bubble_chart Overview

Cerebral contusion and laceration is a collective term for brain contusion and laceration, as from the pathological perspective of brain injury, contusion and laceration often coexist simultaneously, with the distinction lying only in which is more severe or which is milder. Typically, superficial cerebral contusions and lacerations occur at the site of violent impact and the contrecoup site, especially the latter, which is usually more severe and frequently involves the frontal and temporal poles and the base of the brain. This is caused by the sliding and collision of brain tissue within the cranial cavity. Intraparenchymal cerebral contusions and lacerations, on the other hand, are often caused by deformation and shear stress of brain tissue leading to injury, commonly seen between structures of different densities, and primarily manifest as contusions and petechial hemorrhages.

bubble_chart Pathological Changes

The pathological changes of cerebral contusion and laceration, taking contrecoup cerebral contusion and laceration as an example, in mild cases, static blood and edema can be observed on the surface of the frontal and temporal lobes, with patchy hemorrhagic foci under the soft membrane. There are often fissures in the arachnoid membrane or soft membrane, and the cerebrospinal fluid appears bloody. In severe cases, the cerebral cortex and the underlying white matter are crushed and ruptured, with local hemorrhage, edema, and even hematoma formation. The damaged cortical vessels are embolized, the brain tissue becomes eroded and necrotic, and around the contusion and laceration area, there are patchy hemorrhagic foci and softening foci, extending wedge-shaped into the white matter. After 4–5 days, the necrotic tissue begins to liquefy, the blood decomposes, and the surrounding tissue shows rust-colored hemosiderin staining, with black coagulated blood fragments mixed in the eroded tissue. Even 1–3 days after the injury, the areas of local necrosis and liquefaction gradually absorb and form cysts, surrounded by glial cell proliferation for repair. The nearby brain tissue atrophies, the arachnoid membrane thickens and adheres to the dura mater and brain tissue, eventually forming a cerebral membrane scar.

In the early stages of cerebral contusion and laceration, microscopic examination reveals vacuolization of neuronal cytoplasm, disappearance of Nissl bodies, nuclear pyknosis, fragmentation, and dissolution, swelling and rupture of nerve axons, disappearance of the layered structure of the cerebral cortex, blurred boundaries between gray and white matter, swelling of glial cells, capillary congestion, and obvious extracellular space edema. In the following days to weeks, the contused and lacerated tissue gradually liquefies and enters the repair phase. The damaged area shows gitter cells phagocytosing disintegrated debris and myelin sheaths, along with glial cell hyperplasia and hypertrophy, fibroblast infiltration, local disappearance of nerve cells, and eventual replacement by glial scars.

bubble_chart Clinical Manifestations

The clinical manifestations of cerebral contusion and laceration vary greatly depending on the causative factors and the site of injury. In mild cases, there may be no primary disturbance of consciousness, such as in simple closed depressed fractures or crush injuries of the skull. In severe cases, it can lead to deep unconsciousness, severe disability, or even death.

Disturbance of consciousness: This is one of the most prominent clinical manifestations of cerebral contusion and laceration. Unconsciousness often occurs immediately after the injury, and its duration can range from minutes to hours, days, months, or even prolonged unconsciousness, depending on the severity of the injury. Prolonged unconsciousness is often associated with extensive cortical damage or brainstem injury. Generally, unconsciousness lasting more than 30 minutes after the injury is considered a reference criterion for diagnosing cerebral contusion and laceration.

Focal symptoms: These vary depending on the location and severity of the injury. If only the so-called "silent areas," such as the frontal or anterior temporal lobes, are affected, there may be no neurological deficits. However, if the functional areas of the cerebral cortex are damaged, corresponding symptoms such as paralysis, aphasia, visual field deficits, sensory disturbances, or focal seizures may occur. If a patient with cerebral contusion and laceration initially shows no positive neurological signs but later develops new localized symptoms, the possibility of secondary intracranial damage should be considered, and further examination should be conducted promptly.

