Role of TLR5 in the Translocation and Dissemination of Commensal Bacteria in the Intestine after Traumatic Hemorrhagic Shock.

Enterogenous infection is a major cause of death during traumatic hemorrhagic shock (THS). It has been reported that Toll-like receptor 5 (TLR5) plays an integral role in regulating mucosal immunity and intestinal homeostasis of the microbiota. However, the roles played by TLR5 on intestinal barrier maintenance and commensal bacterial translocation post-THS are poorly understood. In this research, we established THS models in wild-type (WT) and Tlr5-/- (genetically deficient in TLR5 expression) mice. We found that THS promoted bacterial translocation, while TLR5 deficiency played a protective role in preventing commensal bacteria dissemination after THS. Furthermore, intestinal microbiota analysis uncovered that TLR5 deficiency enhanced the mucosal biological barrier by decreasing RegIIIγ-mediated bactericidal activity against G+ anaerobic bacteria. We then sorted small intestinal TLR5+ lamina propria dendritic cells (LPDCs) and analyzed TH1 differentiation in the intestinal lamina propria and a coculture system consisting of LPDCs and naïve T cells. Although TLR5 deficiency attenuated the regulation of TH1 polarization by LPDCs, it conferred stability to the cells during THS. Moreover, retinoic acid (RA) released from TLR5+ LPDCs could play a key role in modulating TH1 polarization. We also found that gavage administration of RA alleviated bacterial translocation in THS-treated WT mice. In summary, we documented that TLR5 signaling plays a pivotal role in regulating RegIIIγ-induced killing of G+ anaerobic bacteria, and LPDCs mediated TH1 differentiation via RA. These processes prevent intestinal bacterial translocation and enterogenous infection after THS, suggesting that therapeutically targeting LPDCs or gut microbiota can interfere with bacterial translocation after THS.

The "Two-Step" approach for classifying the severity of acute pancreatitis: A retrospective study.

BACKGROUND: The Revised Atlanta Classification (RAC) and Determinant-Based Classification (DBC) are currently two widely adopted systems for evaluating the severity of acute pancreatitis (AP). This study aimed to overcome the inaccuracies and limitations that existed in them. METHODS: We retrospectively analyzed 298 patients with AP. The "Two-Step" approach was divided into an early organ failure (OF) assessment: (I) none, (II) transient, (III) single persistent, and (IV) multiple persistent; and a later local complications assessment: (A) none, (B) sterile, and (C) infectious. Patients with AP who died before the second step were classified into category X. The "Two-Step" approach was then compared to the RAC and DBC. RESULTS: As the patients' grades increased (I to IV), organ support treatment rates, intensive care unit lengths of stay, and mortalities increased. Invasive intervention rates displayed increasing trends with local complications aggravated (A to C). Patients in category X were older and had higher Marshall scores with the highest grades of severity. CONCLUSIONS: By combining the early OF grades and the late local complications, the "Two-Step" approach represents an accurate classification system required for stratified studies of AP, and introduces the category X as the severest forms of AP.

Systematic Review and Meta-Analysis of the Efficacy of Appropriate Empiric Anti-Enterococcal Therapy for Intra-Abdominal Infection.

Background: Delayed treatment of seriously infected patients results in increased mortality. However, antimicrobial therapy for the initial 24 to 48 hours is mostly empirically provided, without evidence regarding the causative pathogen. Whether empiric anti-enterococcal therapy should be administered to treat intra-abdominal infection (IAI) before obtaining culture results remains unknown. We performed a meta-analysis to explore the effects of empiric enterococci covered antibiotic therapy in IAI and the risk factors for enterococcal infection in IAI. Methods: We searched multiple databases systematically and included 23 randomized controlled trials (RCTs) and 13 observational studies. The quality of included studies was assessed, and the reporting bias was evaluated. Meta-analysis was performed using random effects or fixed effects models according to the heterogeneity. The risk ratio (RR), odds ratio (OR), and 95% confidence interval (CI) were calculated. Results: Enterococci-covered antibiotic regimens provided no improvement in treatment success compared with control regimens (RR, 0.99; 95% CI, 0.97-1.00; p = 0.15), with similar mortality and adverse effects in both arms. Basic characteristic analysis revealed that most of the enrolled patients with IAI in RCTs were young, lower risk community-acquired intra-abdominal infection (CA-IAI) patients with a relatively low APACHE II score. Interestingly, risk factor screening revealed that malignancy, corticosteroid use, operation, any antibiotic treatment, admission to intensive care unit (ICU), and indwelling urinary catheter could predispose the patients with IAI to a substantially higher risk of enterococcal infection. "Hospital acquired" itself was a risk factor (OR, 2.81; 95% CI, 2.34-3.39; p < 0.001). Conclusion: It is unnecessary to use additional agents empirically to specifically provide anti-enterococcal coverage for the management of CA-IAI in lower risk patients without evidence of causative pathogen, and risk factors can increase the risk of enterococcal infection. Thus, there is a rationale for providing empiric anti-enterococcal coverage for severely ill patients with CA-IAI with high risk factors and patients with hospital-acquired intra-abdominal infection (HA-IAI).

