Differences in telomerase activity between colon and rectal cancer.

BACKGROUND: Colorectal cancer is one of the most common cancers and the third leading cause of cancer death in both sexes. The disease progresses as a multistep process and is associated with genetic alterations. One of the characteristic features of cancer is telomerase activation. We sought to evaluate the differences in telomerase activity between colon cancer and adjacent normal tissue and to correlate the differences in telomerase activity between different locations with clinicopathological factors and survival. METHODS: Matched colon tumour samples and adjacent normal mucosa samples 10 cm away from the tumour were collected during colectomy. We assessed telomerase activity using real time polymerase chain reaction. Several pathological characteristics of tumours, including p53, Ki-67, p21, bcl2 and MLH1 expression were also studied. RESULTS: We collected samples from 49 patients. There was a significantly higher telomerase activity in colon cancer tissue than normal tissue. Adenocarcinomas of the right colon express significantly higher telomerase than left-side cancers. Colon cancers and their adjacent normal tissue had significantly more telomerase and were more positive to MLH1 than rectal cancers. The expression of p53 negatively correlated to telomerase activity and was linked to better patient survival. CONCLUSION: Colon and rectal cancers seem to have different telomerase and MLH1 profiles, and this could be another factor for their different biologic and clinical behaviour and progression. These results support the idea that the large bowel cannot be considered a uniform organ, at least in the biology of cancer.

CONTEXTE: Le cancer colorectal est l'un des cancers les plus répandus; il arrive au troisième rang des décès attribuables au cancer chez les hommes et les femmes. La maladie progresse en plusieurs étapes et est associée à des anomalies génétiques. L'une des principales caractéristiques du cancer est l'activation de la télomérase. Nous avons voulu évaluer les différences d'activité de la télomérase entre les tissus touchés par le cancer du côlon et les tissus adjacents normaux afin d'établir une corrélation entre les différences d'activité de la télomérase selon la localisation d'une part et les facteurs clinicopathologiques et la survie d'autre part. MÉTHODES: Lors de colectomies, nous avons recueilli des échantillons tissulaires jumelés de tumeur du côlon et de muqueuse adjacente normale à 10 cm du foyer tumoral. Nous avons mesuré l'activité de la télomérase à l'aide de la réaction en chaîne de la polymérase en temps réel. Plusieurs caractéristiques pathologiques des tumeurs ont aussi été analysées, y compris l'expression des gènes p53, Ki-67, p21, bcl2 et MLH1. RÉSULTATS: Nous avons recueilli des échantillons auprès de 49 patients. Nous avons noté une activité nettement plus intense de la télomérase dans les tissus touchés par le cancer du côlon que dans les tissus normaux. Les adénocarcinomes du côlon ascendant expriment une activité de la télomérase significativement plus intense que les cancers du côlon descendant. Les cancers du côlon et les tissus adjacents normaux présentaient une activité significativement plus intense de la télomérase et étaient plus souvent positifs à l'égard du MLH1 comparativement aux cancers rectaux. L'expression du p53 a été en corrélation négative avec l'activité de la télomérase et a été associée à une meilleure survie chez les patients. CONCLUSION: Les cancers du côlon et du rectum semblent avoir des profils différents au plan de la télomérase et du gène MLH1. Ce facteur pourrait entre autre expliquer leur comportement et leur progression biologiques et cliniques distincts. Ces résultats appuient l'hypothèse selon laquelle le côlon ne peut être considéré comme un organe uniforme, du moins en ce qui concerne la biologie du cancer.

Laparoscopic pancreaticoduodenectomy and distal pancreatectomy: a UK experience and a systematic review of the literature.

BACKGROUND: Advances in operative techniques and technology have facilitated laparoscopic distal pancreatectomy (LDP) and laparoscopic pancreaticoduodenectomy (LPD). METHODS: All distal pancreatectomies were attempted laparoscopically, while selected patients underwent LPD. The literature was systematically reviewed. RESULTS: Between 2002 and 2008, 21 patients underwent LDP (n=14) or LPD (n = 7). The mean operating time, blood loss, and hospital stay after LDP were 265 min, 262 ml, and 7.7 days, respectively, and after LPD they were 628 min, 350 ml, and 11.1 days, respectively. The conversion, morbidity, pancreatic fistula, readmission, reoperation, and mortality after LDP were 7.1, 35.7, 28.4, 28.4, 0, and 7.1% respectively, and after LPD they were 0, 28.6, 14.3, 28.6, 0, and 0% respectively. The literature review identified 987 LDP and 126 LPD. Most LDP were for benign disease (83.9%) while most LPD were for malignancy (91.5%). The mean operating time, morbidity, pancreatic fistula, mortality, and hospital stay after LDP were 221.5 min, 24.7%, 16.4%, 0.4%, and 7.7 days, respectively, and after LPD they were 448.3 min, 28.6%, 11.6%, 2.1%, and 16 days, respectively. CONCLUSION: LDP, particularly for benign disease and low-grade malignancy, is increasingly becoming the gold standard approach in experienced hands. In selected patients, LPD is feasible and safe. Long-term follow-up data are needed.

