Shoelace Breast Cast.

Implant malposition after breast augmentation surgery remains a common complication. Several surgical options exist to correct the resultant deformity; however, all involve additional risks, costs, and the increased potential for patient dissatisfaction. In my practice, I have developed a nonsurgical therapy using shoelaces, which, when tied and placed in a certain fashion, can correct this deformity. When worn continuously, the shoelaces act as an external breast cast that allows the inframammary fold to be set and heal in the correct position. I have achieved great success in using this nonsurgical technique, and it allows me to be aggressive in cases where I need to raise the inframammary fold because I know that I can easily correct if the fold is lowered too much.

Live transference of surgical subspecialty skills using telerobotic proctoring to remote general surgeons.

BACKGROUND: Certain clinical environments, including military field hospitals or rural medical centers, lack readily available surgical subspecialists. We hypothesized that telementoring by a surgical subspecialist using a robotic platform is feasible and can convey subspecialty knowledge and skill to a remotely located general surgeon. STUDY DESIGN: Eight general surgery residents evaluated the effect of remote surgical telementoring by performing 3 operative procedures, first unproctored and then again when teleproctored by a surgical subspecialist. The clinical scenarios consisted of a penetrating right ventricular injury requiring suture repair, an open tibial fracture requiring external fixation, and a traumatic subdural hematoma requiring craniectomy. A robotic platform consisting of a pan-and-tilt camera with laser pointer attached to an overhead surgical light with integrated audio allowed surgical subspecialists the ability to remotely teleproctor residents. Performance was evaluated using an Operative Performance Scale. Satisfaction surveys were given after performing the scenario unproctored and again after proctoring. RESULTS: Overall mean performance scores were superior in all scenarios when residents were proctored than when they were not (4.30 +/- 0.25 versus 2.43 +/- 0.20; p < 0.001). Mean performance scores for individual metrics, including tissue handling, instrument handling, speed of completion, and knowledge of anatomy, were all superior when residents were proctored (p < 0.001). Satisfaction surveys showed greater satisfaction and comfort among residents when proctored. Proctored residents believed the robotic platform facilitated learning and would be feasible if used clinically. CONCLUSIONS: This study supports the use of surgical teleproctoring in guiding remote general surgeons by a surgical subspecialist in the care of a wounded patient in need of an emergency subspecialty operation.

Local secretion of urocortin 1 promotes microvascular permeability during lipopolysaccharide-induced inflammation.

Urocortin 1 (Ucn1) is a neuropeptide that regulates vascular tone and is implicated in both the vascular and immune cell-mediated responses to inflammation. The role of Ucn1 in regulating microvascular permeability has not been determined. We hypothesized that local Ucn1 release promotes microvascular permeability and that this effect augments the local gastrointestinal vascular response to lipopolysaccharide (LPS)-induced systemic inflammation. We measured hydraulic (L(p)) and macromolecule permeability in mesenteric venules. We show that a continuous infusion of 10(-7) m Ucn1 in a postcapillary venule increased L(p) 2-fold over baseline, as did LPS-induced inflammation. However, simultaneous infusion of Ucn1 and LPS markedly increased L(p) by 7-fold. After local knockdown of Ucn1 using RNA interference, infusion of Ucn1 with LPS resulted in return to 2-fold increase, confirming that Ucn1 synergistically augments hydraulic permeability during inflammation. LPS and Ucn1 treatment also resulted in increased numbers of interstitial microspheres, which colocalized with CD31(+) immune cells. Ucn1 activity is mediated through two receptor subtypes, CRH-R(1) and CRH-R(2). CRH-R(1) receptor blockade exacerbated, whereas CRH-R(2) receptor blockade decreased the LPS-induced increase in L(p). Finally, treatment with the c-JUN N-terminal kinase (JNK) antagonist SP600125 during infusion of LPS, but not Ucn1, decreased L(p). These findings suggest that Ucn1 increases microvascular permeability and acts synergistically with LPS to increase fluid and macromolecule losses during inflammation. Knockdown of endogenous Ucn1 during inflammation attenuates synergistic increases in L(p). Ucn1's effect on L(p) is partially mediated by the CRH-R(2) receptor and acts independently of the c-JUN N-terminal kinase signal transduction pathway.

