Chemical burns
Chemical injuries to the skin and mucous membranes occur upon contact with aggressive chemical compounds. The main etiological factors include:
- Concentrated acids and alkalis.
- Heavy metal salts.
- Toxic gases (e.g., lewisite, mustard gas).
The depth of tissue damage directly depends on the characteristics of the agent (the nature of the substance and its concentration), ambient temperature, and the duration of tissue exposure. It is important to remember that exposure (duration of action) is the only parameter that can be influenced at the first aid stage. Rapid removal of the chemical significantly reduces the severity of the injury.
Contact with chemicals leads to necrosis. The action of alkalis is characterized by the formation of wet (colliquative) necrosis. Externally, such an area appears as a gelatinous gray mass that is flush with healthy skin or protrudes above it.
Electrical injury and the effect of electric current
Electrical burns occur when the body is exposed to a current exceeding 24 V. The damaging effect consists of the direct passage of electrons through tissues and intense heat generation (in accordance with Joule's law). Thermal destruction depends on the current magnitude, tissue electrical resistance, and contact duration.
The pathogenesis of electrical injury involves deep tissue damage along the path of the current. Structures with high conductivity (low resistance)—blood vessels and muscles—suffer the most destruction. Damage to large vessels is associated with a high risk of tissue necrosis and organ gangrene.
Local manifestations are referred to as "current marks" and are localized at the entry and exit points of the discharge. These are round or oval wounds 2–3 cm in diameter, featuring a characteristic central depression, covered with a gray or dark brown scab, and surrounded by pronounced edema. Sensitivity in the affected area is reduced. Lightning strikes produce specific dark-brown arborescent stripes on the body.
Radiation burns
Radiation injuries are caused by the local effect of various types of radiant energy (isotope, X-ray, or UV radiation). A key feature of these injuries is the combination of skin damage with a severe general systemic impact on the body (radiation sickness).
The pathogenesis of a local radiation burn includes:
- Impairment of capillary blood flow with erythrocyte stasis.
- Formation of massive edema.
- Degenerative changes in nerve endings.
- Upon exposure to high doses, the development of deep dry tissue necrosis.
The clinical course is divided into three phases: primary reaction, latent period (apparent well-being), and the period of necrotic changes. The duration of the latent period varies from several hours (in solar burns) to long periods (upon exposure to ionizing radiation).
Necrotic phase and treatment of radiation injuries
During the period of necrotic changes, skin hyperemia and persistent dilation of small vessels (telangiectasia) develop. Epidermal detachment occurs with the formation of blisters filled with serous fluid, and areas of necrosis are formed. After the rejection of dead tissues, radiation ulcers remain. They are covered with scant gray discharge and are characterized by a complete loss of regenerative capacity: granulation and epithelialization are absent.
Local symptoms occur against the background of systemic manifestations of radiation sickness: weakness, nausea, and vomiting. Progressive thrombocytopenia, leukopenia, and anemia are observed in the blood. A hemorrhagic syndrome develops (bleeding of mucous membranes with minimal trauma, cutaneous hemorrhages).
Treatment of radiation ulcers is carried out only against the background of systemic therapy for radiation sickness. Without correcting the general condition, local treatment is futile.
- Systemic therapy: use of blood components, bone marrow transplantation.
- Local treatment: necrolytic agents (proteolytic enzymes) and antiseptics during the cleansing phase, followed by ointment dressings with regeneration stimulants.
To remember which tissues are most vulnerable to electricity, keep conductors in mind: current travels where there is an abundance of fluid and electrolytes. Therefore, muscles and blood vessels (tissues with high conductivity) suffer the most damage.
Class and exam questions
What determines the severity of a chemical burn?
By the nature of the substance, its concentration, ambient temperature, and exposure time. The agent's exposure time is the only factor that can be reduced when providing first aid.
What does a concentrated alkali burn look like?
Wet (colliquative) necrosis forms. The wound appears as a gelatinous gray mass that is flush with the skin or protrudes above it.
What are "current marks" and where do they occur?
These are burn wounds at the entry and exit points of electricity: round, 2–3 cm in diameter, with a central depression. They are covered with a gray or dark brown scab, surrounded by edema, and are painless due to reduced sensitivity.
Why do radiation ulcers heal poorly?
Tissues almost completely lose their regenerative capacity due to the systemic effects of radiation (radiation sickness) and deep degeneration of nerve endings. Without treating radiation sickness, local therapy does not work.
What else to study on this topic
- Features of coagulation (dry) necrosis in acid burns.
- Pathogenesis of injuries caused by toxic gases (mustard gas, lewisite).
- Surgical treatment tactics for deep electrical burns and gangrene.
- Management of hemorrhagic syndrome in severe radiation sickness.
Master the entire topic in the "General Surgery" course
This is a summary. The course covers everything tested in classes and exams.
- Complete study guide on "Chemical and Radiation Burns" and 3,335 other subject pages
- Assignments and quizzes after every topic — just like in a colloquium
- AI tutor answers questions on the topic anytime
- 70 video lessons on the subject
Other topics in "CHAPTER 10. GENERAL ISSUES IN TRAUMATOLOGY"
Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.