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Background: Anastomotic leakage (AL) is the most serious complication after rectal cancer surgery. Risk factors associated with AL have been documented in previous studies; however, the consensus is still lacking. In this retrospective study, we aimed to identify risk factors for AL after rectal cancer resection and to create an accurate and effective tool for predicting the risk of this complication. Methods: The study cohort comprised of 276 patients with rectal cancer who had undergone anterior resection between 2015 and 2020. Twenty-four selected variables were assessed by univariate and multivariate logistic regression analyses to identify independent risk factors of AL. A risk assessment model for predicting the risk of AL was established on the basis of the regression coefficients of each identified independent risk factor. Results: Anastomotic leakage occurred in 20 patients (7.2%, 20/276). Multivariate analysis identified the following variables as independent risk or protective factors of AL: perioperative ileus (P < 0.001, odds ratio [OR] = 14.699), tumor size ≥5 cm (P = 0.025, OR = 3.925), distance between tumor and anal verge Conclusions: Our risk assessment model accurately and effectively identified patients at high risk of AL and could be useful in aiding decision-making aimed at minimizing adverse outcomes associated with leakage. Keywords: Anastomotic leakage, rectal cancer, risk assessment model, Author(s): Rui Ding [1]; Ming He [1]; Hong Cen [1]; Zheng Chen [1]; Yonghui Su (corresponding author) [1] Introduction Colorectal cancer is one of the commonest malignant tumors, ranking third [...]

Author(s): Diana Marcela Grajales-Urrego[sup.1], Fabián Mantilla-Sylvain[sup.2], Mariam Carolina Rolon-Cadena[sup.1], William Mauricio Basto-Borbón[sup.3] and Johanna Ãlvarez-Figueroa[sup.1,4] Background Invasive fungal infections are important causes of morbidity and mortality in immunocompromised patients. In [...], Background Mucormycosis is a highly lethal opportunistic fungal disease caused by ubiquitous molds of the order Mucorales, with Rhizopus, Lichtheimia and Mucor being the most common genera. This rare disease primarily affects immunocompromised patients, with presentations ranging from rhino-orbito-cerebral infections to disseminated mucormycosis with angioinvasion, leading to thrombosis and tissue infarction. Gastrointestinal mucormycosis is the least common clinical presentation and is believed to be secondary to spore ingestion. It can involve multiple components of the gastrointestinal tract, such as the stomach, liver, ileum, and colon, with nonspecific manifestations, including pain, nausea, vomiting, and abdominal distension. The initial clinical presentation may even manifest as gastrointestinal bleeding due to gastric ulceration or intestinal perforation. Case presentation Here we present the case of a 48-year-old male patient with a 9-year history of human immunodeficiency virus (HIV) infection who was hospitalized in the context of febrile neutropenia and whose acute respiratory infection was documented; therefore, antibiotic treatment was initiated. However, due to persistent febrile peaks and peripheral blood showing documentation of multilineage cytopenias, a bone marrow biopsy was performed, compatible with presenting features of marrow myelodysplasia. During hospitalization, the patient presented left flank abdominal pain, and an abdominal computed tomography (CT) scan revealed signs of intussusception of a small bowel loop at the distal jejunum level, leading to intestinal obstruction with ischemic progression, requiring ileectomy (60 cm). Histopathological analysis of the resected intestine revealed severe transmural ischemic changes associated with venous thrombosis due to fungal structures, with histochemical studies demonstrating the presence of zygomycete (Mucor) fungal structures, leading to the initiation of treatment with amphotericin B. However, despite treatment, the patient experienced progressive clinical deterioration with persistent fever and ventilatory failure, with follow-up tests showing absolute neutropenia and blood cultures positive for yeast, leading to death 52 days after admission. Conclusions The diagnosis of intestinal mucormycosis may be delayed due to the lack of specificity of the signs and symptoms. Pathologists as well as histopathological studies are essential for timely treatment. Keywords: Mucormycosis, Gastrointestinal mucormycosis, Human immunodeficiency virus, Acute myeloid leukemia, Intestinal ischemia, Venous thrombosis.