Efficacy of Early Percutaneous Catheter Drainage in Acute Pancreatitis of Varying Severity Associated With Sterile Acute Inflammatory Pancreatic Fluid Collection.

OBJECTIVE: The aim of the study was to evaluate the efficacy of early percutaneous catheter drainage (PCD) for sterile acute inflammatory pancreatic fluid collection (AIPFC) in acute pancreatitis (AP) of varying severity. METHODS: Retrospective analyses were performed based on the presence of sterile AIPFC and different AP severities according to 2012 Revised Atlanta Classification. RESULTS: Early PCD contributed to obvious decreases in operation rate (OR, P = 0.006), infection rate (IR, P = 0.020), and mortality (P = 0.009) in severe AP (SAP). In moderate SAP with sterile AIPFCs, however, early PCD was associated with increased OR (P = 0.009) and IR (P = 0.040). Subgroup analysis revealed that early PCD led to remarkable decreases in OR for patients with persistent organ failure (OF) within 3 days (P = 0.024 for single OF, P = 0.039 for multiple OF) and in mortality for patients with multiple OF (P = 0.041 for OF within 3 days and P = 0.055 for 3-14 days). Moreover, lower mortality was found in SAP patients with early PCD-induced infections than with spontaneous infections (P = 0.027). CONCLUSIONS: Early PCD may improve the prognosis of SAP with drainable sterile AIPFCs by reducing the OR, IR, and mortality.

Effects of Short-Peptide-Based Enteral Nutrition on the Intestinal Microcirculation and Mucosal Barrier in Mice with Severe Acute Pancreatitis.

SCOPE: Short-peptide-based enteral nutrition (SPEN) is absorbed more efficiently in patients with severe acute pancreatitis (SAP). More importantly, SPEN decreases SAP-induced enterogenous infection risk. This study aims to investigate whether SPEN alleviates intestinal bacterial translocation in mice with SAP, and the underlying mechanisms. METHODS AND RESULTS: The SAP model is established after pre-treatment with SPEN or intact-protein-based enteral nutrition. Although there is no improvement in pancreas injury, as evaluated through Hematoxylin-Eosin staining or serum amylase, SPEN obviously attenuates intestinal bacterial translocation after SAP. To unveil the mechanisms, it is found that the intestinal mechanical barrier destroyed by SAP is significantly relieved by SPEN, which presents with recovered ZO-1 expression, mucus layer, and goblet cell function. Additionally, SPEN alleviates local CCR6/CCL20 induced CD11c+ dendritic cell infiltration, systemic immunosuppression, and inhibits the secretion of luminal secretory immunoglobulin A. Possibly responsible for SAP-induced mucosal dysfunctions, destroyed intestinal mucosal microcirculation and local hypoxia are largely improved in SAP+SPEN group. CONCLUSION: SPEN can improve downregulated intestinal mucosal microcirculation secondary to SAP, which may be responsible for mucosal inflammation relief, maintenance of the mechanical barrier and mucosal immunity, the correction of systemic immunosuppression, and play a protective role in defending commensal bacterial translocation after SAP.

Dexamethasone protects the glycocalyx on the kidney microvascular endothelium during severe acute pancreatitis.

