BACKGROUND: Children who experience alkaline injury are at risk for the development of esophageal strictures and the need for esophageal dilations.
OBJECTIVE: We aimed to assess predictors for a higher number of esophageal dilatations in children following alkali ingestion.
METHODS: Single-center retrospective cohort study including children who underwent esophagogastroduodenoscopy (EGD) after alkali ingestion. Possible predictive factors for the need for esophageal dilatations were evaluated.
RESULTS: A total of 34 patients were included, and 19 were female (55.9%). The median age at the time of the accidents was 20.6 months (IQR 15-30.7). All alkali ingestions were accidental, in all cases involving liquid products, and most (24/34; 70%) occurred at the child\'s home. Homemade liquid soap was the agent in half of the cases. The most frequently reported symptom at presentation was vomiting (22/34, 64.7%). The median follow-up time was 3.2 years (IQR 1.1-7.4). On follow-up, the median number of esophageal dilatations required for these patients was 12.5 (IQR 0-34). Among demographic factors, male gender (P=0.04), ingestion of homemade products (P<0.01), and accidents happening outside of the household environment (P=0.02) were associated with a greater number of esophageal dilations on follow-up. An endoscopic classification Zargar of 2B or higher (P=0.03), the presence of stricture at the time of the second EGD (P=0.01), and gastroesophageal reflux disease (GERD) as a late complication (P=0.01) were also associated with a greater number of esophageal dilations on long term follow-up.
CONCLUSIONS: Beyond the endoscopic classification severity - a well-known risk factor for the strictures after alkali ingestions, we found that male gender, accidents with homemade products, and accidents occurring outside the household environment were significantly associated with a greater number of esophageal dilatations in the long-term follow-up of children following alkali ingestion.

UNASSIGNED: The integrity of the corneal epithelium is essential in maintaining normal corneal function. Conditions disrupting the corneal epithelial layer range from chemical burns to dry eye disease and may result in impairment of both corneal transparency and sensation. Identifying factors that regulate corneal wound healing is key for the development of new treatment strategies. Here, we investigated a direct role of mitochondria in corneal wound healing via mitochondria transplantation.
UNASSIGNED: Human corneal epithelial cells (hCECs) were isolated from human corneas and incubated with mitochondria which were isolated from human ARPE-19 cells. We determined the effect of mitochondria transplantation on wound healing and proliferation of hCECs. In vivo, we used a mouse model of corneal chemical injury. Mitochondria were isolated from mouse livers and topically applied to the ocular surface following injury. We evaluated the time of wound repair, corneal re-epithelization, and stromal abnormalities.
UNASSIGNED: Mitochondria transplantation induced the proliferation and wound healing of primary hCECs. Further, mitochondria transplantation promoted wound healing in vivo. Specifically, mice receiving mitochondria recovered twice as fast as control mice following corneal injury, presenting both enhanced and improved repair. Corneas treated with mitochondria demonstrated the re-epithelization of the wound area to a multi-layer appearance, compared to thinning and complete loss of the epithelium in control mice. Mitochondria transplantation also prevented the thickening and disorganization of the corneal stromal lamella, restoring normal corneal dehydration.
UNASSIGNED: Mitochondria promote corneal re-epithelization and wound healing. Augmentation of mitochondria levels via mitochondria transplantation may serve as an effective treatment for inducing the rapid repair of corneal epithelial defects.

