Cerebral Contusion

Etiology

The etiology of cerebral contusion is trauma to the head. Most of the time, it is a closed head injury, although open injuries can also result in contusions. Various mechanisms can cause such trauma, including:

• Road traffic accidents (motor vehicle, motorcycle, and pedestrian)
• Falls
• Physical aasault
• Recreation-related head injuries
• Sports injury
• Domestic violence
• Child abuse
• Blast injury
• Penetrating head injuries (missiles and non-missiles)

Epidemiology

TBI is a significant global cause of disability, death, and economic cost. In the United States, approximately 2.8 million TBIs occur annually, with one-third affecting children.[1][2] Over 250,000 patients are hospitalized for nonfatal TBIs, including 10% hospitalizations in children. Over 2.5 million patients are treated in the emergency department, with children comprising 25% of these cases. More than 50,000 patients die from TBI, with 4.5% of deaths related to children.[1] Fatalities in children are more common with falls and road traffic accidents.[4] The mortality rate has steadily declined over the past decades due to improvements in patient management.[5] 

The most common sports-related injuries resulting in emergency department visits are superficial injuries and cerebral contusions.[6] One year after TBI hospitalization, 43% of Americans have a residual disability, including physical, cognitive, behavioral, and psychosocial impairments; the prevalence of residents living with disabilities is 3.2 million.[1][2] The prevalence of self-reported head injury among adults aged 40 or older is 15.7% in the United States.[7] The rate is higher in men (20.0%) compared to women (12.0%), with non-Hispanic White respondents showing the highest (18.0%) compared to non-Hispanic Black respondents (8.9%).[7] 

TBI leads to 1 million hospitalizations per year in the European Union, accounting for the most deaths (50,000) following road traffic accidents.[8][9] Unfortunately, three-fourths of these victims are young people. A Chinese head trauma data bank has shown important information regarding cerebral contusions. The mortality rates of patients with no cerebral contusions, single cerebral contusions, and multiple cerebral contusions are 3.9%, 7.8%, and 14.8%, respectively. The mortality rate of patients with and without traumatic subarachnoid hemorrhage was 9.5% and 5.4%, respectively. The mortality rates for patients with no intracranial hematomas, single intracranial hematomas, and multiple intracranial hematomas were 5.8%, 8.4%, and 20.6%, respectively.[10] Approximately 51.6% of the patients had a cerebral contusion, and 49.9% had a traumatic subarachnoid hemorrhage.[10]

TBI related to recreation most commonly involved cerebral contusion in 29% of the cases, followed by a traumatic subarachnoid hemorrhage in 26%, subdural hematoma in 25%, and epidural hematoma in 23%.[11] In the Netherlands, road traffic accidents resulted in a contusion incidence of 46.6% among cyclists and 74.2% among motorcyclists.[12] A cerebral contusion occurs in over 50% of patients with severe TBI.[12] In adults older than 60 with TBI, cerebral contusions arise in approximately 18% of them.[13] Pediatric TBI frequently shows brain edema (72.9%), skull fracture (69.5%), and brain contusion (55.9%).[14]

The risk of a male patient having a TBI is double that of a female patient. However, after an injury is sustained, there is no statistically significant difference in mortality rates between male (7.5%) and female (7.2%) patients with TBI.[10]

Pathophysiology

Cerebral contusions are typically observed in the temporal and frontal lobes, although other sites can be affected through coup (beneath the impact) and contrecoup (opposite to the impact) mechanisms. The relative motion between the brain and skull produces compressive strains and skull deformation, most pronounced in the orbital roof, the temporal squama, and the ala major of the sphenoid bone.[15]

Different Forms of Cerebral Contusions

• Coup contusions: These contusions result from cavitation that arises due to the elastic movement of the skull following an impact. The negative pressures at the impact site may lead to the formation of gas bubbles, which then collapse rapidly, causing damage to the brain tissue.
• Contrecoup contusions: The distribution of contusions in this category does not align with the anticipated areas of negative pressure as proposed by cavitation theory. Ommaya has attributed these contusions to shear strains and deformation of the skull that act upon bony protuberances.
• Fracture contusions: These contusions occur as a result of intruding bone fragments and associated cavitation that follows blunt trauma.
• Gliding contusions: Frequently observed in the parasagittal regions and associated with diffuse axonal injury.

