URP20 improves corneal injury caused by alkali burns combined with pathogenic bacterial infection in rats.

Corneal alkali burns often occur in industrial production and daily life, combined with infection, and may cause severe eye disease. Oxidative stress and neovascularization (NV) are important factors leading to a poor prognosis. URP20 is an antimicrobial peptide that has been proven to treat bacterial keratitis in rats through antibacterial and anti-NV effects. Therefore, in this study, the protective effect and influence mechanism of URP20 were explored in a rat model of alkali burn together with pathogenic bacteria (Staphylococcus aureus and Escherichia coli) infection. In addition, human umbilical vein endothelial cells (HUVECs) and human corneal epithelial cells (HCECs) were selected to verify the effects of URP20 on vascularization and oxidative stress. The results showed that URP20 treatment could protect corneal tissue, reduce corneal turbidity, and reduce the NV pathological score. Furthermore, URP20 significantly inhibited the expression of the vascularization marker proteins VEGFR2 and CD31. URP20 also reduced the migration ability of HUVECs. In terms of oxidative stress, URP20 significantly upregulated SOD and GSH contents in corneal tissue and HCECs (treated with 200 µM H2O2) and promoted the expression of the antioxidant protein Nrf2/HO-1. At the same time, MDA and ROS levels were also inhibited. In conclusion, URP20 could improve corneal injury combined with bacterial infection in rats caused by alkali burns through antibacterial, anti-NV, and antioxidant activities.

Can we predict the risk of esophageal stricture after caustic injury?

Nonoperative management of severe caustic injuries has demonstrated its feasibility, avoiding the need for emergency esogastric resection and resulting in low mortality rates. However, leaving superficial necrosis in place could increase the risk of esophageal stricture development. Data on the risk factors of esophageal stricture secondary to caustic ingestion are scarce. The aim of our study was to identify the risk factors for esophageal strictures after caustic ingestion at admission. From February 2015 to March 2021, all consecutive patients with esophageal or gastric caustic injury score ≥ II according to the Zargar classification were retrospectively analyzed. For each patient, we collected over 50 criteria at admission to the emergency room and then selected among them 20 criteria with the best clinical relevance and limited missing data for risk factor analyses. Among the 184 patients included in this study, 37 developed esophageal strictures (cumulative rate 29.4%). All esophageal strictures occurred within 3 months. In multivariate analyses, the risk factors for esophageal strictures were voluntary ingestion (cause-specific hazard ratio 5.92; 95% confidence interval 1.76-19.95, P = 0.004), Zargar's esophageal score ≥ III (cause-specific hazard ratio 14.30; 95% confidence interval 6.07-33.67, P < 0.001), and severe ear, nose, and throat lesions (cause-specific hazard ratio 2.15; 95% confidence interval 1.09-4.22, P = 0.027). Intentional ingestion, severe endoscopic grade, and severe ENT lesions were identified as risk factors for esophageal stricture following caustic ingestion. Preventive measures for this population require further evaluation.

Endoscopic Dilatation with Ultrathin Endoscope Assisted Method for Esophageal and Pyloric Stricture related Corrosive Injury: 4 Years Case Series Study.

Corrosive injuries (CI) become medical problems related complications include esophageal, pyloric stricture and squamous cell carcinoma, physical and quality of life. Endoscopic (ED) dilatation is primary therapy. The ultrathin endoscope-assisted method is potentially safe and useful in avoiding technical failure. Describe clinical outcomes of ED ED-related CI including successful, refractory, recurrent, and complications-related procedures. Case series study of esophageal and/or pyloric stricture patients after CI who underwent dilatation at Soetomo General Hospital (July 2018 - July 2022). One - biweekly ED using Through The Scope (TTS) balloon or Savary Bougie dilator. The target diameter is 14mm. Fifteen patients with stricture-related CI. Eleven patients underwent ED with a total of 73 procedures. Mean age 31,45 years, predominantly male patients (6), suicide attempt (7), acid agent (9), located at esophagus (3), pylorus (3), or both (5). Number of esophageal dilatation to achieve the target of 14 mm was 1-2 and 2-15 procedures for simple and complex stricture. Five esophageal strictures were successfully dilated but 2 patients were recurrent and 3 cases were refractory to ED. Pyloric dilatation resulted in a lower success rate. Recurrent and refractory cases were 5 and 3 patients respectively. ED with ultrathin endoscope method is useful for traversing guidewire during ED. Ongoing inflammation and fibrosis were linked to recurrent and refractory stricture.

