An update on chemical eye burns Bizrah, Mukhtar; Yusuf, Ammar; Ahmad, Sajjad
Eye (London),
09/2019, Letnik:
33, Številka:
9
Journal Article
Recenzirano
Odprti dostop
Ocular chemical injuries vary in severity, with the more severe end of the spectrum having profound visual consequences and medicolegal implications. Grading of ocular injuries is critical for ...determining acute treatment and visual prognosis. Poor immediate management results in more challenging treatment of acute disease. Similarly, poorly controlled acute disease results in more treatment-resistant chronic ocular disease. Despite several decades of research and public health initiatives, simple and effective interventions such as wearing protective eyewear and immediate irrigation of eyes remain as key challenges. Education and prevention are therefore important public health messages. Hurdles in the acute management of disease include poor evidence-base for commonly used treatments (e.g. based on experimental animal studies), reduced treatment adherence rates and high clinic non-attendance rates. The evolution of treatment strategies, particularly limbal stem cell transplantation, has revolutionised the visual and cosmetic outcomes in chronic phases of disease. It is therefore increasingly important to consider tertiary referral for patients with limbal stem cell failure or vision-limiting corneal scarring.
Choking agent exposure, among them chlorine gas, occurs in household or industrial accidents, chemical warfare and terrorist attacks.
Review of published animal and human data regarding the history, ...pathophysiology, clinical effects and management of chlorine exposure.
Highly soluble agents cause quick upper respiratory tract symptoms. Chlorine gas has a medium solubility, also causing delayed lower airway symptoms, mainly due to its oxidizing potential by releasing hypochlorous and hydrochloric acid, but also by interacting with Transient Receptor Potential channels.
Eyes may show conjunctival injection, abrasions and corrosions. Burns of the oronasal mucosa and trachea can occur. Dyspnea, bronchospasm and possible retrosternal pain occur frequently. Glottis edema or laryngospasm are acute life-threatening emergencies. Chlorine gas can cause toxic pneumonitis, lung edema and acute respiratory distress syndrome (ARDS).
General management includes physical examination, pulse oximetry and arterial blood gases. Eyes should be irrigated, humidified oxygen and inhalative bronchodilators administered. An EKG, cardiac enzymes and complete-blood-count should be obtained if there is retrosternal pain. Routine chest x-ray is not recommended – except if pulmonary edema is suspected. Laryngoscopy should be performed if glottis edema is suspected. Sodium bicarbonate inhalation after chlorine gas inhalation is discussed controversially. Mechanical ventilation with continuous-positive-airway-pressure or intubation/tracheotomy with high positive-end-expiratory-pressure may be necessary. Glucocorticoids for prevention of pulmonary edema should be applied restrictively. Prophylactic antibiotics are not recommended. In severe ARDS, extracorporeal membrane oxygenation (ECMO) can be considered.
Treatment is mainly symptom oriented. New and promising therapies are in development.
To compare the outcomes of conventional medical treatment vs combined medical treatment and amniotic membrane transplantation (AMT) in the management of patients with Roper-Hall grade IV ocular ...chemical injury.
Randomized, parallel-controlled clinical trial.
Setting: Single tertiary referral hospital. Patients: Sixty eyes of 60 patients with Roper-Hall grade IV ocular chemical injury with a minimum follow-up of 12 months were enrolled in the study. Intervention: Patients were randomly assigned to 2 groups: Group 1 (30 eyes) received topical preservative-free lubricating gel and drops, chloramphenicol, betamethasone, homatropine, oral vitamin C, and doxycycline; Group 2 (30 eyes) received amniotic membrane transplant (AMT) on the entire ocular surface in addition to the medical treatment provided in Group 1. Outcome Measures: The main outcome measure was time to complete corneal epithelialization. Secondary outcome measures were best-corrected visual acuity (BCVA) and neovascularization in the central 5 mm of the cornea.
Mean follow-up time was 20.3 ± 2.5 months (range 13-24 months). Corneal epithelial defects healed within 72.6 ± 30.4 (21-180) days in Group 1 vs 75.8 ± 29.8 (46-170) days in Group 2 (P = .610). Mean BCVA was 2.06 ± 0.67 (0.4-2.6) logMAR vs 2.06 ± 0.57 (1-2.9) logMAR in Groups 1 and 2, respectively (P = .85). Group 1 developed more central corneal neovascularization (22 eyes; 73.3%) compared to Group 2 (16 eyes; 53.3%); however, it was not statistically significant (P = .108).