Headache and vomiting: Headache symptoms can only be reported by the patient after they regain consciousness. If severe headache and frequent vomiting persist after the injury, or if symptoms worsen after initial improvement (Grade I), the cause should be investigated. If necessary, auxiliary examinations should be performed to rule out intracranial hematoma. For unconscious patients, care should be taken to prevent aspiration and the risk of suffocation during vomiting.

Vital signs: Significant changes are often observed. In the early stages, there is usually a drop in blood pressure, weak pulse, and shallow, rapid breathing due to cerebral inhibition after head injury. These symptoms typically gradually recover shortly after the injury. If hypotension persists, the possibility of combined injuries should be considered. Conversely, if vital signs recover quickly and blood pressure continues to rise, with an increased pulse pressure, strong and full pulse, slowed heart rate, and deeper, slower breathing, intracranial hematoma and/or cerebral edema or swelling should be suspected. Patients with cerebral contusion and laceration may also experience a mild fever (Grade I), usually around 38°C. Persistent high fever is often associated with hypothalamic injury.

Meningeal irritation: Due to subarachnoid hemorrhage after cerebral contusion and laceration, patients often exhibit signs of meningeal irritation, such as photophobia with closed eyes, curling up in bed, and early low-grade fever with nausea and vomiting. Neck stiffness usually resolves within about a week. If symptoms persist, the possibility of injury at the craniocervical junction or secondary intracranial infection should be considered.

bubble_chart Diagnosis

Patients with cerebral contusion and laceration often experience impaired consciousness, which frequently complicates neurological examinations. For patients presenting with positive neurological signs, the location and severity of damage can be assessed based on localized symptoms and the state of unconsciousness. In cases where consciousness is severely impaired and the patient exhibits poor responsiveness to external stimuli, identifying neurological deficits becomes challenging, even if they exist. This is particularly true for patients with multiple cerebral contusions and lacerations or deep brain injuries, where localization is difficult. Accurate diagnosis often relies on CT scans and other necessary auxiliary examinations.

bubble_chart Treatment Measures

The treatment of cerebral contusion and laceration should primarily focus on non-surgical methods, aiming to minimize the series of pathophysiological reactions following brain injury, closely monitor for secondary intracranial hematomas, maintain physiological balance in the internal and external environments of the body, and prevent various complications. Unless there is a secondary intracranial hematoma or uncontrollable intracranial hypertension requiring surgery, surgical intervention is generally unnecessary.

1) Non-surgical treatment: The onset of cerebral contusion and laceration coincides with the beginning of secondary brain damage, with the two closely linked and mutually causative. Therefore, initiating reasonable treatment as early as possible is key to reducing disability and mortality rates. The goals of non-surgical treatment are, first, to prevent a series of pathophysiological changes from exacerbating brain damage after injury, and second, to provide a favorable internal environment for the functional recovery of partially damaged brain cells. Thus, proper management should address both intracranial and systemic aspects. ① General management: For patients with mild or some moderate cerebral contusion and laceration with minor traumatic reactions, the focus is on symptomatic treatment, prevention and management of cerebral edema, close observation of the condition, and timely intracranial pressure monitoring and/or repeat CT scans. For patients in an unconscious state with moderate or severe injuries, in addition to non-surgical treatment, intensive care is required. If conditions permit, they should be admitted to the ICU (intensive care unit) for continuous monitoring with multi-channel physiological monitors and specialized nursing care. Patients should be placed in a lateral position to maintain airway patency and receive intermittent oxygen therapy. If the patient is not expected to regain consciousness within a short period (3–5 days), an early tracheostomy should be performed to facilitate timely secretion clearance, reduce airway resistance, and minimize dead space. Simultaneously, the head of the bed should be elevated by 15°–30° to promote intracranial venous return and reduce intracranial pressure. Daily fluid intake and output should be balanced. In the absence of excessive sodium loss, 500 ml/d of saline solution is sufficient, as excessive amounts may promote cerebral edema. When administering glucose-containing fluids, care should be taken to avoid hyperglycemia, which could worsen cerebral ischemia, hypoxia, and acidosis. If necessary, an appropriate dose of insulin should be given for correction, and the dosage should be adjusted promptly based on blood glucose measurements. If the patient remains unable to eat after 3–4 days, a nasogastric tube should be placed to provide liquid nutrition, maintaining daily caloric and nutritional needs. Additionally, for critically ill patients, regular blood tests for generation and transformation and acid-base balance should be conducted to guide treatment. Attention should also be paid to the prevention and management of heart, lung, liver, and kidney functions, as well as complications. ② Special management: Severe cerebral contusion and laceration patients often experience worsening conditions due to agitation, limb rigidity, high fever, and spasms. The underlying causes should be identified and addressed promptly and effectively. For patients presenting with central high fever, frequent decerebrate rigidity, diencephalic seizures, or persistent epilepsy early after injury, hypothermic hibernation therapy and/or barbiturate treatment should be considered. Traumatic acute brain swelling, also known as diffuse brain swelling (DBS), is a widespread cerebral enlargement in the early stages of severe brain injury, possibly related to cerebral vascular paralysis, dilation, or post-ischemic acute edema, and is more common in adolescents. Once it occurs, measures such as hyperventilation, barbiturates, steroids, and aggressive dehydration should be initiated as early as possible. Hypothermic hibernation and blood pressure reduction can also help alleviate vasogenic cerebral edema. Surgery is not beneficial and may even be harmful.