Luteolin ameliorates cornea stromal collagen degradation and inflammatory damage in rats with corneal alkali burn.

Corneal alkali burn (AB) is a blindness-causing ocular trauma commonly seen in clinics. An excessive inflammatory reaction and stromal collagen degradation contribute to corneal pathological damage. Luteolin (LUT) has been studied for its anti-inflammatory effects. In this study, the effect of LUT on cornea stromal collagen degradation and inflammatory damage in rats with corneal alkali burn was investigated. After corneal alkali burn, rats were randomly assigned to the AB group and AB + LUT group and received an injection of saline and LUT (200 mg/kg) once daily. Subsequently, corneal opacity, epithelial defects, inflammation and neovascularization (NV) were observed and recorded on Days 1, 2, 3, 7 and 14 post-injury. The concentration of LUT in ocular surface tissues and anterior chamber, as well as the levels of collagen degradation, inflammatory cytokines, matrix metalloproteinases (MMPs) and their activity in the cornea were detected. Human corneal fibroblasts (HCFs) were co-cultured with interleukin (IL)-1ß and LUT. Cell proliferation and apoptosis were assessed by CCK-8 assay and flow cytometry respectively. Measurement of hydroxyproline (HYP) in culture supernatants was used to quantify the amount of collagen degradation. Plasmin activity was also assessed. ELISA or real-time PCR was used to detect the production of matrix metalloproteinases (MMPs), IL-8, IL-6 and monocyte chemotactic protein (MCP)-1. Furthermore, the immunoblot method was used to assess the phosphorylation of mitogen-activated protein kinases (MAPKs), transforming growth factor-ß-activated kinase (TAK)-1, activator protein-1 (AP-1) and inhibitory protein IκB-α. At last, immunofluorescence staining helped to develop nuclear factor (NF)-κB. LUT was detectable in ocular tissues and anterior chamber after intraperitoneal injection. An intraperitoneal injection of LUT ameliorated alkali burn-elicited corneal opacity, corneal epithelial defects, collagen degradation, NV, and the infiltration of inflammatory cells. The mRNA expressions of IL-1ß, IL-6, MCP-1, vascular endothelial growth factor (VEGF)-A, and MMPs in corneal tissue were downregulated by LUT intervention. And its administration reduced the protein levels of IL-1ß, collagenases, and MMP activity. Furthermore, in vitro study showed that LUT inhibited IL-1ß-induced type I collagen degradation and the release of inflammatory cytokines and chemokines by corneal stromal fibroblasts. LUT also inhibited the IL-1ß-induced activation of TAK-1, mitogen-activated protein kinase (MAPK), c-Jun, and NF-κB signaling pathways in these cells. Our results demonstrate that LUT inhibited alkali burn-stimulated collagen breakdown and corneal inflammation, most likely by attenuating the IL-1ß signaling pathway. LUT may therefore prove to be of clinical value for treating corneal alkali burns.

Complex Refractory Esophageal Stricture Due to Chronic Gasoline Ingestion: A Case Report.

Esophageal stricture is a narrowing of the esophageal lumen which is often characterized by impaired swallowing or dysphagia. It can be induced by inflammation, fibrosis or neoplasia which damages the mucosa and/or submucosa of the esophagus. Corrosive substance ingestion is one of the major causes of esophageal stricture, particularly in children and young adults. For instance, accidental ingestion or attempted suicide with corrosive household products is not uncommon. Gasoline is a liquid mixture of aliphatic hydrocarbons derived from the fractional distillation of petroleum, which is then combined with additives such as isooctane and aromatic hydrocarbons (e.g., toluene and benzene). Gasoline also contains several other additives including ethanol, methanol and formaldehyde, which make it a corrosive agent. Interestingly, to the best of our knowledge, the incidence of esophageal stricture caused by chronic gasoline ingestion has not been reported. In this paper, we report the case of a patient with dysphagia due to complex esophageal stricture due to chronic gasoline ingestion who underwent a series of esophago-gastro-duodenoscopy (EGD) procedures and repeated esophageal dilation.