Computed tomography to detect accessory spleens before laparoscopic splenectomy: is it necessary?

BACKGROUND: Some one-fifth of patients may have accessory spleens (AcS) and require their removal at the time of splenectomy to achieve and maintain hematological response. The purpose of this study was to evaluate the benefit of computed tomography (CT) in patients undergoing laparoscopic splenectomy (LS). METHODS: All patients who required splenectomy were offered LS and underwent preoperative contrast-enhanced CT scan to detect and locate AcS. The surgeon was not blinded to the result of the CT scan. Patients were followed up to determine if there was recurrent disease. RESULTS: Between 2000 and 2007, 58 consecutive patients (31 men) were referred for splenectomy and all underwent LS. Preoperative CT scan detected 11 AcS in 11 patients (19%), of which 9 were confirmed during LS; the remaining 2 patients suffered with ITP preoperatively and had a good hematologic response to LS. At LS, 14 AcS were found in 13 patients (22%), of which 4 patients had negative preoperative CT scan; those additional AcS were readily found and were located close to the lower pole or hilum of the spleen. All removed AcS were confirmed histologically. In one patient who had LS and removal of AcS for ITP a further AcS within the tail of the pancreas was detected 1 year postoperatively on CT after thrombocytopenia relapsed. The sensitivity and specificity of CT scan for the detection of AcS were 60% and 95.6%, and the corresponding values for laparoscopy were 93.3% and 100%, respectively. Pairwise comparison of the ROC curves identified laparoscopy to be associated with a significantly higher area under the curve compared with CT scan (0.967 vs. 0.673; P = 0.004). CONCLUSIONS: Accessory spleens can be readily detected at laparoscopy in the vicinity of the spleen; preoperative CT scan for their detection and localization may not be necessary.

High expression of immune checkpoints is associated with the TIL load, mutation rate and patient survival in colorectal cancer.

Adoptive cell therapy with the use of tumor-infiltrating lymphocytes (TILs) is a very promising immunotherapeutic approach for the treatment of patients with colorectal cancer (CRC). However, within the tumor microenvironment, co­inhibitory immune checkpoints can inactivate TILs. The aim of the present study was to examine the association between the TIL load, the mutation rate and the clinical outcome in the immune landscape of patients with CRC. RNA­seq and whole exome seq data of 453 colon adenocarcinomas (COAD) and rectal adenocarcinomas (READ), along with the TIL load and clinicopathological information of each patient, were extracted from the TCGA GDC Data Portal and analyzed computationally. The expression of immune checkpoint molecules was compared between colon cancer and normal tissue. A total of 9 immune­related gene signatures were investigated in CRC. Spearman's correlation analysis was performed to examine the correlation between the TIL load with the expression of each immune checkpoint molecule. Indoleamine 2,3­dioxygenase 1 (IDO1) was found to be significantly overexpressed in CRC, whereas V­domain Ig suppressor of T cell activation (VISTA) and lymphocyte activating 3 (LAG3) were markedly downregulated. A high expression of cytotoxic T­lymphocyte­associated protein 4 (CTLA­4), IDO1, programmed cell death 1 (PD­1) and T­cell immunoreceptor with Ig and ITIM domains (TIGIT), tended to be associated with a better overall survival of the patients. In COAD, the TIL load positively correlated with the expression of adenosine A2A receptor (ADORA2A), CTLA­4, hepatitis A virus cellular receptor 2 (HAVCR2), lymphocyte activating 3 (LAG3), programmed death­ligand PD­L1, PD­L2, TIGIT and VISTA, whereas in READ, such positive correlations were noted only between the TIL load and LAG3 or PD­L2. The 'central memory T­cell' and 'exhausted T­cell' gene signatures were significantly lower among the READ tumors. The expression of PD­1, PD­L1, PD­L2, CTLA­4 and IDO1 was significantly higher among COAD patients with a high mutation rate (>34 mutations/Mb) compared to those with a lower rate. Somatic mutations in PD­1, PD­L1, CTLA­4 and other checkpoint molecules did not seem to affect their expression levels. On the whole, the data of the present study highlight the association of immune checkpoint molecules with the TIL load, patient survival and a high mutation rate in CRC. The data corroborate that patients with colon cancer with higher PD1, PD­L1/2, CTLA­4 and IDO1 expression, and a high mutation rate, are the ones who will benefit more from the respective immune checkpoint inhibition therapies.