OBJECTIVE: This study demonstrated that dexamethasone (DEX) protects the endothelial glycocalyx from damage induced by the inflammatory stimulus tumor necrosis factor-α (TNF-α) during severe acute pancreatitis (SAP), and improves the renal microcirculation. METHODS: Ninety mice were evenly divided into 3 groups (Sham, SAP, and SAP+DEX). The SAP mice model was established by ligature of pancreatic duct and intraperitoneal injection of cerulein. Renal perfusion and function, and morphological changes of the glycocalyx were evaluated by laser Doppler velocimetry, electron microscopy, and histopathology (hematoxylin and eosin (H&E) staining), respectively. Serum levels of syndecan-1 and TNF-α were assessed by enzyme-linked immunosorbent assay (ELISA). The protective effects of dexamethasone on the glycocalyx and renal microcirculation were evaluated. RESULTS: Significantly high levels of serum TNF-α were detected 3 h after the onset of SAP. These levels might induce degradation of the glycocalyx and kidney hypoperfusion, resulting in kidney microcirculation dysfunction. The application of dexamethasone reduced the degradation of the glycocalyx and improved perfusion of kidney. CONCLUSIONS: Dexamethasone protects the endothelial glycocalyx from inflammatory degradation possibly initiated by TNF-α during SAP. This is might be a significant discovery that helps to prevent tissue edema and hypoperfusion in the future.

Severe traumatic hemorrhagic shock induces compromised immune barrier function of the mesenteric lymph node leading to an increase in intestinal bacterial translocation.

Critically ill patients have increased susceptibility to translocation of gut bacteria. However, the mechanisms are complicated and remain unclear, and the aim of this study was to explore these mechanisms. Rats exposed to different levels of shock were orally administrated with bioluminescent Citrobacter. We found that severe shock caused an increase in bacterial translocation to the visceral organs, such as liver, spleen and blood, compared with mild shock. Surprisingly, bacterial translocation to mesenteric lymph node (MLN) was unchanged between the two shock groups. Various methods, including flow cytometry, a co-culture model and western blots, were used to evaluate MLN-associated immune function. Specifically, we focused on mesenteric lymph node dendritic cells (MLN-DCs), the critical antigen presenting cells involved in the construction of the immune barrier in MLN. We also found that severe shock impaired the phenotypic maturation of MLN-DCs and induced a tolerogenic phenotype. Furthermore, co-culture assays of DCs with naive CD4+ T cells showed that DCs subject to severe shock were more inclined to polarize native CD4+ T cells into Th2 and Treg cells. This study successfully reproduced the clinical phenomenon of severe shock resulting in increased bacterial translocation to extraintestinal tissues, and this may be related to the compromised immune barrier function of MLN, as maturation and function of MLN-DC's were badly impaired.

Clinical characteristics and treatment of thyroid cancer in children and adolescents: a retrospective analysis of 83 patients.

OBJECTIVE: To study the clinical characteristics, treatment, and prognosis of thyroid cancer in children and adolescents. METHODS: We performed a retrospective analysis of clinical data from 83 cases of thyroid cancer in children and adolescents from January 1990 to December 2010. We compared extra-thyroid extension, lymph node metastasis, distant metastasis, and prognosis between pediatric patients ≤12 years of age (27 cases) and those >12 years of age (56 cases). All the patients agreed to undergo thyroidectomy and endocrine therapy, and the consent was obtained from parents or guardians. RESULTS: Histopathology included papillary carcinoma in 67 cases, papillary carcinoma with partial follicular growth pattern in 1 case, papillary carcinoma with squamous metaplasia in 4 cases, follicular carcinoma in 7 cases, medullary carcinoma in 3 cases, and poorly differentiated carcinoma in 1 case. The total lymph node metastasis rate was 78.31%. Patients ≤12 years of age showed a higher rate of lymph node metastasis than the older group (92.59% vs. 71.43%, P=0.028). The incidence rate in females in the older group was higher than that in the younger group (80.36% vs. 59.26%, P=0.041). There were no significant differences in extra-thyroid extension, distant metastasis, survival rate, or recurrent disease between the two groups. CONCLUSIONS: The lymph node metastasis of thyroid cancer is higher in patients ≤12 years of age than in those >12 years of age; the incidence rate is higher in females than in males. Childhood thyroid cancer has a good prognosis, surgery being the most effective treatment. Choosing a reasonable surgery method and comprehensive postoperative treatment can achieve a cure and satisfactory survival rate.

