECEPTOR-␣. T. Suzuki, T. Shimizu, H. Yu, Y. Hsieh, M. A. Choudhry, K. I. Bland, I. H. Chaudry; University of Alabama at Birmingham, Birmingham, AL. Previous studies have shown that Kupffer cells (KC) are main source of circulating cytokines following trauma-hemorrhage (T-H) and 17-estradiol (E2) administration following T-H attenuates the elevation of plasma cytokine levels and KC cytokine production. Since studies indicate that ER-␣ is predominantly expressed in liver and plays a key role in E2-mediated salutary effects on hepatic function following T-H, we hypothesized that the salutary effects of E2 on KC cytokine production following T-H are mediated via ER-␣. Accordingly, we examined whether: 1) the salutary effects of E2 are mediated via estrogen receptor (ER)-␣ or ER-, and 2) MAPK play a role in mediating the salutary effects of E2. Male Sprague-Dawley rats underwent T-H (mean BP 40mmHg for 90min, then resuscitation). ER-␣ agonist propyl pyrazole triol (PPT) (5g/kg), ER- agonist diarylpropionitrile (DPN) (5g/kg), E2 (50g/kg) or vehicle (10% DMSO) was injected subcutaneously at the middle of resuscitation. At 24 hrs after T-H, KC were isolated and their release of IL-6, TNF-␣ and IL-10 in response to LPS (1g/ ml) was determined. In addition, the activation of MAPK (e.g., p38, ERK-1/2 and JNK) in KC was determined. One-way ANOVA and Tukey‘s test were used for analysis. Values are mean ⫾SEM of n ⫽ 5-6/group. As shown in the Figures below, IL-6, TNF-␣ and IL-10 release by KC increased following T-H, however, PPT or E2 administration significantly prevented the increase in KC cytokine production. Although the elevation of IL-6 and IL-10 production by KC was also attenuated by DPN treatment following T-H, KC capacity to produce these cytokines still remained significantly higher compared to sham. Moreover, PPT or E2 treatment prevented T-H-mediated activation of p38, ERK-1/2 and JNK in KC. However, DPN treatment had no significant effect on MAPK activation. Since ER-␣ agonist, PPT administration following T-H was more effective in attenuating the increases in KC cytokine production and the activation of MAPK in KC than ER- agonist DPN, it appears that the salutary effects of E2 on KC functions are mediated predominantly via ER-␣ and that these beneficial effects are likely mediated via an attenuation of MAPK activation following T-H.