Theories Explaining the Formation of Cerebral Contusions

• Vibration theory: According to this theory, an impact generates vibratory waves that exert significant force on the contralateral side of the skull.
• Transmitted wave theory: This theory posits that a wave originating at the impact point can create a vacuum, leading to the disruption of blood vessels and resulting damage to the brain parenchyma.
• Brain displacement theory: This theory advocates that the momentum generated by acceleration-deceleration dynamics can cause the brain to detach from its supporting attachments.
• Skull deformation theory: This theory examines the alterations in skull structure that occur during impact events.
• Pressure gradient theory: This theory suggests that movement between the brain and the skull generates intracranial cavitation as a consequence of a localized, nonuniform pressure gradient.
• Rotational shear force theory: This theory illustrates that rapid rotational movements of the head may contribute to the occurrence of contusive injuries.

Brain contusions are lesions with a hemorrhagic character that typically begin in the brain's cortical area and, more commonly, at the crests of the gyri of the cerebrum. These lesions can progress to the subcortical white matter in the more severe forms of injury. Despite the primary cortical area's preference, they can also develop at the white-gray border with expansion into the overlying gray matter. The occurrence of hemorrhage within the contusion can lead to ischemia and edema in the local area, which progresses to tissue destruction, neuronal necrosis, and cavitation, accompanied by overlying reactive gliosis.

There are many instances where the progression and expansion of the hemorrhagic components in the areas surrounding the initial contusion have been observed. Contusion progression occurred with a frequency of 63% to 70%.[16][17] Progression typically occurs within the first 12 hours but may also develop within 3 to 4 days after TBI.[18] Historically, it was postulated that the hemorrhagic brain contusion progression occurred secondary to a coagulopathic event associated with TBI.[18][19][20] 

Endothelial injury and ruptured microvessels have been implicated in this process. More recently, the concept of traumatic penumbra has been postulated.[15]

In TBI, the contused brain is a major source of tissue factor release. Recent studies have proposed that the cerebrum's vasculature is mechanosensitive, activating endothelial cells in the penumbra that were not initially damaged by the contusion core. In this situation, the contusion penumbra experiences activation of 2 transcription factors (endothelial mechanosensitive mechanisms), which are the specificity protein 1 (transcription factor 1) and nuclear factor kappa B.[21] The importance of these factors in controlling sulfonylurea receptor 1-transient receptor potential melastatin 4, which forms the regulatory subunit of the NCCa-ATP channel, is of interest in the context of the damage cascade.[22][23][24][25] 

The nuclear factor kappa B leads to apoptosis, whereas the specificity factor 1 causes vascular fragmentation. Both factors are associated with dysfunction or damage to vascular entities, resulting in microvascular failure and endothelial necrosis.[18][26] Contusion progression risk factors independently associated with the hematoma growth included an initial volume, cisternal compression, decompressive craniectomy, age, falls as the mechanism of trauma, multiple hematomas, and hypoxia.[16]

The initial trauma from the brain injury can lead to immediate cell death through necrosis. The cell lyses and releases harmful substances, including inflammatory chemokines and cytokines, reactive oxygen species, and proteases. The release of inflammatory mediators, including pro-inflammatory cytokines, as well as the breakdown of the blood-brain barrier, leads to the development of cerebral edema. Secondary injury from excitatory amino acids, including glutamate and aspartate, increased intercellular cytosolic calcium concentration, acidosis, and free radical production. Glutamate excitotoxicity can cause persistent membrane depolarization, which activates ion channels, particularly N-methyl-D-aspartate channels. Secondary to the permanent opening of N-methyl-D-aspartate channels, sodium and calcium ions enter cells, whereas potassium ions are extruded into the extracellular space.[27] A shift of potassium into the extracellular space results in rapid swelling of astrocytes, which absorb potassium to preserve ionic homeostasis.[28] 

Free radicals cause damage to genetic material, leading to the downregulation of genes and mitochondrial disruption. This disruption results in ion dyshomeostasis and consequent neuronal and astrocytic swelling, ultimately leading to cell death. Once the autoregulatory mechanisms have been abolished, cerebral blood flow passively follows changes in arterial blood pressure and impaired cerebral pressure. In the central core area, cerebral blood flow is 4.7 mL/100 g/min, whereas in the peripheral zone, it ranges from 16 to 18 mL/100 g/min.[28] Irreversible neuronal death occurs when cerebral blood flow is below 8 cc/100g/min, whereas neurons can recover if they have a cerebral blood flow of 9 to 18 cc/100g/min.[29]