Salubrinal Ameliorates Inflammation and Neovascularization via the Caspase 3/Enos Signaling in an Alkaline-Induced Rat Corneal Neovascularization Model.

Background and Objectives: Ocular alkaline burn is a clinical emergency that can cause permanent vision loss due to limbal stem cell deficiency and corneal neovascularization (CNV). Although the basic pathogenetic mechanisms are considered to be acute oxidative stress and corneal neovascularization triggered by inflammation, the underlying intracellular mechanisms have not been clearly elucidated. The aim of this study was to investigate the role of endoplasmic reticulum (ER) stress on inflammation and neovascularization, and the effect of the ER stress inhibitor salubrinal (SLB), as a novel treatment in a corneal alkaline burn model in rats. Methods: Chemical burns were created by cautery for 4 s using a rod coated with 75% silver nitrate and 25% potassium nitrate in the corneal center for the corneal neovascularization (CNV) model. Twenty-eight Wistar albino rats were divided into four groups: SHAM, CNV, CNV + SLB, and CNV + bevacizumab (BVC). After the CNV model was applied to the right eye, a single subconjunctival dose (0.05 mL) of 1 mg/kg salubrinal was injected into both eyes in the CNV + SLB group. A total of 1.25 mg/mL of subconjunctival BVC was administered to the CNV + BVC group. Fourteen days after experimental modeling and drug administration, half of the globes were placed in liquid nitrogen and stored at -20 °C until biochemical analysis. The remaining tissues were collected and fixed in 10% buffered formalin for histopathological and immunohistochemical analysis. Three qualitative agents from three different pathways were chosen: TNFR for inflammation, endothelial nitric oxide synthase (e-NOS) for vascular endothelial growth factor (VEGF)-mediated vascular permeability, and caspase-3 for cellular apoptosis. Results: Significantly lower caspase-3 and eNOS levels were detected in the CNV + SLB and CNV + BVC groups than in the CNV group. Additionally, histopathological evaluation revealed a significant decrease in neovascularization, inflammatory cell infiltration, and fibroblast activity in the CNV + SLB and CNV + BVC groups. The endoplasmic reticulum stress inhibitor, salubrinal, administered to the treatment group, attenuated apoptosis (caspase-3) and inflammation (e-NOS). In the control group (left eyes of the SLB group), salubrinal did not have a toxic effect on the healthy corneas. Conclusion: The ER stress pathway plays an important role in angiogenesis after alkaline corneal burns, and treatment with SLB modulates this pathway, reducing caspase-3 and eNOS levels. Further studies are needed to understand the molecular mechanisms altered by SLB-mediated therapy. The fact that more than one mechanism plays a role in the pathogenesis of CNV may require the use of more than one molecule in treatment. SLB has the potential to affect multiple steps in CNV pathogenesis, both in terms of reducing ER stress and regulating cellular homeostasis by inhibiting the core event of integrated stress response (ISR). Therefore, it can be used as a new treatment option and as a strengthening agent for existing treatments. Although blockade of intracellular organelle stress pathways has shown promising results in experimental studies, more in-depth research is needed before it can be used in routine practice. To the best of our knowledge, this study is the first to report the role of ER stress in corneal injury.

[The role of endosonography in the treatment of chemical ulcerative-necrotic burns of the esophagus]. / Rol' endosonografii v opredelenii taktiki lecheniya khimicheskogo yazvenno-nekroticheskogo ozhoga pishchevoda: klinicheskoe nablyudenie.

The authors present ultrasonography-assisted endoscopic diagnosis of chemical burn of the esophagus. This method early predicted decompensated cicatricial stenosis of the esophagus that was valuable to determine treatment strategy. Preventive mini-invasive endoscopic percutaneous gastrostomy provided adequate enteral nutrition in a patient with decompensated esophageal stenosis before reconstructive surgery.

[Histological evaluation of esophageal stricture in children with caustic burn]. / Patogistologicheskaya kharakteristika striktury pishchevoda pri kausticheskom ozhoge u detei.

