Cerebral contusion and laceration refer to primary organic brain injuries caused by violent trauma to the head. These injuries can occur both at the site of impact and in contralateral areas due to coup-contrecoup mechanisms.
Pathology
In mild cases, scattered petechial hemorrhages may be observed in the cerebral cortex beneath the local pia mater. Moderate cases often involve more extensive brain tissue damage, including pia mater tears and involvement of deep white matter. Severe cases are characterized by widespread crushing, rupture, necrosis, localized hemorrhage, and edema of the cerebral cortex and underlying white matter, sometimes leading to intracerebral hematoma formation. Microscopically, cerebral hemorrhage, indistinct or absent cortical layering may be seen.
Clinical Manifestations
Clinical presentations vary depending on the location, extent, and severity of the injury. Mild cases may exhibit minimal symptoms, while severe cases can result in deep coma or immediate death.
Altered Consciousness
Altered consciousness is one of the most prominent symptoms of cerebral contusion and laceration. It occurs immediately after injury, with duration ranging from minutes to months or even persistent coma, correlating with the severity of brain damage.
Headache, Nausea, and Emesis
These are the most common symptoms. Headaches may localize to the impact site or involve the entire head, presenting as intermittent or persistent pain, most pronounced within the first 1-2 weeks after injury. This is likely associated with subarachnoid hemorrhage, increased intracranial pressure, or cerebrovascular dysfunction. Early post-injury nausea and emesis may result from the forceful impact of cerebrospinal fluid on the brainstem vomiting center (located at the floor of the fourth ventricle), meningeal irritation from subarachnoid hemorrhage, or vestibular system stimulation. Delayed vomiting may arise from progressive intracranial pressure elevation.
Vital Signs
Patients with mild to moderate injuries typically exhibit stable blood pressure, pulse, and respiration. Severe cases may demonstrate elevated blood pressure, bradycardia, and deep, slow breathing due to intracranial hypertension caused by cerebral hemorrhage and edema. Critical cases may develop pathological breathing patterns.
Focal Neurological Deficits
Immediate post-injury neurological dysfunction corresponding to the lesion site may occur. Examples include contralateral limb paralysis from motor cortex damage or aphasia from language center injury. Injuries to the frontal or temporal poles may show no obvious neurological deficits.
Diagnosis
A diagnosis of cerebral contusion and laceration can often be made based on immediate post-injury signs, including disturbances of consciousness, focal symptoms and signs, as well as prominent manifestations such as headache, nausea, and vomiting. Neurological examination may be challenging in patients with impaired consciousness. When the injury involves the frontal pole, temporal pole, or basal surfaces of the frontal and temporal lobes, there may be no focal symptoms or signs, and a definitive diagnosis often requires auxiliary examinations such as CT scans.
A head CT scan effectively reveals the location, extent, and severity of cerebral contusion and laceration and is currently the most commonly used diagnostic tool. Typical CT findings include areas within the brain showing mixed high and low densities, where patchy high-density areas correspond to hemorrhagic foci, and low-density areas correspond to regions of edema. CT can also provide information on ventricular compression and midline shift. While MRI is rarely employed in the diagnosis of acute traumatic brain injuries due to its longer scan times, it is superior to CT in detecting milder contusion lesions.
Lumbar puncture can assess whether cerebrospinal fluid (CSF) contains blood, measure intracranial pressure, and drain hemorrhagic CSF to alleviate symptoms. However, lumbar puncture should be performed cautiously or avoided in patients with significantly elevated intracranial pressure.
Treatment
Close Monitoring of the Condition
Early-stage cerebral contusion and laceration patients frequently experience significant changes in their condition. Such patients require dedicated care, and those in severe condition should be admitted to a neurological intensive care unit (NICU) for close monitoring of vital signs, consciousness, pupil response, and limb activity. Intracranial pressure monitoring or repeat imaging studies, such as head CT scanning, may be necessary.
General Management
Positioning
The head of the bed is elevated to 15°–30° to promote venous blood return from the brain. For unconscious patients, the head is turned to one side, and they are placed in a lateral or semiprone position to prevent aspiration of saliva or vomitus.
Maintaining Airway Patency
Ensuring a clear airway is a crucial aspect of treatment. Airway obstruction can exacerbate brain edema, increase intracranial pressure, and worsen the patient’s condition. For unconscious patients, airway secretions must be promptly cleared. For patients unable to regain consciousness in the short term, early tracheostomy may be appropriate. Patients with respiratory depression or inadequate tidal volume may require ventilatory support.
Management of Agitation and Seizures
The causes of agitation, such as pain, urinary retention, increased intracranial pressure, uncomfortable positioning, or hypoxia, should be identified and addressed. It is particularly important to watch for agitation as a possible precursor to brain herniation. Seizures following cerebral contusion can worsen cerebral hypoxia and, in cases of status epilepticus, can be life-threatening. Seizures should be considered an emergency and managed with sedation and anticonvulsant therapy as needed.
Management of Hyperthermia
Elevated body temperature can increase metabolic rates, exacerbate cerebral hypoxia, and worsen cerebral edema. Hyperthermia requires timely management. For central fever, mild hypothermia therapy may be applied. For fever caused by other factors (e.g., infection), treatment should target the underlying cause.
Sedation and Analgesia
Medications such as opioids, benzodiazepines, GABA receptor agonists, and α2-receptor agonists lower cerebral metabolism and oxygen consumption, reduce stress and neuroinflammation, and improve cerebral ischemia and hypoxia, providing neuroprotective effects.
Prevention of Cerebral Edema or Swelling
Secondary cerebral edema or swelling and intracerebral hematoma are major causes of early death in patients with cerebral contusion and laceration. Controlling cerebral edema or swelling is therefore one of the most critical aspects of treatment.
Surgical Treatment
Surgical intervention should be considered under the following circumstances:
- Severe secondary cerebral edema that does not respond to dehydration therapy and results in worsening of the condition.
- Persistent intracranial hypertension following hematoma evacuation, with sustained edema or swelling of the injured brain tissue and no evidence of hematoma formation in other areas of the brain.
- Postoperative improvement following removal of contusion lesions and hematomas, followed by subsequent deterioration with signs of brain herniation.
Surgical options include removal of contused brain tissue, resection of the frontal or temporal poles, subtemporal decompression, and decompressive craniectomy.