This disease is caused by the scalp and skull {|###|}injury{|###|} due to exposure to high temperatures, electric shocks, and chemical substances. Depending on the duration, concentration, intensity, location, and extent of head contact, the severity of the {|###|}injury{|###|} varies. It is not uncommon clinically, but large-scale reports are rare. Before the application of conservative treatment and antibiotics Suwen, it often led to tissue degeneration, necrosis, and exudation, causing bacterial infections that worsened the condition and even endangered life. In modern times, the removal of necrotic tissue followed by tension-reducing wound suturing, flap transfer, and skin grafting, along with antibiotic therapy, has yielded good results and remains in use today. With advancements in microsurgical techniques, some now perform thorough excision of necrotic tissue and use free greater omentum {|###|}membrane{|###|} to anastomose its blood vessels with those of the scalp, achieving new progress.

bubble_chart Etiology

Scalp and skull burns have various causes, primarily resulting from the head's proximity to or contact with harmful substances, leading to a series of pathological changes. High-temperature sources include hot water, hot oil, high-temperature stoves, molten glass, asphalt, molten iron, burning coal, and high-pressure steam. Electrical injuries involve lightning strikes and high-voltage arc burns. Chemical burns are even more diverse, caused by strong acids, strong alkalis, and flammable or explosive substances such as ethers, alcohols, acetone, acetylene, gasoline, natural gas, gunpowder, and explosives, which can lead to explosions and burns. Additionally, radiation injuries, such as those from deep X-rays and particle radiation from nuclear fission—particularly alpha particles, proton beams, and neutron beams—cause severe tissue damage. A common characteristic of burns from these causes is that the longer the exposure, the larger the affected area, and the higher the concentration, temperature, or dose, the more severe the burn becomes.

The main pathological changes include coagulation of injured tissue proteins, vascular occlusion and destruction, cell lysis and liquefaction, and in severe cases, carbonization. Depending on the severity of the burn, mild cases may show scalp redness and swelling, while severe cases may exhibit the scalp and skull turning brown-gray or black. Microscopically, mild cases present with scalp vascular congestion and cellular edema; more severe cases may show partial cell lysis, liquefaction, and exudation, with the normal structure of bone trabeculae being disrupted and indistinct. In the most severe cases, the scalp and skull appear black, with the normal structure completely disappearing and turning into carbonized fragments, accompanied by involvement of brain tissue.

bubble_chart Clinical Manifestations

Due to differences in the location, extent, and severity of burns, their clinical manifestations vary. In grade I burns, there may be localized pain, redness, and swelling, with a slightly elevated body temperature, generally below 38°C. The peripheral blood count may show white blood cells at around (10–15) × 10⁹/L (10,000–15,000/mm³). In severe cases, all layers of the scalp, muscles, skull, and even brain tissue may be affected simultaneously, appearing brown-gray or black, with the tissue becoming loose, easily sloughing off, or even missing. During the acute phase, patients may experience shock due to localized pain or bleeding, with body temperature potentially rising above 38°C. The peripheral blood count may show white blood cells at (12–20) × 10⁹/L, predominantly polymorphonuclear cells. In severe electrical burns or lightning injuries, the philtrum is often accompanied by myocardial injury, presenting with symptoms such as decreased blood pressure and arrhythmias. When large areas of deep burns occur on the scalp, the wound may crack, leading to bleeding and exudate. If accompanied by severe skull burns, the affected skull may appear brown-gray or black, or even slough off or become missing. On X-ray plain films, the local skull may show low-density shadows or defects. Severe burns often involve local brain tissue, causing cerebral edema, increased intracranial pressure, and corresponding localized neurological signs, such as headache, vomiting, hemiplegia, aphasia, and other manifestations.