OBJECTIVE: To analyze histological features of esophageal strictures in children with chemical burn following ingestion of household products containing sodium (potassium) hypochlorite, sodium (potassium) hydroxide. MATERIAL AND METHODS: We analyzed 3 children with complicated caustic esophageal burns. Children at the time of swallowing the caustic were 26.3±4.1 months. Multiple dilatations of esophageal stricture were ineffective. Therefore, extirpation or subtotal resection of the esophagus and esophagocoloplasty were performed. We stained specimens using hematoxylin and eosin, as well as Masson's trichrome. RESULTS: Severe esophageal burns caused by sodium (potassium) hydroxide and/or sodium hypochlorite are followed by irreversible tissue lesions and non-dilatable stricture. Strictures are localized in the areas of physiological narrowing of the esophagus. The longest stricture follows ingestion of liquid substance. Histological properties include atrophy of glands and mucous membrane, muscle layer substitution by connective tissue and diffuse sclerosis of esophageal wall. CONCLUSION: Non-dilatable esophageal stricture following caustic burn in children is due to irreversible morphological lesion of esophageal wall with mucous layer atrophy and sclerosis of all layers.

AIP1 suppresses neovascularization by inhibiting the NOX4-induced NLRP3/NLRP6 imbalance in a murine corneal alkali burn model.

BACKGROUND: Apoptosis signal-regulating kinase 1-interacting protein 1 (AIP1) participates in inflammatory neovascularization induction. NADPH oxidase 4 (NOX4) produces reactive oxygen species (ROS), leading to an imbalance in nucleotide-binding oligomerization domain-like receptor family pyrin domain containing 3 (NLRP3) and NLR family pyrin domain containing 6 (NLRP6) expression. The mechanisms of AIP1, NOX4, ROS and inflammasomes in corneal neovascularization were studied herein. METHODS: C57BL/6 and AIP1-knockout mice were used in this study. The alkali burn procedure was performed on the right eye. Adenovirus encoding AIP1 plus green fluorescence protein (GFP) (Ad-AIP1-GFP) or GFP alone was injected into the right anterior chamber, GLX351322 was applied as a NOX4 inhibitor, and then corneal neovascularization was scored. The expression of related genes was measured by quantitative real-time polymerase chain reaction, western blotting and immunofluorescence staining. 2',7'-Dichlorofluorescin diacetate staining was used to determine the ROS levels. RESULTS: The expression of AIP1 was decreased, while that of cleaved interleukin-1ß (clv-IL-1ß) and vascular endothelial growth factor A (VEGFa) was increased after alkali burn injury. NOX4 expression was increased, the imbalance in NLRP3/NLRP6 was exacerbated, and corneal neovascularization was increased significantly in AIP1-knockout mice compared with those in C57BL/6 mice after alkali burns. These effects were reversed by AIP1 overexpression. NLRP3/NLRP6 expression was imbalanced after alkali burns. GLX351322 reversed the imbalance in NLRP3/NLRP6 by reducing the ROS levels. This treatment also reduced the expression of clv-IL-1ß and VEGFa, suppressing neovascularization. CONCLUSIONS: AIP1 and NOX4 can regulate corneal inflammation and neovascularization after alkali burn injury. Based on the pathogenesis of corneal neovascularization, these findings are expected to provide new therapeutic strategies for patients. Corneal alkali burn injury is a common type of ocular injury that is difficult to treat in the clinic. The cornea is a clear and avascular tissue. Corneal neovascularization after alkali burn injury is a serious complication; it not only seriously affects the patient's vision but also is the main reason for failed corneal transplantation. Corneal neovascularization affects approximately 1.4 million patients a year. We show for the first time that AIP1 and NOX4 can regulate corneal inflammation and neovascularization after alkali burns. The expression of AIP1 was decreased, while that of clv-IL-1ß and VEGFa was increased after alkali burns. We tried to elucidate the specific molecular mechanisms by which AIP1 regulates corneal neovascularization. NOX4 activation was due to decreased AIP1 expression in murine corneas with alkali burns. NOX4 expression was increased, the imbalance in NLRP3/NLRP6 was exacerbated, and corneal neovascularization was increased significantly in AIP1-knockout mice compared with those in C57BL/6 mice after alkali burns. These effects were reversed by AIP1 overexpression. Additionally, NLRP3/NLRP6 expression was unbalanced, with NLRP3 activation and NLRP6 suppression in the corneal alkali burn murine model. Eye drops containing GLX351322, a NOX4 inhibitor, reversed the imbalance in NLRP3/NLRP6 by reducing ROS expression. This treatment also reduced the expression of clv-IL-1ß and VEGFa, reducing neovascularization. Therefore, we provide new gene therapeutic strategies for patients. With the development of neovascularization therapy, we believe that in addition to corneal transplantation, new drug or gene therapies can achieve better results. Video Abstract.