Disseminated intravascular coagulation (DIC) is a coagulation disorder secondary to brain injury. The cause lies in the high concentration of thromboplastin in brain tissue, which is released into the bloodstream after trauma, activating the coagulation system. Due to abnormal platelet aggregation, microthrombi may form in small blood vessels of the cerebral cortex, basal ganglia, white matter, and brainstem, followed by secondary hemorrhage caused by fibrinogenolysis. Delayed intracranial hematoma may also be related to this (Touho, 1986). Diagnosis of intravascular coagulation relies on laboratory tests, including thrombocytopenia, decreased fibrinogen, and prolonged prothrombin time. Once it occurs, fresh blood transfusion should be administered alongside active treatment of the brain injury to replenish clotting factors and platelets. Some authors also employ heparin anticoagulation therapy or antifibrinolytic agents to counteract excessive fibrinolysis. ③Reducing intracranial hypertension: Almost all patients with cerebral contusion and laceration experience varying degrees of increased intracranial pressure. Mild cases may be treated with bed rest, oxygen therapy, hormones, and dehydration as appropriate. Severe cases should undergo hyperventilation, high-dose hormone therapy, and dehydration treatment under intracranial pressure monitoring as early as possible. In critical conditions, hibernation cooling and barbiturate therapy should also be considered. Furthermore, severe brain trauma leads to significant changes in hemorheology, manifested by increased whole blood viscosity, plasma viscosity, hematocrit, erythrocyte aggregation, and fibrinogen, along with reduced erythrocyte deformability, the severity of which correlates positively with the injury. Enhanced erythrocyte aggregation and decreased deformability cause erythrocytes to stack into three-dimensional networks, increasing shear stress and blood viscosity, leading to microcirculatory stasis and microthrombi formation, thereby exacerbating secondary brain damage. Therefore, hemorheological changes should be monitored and corrected during the treatment of severe cerebral contusion and laceration. Currently, the commonly used neurosurgical dehydrating agent mannitol has a biphasic effect on hemorheology: early administration increases blood volume and dilutes the blood, while in the late stage [third stage], blood volume decreases, and blood viscosity rises relatively. Repeated use of mannitol may thus significantly increase blood viscosity, causing a so-called "rebound phenomenon" and even worsening vasogenic brain edema. To address this, some authors use hematocrit as an indicator during dehydration therapy for brain injury patients, maintaining a "optimal hematocrit" of 0.3–0.4. Low-molecular-weight dextran (Dextranum-40) is administered intravenously at 0.5g/kg/day for isovolemic or hypervolemic hemodilution therapy, keeping blood viscosity at the "optimal hematocrit" level to alleviate brain edema and secondary damage. ④Brain function recovery therapy: The goal is to reduce disability rates and improve quality of life, enabling traumatic brain injury patients to achieve as much independence as possible in daily life, work, and social interactions. Although brain function recovery primarily addresses late-stage [third stage] complications or sequelae such as paralysis, aphasia, epilepsy, and cognitive impairments, the importance of early preventive treatment must be emphasized. Brain function protection should be prioritized during the acute phase of traumatic brain injury to minimize deficits. Once the critical period has passed and the condition stabilizes, neurorestorative medications should be administered promptly, alongside functional rehabilitation, including physiotherapy, tuina, acupuncture, and passive or active exercise training.