Background Intussusception, a common cause of abdominal pain in children, often lacks clear underlying causes and is mostly idiopathic. Recurrence, though rare, raises clinical concerns, with rates escalating after each episode. Factors like pathological lead points and Henoch-Schönlein purpura (HSP) are associated with recurrent cases. On the other hand, the prevalence of Helicobacter pylori (H. pylori), often asymptomatic, in children has been declining. Although its infection is reported to be linked with HSP, its role in recurrent intussusception remains unexplored. Further research is needed to understand the interplay among H. pylori (culprit pathogen), HSP (trigger), and intractable intussusception so as to develop effective management strategies. Case presentation A two-year-old girl experienced four atypical episodes of intussusception at distinct locations, which later coincided with HSP. Despite treatment with steroids, recurrent intussusception persisted, suggesting that HSP itself was not a major cause for intractable presentations. Subsequent identification of H. pylori infection and treatment with triple therapy resulted in complete resolution of her recalcitrant intussusception. Conclusion This instructive case underscored a sequence wherein H. pylori infection triggered HSP, subsequently resulting in recurrent intussusception. While H. pylori infection is not common in young children, the coexistence of intractable intussusception and steroid-resistant recurrent HSP necessitates consideration of H. pylori infection as a potential underlying pathogen. Keywords: Intussusception, Helicobacter pylori, Henoch-schönlein purpura, Triple therapy, Author(s): Kuan-Chieh Wang[sup.1,2], Chun-Hao Chu[sup.3,4], Che-Ming Chiang[sup.4], Fu-Ruei Zeng[sup.4], Ching-Wen Huang[sup.4] and Chien-Ming Lin[sup.4] Background Intussusception is the second most common cause of abdominal pain in children but the underlying [...]

Background: Surgical site infection (SSI) is one of the most common sources of morbidity after pancreaticoduodenectomy. Surgical site infections are associated with readmissions, prolonged length of stay, delayed initiation of adjuvant chemotherapy and negative effects on quality of life. Incisional vacuum-assisted closure (iVAC) devices applied on closed incisions may reduce SSI rates. The objective of this retrospective review is to evaluate the impact of iVAC on SSI rate after pancreaticoduodenectomy. Methods: A cohort of patients undergoing pancreaticoduodenectomy at a single institution who had at least 1 risk factor for SSI and who received an iVAC were compared with a historical cohort of high-risk patients who received conventional dressings after pancreaticoduodenectomy. The primary outcome was incidence of SSI within 30 days, abstracted from chart review. Secondary outcomes were 30-day readmission, 90-day mortality, rate of postoperative pancreatic fistula and rate of delayed gastric emptying. Results: In total, 175 patients were included, of whom 61 received an iVAC. The incidence of SSI was 13% (8 of 61 patients) and 16% (18 of 114 patients) in the iVAC and conventional dressing groups, respectively (odds ratio 0.81, 95% confidence interval 0.33-1.98). Preoperative biliary drainage was the most frequent SSI risk factor. Binary logistic regression using SSI as the outcome demonstrated no significant association with iVAC use when adjusted for SSI risk factors. There were no differences in rates of postoperative pancreatic fistula, delayed gastric emptying or 90-day mortality. Conclusion: This report describes the outcomes of the integration of iVAC devices into routine clinical practice at a high-volume institution. Application of this device after pancreaticoduodenectomy for patients at elevated risk of SSI was not associated with a reduction in the rate of SSis. Contexte : L'infection de la plaie opératoire (IPO) est l'une des principales causes de morbidité après la pancréatoduodénectomie. Les IPO sont associées à des réadmissions, au prolongement des séjours hospitaliers et au report de la chimiothérapie adjuvante, en plus de nuire à la qualité de vie. Le traitement des plaies par pression négative (TPN) appliqué sur des incisions refermées pourrait réduire les taux d'IPO. Cette étude rétrospective avait pour objectif de mesurer l'impact du TPN sur le taux d'IPO après la pancréatoduodénectomie. Méthodes : Dans un seul et même établissement, une cohorte de malades soumis à une pancréatoduodénectomie présentant au moins 1 facteur de risque d'IPO et ayant bénéficié du TPN a été comparée à une cohorte historique de cas à risque élevé chez qui on a appliqué des pansements classiques après la pancréatoduodénectomie. Le paramètre principal était l'incidence des IPO dans les 30 jours suivant l'intervention, selon la revue des dossiers. Les paramètres secondaires étaient les réadmissions dans les 30 jours, la mortalité dans les 90 jours, et les taux de fistules postopératoires et de retards de la vidange gastrique. Résultats : En tout, 175 malades ont été inclus, dont 61 ont reçu le TPN. L'incidence des IPO a été de 13% (8 malades sur 61) et de 16% (18 malades sur 114) dans les groupes ayant reçu le TPN et les pansements classiques, respectivement (rapport des cotes 0,81, intervalle de confiance de 95% 0,33-1,98). Le drainage biliaire préopératoire était le facteur de risque d'IPO le plus fréquent. La régression logistique binaire avec l'IPO comme paramètre n'a permis d'établir aucun lien significatif avec le TPN après ajustement pour tenir compte des facteurs de risque d'IPO. On n'a noté aucune différence quant aux taux de fistules pancréatiques postopératoires, aux retards de la vidange gastrique ou à la mortalité à 90 jours. Conclusion : Ce rapport décrit l'impact de l'intégration des systèmes de TPN dans la pratique clinique habituelle d'un établissement achalandé. L'utilisation de tels dispositifs après la pancréatoduodénectomie en présence d'un risque élevé d'IPO n'a pas été associée à une réduction du taux d'IPO., Surgical site infection (SSI) is one of the most common causes of morbidity after pancreaticoduodenectomy, affecting 10%-30% of patients. (1) Preoperative risk factors, such as biliary stenting and neoadjuvant chemotherapy, [...]