Emergency computed tomography evaluation of caustic ingestion.

Computed tomography (CT) is used increasingly for the emergency assessment of caustic injuries and the need for emergency endoscopy has been challenged. The study evaluates outcomes of caustic ingestion in the modern era and the feasibility of abandoning emergency endoscopy. Between 2013 and 2019, 414 patients (197 men, median age 42 years) were admitted for caustic ingestion. Emergency and long-term outcomes of patients managed by CT and endoscopy (n = 120) and by CT alone (n = 294) were compared. Propensity score-based analysis was performed to limit bias of between-group comparison. A standard mortality ratio (SMR) was used to compare the observed mortality with the expected mortality in the general French population. Complications occurred in 97 (23%) patients and 17 (4.1%) patients died within 90 days of ingestion. Among 359 patients who underwent nonoperative management, 51 (14%) experienced complications and 7 (2%) died. Of 55 patients who underwent emergency surgery, 46 (84%) experienced complications and 10 (18%) died. The SMR was 8.4 for whole cohort, 5.5 after nonoperative management, and 19.3 after emergency surgery. On multivariate analysis, intentional ingestion (P < 0.016), age (P < 0.0001) and the CT grade of esophageal injuries (P < 0.0001) were independent predictors of survival. The CT grade of esophageal injuries was the only independent predictor of success (P < 0.0001). Crude and propensity match analysis showed similar survival in patients managed with and without endoscopy. CT evaluation alone can be safely used for the emergency management of caustic ingestion.

Outcomes of the management of corrosive injuries of the upper digestive tract in a tertiary care center.

Esophageal stricture is the most common delayed sequelae of aerodigestive tract corrosive injuries. Early endoscopic dilatation is an integral part of corrosive injury management. Self-dilatation of the esophagus is effective in preventing stricture recurrence. In this prospective study, we included patients with corrosive aerodigestive tract injury from January 2009 to December 2020. We analyzed the outcome of the endoscopic dilatation and self-dilatation treatments administered to patients with a corrosive esophageal stricture. Among 295 patients, 164 had an esophageal injury, 73 had esophago-gastric injury, 55 had a gastric injury, and 3 had the pharyngeal injury. Of the 295 patients, 194 (81.85%) underwent dilatation, and 13 patients with diffuse esophageal injury underwent upfront surgery. Successful dilatation was performed in 169 (87.11%) patients. Of the 68 patients undergoing self-dilatation, 63 patients achieved nutritional autonomy by 28 days. Early endoscopic dilatation effectively prevents surgery, and self-dilatation appears promising to prevent recurrent esophageal stricture.

Unusual wound with increasing prevalence caused by artificial fingernail glue.

Clinical introductionA healthy 17-year-old girl presents with a wound on her left medial thigh (figure 1). Two days earlier while applying acrylic nail tips, she spilled nail glue on her jeans in the area of concern. Despite noticing an immediate irritable sensation, she did not perform any first aid nor did she remove her clothing to check the underlying skin.emermed;39/3/185/F1F1F1Figure 1Wound left medial thigh. QUESTION: What is the pathological process of this wound?De-epithelialisation due to removal of clothing glued to skin.Chemical burn.Partial thickness thermal burn.Allergic reaction to nail glue. For answer see page 02.

The effects of hesperidin on stricture formation in corrosive esophageal burns: an experimental study.