Single-contrast computed tomography for the triage of patients with penetrating torso trauma.

BACKGROUND: We have used single-contrast (intravenous contrast only) computed tomography (SCCT) for triaging hemodynamically stable patients with penetrating torso trauma. We hypothesized that SCCT safely determines the need for operative exploration. Furthermore, trauma surgeons without specialized training in body imaging can accurately apply this modality. METHODS: We retrospectively reviewed the records of patients with penetrating torso injuries at a university-based urban trauma center to establish the accuracy of SCCT in determining the need for exploratory laparotomy. The scan was considered positive or negative with respect to the need for exploratory laparotomy as documented by the attending surgeon, who may have considered the read of the on call radiologist if available. In a separate study, four trauma surgeons independently reviewed 42 SCCT scans to establish whether the scans alone could be used to determine whether operative exploration was necessary. RESULTS: Between 1997 and 2008, 306 hemodynamically stable patients with penetrating torso trauma were triaged by SCCT. Overall, SCCT predicted the need for laparotomy with 98% sensitivity and 90% specificity. The positive predictive value was 84% and the negative predictive value (NPV) was 99%. In the 222 patients with gunshot wounds, SCCT had 100% sensitivity and 100% NPV. In the 84 patients with stab wounds, SCCT had 92% sensitivity and 97% NPV. Trauma surgeon agreement in the retrospective review of 42 computed tomography scans was "nearly perfect": positive predictive value was 93% and NPV was 92% for determining the need for exploratory laparotomy surgery. CONCLUSIONS: SCCT is safe and effective for triaging hemodynamically stable patients with penetrating torso trauma. It successfully determined the need for operative intervention with appropriate clinical accuracy without the additional costs, morbidity, and delay of oral and rectal contrast. Trauma surgeons can reproducibly interpret SCCT with high-predictive accuracy as to whether patients with penetrating torso trauma require operative exploration.

Lipoxin a(4) attenuates microvascular fluid leak during inflammation.

BACKGROUND: The release of proinflammatory cytokines during inflammation disturbs the endothelial barrier and can initiate significant intravascular volume loss. Proinflammatory cytokines also induce the expression of anti-inflammatory mediators, such as lipoxin, which promote the resolution of inflammation. Our hypothesis is that lipoxin A(4) (LXA(4)) reverses the increased microvascular fluid leak observed during inflammatory conditions. MATERIALS AND METHODS: Microvascular fluid leak (L(p)) was measured in rat mesenteric venules using a micro-cannulation technique. L(p) was measured under the following conditions: (1) LXA(4) (100 nM) alone (n = 5), (2) LXA(4) (100 nM) administered after endothelial hyperpermeability induced by a continuous perfusion of 10 nM platelet activating factor (PAF) (n = 5), (3) LXA(4) (100 nM) perfused after inflammation induced by a systemic bolus of 10 mg/kg lipopolysaccharide (LPS) (n = 5), and (4) LXA(4) (100 nM) perfused after LPS-induced inflammation during inhibition of c-Jun N-terminal kinase (n = 4). RESULTS: LXA(4) alone slightly increased L(p) from baseline (L(p)-baseline = 1.05 +/- 0.03, L(p)-LXA(4) = 1.55 +/- 0.04; P < 0.0001). PAF increased L(p) 4-fold (L(p)-baseline = 1.20 +/- 0.10, L(p)-PAF = 4.49 +/- 0.95; P < 0.0001). LXA(4) administration after PAF decreased L(p) 66% versus PAF alone (from 4.49 +/- 0.95 to 1.54 +/- 0.13; P = 0.0004). LPS-induced inflammation increased L(p) over 2-fold (L(p)-baseline = 1.05 +/- 0.03, L(p)-LPS = 2.27 +/- 0.13; P < 0.0001). LXA(4) administration after LPS decreased L(p) 42% versus LPS alone (from 2.27 +/- 0.13 to 1.31 +/- 0.05; P < 0.0001). The effect of c-Jun N-terminal kinase inhibition during LPS-induced inflammation attenuated the decrease in leak cause by LXA(4) by 51% (P = 0.0002). CONCLUSION: After either LPS or PAF, LXA(4) attenuated the intravascular volume loss caused by these inflammatory mediators. The activity of LXA(4) may be partly mediated by the c-Jun N-terminal kinase signaling pathway. These data support an anti-inflammatory role for LXA(4) and suggests a potential pharmacologic role for LXA(4) during inflammation.

