Acid burn

Introduction Acid burn is characterized by acid dehydration and protein coagulation and degeneration associated with acid chemicals in contact with the skin, accompanied by thermal burns. There are few blisters in acid burns, the wounds are dry, the edges are clearly defined, and the swelling is lighter. Due to protein coagulation, in addition to hydrofluoric acid, lesions often do not invade the deep layer.

Cause

Acid burn refers to the damage caused by high concentration of strong acid acting on the tissue, causing tissue dehydration and protein denaturation. The main causes of burns are strong acids such as sulfuric acid, nitric acid and hydrochloric acid. Acid burns can cause localized pain and coagulative necrosis. Many acids are flammable, explosive, corrosive and toxic, which can cause great harm. Commonly used are sulfuric acid, nitric acid, and hydrochloric acid burns. They are characterized by dehydration of tissues, coagulation of tissue protein precipitates, and therefore few blisters, which quickly become sputum. In general, the deeper the burn, the harder the toughness and the darker the color (brown, yellowish brown), but the depth is often difficult to judge due to the concealment of the twilight. Early infection is lighter. Deep acid burns are delayed and healed slowly.

an examination

Related inspection

Skin lesion

1. History of exposure to strong acids.

2. The wound is quickly scarred, generally without bubbles. Except for hydrofluoric acid, it does not generally invade deep tissues.

3. Sulfuric acid burns appear dark brown or black enamel; nitric acid is brownish yellow enamel; hydrochloric acid or carbolic acid is yellow or white enamel.

4. The carbolic acid burn wound began to appear white, then turned gray or blue-gray. This acid dehydration is not as strong as the above, but it can penetrate into the blood circulation and damage the kidney.

5. Fluorohydrogen burn wounds begin to show erythema or blisters. In addition to the deterioration of the protein, the acid also dissolves the lipid, destroys the cell membrane, decalcifies (destroy the bone), etc., so the tissue necrosis will continue to expand and deepen, the pain is more dramatic, and ulcers can form.

Differential diagnosis

(1) Burning of sulfuric acid, hydrochloric acid and nitric acid

Triacids can cause skin burns when in a liquid state, and can cause inhalation damage in a gaseous state.

diagnosis

1. History of exposure to sulfuric acid or hydrochloric acid or nitric acid. In particular, ask about the type of acid, contact time, burn first aid and whether there is history of acid mist inhalation; local wounds are tested for strong acidity with pH test paper.

2. Burn wound characteristics: sulfuric acid burn wounds are generally black or brownish black; hydrochloric acid burn wounds are yellowish blue; nitric acid burned wounds are yellow or yellowish brown. The wound is soft and moist, and the light color is light burn; the burned skin is leathery and the color is deep burn. Acid burns the skin to dry, so the infection under the skin is generally less.

3. Often accompanied by upper respiratory tract irritation or laryngeal edema, chest tightness, and even pulmonary edema.

[First Aid Treatment]

1. Rinse immediately with plenty of water, not less than 20 minutes, and then neutralize with 3%~5% sodium bicarbonate solution. Neutralization with soap can also be done without any conditions.

2. Exposure therapy for wounds: Patients with grade III burns should have early escharectomy, autologous skin grafting and skin grafting to eliminate the wound at an early stage.

3. Large area acid burns should be treated with anti-shock.

4. Early injection of procaine penicillin 1.6 million u / d intramuscularly, to fight infection, after 3 ~ 5d, depending on the wound surface and the patient's general condition decided to disable or switch to sensitive antibiotics.

(two) hydrofluoric acid burns

In addition to the characteristics of acid burns, it also has a strong corrosive effect, which can dissolve fat and decalcification, resulting in longer-lasting local tissue necrosis. If the severe ulcer is not cured for a long time, if it is not treated in time, the damage can reach the periosteum, causing aseptic necrosis of the bone.

diagnosis

1. Have a history of exposure to hydrofluoric acid.

2. Local wounds: early asymptomatic, severe pain after 1~8h. The initial skin flushed, then gradually turned dark red, dry, followed by pale, necrotic wounds, and finally purple black or black. There are also local blisters, the blisters are brown, and the wounds are not easy to heal.

3. Inhalation of hydrofluoric acid smoke may have respiratory irritation and pulmonary edema. In severe cases, asphyxia may occur.

4. According to the degree of burn, the patient has symptoms of fluorosis such as headache, fatigue, nausea, vomiting, convulsions, coma, circulatory failure and kidney damage.

[First Aid Treatment]

1. Rinse immediately with plenty of running water for 20 to 30 minutes.

2. Wash or soak for 1 h with 3%~10% sodium bicarbonate solution, then soak for 1 h with 50% magnesium sulfate.

3. Mild burns with or without 10% calcium gluconate in the surrounding area or with 5% to 10% calcium chloride for DC calcium penetration therapy. The latter has quick pain and less sequelae.

4. In severe cases, local surgery can be performed to remove normal tissue, and then the skin is removed with skin graft or flap.

5. Large areas of hydrofluoric acid burns should be supplemented with calcium, with 10% calcium gluconate 10ml or 5% calcium chloride 20ml added to 25% glucose injection 20ml slow intravenous injection. The patient's blood calcium ion concentration and renal function changes were measured daily, and those with respiratory damage should be analyzed for blood gas.

6. A wide range of hydrofluoric acid burns should be treated with anti-burn shock (2% area of hydrofluoric acid burns can cause shock). In case of vapor inhalation, it can be inhaled by 2% sodium bicarbonate solution. In severe cases, tracheotomy should be performed.

7. Give antibiotics to prevent infection.

(three) chromic acid burns

Contact with the skin causes local tissue corrosion and causes the protein to coagulate. If not handled properly, chromium ions can be absorbed from the wound surface, causing poisoning.

diagnosis

1. History of exposure to chromic acid.

2. Local wounds are ulcerated, blisters, and the surface is yellow. The wound can reach the periosteum and is not easy to heal.

3. Prolonged exposure to chromic acid mist can cause ulceration and perforation of the nasal septum.

4. When the wound area is large, it can cause methemoglobinemia, hypoxia, renal function damage and various tube types and hemoglobinuria.

[First Aid Treatment]

1. Rinse immediately with plenty of water for 20~30min.

2. Rinse or wet with 5%~10% sodium thiosulfate or phosphate buffer. It can also be rinsed with 10% EDTA solution to reduce the chromium ion absorption of the wound.

3. Early cutting defects can be considered.

4. Early hemodialysis or exchange of blood in the event of poisoning.

(4) oxalic acid burns

diagnosis

1. Have a history of oxalic acid exposure.

2. Partial wound skin produces powdery white intractable ulceration.

3. Hypercalcemia, convulsions and kidney damage can occur with a large burn area.

[First Aid Treatment]

1. Rinse immediately with plenty of running water.

2. The wound is partially applied with calcium gluconate solution.

3. Appropriate calcium supplementation, rehydration, diuresis, prevention and treatment of acute renal failure.

The material in this site is intended to be of general informational use and is not intended to constitute medical advice, probable diagnosis, or recommended treatments.