AIM/BACKGROUND: Esophageal strictures in children that develop as a result of accidental ingestion of corrosive substances remain an important health problem. The purpose of this study is to determine the effects of Hesperidin, an effective bioflavonoid in the proliferative and exudative phase of inflammation, on the stricture formation in corrosive esophageal burns. METHODS: Experimental esophageal burns in rats were created using a modified Gehanno and Guedon model with 20% NaOH. Rats were divided into 5 groups. In the Sham group, the distal esophagus was prepared and cannulated according to the model, but no NaOH was administrated. The esophageal burn was created with NaOH in the other groups. The burned groups were divided into two groups as untreated (T14, T21) and treated with 100 mg/kg/day Hesperidin (H14, H21) intraperitoneally, and these groups were divided into two according to their sacrification periods (14 and 21 days). Inflammation, fibrosis, and necrosis were graded by histopathological evaluation in all groups. The efficacy of treatment was evaluated using the weight of rats, stenosis index, and histopathological parameters. RESULTS: Histopathologic damage scores such as inflammation, necrosis, and fibrosis were lower in the H14 and H21 groups and higher in the T14 and T21 groups. And also stenosis index was found higher in T14 and T21 groups (p < 0.05), while it was similar to the Sham group in H14 and H21 groups. No statistically significant difference was found between the H14 and H21 groups in terms of stenosis index. When weights of the rats at the beginning and end of the experiment were compared, weights of the H14 and H21 groups and the Sham group were similar. There was a significant decrease in the weight of the rats in the T14 and T21 groups (p < 0.001). CONCLUSIONS: This study is the first to use Hesperidin in preventing esophageal damage in an esophageal caustic burn model. It was shown that Hesperidin was effective in reducing macroscopic and microscopic histopathologic damage in the corrosive esophageal burn model, preventing the stricture formation, and has positive effects on nutrition in rats with an esophageal burn.

A prospective randomized controlled trial of omeprazole for preventing esophageal stricture in grade 2b and 3a corrosive esophageal injuries.

OBJECTIVES: Esophageal stricture is a significant complication of grade 2b and 3a esophageal injuries and causes much patient suffering. Preventing strictures would be beneficial to patients but there are currently no proven effective drugs. This study aimed to evaluate the effect of omeprazole for preventing esophageal stricture in adults with grade 2b and 3a corrosive esophageal injuries. METHODS: This study was an open single-center prospective randomized controlled trial that took place from April 2018 to January 2020. Patients were randomized to standard treatment or 80 mg/day intravenously × 3 days followed by 40 mg/day orally for 4 weeks. They were endoscoped at baseline and 4 weeks post discharge. Strictures were confirmed radiologically. RESULTS: 20 patients were enrolled: 15 with grade 2b and five with grade 3a injuries. Standard care and omeprazole groups numbered 10 each. At 1 month, seven and two patients developed strictures in the standard and omeprazole groups, respectively, p = 0.024, for a risk reduction of 71.4%. CONCLUSIONS: Omeprazole reduced the risk of short-term developing esophageal strictures following grade 2b and 3a corrosive esophageal injuries. Larger studies are needed to reconfirm this finding. Thai Clinical Trials Registry (TCTR) number TCTR20190504001.

COMPLETE THORACIC ESOPHAGUS OBLITERATION: CLINICAL CASE REPORT.

Using the example of a clinical case, to present the management features of a patient with complete esophageal obliteration as a chemical burn result, the surgical intervention features in case of a non-standard situation during the operation, and the treatment results analyze. It was described a clinical case of 41-year-old patient with thoracic esophagus obliteration due to extended post-burn cicatricial esophageal stricture, dysphagia of IV degree in very severe general condition. Stamm-Senn-Kader's gastrostomy was performed as a first step of surgical treatment. Angiography and embolization of the right colic artery and it's branches was performed in 8 months while preserving the middle colic artery. In 20 days the cologastroanastomosis and feeding colostomy on the right chest wall were performed. In 10 days after the colostomy was disattached from the chest wall, the end-to-side esophagocoloanastomosis was performed intrapleurally. In one month after the third surgery and restoration of the food passage by the natural way, closure of the contact gastrostomy was performed. During the observation over the patient (8 years) the postoperative complications were not observed. The patient survived. The proposed staged surgical treatment tactics of patients with complete esophageal obliteration due to post-burn esophageal stricture, dysphagia of IV degree presents effective treatment results and a significant improvement in the patient's life quality.