Usability of robotic platforms for remote surgical teleproctoring.

Military field hospitals and rural medical centers may lack surgical subspecialists. Robotic technology can enable proctoring of remotely located general surgeons by subspecialists. Our objective compared three proctoring platforms: (1) 6-degree-of-freedom (DOF) computer input devices controlling a camera and laser pointer mounted on robotic arms, (2) a computer mouse controlling a pan-tilt-zoom (PTZ) camera and robotic laser scanner, and (3) a computer pen/tablet controlling a PTZ-camera and robotic laser scanner. Our hypothesis was that a pen/tablet or mouse platform would be superior to the 6-DOF-input device platform. Five surgeons used each platform by simulating the creation of operative incisions. Qualitative (instrument handling, time, motion, spatial awareness) and quantitative performance (accuracy, speed) was assessed on a five-point scale. Each surgeon completed a satisfaction survey. Both mouse and pen/tablet had higher mean performance scores than the 6-DOF-input device in all quantitative (6-DOF = 1.7 +/- 0.8, mouse = 4.3 +/- 0.2, pen = 4.1 +/- 0.6; p < 0.001) and qualitative measures (6-DOF = 1.7 +/- 0.2, mouse = 4.8 +/- 0.0, pen = 4.6 +/- 0.1; p < 0.001). Handling, motion, and instrument awareness were superior with the mouse and pen/tablet versus 6-DOF-input devices (p < 0.0001). Speed and accuracy were also superior using the mouse or pen/tablet versus 6-DOF-input devices (p < 0.0001). Surgeons completed tasks faster using the mouse versus pen/tablet (p = 0.02). Satisfaction surveys revealed a preference for the mouse. This study demonstrates the superiority of a mouse or pen/tablet controlling a PTZ-camera and robotic laser scanner for remote surgical teleproctoring versus 6-DOF-input devices controlling a camera and laser pointer. Either a mouse or pen/tablet platform allows subspecialists to proctor remotely located surgeons.

The number of gunshot wounds does not predict injury severity and mortality.

It is presumed that as the number of gunshot wounds (GSWs) increases, so do the Injury Severity Score (ISS) and mortality risk. We hypothesized that the number of bullet wounds relates to ISS and death; however, a single GSW to the head is ominous. We reviewed the charts of all GSW patients admitted to a trauma center from 2004 to 2006 (n = 531). We analyzed patient demographics, ISS, and mortality. There was no correlation with the number of GSWs with either ISS or mortality. There was only a 0.3 per cent increased risk of death for each additional GSW (r2 = 0.12). Patients with a single GSW versus multiple GSWs had no difference in mortality (9.1 vs 8.4%, P = 0.8). A single GSW to the head carried a 50 per cent mortality risk. For those who sustained both head and body GSWs, each additional GSW did not increase mortality (r2 = 0.007). Our study shows that the number of GSWs has no affect on mortality or ISS. Internal triage and management of gunshot victims should not be affected by the categorization of patients as having a single versus multiple GSWs.