Role of laparoscopic right portal vein ligation in planning staged or major liver resection.

BACKGROUND AND AIMS: Right portal vein ligation (PVL) has its recognized role in inducing hypertrophy of future liver remnant (FLR) prior to major liver resection. The aim of this study was to evaluate the safety, feasibility, and effectiveness of laparoscopic right PVL and to explore its applications. METHODS: Laparoscopic right PVL was employed either during staging laparoscopy when a right hepatic trisectionectomy was indicated, leaving a small (<25%) FLR (indication 1), or during a laparoscopic left hepatic lobectomy (left lateral sectionectomy) when a second-stage right hemihepatectomy was to follow (indication 2). A follow up cross-sectional liver imaging was performed 4-6 weeks later with liver volumetry to confirm hypertrophy of the FLR before proceeding to major hepatectomy. RESULTS: Six patients (female, 5), 74-83 years old, underwent a laparoscopic right PVL, of whom 4 patients fulfilled indication 1 while 2 patients fulfilled indication 2. The median operating time for indication 1 was 60 minutes. There were no intra- or postoperative complications, and all procedures were completed laparoscopically. Repeat imaging of the liver demonstrated a median (range) hypertrophy of FLR of 24.5% (range, 20.7-33.1%). The right liver experienced atrophy. CONCLUSIONS: In the hands of the experienced laparoscopic hepatobiliary surgeon, laparoscopic right PVL is feasible and safe, and induces adequate regeneration of the FLR. Laparoscopic right PVL has its applications at the time of staging laparoscopy in patients requiring a right hepatic trisectionectomy in the presence of a small FLR and as part of a staged liver resection in patients with bilobar liver disease that spares segments 1 and 4.

Laparoscopic revision of failed fundoplication and hiatal herniorraphy.

OBJECTIVE: The aim of this study was to evaluate the mechanisms of failure after laparoscopic fundoplication and the results of revision laparoscopic fundoplication. BACKGROUND: Laparoscopic Nissen fundoplication has become the most commonly performed antireflux procedure for the treatment of gastroesophageal reflux disease, with success rates from 90 to 95%. Persistent or new symptoms often warrant endoscopic and radiographic studies to find the cause of surgical failure. In experienced hands, reoperative antireflux surgery can be done laparoscopically. We performed a retrospective analysis of all laparoscopic revision of failed fundoplications done by the principle author and the respective fellow within the laparoscopic fellowship from 1992 to 2006. METHODS: A review was performed on patients who underwent laparoscopic revision of a failed primary laparoscopic fundoplication. RESULTS: Laparoscopic revision of failed fundoplication was performed on 68 patients between 1992 and 2006. The success rate of the laparoscopic redo Nissen fundoplication was 86%. Symptoms prior to the revision procedure included heartburn (69%), dysphagia (8.8%), or both (11.7%). Preoperative evaluation revealed esophagitis in 41%, hiatal hernia with esophagitis in 36%, hiatal hernia without esophagitis in 7.3%, stenosis in 11.74%, and dysmotility in 2.4%. The main laparoscopic revisions included fundoplication alone (41%) or fundoplication with hiatal hernia repair (50%). Four gastric perforations occurred; these were repaired primarily without further incident. An open conversion was performed in 1 patient. Length of stay was 2.5 +/- 1.0 days. Mean follow-up was 22 months (range, 6-42), during which failure of the redo procedure was noted in 9 patients (13.23%). CONCLUSION: Laparoscopic redo antireflux surgery, performed in a laparoscopic fellowship program, produces excellent results that approach the success rates of primary operations.

Cytolytic activity correlates with the mutational burden and deregulated expression of immune checkpoints in colorectal cancer.

