Volvulus caused by a free intraperitoneal staple after laparoscopic appendectomy: A case report.

INTRODUCTION: Laparoscopic appendectomies are routinely performed using linear staplers. Few case reports have discussed complications from free intraperitoneal staples after appendectomy. We present the first case of a volvulus caused by a free staple that subsequently required bowel resection. PRESENTATION OF CASE: A 27-year-old female underwent laparoscopic appendectomy for uncomplicated appendicitis. The base of the appendix was divided using a laparoscopic gastrointestinal anastomosis (GIA) stapler and the mesoappendix was divided using a LigaSure device. The patient was discharged the following day. Eight days later, the patient returned to the emergency department with severe abdominal pain, emesis, and peritoneal signs. Computed tomography (CT) showed significant pneumoperitoneum and nonspecific small bowel edema. Exploratory laparotomy was performed revealing a necrotic small bowel segment from a malformed, free staple caught on the peritoneum of the small bowel mesentery causing a closed loop obstruction. After reduction and detorsion, the small bowel segment was not viable and required resection. She was discharged on postoperative day four with no additional perioperative complications. DISCUSSION: Mechanical staplers are commonly used in laparoscopic appendectomy and free intraperitoneal staples are generally considered inert. A high index of suspicion should be maintained for the early postoperative appendectomy patient with obstructive symptoms. CONCLUSION: Inspection of the staple line, choosing the appropriate staple size and cartridge, and removing free malformed staples if seen should be employed during appendectomy to prevent rare but devastating complications.

Outcomes in Trauma Patients With Behavioral Health Disorders.

BACKGROUND: The relationship between behavioral health disorders (BHDs) and outcomes after traumatic injury is not well understood. The objective of this study was to evaluate the association between BHDs and outcomes in the trauma patient population. MATERIALS AND METHODS: We performed a review of the Trauma Quality Improvement Program database from 2013 to 2016 comparing patients with and without a BHD, which was defined as a psychiatric disorder, alcohol or drug use disorders, dementia, or attention deficit hyperactivity disorder. Outcomes of interest were mortality, length of stay (LOS), and inpatient complications. RESULTS: In the study population, 254,882 patients (25%) had a BHD. Of these, psychiatric disorders comprised 38.3% (n = 97,668) followed by alcohol (33.3%, n = 84,845) and drug (26.4%, n = 67,199) use disorders, dementia (20.2%, n = 51,553), and attention deficit hyperactivity disorder (1.7%, n = 4301). On multivariable analysis, overall mortality was lower in the BHD group (odds ratio [OR] 0.83, confidence interval [CI] 0.79-0.83; P < 0.001). Patients with dementia had higher mortality when controlling for other risk factors (OR 1.62, CI 1.56-1.69; P < 0.001). LOS was 8.5 d (s = 0.02) for patients with a BHD versus 7.4 d (s = 0.01) for patients without a BHD (P < 0.001). Comorbid BHD was associated with any inpatient complication (OR 1.19, CI 1.18-1.20; P < 0.001). CONCLUSIONS: Trauma patients with a BHD had lower overall mortality compared with those without a BHD. However, on subgroup analysis, those with dementia had increased mortality. BHDs increased risk for any inpatient complication and prolonged LOS. Trauma patients with BHDs represent a vulnerable population and warrant special attention to minimize harm and improve outcomes.

Trauma-hemorrhagic shock induces a CD36-dependent RBC endothelial-adhesive phenotype.

OBJECTIVE: Microvascular dysfunction is a key element in the development of the multiple organ dysfunction syndrome. Although the mechanisms for this response are unclear, RBC adhesion to endothelium may initiate intravascular occlusion leading to ischemic tissue injury. Thus, we tested the hypothesis that trauma-hemorrhage induces RBC-endothelial cell adhesion. DESIGN: Prospective in vivo and in vitro animal study and analysis of patient blood samples. SETTING: University research laboratory and hospital emergency and trauma units. INTERVENTION: We initially assayed RBC adhesion to endothelial cells in vitro using RBCs obtained from rats subjected to trauma-hemorrhagic shock or sham shock as well as from severely injured trauma patients. Subsequently, we measured the role of putative RBCs and endothelial cell receptors in the increased RBC-endothelial cell adhesive response. MAIN RESULTS: In both rats and humans, trauma-hemorrhagic shock increased RBC adhesion to endothelium as well as increasing several putative RBC surface adhesion molecules including CD36. The critical factor leading to RBC-endothelial cell adhesion was increased surface RBC CD36 expression. Adhesion of trauma-hemorrhagic shock RBCs was mediated, at least in part, by the binding of RBC CD36 to its cognate endothelial receptors (αVß3 and VCAM-1). Gut-derived factors carried in the intestinal lymphatics triggered these trauma-hemorrhagic shock-induced RBC changes because 1) preventing trauma-hemorrhagic shock intestinal lymph from reaching the systemic circulation abrogated the RBC effects, 2) in vitro incubation of naïve whole blood with trauma-hemorrhagic shock lymph replicated the in vivo trauma-hemorrhagic shock-induced RBC changes while 3) injection of trauma-hemorrhagic shock lymph into naïve animals recreated the RBC changes observed after actual trauma-hemorrhagic shock. CONCLUSIONS: 1) Trauma-hemorrhagic shock induces rapid RBC adhesion to endothelial cells in patients and animals. 2) Increased RBC CD36 expression characterizes the RBC-adhesive phenotype. 3) The RBC phenotypic and functional changes were induced by gut-derived humoral factors. These novel findings may explain the microvascular dysfunction occurring after trauma-hemorrhagic shock, sepsis, and other stress states.