Background Dyspepsia is a common gastrointestinal illness sometimes associated with Helicobacter pylori (H. pylori) infection. Screening and eradicating the bacterium reduces the risk of infection-related complications. The aim of this study was to determine the magnitude of H. pylori infection among dyspeptic patients and the effectiveness of triple eradication therapy at hospitals in Hawassa city, Ethiopia. Results The prevalence of H. pylori infection was 48.5%. The H. pylori eradication rate using first-line triple therapy was 83.8%. Eradication therapy failure is associated with previous exposure compared to no exposure (AOR: 4.8, 95% CI: 1.37-10.97), a regimen for 10-days compared to 14-days (AOR: 4.05, 95% CI: 1.42-11.55), and self-reported side effects compared to no report (AOR: 2.5, 95% CI: 1.12-5.97). Based on Morisky-eight scale 230 (79.0%) patients were adherent to their triple therapy. Participants with no reports of adverse effects showed increased odds of adherence to triple therapy compared to those who had reports (AOR = 2.45, 95% CI: 1.29-4.62). Conclusions This study demonstrated that about half of adult dyspeptic patients were infected with H. pylori, and moderate eradication was observed. Factors such as previous history of eradication therapy, duration of the eradication regimen, and perception of potential adverse effects are associated with eradication rate and should be considered during the initiation of eradication therapy. Keywords: Dyspepsia, H. Pylori, Eradication therapy, Fecal-antigen test, Hawassa, Author(s): Sintayehu Fekadu[sup.1], Seyife Kibru[sup.2], Sisay Tesfaye[sup.2], Tariku Egeno[sup.3], Alemu Tamiso[sup.4], Hizkel Engiso[sup.5] and Serawit Deyno[sup.5] Background Dyspepsia is a complex disorder with several distinct pathophysiologic mechanisms. 70% of cases [...]

Byline: Nitin. Vashistha, Siddharth. Singhal, Sandeep. Budhiraja, Dinesh. Singhal Background: Several risk calculating tools have been introduced into clinical practice to provide patients and clinicians with objective, individualised estimates of [...]

Mucormycosis, caused by fungi of order Mucorales, is a rare, life-threatening fungal infection whose incidence has been rising since the late 1990s (1). The main infection locations are pulmonary, rhino-orbito-cerebral, [...]

Byline: Jayaraman. Bharath, Dinesh. Niti, Supriya. Chauhan, Mani. Kumari, Vellathussery. Sunitha, K. Nagarajan Sir, Infratentorial empyemas are one of the most dreaded complications of chronic suppurative otitis media. The infratentorial [...]

Background Clarithromycin-containing triple therapy is commonly used to treat Helicobacter pylori infections. Clarithromycin resistance is the leading cause of H. pylori treatment failure. Understanding the specific mutations that occur in H. pylori strains that have evolved antibiotic resistance can help create a more effective and individualised antibiotic treatment plan. However, little is understood about the genetic reprogramming linked to clarithromycin exposure and the emergence of antibiotic resistance in H. pylori. Therefore, this study aims to identify compensatory mutations and biofilm formation associated with the development of clarithromycin resistance in H. pylori. Clarithromycin-sensitive H. pylori clinical isolates were induced to develop clarithromycin resistance through in vitro exposure to incrementally increasing concentration of the antibiotic. The genomes of the origin sensitive isolates (S), isogenic breakpoint (B), and resistant isolates (R) were sequenced. Single nucleotide variations (SNVs), and insertions or deletions (InDels) associated with the development of clarithromycin resistance were identified. Growth and biofilm production were also assessed. Results The S isolates with A2143G mutation in the 23S rRNA gene were successfully induced to be resistant. According to the data, antibiotic exposure may alter the expression of certain genes, including those that code for the Cag4/Cag protein, the vacuolating cytotoxin domain-containing protein, the sel1 repeat family protein, and the rsmh gene, which may increase the risk of developing and enhances virulence in H. pylori. Enhanced biofilm formation was detected among R isolates compared to B and S isolates. Furthermore, high polymorphism was also detected among the genes associated with biofilm production. Conclusions Therefore, this study suggests that H. pylori may acquire virulence factors while also developing antibiotic resistance due to clarithromycin exposure. Keywords: Helicobacter pylori, Whole genome sequencing, Virulence, Biofilm formation, Antibiotic resistance, Clarithromycin, Author(s): Naim Asyraf Rosli[sup.1], Anis Rageh Al-Maleki[sup.1,2], Mun Fai Loke[sup.3], Eng Guan Chua[sup.4], Mohammed Abdelfatah Alhoot[sup.5,6] and Jamuna Vadivelu[sup.7] Introduction Helicobacter pylori is a spiral-shaped Gram-negative bacteria that thrives in [...]