Esophageal chemical burns
Introduction
Introduction to esophageal chemical burns Esophageal chemical burns, also known as acute corrosive esophagitis (acutecorrosiveesophagitis) is caused by strong acid, strong alkali and other chemical corrosive agents caused by severe damage to the esophagus. The type, concentration and amount of corrosive agents are closely related to the severity of esophagitis. basic knowledge The proportion of illness: 0.001% Susceptible people: no special people Mode of infection: non-infectious Complications: esophageal perforation, tracheoesophageal fistula, peritonitis, bronchiectasis
Cause
Causes of esophageal chemical burns
(1) Causes of the disease
Esophageal chemical burns are clinically divided into acidic and alkaline corrosion. Acidic chemicals such as strong acid (with sulfuric acid, nitric acid, hydrochloric acid, carbolic acid, etc.) can cause coagulative necrosis with the tissue contact surface due to esophageal squamous epithelial surface. The attached mucus has strong acid resistance, which can prevent acid from penetrating into deep tissues, so it can be absorbed into the stomach. Alkaline chemicals such as potassium hydroxide, sodium hydroxide, sodium sulphate, brine, dilute ammonia Solution (ammonia) and lime water can dissolve protein, collagen and fat. After swallowing, it mainly produces liquefaction necrosis and penetrates into deep tissues, causing extensive tissue damage. Liquid base is easy to pass through the pharynx and enter the esophagus because of its high specific gravity. And the stomach; the solid base is often confined to a certain area of the pharynx or esophagus because of its easy adhesion.
(two) pathogenesis
The esophageal injury and healing caused by alkaline substances are divided into three phases, namely the acute phase (1st to 4th days): liquefaction, necrosis, intravascular thrombosis and progressive inflammatory changes, mucosal congestion, edema, no mucosa within 24h Shedding and necrosis; subacute phase (5th to 14th day): mucosal detachment in necrotic area, formation of ulcer with granulation tissue formation, fibroblasts and collagen deposition begin to appear, and the esophageal wall is thinner and most easily perforated; scar formation period (15 days to 3 months): fibrous tissue formation, collagen deposition, collagen contraction at week 3, causing esophageal stricture, regeneration of esophageal mucosa completed within 4 weeks to 3 months after swallowing corrosive lye, severe The late complication of esophageal chemical injury is esophageal stricture, and the stenosis is mostly located in the most severe part of the esophageal injury. The physiological stenosis of the esophagus is likely to cause the corrosion of the substance to stay, and it is also the heaviest part of the esophageal injury.
Prevention
Esophageal chemical burn prevention
1. Strict management to prevent esophageal damage caused by eating strong acid and alkali.
2. Strengthen education to prevent adolescents and adults from having suicidal intentions and ingesting strong acid and alkali.
Complication
Esophageal chemical burn complications Complications Esophageal perforation Tracheal esophageal fistula Peritonitis Bronchiectasis
Complications after swallowing corrosive agents can be divided into local and systemic.
1. Systemic complications: If the amount of poison is high, there will be systemic poisoning, and the severe ones will die within a few hours or within 1-2 days.
2. Local complications:
(1) Bleeding: A small amount of vomiting may occur within a few days after taking the poison, but a large amount of bleeding is caused by the shedding of necrotic tissue, which often occurs within 1 to 2 weeks. Generally, a large amount of bleeding suddenly occurs in about 10 days. Because of the inability to stop and die, it is better for patients with severe symptoms to disappear after 1 week. It is best to stay in bed and go to the fluid diet until 2 weeks, so that there is not much bleeding.
(2) esophageal perforation and mediastinal inflammation: only in patients with swallowed venom is too thick and large, generally alkaline corrosion is more likely to occur in the esophageal perforation, more at the lower end of the esophagus rupture to the left chest cavity, sometimes through to The trachea forms a tracheal esophageal fistula, and there have been reports of accidental rupture to the aortic arch in the literature.
(3) Gastric burns, gastric perforation and peritonitis: more complicated with acidic corrosive agents, showing acute abdominal symptoms and critical illness.
(4) laryngeal edema, aspiration pneumonia, lung abscess and bronchiectasis: can be complicated by acute corrosive esophagitis and scar stenosis, especially in children.
(5) esophageal scar stenosis: often an inevitable complication, only early prevention can prevent it, stomach scar stenosis is often complicated in patients swallowing acidic corrosive agents.
Symptom
Symptoms of esophageal chemical burns Common symptoms Asphalt burns, cheeks, cheeks, burns, esophageal obstruction, acute sternal pain, fever, hooliganism, dysphagia, edema
The early symptoms were salivation, vomiting, fever and swallowing pain and difficulty, pain in the back of the sternum and under the xiphoid. The symptoms disappeared after about 2 weeks, and the dysphagia again occurred after the burn (about 1 month later), and gradually increased. Trends, partial or complete esophageal obstruction, can be complicated by cough, shortness of breath and respiratory aspiration pulmonary edema or infection.
Examine
Examination of esophageal chemical burns
When combined with esophageal perforation and respiratory infection, the white blood cell count increased and hemoglobin decreased.
X-ray inspection
X-ray examination should be after the acute inflammation subsides, the patient can swallow the food for esophagography, if there is suspected esophageal fistula or perforation, the contrast agent can flow into the respiratory tract, preferably using lipiodol angiography, according to the different stages of the development of the lesion and The degree of injury is different, lighter: early is the secondary esophageal sputum, mucosal texture is still normal, can also be slightly thickened, twisted, late scar, stenosis is not obvious, moderate: esophageal involvement length increased, secondary sputum significantly The mucosal texture is irregularly jagged or beaded. In severe cases, the lumen is significantly reduced, even in the shape of a rat tail.
2. Esophagoscopy
In addition to shock or perforation, it should be implemented as soon as possible to determine the extent of the lesion, to prevent obstruction due to stenosis, regular endoscopic reexamination, in addition to the dilated esophagus, early detection of esophageal cancer, because the incidence of cancer is more than normal esophagus High, especially the thickening of the esophagus caused by strong alkali.
Diagnosis
Diagnosis and diagnosis of esophageal chemical burns
diagnosis
Mainly rely on medical history, the first detection of pharyngeal cheek burns during physical examination, according to the degree of burn and the dose and traits of corrosive agents and the difficulty of swallowing to determine whether there is esophageal burn.
Differential diagnosis
Esophageal chemical burns are generally not difficult to diagnose according to their medical history, symptoms and signs, and often coexist with corrosive gastritis, but in the clinical should pay attention to whether there are other lesions with esophagus.
For middle-aged and elderly men, it is necessary to pay attention to the identification of esophageal cancer. Esophageal cancer is mainly characterized by difficulty in swallowing and weight loss. The condition is progressively worsened. X-ray and gastroscopy combined with biopsy can confirm the diagnosis.