Outcomes of Endoscopic Dilation in Patients with Esophageal Anastomotic Strictures: Comparison Between Different Etiologies.

BACKGROUND AND AIMS: This retrospective study was aimed at assessing the efficacy of endoscopic dilation for esophageal anastomotic strictures, and to compare response between caustic anastomotic strictures (CAS) and non-caustic anastomotic strictures (NCAS). MATERIALS AND METHODS: Patients with anastomotic strictures (enrolled during January 1996-December 2015) were analyzed. Short- and long-term outcomes of dilation, in terms of clinical success, refractory, and recurrent strictures were compared between NCAS and CAS. Patients with refractory and recurrent strictures were managed with adjunctive therapy including intralesional steroids. Factors predicting refractoriness at start of dilation and reasons for more than ten lifetime dilations were also evaluated. RESULTS: Of the 142 patients, 124 (mean age-44.02; males-74) underwent dilation. Clinical success was achieved in 113 (91.3%) patients requiring a median [Interquartile range (IQR)] of 4 (2-10) sessions. The number of dilations to achieve clinical success, refractory strictures, and recurrent strictures, and the use of adjunctive therapy were significantly higher for CAS than for NCAS. Intralesional steroid use decreased periodic dilation index (PDI) significantly in CAS. Caustic etiology and starting dilation diameter of < 10 mm were found to be predictors of refractoriness, with the former alone being an independent predictor of more than ten lifetime dilations. No patient had free perforation; however, five required revision surgery. CONCLUSION: Patients with CAS fared worse than those with NCAS in terms of number of dilations, refractoriness, recurrence of strictures, and need of adjunctive therapy. Endoscopic dilation can successfully ameliorate dysphagia due to anastomotic strictures in a majority of patients.

Factors affecting the outcome of endoscopic dilatation in refractory post-corrosive oesophageal stricture in Egyptian children: a single-centre study.

BACKGROUND: An important complication of corrosive ingestion is oesophageal stricture. Improvements in endoscopes and accessories have supported an increase in the number of patients who are conservatively treated with endoscopic dilations. In this study, we aimed to detect factors affecting the outcome of endoscopic dilatation for refractory post-corrosive oesophageal stricture. METHODS: This study was carried out in the Paediatric Endoscopy Unit in the Children's Hospital and included 100 children older than 2 years of age of both sexes who had an established diagnosis of post-corrosive oesophageal stricture on repeated endoscopic dilatation sessions. The duration of the condition was more than 6 months, and dilatation failed to achieve a diameter of 14 mm during the first five sessions at 2-week intervals (refractory), excluding other causes of oesophageal stricture. RESULTS: Males represented 63% of patients. The mean age of enrolled children was 5.9 ± 2.6 years; 90% of patients ingested an alkaline corrosive substance (potash). The total number of dilatation sessions ranged from 16 to 100, with a mean number of sessions ranging from 37.2 ± 14.9. Fifty-four patients (54%) were well controlled by regular endoscopic dilatation with good clinical and endoscopic outcomes, and no more dilatations were needed. CONCLUSION: Endoscopic dilation is an effective method for managing refractory post-corrosive oesophageal strictures that require a long follow-up period. There are a lot of factors affecting the outcome.

Emergency Computed Tomography Predicts Caustic Esophageal Stricture Formation.