BACKGROUND: Microsatellite unstable colorectal cancers (MSI+ CRCs) expressing PD-L1, respond to anti-PD-1 or anti-PD-L1 checkpoint blockade, whereas microsatellite-stable tumors do not respond the same. Our aim was to examine how the immune landscape relates to different aspects of the CRC's biology, including neoepitope burden. METHODS: We used TCGA data to stratify patients based on a cytolytic T-cell activity expression index and correlated immune cytolytic activity (CYT) with mutational, structural, and neoepitope features of each tumor sample. The expression of several immune checkpoints was verified in an independent cohort of 72 CRC patients, relative to their MSI status, using immunohistochemistry and RT-qPCR. RESULTS: CRC exhibits a range of intertumoral cytolytic T-cell activity, with lower cytolytic levels in the tumor, compared to the normal tissue. We separated CRC patients into CYT-high and CYT-low subgroups. High cytolytic activity correlated with increased mutational load in colon tumors, the count of MHC-I/-II classically defined and alternatively defined neoepitopes, high microsatellite instability and deregulated expression of several inhibitory immune checkpoints (VISTA, TIGIT, PD-1, IDO1, CTLA-4, and PD-L1, among others). Many immune checkpoint molecules (IDO1, LAG3, TIGIT, VISTA, PD-1, PD-L1 and CTLA-4) expressed significantly higher in MSI+ CRCs compared to MSS tumors. The expression of Treg markers was also significantly higher in CYT-high tumors. Both individual and simultaneous high levels of CTLA-4 and PD-L1 had a positive effect on the patients' overall survival. On the reverse, simultaneous low expression of both genes led to a significant shift towards negative effect. Assessed globally, CYT-low CRCs contained more recurrent somatic copy number alterations. PD-L1 protein was absent in most samples in the independent cohort and stained lowly in 33% of MSI CRCs. PD-L1+ CRCs stained moderately for CD8 and weakly for FOXP3. CYT-high colon tumors had higher TIL load, whereas CYT-high rectum tumors had higher TAN load compared to their CYT-low counterparts. CONCLUSIONS: Overall, we highlight the link between different genetic events and the immune microenvironment in CRC, taking into consideration the status of microsatellite instability. Our data provide further evidence that MSI+ and CYT-high tumors are better candidates for combinatorial checkpoint inhibition.

Understanding the Interplay between COX-2 and hTERT in Colorectal Cancer Using a Multi-Omics Analysis.

BACKGROUND: Cyclooxygenase 2 (COX-2) is involved in the initial steps of colorectal cancer (CRC) formation, playing a key role in the catalysis of arachidonic acid to prostaglandin E2 (PGE2). The human telomerase reverse transcriptase (hTERT or TERT) also plays an important role in colorectal cancer growth, conferring sustained cell proliferation and survival. Although hTERT induces COX-2 expression in gastric and cervical cancer, their interaction has not been investigated in the context of CRC. METHODS: COX-2, PGE2 levels, and telomerase activity were evaluated by immunohistochemistry, ELISA, and TRAP assay in 49 colorectal cancer samples. PTGS1, PTGS2, PTGES3, TERT mRNA, and protein levels were investigated using RNA-seq and antibody-based protein profiling data from the TCGA and HPA projects. A multi-omics comparison was performed between PTGS2 and TERT, using RNAseq, DNA methylation, copy number variations (CNVs), single nucleotide polymorphisms (SNPs), and insertions/deletions (Indels) data. RESULTS: COX-2 expression was positive in 40/49 CRCs, bearing cytoplasmic and heterogeneous staining, from moderate to high intensity. COX-2 staining was mainly detected in the stroma of the tumor cells and the adjacent normal tissues. PGE2 expression was lower in CRC compared to the adjacent normal tissue, and inversely correlated to telomerase activity in right colon cancers. COX-1 and COX-2 were anticorrelated with TERT. Isoform structural analysis revealed the most prevalent transcripts driving the differential expression of PTGS1, PTGS2, PTGES3, and TERT in CRC. COX-2 expression was significantly higher among B-Raf proto-oncogene, serine/threonine kinase, mutant (BRAFmut) tumors. Kirsten ras oncogene (KRAS) mutations did not affect COX-2 or TERT expression. The promoter regions of COX-2 and TERT were reversely methylated. CONCLUSIONS: Our data support that COX-2 is involved in the early stages of colorectal cancer development, initially affecting the tumor's stromal microenvironment, and, subsequently, the epithelial cells. They also highlight an inverse correlation between COX-2 expression and telomerase activity in CRC, as well as differentially methylated patterns within the promoter regions of COX-2 and TERT.