Allicin ameliorates intraintestinal bacterial translocation after trauma/hemorrhagic shock in rats: The role of mesenteric lymph node dendritic cell.

BACKGROUND: Intestinal dendritic cells play important roles in regulating the function of the intestinal immune barrier and the intestinal bacterial translocation. In this study, we aim to investigate the effects of allicin on the function of mesenteric lymph node-dendritic cells after trauma/hemorrhagic shock. METHODS: One hundred and eight-four Sprague-Dawley rats were randomly assigned into a sham group (n = 46), sham + allicin group (n = 46), trauma/hemorrhagic shock group (n = 46), and trauma/hemorrhagic shock + allicin group (n = 46). Studies were performed on an in vivo model of spontaneously breathing rats with induced trauma/hemorrhagic shock. Allicin was diluted in resuscitation fluid and was administered through the right jugular vein. Flow cytometry was used to determine the expression of CD80, CD86, and major histocompatibility complex II (MHC II) on the surface of mesenteric lymph node-dendritic cells, as well as apoptosis. Intraintestinal bacterial translocation was monitored by using bioluminescent citrobacter. Intestinal permeability tests were conducted by using both FITC-Dextran and Ussing-Chember assay. RESULT: CD80 and MHC-II expression levels were downregulated in the trauma/hemorrhagic shock group compared with the sham and sham + allicin groups; however, the expression was upregulated after allicin treatment. Also, allicin could ameliorate the trauma/hemorrhagic shock-induced increase in early apoptosis of mesenteric lymph node-dendritic cells. A significant increase was observed in the permeability of the intestinal barrier after severe traumatic shock, along with an obvious intraintestinal bacterial translocation to mesenteric lymph node. No difference was noticed in the bacterial translocation in mesenteric lymph node in the trauma/hemorrhagic shock group compared with trauma/hemorrhagic shock + allicin group (P = .589), which indicated allicin could not block bacterial translocation into mesenteric lymph node after trauma/hemorrhagic shock. However, it may increase the capacity of mesenteric lymph node to block intraintestinal bacterial translocation to extraintestinal organs as a statistical difference was noticed in the bacterial translocation in liver, blood, and spleen between trauma/hemorrhagic shock and trauma/hemorrhagic shock + allicin groups (P < .05). CONCLUSION: Trauma/hemorrhagic shock resulted in a decrease of mature mesenteric lymph node-dendritic cells. Allicin treatment could block intraintestinal bacterial translocation through increasing the immunologic barrier function of mesenteric lymph node by modulating dendritic cells maturation.

Impact of misplaced subclavian vein catheter into jugular vein on transpulmonary thermodilution measurement variables.

OBJECTIVE: The subclavian vein (SCV) is usually used to inject the indicator of cold saline for a transpulmonary thermodilution (TPTD) measurement. The SCV catheter being misplaced into the internal jugular (IJV) vein is a common occurrence. The present study explores the influence of a misplaced SCV catheter on TPTD variables. METHODS: Thirteen severe acute pancreatitis (SAP) patients with malposition of the SCV catheter were enrolled in this study. TPTD variables including cardiac index (CI), global end-diastolic volume index (GEDVI), intrathoracic blood volume index (ITBVI), and extravascular lung water index (EVLWI) were obtained after injection of cold saline via the misplaced SCV catheter. Then, the misplaced SCV catheter was removed and IJV access was constructed for a further set of TPTD variables. Comparisons were made between the TPTD results measured through the IJV and misplaced SCV accesses. RESULTS: A total of 104 measurements were made from TPTD curves after injection of cold saline via the IJV and misplaced SCV accesses. Bland-Altman analysis demonstrated an overestimation of +111.40 ml/m(2) (limits of agreement: 6.13 and 216.70 ml/m(2)) for GEDVI and ITBVI after a misplaced SCV injection. There were no significant influences on CI and EVLWI. The biases of +0.17 L/(min·m(2)) for CI and +0.17 ml/kg for EVLWI were revealed by Bland-Altman analysis. CONCLUSIONS: The malposition of an SCV catheter does influence the accuracy of TPTD variables, especially GEDVI and ITBVI. The position of the SCV catheter should be confirmed by chest X-ray in order to make good use of the TPTD measurements.

