settingsJavascript is not enabled in your browser! This website uses it to optimize the user's browsing experience. If it is not enabled, in addition to causing some web page functions to not operate properly, browsing performance will also be poor!
Yaozi
search
diseasePost-traumatic Encephalocele
aliasBrain Mushrooms, Post-traumatic Fungus of the Brain
smart_toy
bubble_chart Overview

Open brain injuries, especially penetrating gunshot wounds, cause the scalp, skull, and dura mater to become exposed or even damaged. If intracranial bleeding, brain edema, or swelling leads to increased intracranial pressure early after the injury, brain tissue may protrude outward through the skull defect, resembling a mushroom—hence the term "brain fungus." If the brain herniation occurs within the first week post-injury without significant infection (early-stage herniation), it often resolves on its own with appropriate antibiotic treatment and measures to reduce intracranial pressure, allowing the herniated brain tissue to retract into the cranial cavity. This is referred to as benign brain herniation. However, if the herniation occurs more than a week after the injury—due to incomplete initial debridement or delayed medical intervention—the intracranial cavity may contain necrotic tissue, blood clots, bone fragments, or foreign bodies that are prone to infection. Once the protruding brain tissue becomes infected, secondary intracranial infections such as purulent meningitis, encephalitis, brain abscess, subdural empyema, or even ventriculitis and thrombophlebitis may develop. If intracranial lesions continue to elevate pressure, conservative treatments often fail. The herniated brain tissue becomes incarcerated, necrotic, and infected, leading to further complications such as venous congestion, edema, and necrosis in adjacent brain tissue. This exacerbates intracranial pressure, worsening the brain fungus. Without prompt and effective intervention, the patient's life is at risk—a condition known as malignant brain herniation.

bubble_chart Clinical Manifestations

In the early stage of brain fungus, the duration is relatively short, and the local appearance presents in two forms: For moist wounds, bloody cerebrospinal fluid or plasma-like exudate can be seen, with pulsation, a small amount of discharge on the surface without obvious pus, appearing pink, and no necrotic tissue; for dry wounds, there is a thin layer of epidermal-like tissue on the brain fungus, but there is often a small amount of discharge at the junction between the base of the brain herniation and the scalp. In the advanced stage, brain fungus is often severely infected, with ischemic and necrotic surface tissue appearing gray-white, accompanied by a large amount of purulent discharge, and pus accumulation often occurs in the crevices where the base meets the scalp. Due to incarceration and adhesion, no pulsation is visible. In cases of severe infection, in addition to symptoms of intracranial hypertension, there may also be accompanying signs such as fear of cold, fever, and corresponding focal neurological deficits.

bubble_chart Treatment Measures

The treatment of cerebral fungus varies depending on the stage of infection. For early-stage cases with mild infection and no secondary intracranial lesions, the first step is to clean and disinfect the surrounding scalp. The herniated brain tissue is then rinsed with saline, hydrogen peroxide, and antibiotic solutions, followed by coverage with sterile petrolatum gauze for protection. Dressings should be changed regularly based on infection status. Concurrently, high-dose systemic antibiotics and appropriate dehydration therapy should be administered. Lumbar puncture for cerebrospinal fluid drainage may be performed if necessary to facilitate the reduction of the cerebral fungus. For dry cerebral fungus with epidermization, if bacterial cultures from the junction of the scalp and herniated brain tissue are negative three consecutive times, early surgical reduction of the fungus, along with repair of the dural and scalp defects, should be pursued. In advanced cases with significant infection, in addition to anti-infective and intracranial pressure-lowering treatments, mild disinfectants such as hydrogen peroxide, 0.1% potassium permanganate, 1% acetic acid solution, 4% boric acid solution, Dakin's solution, or 2.5% silver nitrate should be used to clean the cerebral fungus. This helps debride the infected wound and stimulate granulation tissue growth. Once a new granulation layer forms, pinch grafting can be performed to eliminate the infected wound, followed by scheduled reduction of the fungus and repair of the dural and scalp defects. For severely infected cerebral fungus with secondary intracranial lesions, the underlying cause of increased intracranial pressure must be addressed first. This may include abscess drainage, residual hematoma evacuation, hydrocephalus shunting, or foreign body removal. Only after intracranial hypertension is relieved can the cerebral fungus subside and the wound begin to heal. Performing surgery without proper preparation is not only ineffective but harmful, often leading to infection spread and worsening of the condition.

AD
expand_less