A pulseless limb poorly predicts an arterial injury in combat trauma.

BACKGROUND: A pulseless limb is considered a hard sign of an arterial injury after penetrating trauma in the civilian population. However, the reliability of this finding has never been examined in combat trauma. The purpose of this study was to examine the reliability of the pulseless limb in the combat trauma population. Reasons for false positive physical examination findings were also identified. METHODS: The Joint Theater Trauma Registry identified all patients who presented to a military treatment facility (MTF) in Kandahar, Afghanistan, with a penetrating extremity injury over a 2-year period. Patients found to have a pulse deficit on initial physical examination were followed, and the results of the subsequent computed tomographic angiogram or arteriogram recorded. Patient demographics, injury patterns, and physiological data were examined. Standard statistical analysis was performed. RESULTS: From 2011 to 2012, 644 patients were treated at a single MTF for lower extremity penetrating injuries. The most common mechanisms of injury were explosions (62%) and gunshot wounds (20%). Of the 577 patients with complete medical records, 448 patients (78%) presented with palpable pulses, 115 patients (20%) presented with a pulseless limb, and 14 (2%) presented with hard signs of vascular injury. Of those with a pulseless limb and abnormal ankle-brachial index (ABI) or no ABI obtained who underwent further radiologic imaging, 38 patients (77%) had no arterial injury identified. Compared with those with a palpable pulse, patients with a pulseless limb without an arterial injury were more likely to have a higher Injury Severity Score (ISS), lower hematocrit, lower pH, greater base deficit, higher heart rate, more frequent use of tranexamic acid, and received greater volumes of packed red blood cells, plasma, and crystalloids. CONCLUSIONS: Our results demonstrate that a pulseless limb is a poor predictor of arterial injury and should not be considered a hard sign of vascular injury in the combat population. Variables including a high ISS, anemia, acidosis, and need for resuscitation products, each a surrogate for injury severity, may contribute to the decreased accuracy of the physical examination in our troops. This may translate into unnecessary immediate exploration or other interventions in patients who present with more significant injuries from the battlefield. Future studies must continue to focus on improved algorithms for diagnostic accuracy of extremity vascular injuries in this population.

Hydatidosis of the liver and posterior mediastinum.

INTRODUCTION: Cystic echinococcus (CE) is an endemic zoonosis secondary to infection by the larval form of the cestode Echinococcus granulosus. An intermediate host, humans enter the organism's life cycle by exposure to infected canid feces. The liver is the most common location of CE while mediastinal hydatid cysts are rarely reported. PRESENTATION OF CASE: We report a case of synchronous CE of the liver and posterior mediastinum treated sequentially using chemotherapy, percutaneous aspiration with injection of a scolicidal agent and re-aspiration (PAIR) and then staged minimally-invasive surgeries. DISCUSSION: Synchronous CE involving the liver and posterior mediastinum is rare. The treatment of hydatid liver and mediastinal disease is multimodal including chemotherapy, percutaneous and laparoscopic or open surgical interventions. One option for controlled puncture of hepatic and mediastinal CE includes PAIR followed by surgery. CONCLUSION: The sequential use of chemotherapy and PAIR followed by surgery provides another treatment strategy for management of CE. We believe this strategy may be used safely in locations without endemic CE, including most regions of the United States.

Thoracic gallstones: a delayed complication of laparoscopic cholecystectomy.

BACKGROUND: Thoracic complications resulting from gallstone spillage during laparoscopic cholecystectomy are rare and may occur years after the index surgery. We present the case of a chronic lung abscess resulting from trans-diaphragmatic migration of gallstones spilled and "lost" during a laparoscopic cholecystectomy. METHODS: Case report and literature review. CASE REPORT: A 66-year-old female who had undergone a laparoscopic cholecystectomy 5 y previously presented with hemoptysis and was found to have a chronic lung abscess caused by "lost" gallstones. Her symptoms resolved with video-assisted thorascopic surgery, pulmonary decortication, and wedge resection. CONCLUSIONS: Thoracic complications from "lost" gallstones following laparoscopic cholecystectomy include empyema, hemoptysis, and cholelithoptysis. These rare complications sometimes require surgery but not all presentations of thoracic gallstones mandate operative intervention. Because of these potential complications of "lost" gallstones, reasonable efforts should be made to retrieve gallstones spilled during cholecystectomy. Persistent pulmonary symptoms following laparoscopic cholecystectomy mandate further radiologic examination and a review of the patient's operative report for "lost" gallstones.

Characterization of a monoclonal antibody capable of reliably quantifying expression of human Copper Transporter 1 (hCTR1).

Human copper transporter 1 (hCTR1) is the high-affinity copper influx transporter in mammalian cells that also mediates the influx of cisplatin. Loss of hCTR1 expression has been implicated in the development of resistance to this cancer chemotherapeutic agent. It has turned out to be very difficult to develop antibodies to hCTR1 and polyclonal antibodies produced by different laboratories have yielded conflicting results. We have characterized a newly-available rabbit monoclonal antibody that reacts with an epitope on the N-terminal end of hCTR1 that now permits rigorous identification and quantification of hCTR1 using Western blot analysis. Postnuclear membrane (PNM) preparations made from cells engineered to express high levels of myc-tagged hCTR1, and cells in which the expression of hCTR1 was knocked down, were used to characterize the antibody. The identity of the bands detected was confirmed by immunoprecipitation, surface biotinylation and deglycosylation of myc-tagged hCTR1. Despite the specificity expected of a monoclonal antibody, the anti-hCTR1 detected a variety of bands in whole cell lysates (WCL), which made it difficult to quantify hCTR1. This problem was overcome by isolating post-nuclear membranes and using these for further analysis. Three bands were identified using this antibody in PNM preparations that migrated at 28, 33-35 and 62-64kDa. Multiple lines of evidence presented here suggest that the 33-35 and 62-64kDa bands are hCTR1 whereas the 28kDa band is a cross-reacting protein of unknown identify. The 33-35kDa band is consistent with the expected MW of the glycosylated hCTR1 monomer. This analysis now permits rigorous identification and quantification of hCTR1.