Early trauma-hemorrhage-induced splenic and thymic apoptosis is gut-mediated and toll-like receptor 4-dependent.

Immune depression after trauma-hemorrhage has been implicated as an important factor in the pathogenesis of sepsis and septic-organ failure. Although recent studies have implicated immune-cell apoptosis as an important factor in the evolution of this posttrauma immune-suppressed state, neither the initial triggers that induce this response nor the cellular pathways through which these triggering pathways act have been fully defined. Thus, the current study tests the hypothesis that acute splenic and thymic immune-cell apoptosis developing after trauma-hemorrhagic shock (T/HS) is due to gut-derived factors carried in intestinal lymph and that this T/HS lymph-induced immune depressed state is mediated through Toll-like receptor 4 (TLR4). The first set of experiments documented that T/HS caused both thymic and splenic immune-cell apoptosis as measured by TUNEL (terminal deoxynucleotidyl transferase dUTP nick end labeling) and caspase-3 immunohistochemistry and that this increase in apoptosis was totally abrogated by mesenteric lymph duct ligation. In subsequent experiments, mesenteric lymph collected from animals subjected to T/HS or trauma-sham shock were injected into TLR4-deficient (TLR4mut) mice or their wild-type (WT) littermates. Trauma-hemorrhagic shock, but not trauma-sham shock, lymph caused splenic apoptosis in the WT mice. However, the TLR4mut mice were resistant to T/HS lymph-induced splenic apoptosis. Furthermore, the WT, but not the TLR4mut mice developed splenic apoptosis after actual T/HS. In conclusion, gut-derived factors appear to initiate a sequence of events that leads to an acute increase in splenic and thymic immune-cell apoptosis, and this process is TLR4-dependent.

Intravenous injection of mesenteric lymph produced during hemorrhagic shock decreases RBC deformability in the rat.

OBJECTIVE: To test the hypothesis that gut-derived factors carried in trauma-hemorrhagic shock (T/HS) lymph are sufficient to induce red blood cells (RBC) injury, to investigate their potential mechanisms of action, and to define the time post-T/HS that these factors appear in the lymph. METHODS: Mesenteric lymph collected from T/HS or trauma-sham shock (T/SS) rats over different time periods was injected intravenously into male rats at a rate of 1 mL/h for 3 hours. RBC deformability was measured using laser-assisted ektacytometer to calculate the elongation index. From the shear-stress elongation curve, the stress required for the erythrocytes to reach 50% of their maximal elongation was also determined. RBC deformability was measured before lymph infusion and at 1 hour and 3 hours after the initiation of lymph infusion. The effect of the lymph samples (5% v/v) was also determined in vitro by incubating naïve whole blood with the lymph samples. The potential role of T/HS lymph-induced RBC oxidant injury mediated by inducible nitric oxide synthase (iNOS)-generated oxidants and/or white blood cells (WBC) was investigated using iNOS inhibitors and WBC depletion, respectively. In all the in vivo studies, five to seven rats were studied per group. RESULTS: The intravenous injection of T/HS lymph but not T/SS lymph caused in vivo RBC injury. The biological activity of T/HS lymph varied over time with the RBC-injurious factors being produced only during the first 3 hours postshock. The in vivo inhibition of iNOS did not prevent lymph-induced RBC injury. T/HS lymph incubated in vitro with naïve whole blood resulted in RBC injury, but this injury was not observed in blood depleted of WBC. CONCLUSIONS: These results indicate that T/HS lymph produced during the initial 3-hour postshock period is sufficient to induce RBC injury in otherwise normal rats and that the lymph-induced RBC injury is not dependent on activation of the iNOS pathway but seems to require WBC.