Effects of intravenous versus epidural lidocaine infusion on pain intensity and bowel function after major large bowel surgery: a double-blind randomized controlled trial.

BACKGROUND: We compared the effects of intravenous lidocaine (IVL) with lumbar epidural lidocaine analgesia (LEA) on pain and ileus after open colonic surgery. METHODS: Between December 2011 and February 2013, 60 patients were randomly allocated to IVL, LEA, or control group. The IVL group received intraoperatively lidocaine 2 % intravenously (1.5 mg/kg bolus, 2 mg/kg/h infusion) and normal saline (NS) epidurally. The LEA group received lidocaine epidurally (1.5 mg/kg bolus, 2 mg/kg/h infusion) and NS intravenously. The control group received NS both intravenously and epidurally, as bolus and infusion. All NS volumes were calculated as if containing lidocaine 2 % at the aforementioned doses. We assessed pain intensity at rest/cough at 1, 2, 4, 12, 24, and 48 h postoperatively (numerical rating scale 0-10), 48-h analgesic consumption, and time to first flatus passage. RESULTS: Data from 60 patients (20 per group) were analyzed. The IVL group had significantly lower pain scores at rest and cough compared to LEA or control group only at 1, 2, and 4 h postoperatively (P < 0.005 for all comparisons). The 48-h analgesic requirements and time to first flatus passage did not differ significantly between IVL group and LEA or control group (P > 0.05). CONCLUSIONS: Compared with LEA-lidocaine or placebo, intravenous lidocaine offered no clinically significant benefit in terms of analgesia and bowel function.

Effects of octreotide and insulin on colon cancer cellular proliferation and correlation with hTERT activity.

Peptide hormone somatostatin and its receptors have a wide range of physiological functions and play a role in the treatment of numerous human diseases, including colorectal cancer. Octreotide, a synthetic somatostatin-analog peptide, inhibits growth of colonic cancer cells primarily by binding to G-protein coupled receptors and elicits cellular responses through second-messenger systems. Insulin also initiates mitogenic signals in certain cell types. The objective of the present study was to explore the effects of octreotide with or without insulin treatment, on Caco-2 and HT-29 human colon-cancer cell proliferation and to correlate their effects with the activation of telomerase reverse transcriptase (hTERT). The involvement of protein tyrosine phosphatases in the regulation of the anti-proliferative effect of octreotide was also evaluated. Sodium orthovanadate was used to reverse the anti- proliferative effect of octreotide. Telomerase activity was determined for each time point under octreotide and/or insulin treatment. Elevated expression of sst1, sst2 and sst5 was confirmed in both cell lines by RT-PCR. Immunocytochemistry detected sst1, sst2A, sst2B, sst3, sst4 and sst5 protein expression in the membranes of both cell lines. Octreotide inhibited the proliferation of Caco-2 and HT-29 cells in a time and dose-dependent manner. Insulin exerted proliferative effects in Caco-2 cells and octreotide reversed its effect in both cell lines. Sodium orthovanadate suppressed the anti-proliferative effect of octreotide both in Caco-2 and HT-29 cells. Telomerase activity was significantly reduced when Caco-2 cells were exposed to octreotide, under serum-free cultured medium. On the other hand, telomerase attenuation after octreotide treatment could not counteract the actions of insulin on both cells. Our data indicate that the use of octreotide could provide a possible therapeutic approach to the management of certain patients who suffer from colon cancer.

Tacks-free transabdominal preperitoneal (TAPP) inguinal hernioplasty, using an anatomic 3-dimensional lightweight mesh with peritoneal suturing: pain and recurrence outcomes-initial experience.