In comparison to conventional medical therapy, combined amniotic membrane transplantation and medical therapy does not accelerate corneal epithelialization or affect final visual acuity in severe chemical injuries.
Alkali burns to the eye constitute a leading cause of worldwide blindness. In recent case series, corneal transplantation revealed unexpected damage to the retina and optic nerve in chemically burned ...eyes. We investigated the physical, biochemical, and immunological components of retinal injury after alkali burn and explored a novel neuroprotective regimen suitable for prompt administration in emergency departments. Thus, in vivo pH, oxygen, and oxidation reduction measurements were performed in the anterior and posterior segment of mouse and rabbit eyes using implantable microsensors. Tissue inflammation was assessed by immunohistochemistry and flow cytometry. The experiments confirmed that the retinal damage is not mediated by direct effect of the alkali, which is effectively buffered by the anterior segment. Rather, pH, oxygen, and oxidation reduction changes were restricted to the cornea and the anterior chamber, where they caused profound uveal inflammation and release of proinflammatory cytokines. The latter rapidly diffuse to the posterior segment, triggering retinal damage. Tumor necrosis factor-α was identified as a key proinflammatory mediator of retinal ganglion cell death. Blockade, by either monoclonal antibody or tumor necrosis factor receptor 1 and 2 gene knockout, reduced inflammation and retinal ganglion cell loss. Intraocular pressure elevation was not observed in experimental alkali burns. These findings illuminate the mechanism by which alkali burns cause retinal damage and may have importance in designing therapies for retinal protection.
Objectives/Hypothesis
Button battery (BB) injuries continue to be a significant source of morbidity and mortality, and there is a need to confirm the mechanism of injury for development of additional ...mitigation strategies.
Study Design
Cadaveric piglet esophageal model.
Methods
Lithium, silver oxide, alkaline, and zinc–air BBs were placed in thawed sections of cadaveric piglet esophagus, bathed in normal saline. Severity of gross visual burn, pH, and temperature were recorded every 30 minutes for 6 hours. In other esophageal tissue specimens, the lithium BB was removed after 24, 36, and 48 hours and the site was irrigated with either 0.25% or 3% acetic acid. Separately, ReaLemon® juice, orange juice, Coke®, Dasani® water, Pepsi®, and saline were infused over a vertically suspended esophagus with a CR2032 lithium battery every 5 minutes for 2 hours while tissue temperature and pH were measured.
Results
A gradual rise in tissue pH and minimal change in temperature was noted for all BBs. ReaLemon® and orange juice applied every 5 minutes were most effective at neutralization of tissue pH with minimal change in tissue temperature. After BB removal (24, 36, 48 hours), irrigation of esophageal tissue specimens with 50–150 mL 0.25% acetic acid neutralized the highly alkaline tissue pH.
Conclusions
BB appear to cause an isothermic hydrolysis reaction resulting in an alkaline caustic injury. Potential new mitigation strategies include application of neutralizing weakly acidic solutions that may reduce esophageal injury progression.
Level of Evidence
NA Laryngoscope, 127:1276–1282, 2017
Ingestion of Caustic Substances Hoffman, Robert S; Burns, Michele M; Gosselin, Sophie
The New England journal of medicine,
04/2020, Letnik:
382, Številka:
18
Journal Article
Recenzirano
Acids and alkalis can cause tissue damage on contact. Accidental and intentional ingestions of caustic materials in adults and children are a worldwide health issue. Acids act in part by denaturing ...proteins, and alkalis by saponifying fats. Approaches to management are outlined.
BACKGROUND:Endoscopy is the standard of care for emergency patient evaluation after caustic ingestion. However, the inaccuracy of endoscopy in determining the depth of intramural necrosis may lead to ...inappropriate decision-making with devastating consequences. Our aim was to evaluate the use of computed tomography (CT) for the emergency diagnostic workup of patients with caustic injuries.
METHODS:In a prospective study, we used a combined endoscopy–CT decision-making algorithm. The primary outcome was pathology-confirmed digestive necrosis. The respective utility of CT and endoscopy in the decision-making process were compared. Transmural endoscopic necrosis was defined as grade 3b injuries; signs of transmural CT necrosis included absence of postcontrast gastric/ esophageal-wall enhancement, esophageal-wall blurring, and periesophageal-fat blurring.