Caustic ingestion in children is a public health problem; it is mainly due to domestic accidents due to improper packaging and storage of caustic products. It is a medical and surgical emergency whose management is multidisciplinary. The lesions caused by the accidental ingestion of caustics can affect the functional and vital prognosis in 10% of cases.
A retrospective, descriptive study from January 2020 to December 2022 (2 years), carried out in the emergency department of the General Reference Hospital of Niamey (Niger). The study included patients less than 15 years old admitted for ingesting a caustic product.
Our study included 17 patients. The average age was 5 years, with age extremes of 2 to 11 years. We noted a male predominance with a sex ratio (M/F) of 2.4. Ingestion of caustic products was accidental in all cases. The caustic product was caustic soda in 59%. The average quantity of product ingested was 5 ml (2 ml to 20 ml). The average consultation time was 3 days (3 hours to 15 days). Clinically, dysphagia was the most functional sign, represented by 13 cases, or 76%. Regarding general signs, 3 patients (18%) were admitted with fever; blood pressure was normal in 15 patients (88%); and 2 patients (18%) were admitted in a state of shock. The respiratory rate was normal in 14 patients (82%). Four patients (24%) were admitted in a state of deterioration in the general condition associated with severe malnutrition and dehydration. On physical examination, 2 patients (12%) presented with abdominal defense at the epigastric level. Examination of the ENT sphere revealed benign buccopharyngeal ulcerations in 2 patients (12%). Esogastroduodenal fibroscopy was performed in 4 patients (24%). The caustic lesions observed in the esophagus were: Zargar stage I at 25%, stage Ila at 50%, and stage Illb at 25%. In the stomach, the lesions were Zargar stage I in 75% of cases and stage III in 25% of cases. An injected thoracic-abdominopelvic computed tomography (CT) was performed in 3 patients (18%). It revealed a lack of enhancement of the esophageal wall compatible with esophageal necrosis in one patient. An esophagogastroduodenal transit was performed in 8 patients (47%) admitted more than 72 hours after ingestion of the caustic. They showed esophageal stenoses longer than 3 cm in 3 patients, multiple esophageal stenoses in 2 patients, a single esophageal stenosis in 2 patients, and a single antropyloric stenosis in 1 patient. Therapeutically, all patients benefited from antiemetics to avoid vomiting and proton pump inhibitors. Intravenous antibiotic prophylaxis with third-generation cephalosporin was administered to 12 patients (71%). Corticosteroid therapy based on IV prednisolone at a dose of 1 g/1.73 m2 per day was used to limit or prevent stenoses in 9 patients (53%). Parenteral nutrition was administered to 7 patients (41%). Endoscopic dilations were performed in 2 patients (12%). Emergency surgical treatment was performed in 7 patients (41%): 3 patients underwent transitional feeding gastrostomies; in 3 others, esophagoplasties by colon transplant were performed, and 1 patient was treated by stripping of the esophagus associated with total gastrectomy. The postoperative course was marked by a leak of esocolic anastomosis in one patient for whom conservative treatment was performed with good progress. The average length of hospital stay was 5 days (1-32 days).
Accidental caustic ingestions can have serious consequences. Preventing these accidents relies on raising public awareness of the dangers associated with improper storage of these products.

Severe corneal injury can lead to blindness even after prompt treatment. 14-3-3zeta, a member of an adaptor protein family, contributes to tissue repair by enhancing cellular viability and inhibiting fibrosis and inflammation in renal disease or arthritis. However, its role in corneal regeneration is less studied. In this study, filter disc of 2-mm diameter soaked in sodium hydroxide with a concentration of 0.5 N was placed at the center of the cornea for 30 s to establish a mouse model of corneal alkali injury. We found that 14-3-3zeta, which is mainly expressed in the epithelial layer, was upregulated following injury. Overexpression of 14-3-3zeta in ocular tissues via adeno-associated virus-mediated subconjunctival delivery promoted corneal wound healing, showing improved corneal structure and transparency. In vitro studies on human corneal epithelial cells showed that 14-3-3zeta was critical for cell proliferation and migration. mRNA-sequencing in conjunction with KEGG analysis and validation experiments revealed that 14-3-3zeta regulated the mRNA levels of ITGB1, PIK3R1, FGF5, PRKAA1 and the phosphorylation level of Akt, suggesting the involvement of the PI3K-Akt pathway in 14-3-3zeta-mediated tissue repair. 14-3-3zeta is a potential novel therapeutic candidate for treating severe corneal injury.

Alkaline burns to the cornea lead to loss of corneal transparency, which is essential for normal vision. We used a rat corneal alkaline burn model to investigate the effect of ophthalmic trimebutine solution on healing wounds caused by alkaline burns. Trimebutine, an inhibitor of the high-mobility group box 1-receptor for advanced glycation end products, when topically applied to the burned cornea, suppressed macrophage infiltration in the early phase and neutrophil infiltration in the late phase at the wound site. It also inhibited neovascularization and myofibroblast development in the late phase. Furthermore, trimebutine effectively inhibited interleukin-1β expression in the injured cornea. It reduced scar formation by decreasing the expression of type III collagen. These findings suggest that trimebutine may represent a novel therapeutic strategy for corneal wounds, not only through its anti-inflammatory effects but also by preventing neovascularization.