BACKGROUND: Endoscopy is the best predictor of stricture formation after caustic ingestion. OBJECTIVE: Our aim was to compare the accuracy of emergency computed tomography (CT) and endoscopy in predicting risks of esophageal stricture. METHODS: We describe a CT classification of esophageal caustic injuries: Grade I show normal esophagus; Grade IIa display internal enhancement of the esophageal mucosa and enhancement of the outer wall conferring a "target" aspect; Grade IIb present as a fine rim of external esophageal wall enhancement. In 152 patients (56 males, median age 45) who underwent esophageal preservation after caustic ingestion we compared the accuracy of the CT and endoscopic (Zargar) classifications in predicting esophageal stricture. RESULTS: On endoscopy esophageal injuries were classified as grade 1 (n = 50; 33%), grade 2a (n = 11; 7%), grade 2b (n = 19; 13%), grade 3a (n = 14; 9%), and grade 3b (n = 58; 38%). On CT, 47 (31%) patients had grade I, 47 (31%) had grade IIa and 58 (38%) had grade IIb esophageal injuries. Fifty-six (37%) patients developed esophageal strictures. The risk of esophageal stricture formation was 0%, 17%, and 83%, for grade I, IIa, and IIb CT injuries and 0, 0, 28, 50, and 76% for endoscopic grade 1, 2a, 2b, and 3a and 3b injuries, respectively. ROC curve analysis at 120 days after ingestion showed that CT outperformed endoscopy in predicting stricture formation (AUC: 85.1 [95% CI, 74.9-95.3] vs 77.8 [95% CI, 66.5-89.0], P = 0.047) and did just as well as a combined CT-endoscopy algorithm (AUC: 85.8 [95% CI, 76.5-95.0] vs 85.1 [95% CI, 74.9-95.3], P = 0.73). CONCLUSION: Emergency CT outperforms endoscopy in predicting esophageal stricture formation after caustic ingestion. Emergency endoscopy evaluation after caustic ingestion is not indispensable.

The Role of Microglia and Peripheral Monocytes in Retinal Damage after Corneal Chemical Injury.

Eyes that have experienced alkali burn to the surface are excessively susceptible to subsequent severe glaucoma and retinal ganglion cell loss, despite maximal efforts to prevent or slow down the disease. Recently, we have shown, in mice and rabbits, that such retinal damage is neither mediated by the alkali itself reaching the retina nor by intraocular pressure elevation. Rather, it is caused by the up-regulation of tumor necrosis factor-α (TNF-α), which rapidly diffuses posteriorly, causing retinal ganglion cell apoptosis and CD45+ cell activation. Herein, we investigated the involvement of peripheral blood monocytes and microglia in retinal damage. Using CX3CR1+/EGFP::CCR2+/RFP reporter mice and bone marrow chimeras, we show that peripheral CX3CR1+CD45hiCD11b+MHC-II+ monocytes infiltrate into the retina from the optic nerve at 24 hours after the burn and release further TNF-α. A secondary source of peripheral monocyte response originates from a rare population of patrolling myeloid CCR2+ cells of the retina that differentiate into CX3CR1+ macrophages within hours after the injury. As a result, CX3CR1+CD45loCD11b+ microglia become reactive at 7 days, causing further TNF-α release. Prompt TNF-α inhibition after corneal burn suppresses monocyte infiltration and microglia activation, and protects the retina. This study may prove relevant to other injuries of the central nervous system.

Short-term Effects of Mitomycin C Infiltration for Caustic Oesophageal Strictures in Children.

OBJECTIVES: The aim of this study was to investigate the efficacy and safety of endoscopic local infiltration of mitomycin C (MMC) after oesophageal dilation for children suffering from refractory postcorrosive oesophageal stricture (OS). METHODS: Children referred to Cairo University Specialized Paediatric Hospital with refractory postcorrosive OS during the period from March 2016 to August 2017 were included in this study. MMC was infiltrated endoscopically at the stricture site by the end of the dilation session. The measured outcomes were dysphagia score (DS) and periodic dilation index (PDI). RESULTS: During the inclusion period of the presented study, 17 children met the inclusion criteria. There were 7 boys and 10 girls. During the follow-up period, an average of 3.8 dilation sessions with MMC infiltration per case were performed, using a total dose of 1 mg each session. The median follow-up period was 9.5 months. The median DS improved from DS 3 before application of MMC to DS 0 at the last follow-up (P < 0.001). Additionally, the median PDI declined from 1 to 0.75 after MMC application (P = 0.052). Sixteen cases (94%) became dysphagia free after 6 months. Seven patients experienced postdilation minor bleeding that was spontaneously resolved, not triggering blood transfusion. There were no infiltration-related complications in the included series. CONCLUSION: Stricture-site MMC endoscopic infiltration by the end of a dilation session proved to be safe and effective in improving the DS and PDI.