2) Surgical treatment: Primary cerebral contusion and laceration generally do not require surgical intervention. However, surgery becomes necessary when secondary damage leads to intracranial hypertension or even brain herniation. Craniotomy for hematoma evacuation should be promptly performed in cases accompanied by intracranial hematoma exceeding 30ml, CT showing mass effect, poor response to non-surgical treatment, intracranial pressure monitoring exceeding 4.0kPa (30mmHg), or poor compliance. For severe cerebral contusion and laceration where progressive intracranial hypertension occurs due to pulped tissue and cerebral edema, and when intracranial pressure reduction measures prove ineffective with pressure reaching 5.33kPa (40mmHg), craniotomy should be performed to remove necrotic tissue, followed by internal or external decompression, with placement of basal cistern or ventricular drainage. In late-stage [third stage] cerebral contusion and laceration complicated by hydrocephalus, ventricular drainage should be performed first to identify the cause before providing corresponding treatment.

bubble_chart Differentiation

X-ray plain film: When the injury condition permits, X-ray skull plain film examination still holds significant value. It not only helps understand the specific situation of the fracture but also has special significance in analyzing the injury mechanism and assessing the injury severity.

CT scan: It can provide a clear differential diagnosis between cerebral contusion and concussion, and clearly display the location, extent, and presence of secondary damage such as hemorrhage and edema. Additionally, it can indirectly estimate intracranial pressure based on the size, shape, and displacement of the ventricles and cisterns. Most importantly, for atypical cases, regular CT scans can dynamically observe the evolution of cerebral edema or the occurrence of delayed hematomas. In recent years, CT has become a routine examination for acute head injuries in hospitals equipped with the technology, as early diagnosis is difficult to achieve based solely on injury history and physical examination. Stein et al. (1990) pointed out that in mild head injuries with GCS scores of 13–15, the positive detection rate of initial CT scans was as high as 18%, with 5% requiring surgical intervention, emphasizing the necessity of early CT examination.

MRI (Magnetic Resonance Imaging): It is generally less used for diagnosing acute cranial injuries. MRI requires longer imaging times, certain metal emergency equipment cannot be brought into the scanning room, and agitated patients may struggle to cooperate, making CT the preferred choice. However, under certain specific circumstances, MRI outperforms CT, such as in visualizing the brainstem, corpus callosum, and cranial nerves; detecting small cerebral contusion foci, axonal injuries, and early cerebral infarctions; and identifying hematomas in the CT isodense phase. MRI has unique advantages in these areas where CT is deficient.

Lumbar puncture: It helps determine the presence of blood in the cerebrospinal fluid, aiding in the differentiation from concussion. Additionally, it can measure intracranial pressure and drain bloody cerebrospinal fluid. However, it is contraindicated in patients with significant intracranial hypertension to avoid triggering brain herniation.

Other auxiliary examinations: For example, cerebral angiography is now less commonly used, but in hospitals or regions without CT, it remains necessary for auxiliary diagnosis. Electroencephalography (EEG) is primarily used for prognosis assessment or epilepsy monitoring. Brainstem auditory evoked potential (BAEP) testing is highly valuable for analyzing the extent of brain function impairment, especially in determining the level of brainstem injury. Furthermore, radionuclide examinations are important for diagnosing late-stage [third-stage] complications of cerebral contusion, such as vascular embolism, arteriovenous fistula, cerebrospinal fluid fistula disease, and hydrocephalus.