Metformin (MET) can be an alternative therapeutic strategy for managing ocular burn primarily because of its pleiotropic mechanism. Longer retention on the ocular surface and sustained release are necessary to ensure the efficacy of MET for ocular application. Although the high aqueous solubility of MET is good for formulation and biocompatibility, it makes MET prone to high nasolacrimal drainage. This limits ocular residence and may be a challenge in its application. To address this, polymers approved for ophthalmic application with natural origin were analyzed through in silico methods to determine their ability to bind to mucin and interact with MET. An ocular insert of MET (3 mg/6 mm) was developed using a scalable solvent casting method without using preservatives. The relative composition of the insert was 58 ± 2.06 %w/w MET with approximately 14 %w/w tamarind seed polysaccharide (TSP), and 28 %w/w propylene glycol (PG). Its stability was demonstrated as per the ICH Q1A (R2) guidelines. Compatibility, ocular retention, drug release, and other functional parameters were evaluated. In rabbits, efficacy was demonstrated in the \'corneal alkali burn preclinical model\'. TSP showed potential for mucoadhesion and interaction with MET. With adequate stability and sterility, the insert contributed to adequate retention of MET (10-12 h) in vivo and slow release (30 h) in vitro. This resulted in significant efficacy in vivo.

Limbal stem cell deficiency (LSCD) is a clinically challenging eye disease caused by damage to limbal stem cells (LSCs). Currently, the international consensus classifies LSCD into three clinical stages based on the disease severity. However, no existing animal models attempt to replicate the varying degrees of LSCD observed in clinical cases. The present study demonstrates an easy-to-create, reproducible, and reliable mouse model of graded LSCD. To achieve mild, moderate, or severe LSCD, filter paper rings with a variety of central angles (90°, 180°, or 270°) are utilized to deliver alkali burns to different sizes of the limbal area (1, 2, or 3 quarters). The animal model has successfully resulted in the development of clinical signs and pathological manifestations in escalating severity that are similarly observed in the three clinical stages of LSCD. Our study thus provides new insights into distinct pathological features underlying different grades of LSCD and serves as a new tool for further exploring the disease mechanisms and developing new effective therapeutics for repairing damaged LSCs.

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OBJECTIVE: To review the management of a patient with a chemical burn from wet cement.
BACKGROUND: This continuing education activity is intended for physicians, physician assistants, nurse practitioners, and registered nurses with an interest in skin and wound care.
OBJECTIVE: After participating in this educational activity, the participant will:1. Recognize the clinical presentation of a patient with a chemical burn from contact with wet cement.2. Describe features related to the pathophysiology of alkali burns from wet cement.3. Select the proper decontamination procedure after exposure to wet cement.4. Identify steps in the treatment of a patient with a chemical burn from contact with wet cement.
Alkali burn from wet cement is an often unrecognized and completely preventable chemical injury. The prevalence of cement burns is likely underestimated because of a lack of awareness and knowledge among both individuals who work with cement and healthcare providers. Chemical injuries have important differences compared with thermal burns: they are usually produced by longer exposure to noxious agents as opposed to short-term exposure that is quickly stopped. As a result, first aid approaches are different. Chemical burns from cement can be avoided with adequate skin and eye protection as well as immediate first aid if contact occurs. Manufacturers of bagged cement place warning notices on packaging, but these can be small and go unnoticed by consumers. Construction workers and amateur do-it-yourselfers should avoid direct contact with cement for any prolonged amount of time. Watertight boots, gloves, and clothing will prevent contact, and any accidental splash on exposed skin should be immediately washed away. Education and awareness of the consequences of cement burns are the best prevention.

We present two cases which underwent complex ocular surface reconstruction to achieve a stable ocular surface. Conjunctival autograft (CAG) procedure was required more than once, in addition to simple limbal epithelial transplantation to address extensive symblepharon in the eyes with total unilateral limbal stem cell deficiency secondary to acid ocular burns. These cases demonstrate that multiple CAGs may be harvested from the contralateral unaffected eye to correct recurrent symblepharon without any donor site complications if the correct surgical technique is adopted.