The effect of hypoxia, reoxygenation, ischemia, and reperfusion on hydraulic permeability in rat mesenteric venules.

Little is known regarding the effects of I/R on hydraulic permeability (Lp). We sought to compare the individual influences of hypoxia, ischemia, reoxygenation, and reperfusion on Lp. We hypothesized that (1) hypoxia increases Lp; (2) reoxygenation further increases Lp; (3) ischemia results in greater increases in Lp compared with hypoxia; (4) reperfusion causes additional increases in Lp compared with hypoxia, ischemia, and reoxygenation; and (5) xanthine oxidase (XO) and white blood cell adherence play important roles in hypoxia, ischemia, and reperfusion. Hydraulic permeability was measured by an in vivo microcannulation technique during hypoxia, reoxygenation, ischemia, and reperfusion in rat mesenteric postcapillary venules. Additional rats were fed a Tungsten-enriched diet to inhibit XO activity, and the studies were repeated. White blood cell adherence was also documented. Hypoxia and ischemia both increased Lp 2-fold from baseline levels (P < 0.001). Reoxygenation did not alter Lp compared with 15 min of hypoxia alone (P > 0.07). Reperfusion after hypoxia increased Lp 6-fold (P < 0.001). Reperfusion after ischemia also increased Lp 6-fold (P < 0.001). Inhibition of XO had no effect on the increase in Lp after both hypoxia and ischemia. However, inhibition of XO attenuated the 6-fold increase in Lp observed during reperfusion after both hypoxia and ischemia by approximately 50% (P < 0.001). White blood cell adherence increased during reperfusion but not hypoxia or ischemia. The complexity of I/R injury makes it a difficult clinical scenario to model for research. We have demonstrated in an in vivo model that hypoxia and ischemia increase Lp similarly, and that reperfusion has a profound deleterious effect on Lp. These changes in Lp seem to be XO and white blood cell dependent.

Angiotensin II type 2 receptor provides an endogenous brake during inflammation-induced microvascular fluid leak.

BACKGROUND: The dual actions of angiotensin II (AngII) on microvascular fluid leak remain enigmatic. Our hypothesis was that the AngII type 2 (AT2) receptor decreases microvascular fluid leak during inflammation. The purposes of this study were to determine the activity of the AT2 receptor during stimulation by endogenous AngII, during stimulation by exogenous AngII, and during inflammation. STUDY DESIGN: Hydraulic permeability (L(p)) of rat mesenteric venules was measured using a microcannulation technique. L(p) was measured during perfusion with the AT1 receptor antagonist, ZD7155, and also with exogenous AngII during AngII type 1 receptor (AT1) blockade. Inflammation was induced with platelet activating factor (PAF), and L(p) was measured during perfusion of AngII with AT1 blockade and also with an AT2 receptor agonist, CGP42112. RESULTS: AT2 receptor activation by endogenous AngII slightly decreased L(p) over that of the control (p=0.02). Exogenous AngII increased L(p) fivefold (L(p)=4.83+/-1.32; p < 0.001). Addition of AT1 receptor blockade decreased L(p) by 74% (to 1.24+/-0.03; p < 0.01). PAF activation increased L(p) fourfold (L(p)=4.49+/-0.74; p < 0.0001). After PAF activation, exogenous AngII then decreased L(p) by 39% (to 2.74+/-0.12; p < 0.01). Exogenous AngII during AT1 receptor blockade after PAF activation decreased L(p) by 61% (from 4.49+/-0.74 to 1.77+/-0.22; p < 0.0001), and selective AT2 receptor stimulation after PAF activation decreased L(p) by 69% (from 4.49+/-0.74 to 1.40+/-0.04; p < 0.001). CONCLUSIONS: This study further supports a dual role for AngII. AngII increases microvascular fluid leak during basal conditions but appears to decrease it during inflammation. Alterations in AT2 receptor activity may be responsible for these different effects.