RESULTS:We included 120 patients (59 men, median age 44 years). Emergency surgery was performed in 24 patients (20%) and digestive resection was completed in 16. Three patients (3%) died and 28 patients (23%) experienced complications. Pathology revealed transmural necrosis in 9/11 esophagectomy and 16/16 gastrectomy specimens. Severe oropharyngeal injuries (P = 0.015), increased levels of blood lactate (P = 0.007), alanine aminotransferase (P = 0.027), bilirubin (P = 0.005), and low platelet counts (P > 0.0001) were predictive of digestive necrosis. Decision-making relying on CT alone or on a combined CT–endoscopy algorithm was similar and would have spared 19 unnecessary esophagectomies and 16 explorative laparotomies compared with an endoscopy-alone algorithm. Endoscopy did never rectify a wrong CT decision.
CONCLUSIONS:Emergency decision-making after caustic injuries can rely on CT alone.
Background
Esophagectomy is the standard of care for high-grade corrosive esophageal necrosis as assessed endoscopically. However, the inaccuracy of endoscopy in determining the depth of intramural ...necrosis may lead to unnecessary esophageal resection, with devastating consequences. Our aim was to evaluate the use of computed tomography (CT) for the emergency diagnostic workup of endoscopic high-grade corrosive esophageal necrosis.
Methods
In a before (2000–2007)/after (2007–2012) study of patients with grade 3b endoscopic esophageal necrosis, we compared outcomes after routine emergency esophagectomy versus selection for emergency esophagectomy based on CT evidence of transmural necrosis, defined as at least two of the following: esophageal-wall blurring, periesophageal-fat blurring, and the absence of esophageal-wall enhancement. Survival estimated using the Kaplan–Meier method was the primary outcome.
Results
Compared to the routine-esophagectomy group (
n
= 125), the CT group (
n
= 72) had better overall survival in the crude analysis (hazard ratio HR, 0.43; 95 % confidence interval 95 %CI, 0.21–0.85;
P
= 0.015) and in the analysis matched on gender, age, and ingested agent (HR, 0.36; 95 %CI, 0.16–0.79;
P
= 0.011). No deaths occurred among patients managed without emergency esophagectomy based on CT findings, and one-third of CT-group patients had their functioning native esophagus at last follow-up. Self-sufficiency for eating and breathing was more common (84 % vs. 65 %; relative risk RR, 1.27; 95 %CI, 1.04–1.55;
P
= 0.016) and repeat suicide less common (4 % vs. 15 %; RR, 0.27; 95 %CI, 0.09–0.82;
P
= 0.019) in the CT group.
Conclusion
The decision to perform emergency esophagectomy for endoscopic high-grade corrosive esophageal injury should rely on CT findings.
Chemical burns are a major cause of corneal injury. Oxidative stress, inflammatory responses and neovascularization after the chemical burn aggravate corneal damage, and lead to loss of vision. ...Although NADPH oxidases (Noxs) play a crucial role in the production of reactive oxygen species (ROS), the role of Noxs in chemical burn-induced corneal injury remains to be elucidated. In the present study, the transcription and expression of Noxs in corneas were examined by RT-qPCR, western blot analysis and immunofluorescence staining. It was found that alkali burns markedly upregulated the transcription and expression of Nox2 and Nox4 in human or mouse corneas. The inhibition of Noxs by diphenyleneiodonium (DPI) or apocynin (Apo) effectively attenuated alkali burn-induced ROS production and decreased 3-nitrotyrosine (3-NT) protein levels in the corneas. In addition, Noxs/CD11b double-immunofluorescence staining indicated that Nox2 and Nox4 were partially co-localized with CD11b. DPI or Apo prevented the infiltration of CD11b-positive inflammatory cells, and inhibited the transcription of inflammatory cytokines following alkali burn-induced corneal injury. In our mouse model of alkali burn-induced corneal injury, corneal neovascularization (CNV) occurred on day 3, and it affected 50% of the whole area of the cornea on day 7, and on day 14, CNV coverage of the cornea reached maximum levels. DPI or Apo effectively attenuated alkali burn-induced CNV and decreased the mRNA levels of angiogenic factors, including vascular endothelial growth factor (VEGF), VEGF receptors and matrix metalloproteinases (MMPs). Taken together, our data indicate that Noxs play a role in alkali burn-induced corneal injury by regulating oxidative stress, inflammatory responses and CNV, and we thus suggest that Noxs are a potential therapeutic target in the future treatment of chemical-induced corneal injury.
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