Successful Resolution of Gastric Outlet Obstruction Caused by Pancreatic Pseudocyst or Walled-Off Necrosis After Acute Pancreatitis: The Role of Percutaneous Catheter Drainage.

OBJECTIVE: Delayed gastric emptying (DGE) in patients with acute pancreatitis (AP) can be caused by gastroparesis or gastric outlet obstruction, which may occur when pancreatic pseudocyst (PP) or walled-off necrosis (WON) compresses the stomach. The aim of the study was to explore a proper surgical treatment. METHODS: From June 2010 to June 2013, 25 of 148 patients with AP suffered DGE. Among them, 12 were caused by gastroparesis, 1 was a result of obstruction from a Candida albicans plug, and 12 were gastric outlet obstruction (GOO) compressed by PP (n = 8) or WON (n = 4), which were treated by percutaneous catheter drainage (PCD). RESULTS: All 12 cases of compressing GOO achieved resolution by PCD after 6 [1.86] and 37.25 [12.02] days for PP and WON, respectively. Five cases developed intracystic infection, 3 cases had pancreatic fistulae whereas 2 achieved resolution and 1 underwent a pseudocyst jejunostomy. CONCLUSIONS: Gastric outlet obstruction caused by a PP or WON is a major cause of DGE in patients with AP. Percutaneous catheter drainage with multiple sites, large-bore tubing, and lavage may be a good therapy due to high safety and minimal invasiveness.

The hydrocortisone protection of glycocalyx on the intestinal capillary endothelium during severe acute pancreatitis.

Malfunctioning of the intestinal microcirculation secondary to severe acute pancreatitis (SAP) can cause injuries to the intestinal mucosal barrier, translocation of gut flora, and sepsis. The glycocalyx on the vascular endothelium helps maintain its normal function through multiple mechanisms, including regulation of vascular permeability and inhibition of intercellular adhesion. It is unknown that whether pancreatitis inflicts injuries to the intestinal mucosal barrier through damaging glycocalyx or stabilizing glycocalyx can be a potential therapeutic target in maintaining the integrity of the intestinal mucosal barrier during SAP. Injecting sodium taurocholate into the pancreatic duct of Sprague-Dawley rats induced SAP. Intestinal perfusion, changes in endothelial glycocalyx, and the associated molecular mechanisms were assessed by laser Doppler velocimetry, electron microscopy, and the levels of heparan sulfate, syndacan-1, and tumor necrosis factor-α (TNF-α) in the superior mesenteric vein. Protective effects of hydrocortisone treatment in the intestinal microcirculation during SAP were evaluated. Degradation of the glycocalyx in intestinal vascular endothelium developed 3 h after the onset of SAP in rats. By 12 h, significant reduction of intestinal perfusion was observed. The concomitant elevated levels of TNF-α in the superior mesenteric vein suggest that TNF-α is involved in the degradation of the glycocalyx. With the use of hydrocortisone, intestinal perfusion was improved and the degradation of glycocalyx was reduced. The degradation of glycocalyx is involved in the malfunction of the intestinal microcirculation. The massive release of TNF-α participates in this process and leads to glycocalyx degradation. Hydrocortisone may be a good therapy to prevent this process.

Full Airway Drainage by Fiber Bronchoscopy Through Artificial Airway in the Treatment of Occult Traumatic Atelectasis.

The objective of this study is to investigate the effects of full airway drainage by fiber bronchoscopy through artificial airway in the treatment of traumatic atelectasis with occult manifestations. From May 2006 to May 2011, 40 cases of occult traumatic atelectasis were enrolled into our prospective study. Group A (n = 18) received drainage by nasal bronchoscope; group B underwent airway drainage by fiber bronchoscopy through artificial airway (n = 22). The effects of treatment were evaluated by the incidence of adult respiratory distress syndrome (ARDS), lung abscess, and the average length of hospital stay. Compared with nasal fiber-optic treatment, airway drainage by fiber bronchoscopy through artificial airway reduced the incidence of ARDS (p = 0.013) and lung abscess (p = 0.062) and shortened the mean length of stay (p = 0.018). Making the decision to create an artificial airway timely and carry out lung lavage by fiber bronchoscopy through artificial airway played a significant role in the treatment of occult traumatic atelectasis.