Based on the patient's history of exposure to harmful substances such as high temperature, high voltage, or chemical agents, along with the duration and intensity of exposure, as well as systemic and local manifestations post-injury, combined with the results of auxiliary examinations, determining the nature, extent, and severity of the burn is generally not difficult.

bubble_chart Treatment Measures

The treatment of this condition varies depending on the location, extent, nature, and severity of the burn, but the principles remain consistent. These include promptly removing the source of contact, cooling and neutralizing or rinsing off acidic or alkaline substances, cutting off electrical power, treating shock, and controlling local bleeding. In the acute phase, some patients require emergency interventions. For instance, if there is significant bleeding from the wound, immediate hemostatic measures should be taken. If the patient is in shock, rapid blood transfusion, fluid infusion, and appropriate use of vasopressors for anti-shock therapy are necessary. In cases of severe myocardial damage leading to hypotension or arrhythmias, vasopressors and cardiac stimulants should be administered as needed. Following these emergency measures, early antibiotic therapy should be initiated to prevent infection. For deep or heavily contaminated wounds, an intramuscular injection of TAT 1500 units is required. Simultaneously, the burned area should be cooled with sterilized saline or rinsed with diluted acid or alkaline solutions to prevent further damage. Intramuscular analgesics may be administered to alleviate pain. Once shock is corrected and the patient's condition stabilizes, local wound management should be performed as soon as possible. For minor scalp burns without tissue necrosis, the hair should be shaved, the area disinfected, and covered with petrolatum gauze or topical Chinese medicinal ointments such as "Tanshang Zi" or "Jing Wan Hong," followed by bandaging. Dressings should be changed every 3–5 days, accompanied by intramuscular antibiotics to prevent infection. If the patient presents in the chronic phase with abscess formation beneath the scalp, incision and drainage should be performed to prevent the spread of inflammation to the skull. For more severe burns, if the affected area is small, the wound edges should be incised under local anesthesia until healthy tissue is reached. Nonviable tissue should be completely excised from the base, followed by antibiotic application and tension-relieving sutures with drainage strips. For larger and deeper soft tissue burns, early excision of nonviable tissue is also recommended. If the skull is exposed but still viable, multiple holes can be drilled into the outer table to the diploë layer, followed by antibiotic and petrolatum gauze packing and bandaging. Dressings should be changed every 2–3 days until granulation tissue forms, at which point intermediate-thickness skin grafts or stamp grafts can be prepared. Recently, microsurgical techniques have been used to anastomose the vascular supply of a free omental flap with scalp vessels, followed by skin grafting once the flap survives. If the skull is severely burned and turns dark brown, indicating nonviability, the necrotic bone should be completely removed, followed by wound care until granulation tissue forms, after which skin grafting can be performed. If the patient presents in the chronic phase with wound infection, early incision and drainage or debridement should be performed.

In the early stages of severe large-area burns to the scalp and skull, shock can occur due to pain and bleeding from the wounds. Electric injury can cause myocardial damage, manifesting as arrhythmias, and in severe cases, may lead to heart failure. In the advanced stage, sepsis can result from wound infection and exudation. If these post-injury changes are inadequately managed, serious consequences may follow. When deep burns involve brain tissue, varying degrees of neurological symptoms such as limb paralysis and epilepsy may persist despite aggressive treatment. For superficial burns or deeper but smaller-area burns, timely and proper management generally leads to a better prognosis.

bubble_chart Complications

The main complications are scalp and skull infections. When both the scalp and skull are severely burned, it can affect local brain tissue, leading to cerebral edema, increased intracranial pressure, and neurological dysfunction, clinically manifested as headache, nausea, vomiting, limb paralysis, aphasia, epilepsy, etc. Electrical burns and lightning injuries can simultaneously cause myocardial damage, presenting as decreased blood pressure, arrhythmias, etc. If combined with extensive burns in other parts of the body, symptoms may include high fever, significant exudation from the wound, and hypoalbuminemia. Skull defects and epilepsy are the main sequelae.

bubble_chart Differentiation

Grade I scalp burns need to be distinguished from those caused by other factors such as violent contusion or scalp infection. Generally, differentiation based on medical history is not difficult.