BACKGROUND: The emphasis for research in inguinal hernia repair has shifted from hernia recurrence to groin pain, which is considered the most important factor for poor quality of life. AIM: : To evaluate hernia recurrences and pain at trocar site and at inguinal hernia site, in patients who underwent tacks-free transabdominal preperitoneal inguinal hernia repair, using a lightweight nonfixed 3-dimensional mesh with peritoneal suturing. MATERIALS AND METHODS: Between 2009 and 2011, 32 patients (2 female) with mean age 51 years underwent hernia repair. The mean follow-up period was 12.4 months. RESULTS: The mean operative time was 84 minutes. There was minimal blood loss. No bowel or urinary bladder injury had occurred. Mean hospital stay was 1 day. One patient developed seroma 4 months postoperatively. There were no conversions to open repair, no hernia recurrence, and no deaths. The mean value of pain at trocar site and inguinal hernia site 12 hours postoperatively was 1.469 and 0.875, respectively. The pain was more intense bearing a peak at 12 hours postoperatively at the trocar site, compared with the inguinal site. CONCLUSIONS: It is demonstrated with this technique that there are no recurrences and the chronic pain is negligible. These findings call for confirmatory randomized trials in larger series with longer follow-up.

Laparoscopic repair of congenital diaphragmatic hernia complicated with sliding hiatal hernia with reflux in adult.

INTRODUCTION: Congenital diaphragmatic hernia (CDH) in adults is a relatively rare condition being asymptomatic in the majority of cases. Symptomatic CDH should prompt surgical management because they may lead to intestinal obstruction or severe pulmonary disease. This is the first reported case of a symptomatic CDH complicated with sliding hiatal hernia (SHH). PRESENTATION OF CASE: A 65 years old women with reflux and dysphagia was complaining of postprandial paroxysmal dyspnea and epigastric pain radiating to her back. Upper endoscopy diagnosed sliding and para-esophageal diaphragmatic hernia with severe esophagitis. Computed tomography-scan revealed a large Bochdalek hernia at the left diaphragm. DISCUSSION: Diagnostic laparoscopy was decided, which confirmed the SHH, but also revealed a CDH defect at the tendonous part of the left diaphragm. The left bundle of the right crus was intact, separating the two hernia components (sliding and congenital). Extensive adhesiolysis was performed, dissecting and separating the stomach away from the diaphragm. Posterior cruroplasty at the esophageal hiatus was performed for the SHH with Nissen fundoplication as antireflux procedure. Primary continuous suture repair was performed for the CDH, reinforced with prosthetic mesh on top. Operative time was 150min with no morbidity. The patient was discharged home uneventfully the third postoperative day. On 12-months follow-up, she reported no symptoms and improvement in quality of life. CONCLUSION: Laparoscopy is a unique method for a precise diagnosis of symptomatic congenital diaphragmatic hernia in adults being also a safe and viable technique for a successful repair at the same time. Experience of advanced laparoscopic surgery is required.

Spontaneous rupture of the splenic capsule with massive bleeding subsequent to the pringle maneuver during laparoscopic liver resection.

BACKGROUND: The Pringle maneuver has its applications to minimize blood loss during hepatic resection. Splenic rupture during the Pringle maneuver in open liver surgery was described only in few cases. This is the first report of such a complication during laparoscopic surgery. CASE REPORT: A 58-year-old woman sustained major splenic capsular rupture during laparoscopic right lateral hepatic sectionectomy (resection of segments VI to VII) for a colorectal metastasis. Surgery was carried out with the patient in the left lateral position. She became hypotensive during the second application of the Pringle maneuver secondary to spontaneous rupture of the splenic capsule. This was controlled with application of thrombogenic hemostatic agents. The patient received 12 units of blood transfusion. Her subsequent recovery was uneventful, and she was discharged on the sixth postoperative day. CONCLUSIONS: Unexplained hypotension during laparoscopic liver resection and the application of the Pringle maneuver should raise suspicion of splenic hemorrhage and prompt a timely and adequate intervention.

Emergency laparoscopic splenectomy for splenic trauma in a Jehovah's Witness patient.

The safety and efficacy of laparoscopic splenectomy in the management of benign hematologic diseases is well established. However, most consider the laparoscopic approach to splenectomy in trauma patients contraindicated. We present a 76-year-old Jehovah's Witness who sustained a blunt abdominal trauma, rib fractures, and grade III splenic injury. She continued to lose blood, albeit slowly, for which she underwent preemptive urgent laparoscopic splenectomy with the use of the red cell saver. The operating time was 65 minutes. She was discharged on the 16th postoperative day after recovering from fractured ribs with subsequent pulmonary atelectasis and basal pneumonia. Whereas the majority of grade I to III splenic injuries in adults can be managed conservatively, some 20% will fail and require emergency splenectomy for delayed rupture of the spleen. In a Jehovah's Witness patient, early splenectomy for injury with the use of red cell saver is advised. This may be accomplished laparoscopically in the hemodynamically noncompromised patient.