Delayed admission to ICU does not increase the mortality of patients post neurosurgery.

Increasing shortage of intensive care resources is a worldwide problem. While routine postoperative admission to the intensive care unit (ICU) of patients undergoing neurosurgery is a long established practice for many hospitals. Therefore, some neurosurgical patients have to be cared in post anesthesia care unit (PACU) before ICU admission during high ICU occupancy. The aim of this study was to compare the outcome of neurosurgical patients immediately admitted to the ICU post operation with those who were required to wait for ICU bed in PACU and managed by anesthesiologists before ICU admission. All adult neurosurgical patients admitted to our ICU between January 2010 and July 2013 were retrospectively analyzed. Recorded data included demographic data, surgical categories, end time of operation, operation hours, postoperative complication, hospital/ICU length of stay and cost, Glasgow coma score (GCS) on ICU discharge and ICU mortality. A total of 989 neurosurgical patients were evaluated. Nine hundred thirty-seven (94.7%) patients were immediately admitted and 52 (5.3%) patients had delayed ICU admission. Median PACU waiting hours was 4.3 h (interquartile range: 2.0-10.2 h). Delayed ICU admission post neurosurgery was highly associated with the end time of operation (p = 0.019) and high ICU occupancy (p < 0.0001). Average GCS on ICU discharge was higher in immediately admitted group (13.0 ± 3.5 vs. 11.4 ± 4.5, p = 0.012). However, delayed admission to ICU post neurosurgery was not associated with prolonged ICU length of stay, increased ICU mortality, increased postoperative complication and hospital/ICU cost (all p > 0.05). Thus, an algorithm for appropriate disposition of neurosurgical patients is warranted so as to balance the quality of care and control of scarce intensive resources.

Six cases of severe acute pancreatitis complicated with vancomycin-resistant enterococcus enteritis.

OBJECTIVE: The objective of this study was to explore the clinical manifestations and possible mechanisms of vancomycin-resistant enterococcus (VRE)-induced severe enteritis and extraenteric disseminations. METHODS: In six patients with severe acute pancreatitis (SAP) complicated with acute infectious diarrhea, VRE was confirmed by bacterial genotyping, minimum inhibitory concentration testing, and empiric linezolid treatment. Samples collected from stools and peripancreatic effusions were used to compare the genotypes of VRE by pulsed-field gel electrophoresis and multilocus sequence typing and to validate the suspected extraenteric disseminations caused by VRE. To further elucidate the mechanisms of VRE-inflicted enteric mucosal injury, in vitro infection of human intestinal Caco-2 cell line with VRE was performed followed by inflammatory cytokine assays and morphological characterization by electron microscopy. RESULTS: All six VRE strains isolated from stool samples caused severe enteritis in SAP patients. The same strains further inflicted significant damage and induced inflammatory reactions in Caco-2 cells. Homologous assays demonstrated high homology between samples from stool and peripancreatic effusions in two patients, indicating the occurrence of extraenteric disseminations. CONCLUSIONS: Alterations in drug resistance and virulence of enterococci, part of the symbiotic bacteria, during the course of SAP may cause inflammatory injuries to enteric epithelium, resulting in enteritis and extraenteric disseminations.

Early enteral nutrition with polymeric feeds was associated with chylous ascites in patients with severe acute pancreatitis.

OBJECTIVE: Chylous ascites (CA) may be involved in the pathological process of severe acute pancreatitis (SAP), but the underlying mechanisms remain unknown. This study investigated the incidence of CA in patients with SAP and its relationship with enteral nutrition (EN). METHODS: A retrospective review of 85 patients with SAP admitted to our hospital was performed. Patients starting EN within 72 hours after the onset of SAP were classified as the early EN (EEN) group, and others, as the later EN group. The incidences of CA and prognosis in the EEN and later EN groups were examined with nutrition preparation of polymeric formula or semielemental feed. RESULTS: Thirteen (15.29%) of 85 patients were identified with CA. A higher incidence of CA was observed in EEN patients who received polymeric formula (9 of 33, P < 0.05). All patients with CA were successfully treated with a modified medium-chain triglyceride diet. Consequently, there were no differences in intensive care unit stay and in mortality rates in patients with or without CA. CONCLUSIONS: There was a higher incidence of CA associated with early enteral feeding of polymeric formula in patients with SAP. Future studies are warranted to confirm our findings and evaluate better enteral feeding options to avoid CA.

Incidence of unexplained intra-abdominal free fluid in patients with blunt abdominal trauma.

BACKGROUND: Intra-abdominal free fluid is commonly caused by injuries of solid or hollow organs in patients suffering from blunt abdominal trauma (BAT). However, it presents a diagnostic dilemma for surgeons when free fluid is unexplained, especially in stable BAT patients. This study was to analyze the incidence of such unexplained free fluid in BAT patients and its diagnostic value in abdominal organ injury. METHODS: Altogether 597 patients with BAT who had been treated at our trauma center over a 10-year period were reviewed. Stable patients with free fluid but without free air or definite organ injury on abdominal computed tomography were studied. Clinical management and operative findings were analyzed. RESULTS: Thirty-four (5.70%) of the 597 patients met the inclusion criteria: 24 (4.02%) underwent therapeutic exploratory laparotomy: bowel injuries were found in 13, hepatic rupture in 3, colon rupture in 3, duodenal rupture in 2, spleen rupture in 1, pancreas rupture in 1, and gallbladder perforation in 1. In 2 patients, laparotomy was nontherapeutic. Those with moderate or large amounts of free fluid were more likely to suffer from a hollow viscus injury and have a therapeutic procedure. The mean time of hospital stay for the delayed laparotomy group was longer than that for the emergency group (19+/-5.12 vs. 12+/-2.24 days; t=2.73, P<0.01). CONCLUSIONS: There was a positive correlation between the amount of unexplained free fluid and the determination of intra-abdominal organ injury. The proportion of BAT patients who required surgical intervention was high, particularly those with a moderate or large amount of free fluid, and most of them suffered from a hollow organ injury. Emergency laparotomy is recommended for these patients.

Familial and genetic researches on three Chinese families with von Hippel-Lindau disease.

OBJECTIVE: Hemangioblastoma of the central nervous system (CNS) occur as sporadic tumors or as a part of von Hippel-Lindau (VHL) disease, an autosomal dominant hereditary tumor syndrome caused by germline mutation of the VHL tumor suppressor gene. This study shows the clinical characteristics of three large Chinese families with VHL disease and evaluates the consequence of the genetic test for the diagnosis of VHL disease and clinical screening of the family members. METHODS: DNA is extracted from peripheral blood in 43 members from three large families with VHL disease and amplified by PCR to three exons of the VHL gene. The PCR products were directly sequenced and the mutations compared with the Human Gene Mutation Database. RESULTS: The ages of the patients who are given the initial diagnosis ranged from 16 to 47 years (mean: 31 years), and the mean time was 17.3 months (2-30 months) from the emergence of the symptom to patients' first visit. Furthermore, the gender distribution was 20% female (4) and 80% male (16). Twenty VHL disease patients in the three families have the most common manifestation of CNS hemangioblastoma. The cytosine replaced the 716th guanine on four patients and three carriers of virulence gene from the first family, which made the 168th serine replaced by threonine. And no mutation was found on the 22 members of the second family. Meanwhile, it was also found that the guanine replaced the 559th cytosine on one patient and two carriers from the third family, which made the 116th leucine replaced by valine. CONCLUSION: The DNA analysis of VHL germline mutations is clearly superior to clinical information to diagnose VHL disease. The CNS hemangioblastoma is the early manifestation in VHL disease. It is recommended that every patient with CNS hemangioblastoma should be screened for VHL gene mutation. The test for the VHL gene plays a key role in the discovery of asymptomatic patients and the carriers of virulence gene.