Brain edema formation begins with vasogenic edema, resulting from the breakdown of the blood-brain barrier and the extravasation of fluid into the extracellular space, which typically occurs within 12 to 24 hours after injury. Then, a secondary injury caused by a cascade of mechanisms initiated at the moment of injury sets in after 24 to 72 hours and progresses for 7 to 10 days. A third phase occurs with the lysis of red blood cells in the intracerebral clot.

Histopathology

Edema is a rapid response that typically begins within minutes of an injury, peaks over several days, and resolves within 6 days. In contrast, hemorrhage initiates and expands within hours, particularly around perivascular areas, reaching maximum accumulation within just 24 hours. Notably, red blood cells retain their viability for up to 5 to 6 months after the injury. Polymorphonuclear leukocytes act quickly, initiating their response within hours of the injury and remaining visible for up to a month. Within just 2 hours, degenerated neurons, including red neurons, become apparent, signaling the immediate impact of injury. Macrophages and scavenger cells emerge within 24 hours, reach their peak between 7 and 14 days, and then gradually decline, illustrating the body's dynamic response to the healing process. Hemosiderin and siderophages can be detected as early as 5 days post injury and can persist for years as indicators of the body's healing trajectory. Hematoidin pigment appears 10 to 12 days after the injury and persists for years within hemorrhagic lesions. Angiogenesis, the formation of new blood vessels, begins 5 to 7 days post injury and reaches its peak by 3 weeks, illustrating the body's remarkable capacity for regeneration. The astrocytic reaction involves initial protoplasmic astroglial proliferation starting 4 to 5 days post injury, followed by fibrillary astroglial proliferation from 7 to 10 days, culminating in the formation of a glial scar that is crucial for restoring the blood-brain barrier. Additionally, fibroblasts appear within 1 week of the injury and can persist for months or even years, playing a vital role in collagen production and the development of fibrosis. This complex interplay of cellular responses highlights the body's remarkable ability to respond to injury and facilitate healing.

History and Physical

An initial trauma assessment is performed. Rapid imaging studies, with identification of possible surgical injuries, are performed after adequate resuscitation. Proper immobilization should be maintained until the stability of the entire spine has been confirmed. The mechanism of trauma is obtained from the patient, relatives, or paramedics.

A detailed neurologic examination is performed. If sedation was given, it should be stopped for an adequate neurological assessment. The patient is evaluated for response to stimuli in eye, motor, and verbal forms. The Glasgow Coma Scale (GCS) was established by Teasdale and Jennett in 1974.[30] This tool helps obtain the best response from a patient and presents the status to the healthcare team. Additionally, GCS helps in comparing future evaluations. The pupillary response is critical in the initial assessment.

Evaluation

X-rays should routinely be performed for a trauma workup. Imaging of the entire spine, chest, and pelvis should be obtained along with any other evident bones involved. Laboratories should include a complete blood count, a comprehensive metabolic panel, an international normalized ratio, and toxicology testing. Arterial blood gases are required for intubated patients and those with respiratory distress.

A head computed tomography (CT) scan should be performed for patients with impaired consciousness or history of loss of consciousness, focal neurologic findings, persistent vomiting, seizures, and an abnormal GCS score.[31] Initially, the CT scan may show isodense or hypodense areas, sometimes mixed-density lesions, commonly surrounded by perilesional hypodense regions. However, as time progresses, more surrounding edema develops. Multiple focal contusions may have a salt-and-pepper appearance. The bone window is used for evaluating skull fractures. A minor contusion near the skull base may be missed due to partial volume averaging. Models such as Brain Lesion Analysis and Segmentation Tool for Computed Tomography (BLAST-CT) help better categorize and quantify the cerebral contusions.[32]

Brain magnetic resonance imaging (MRI) is not indicated in the acute management of TBI.[31] If acutely performed, there are isointense to hyperintense areas on T1-weighted images and hyperintense on T2-weighted images. Fluid-attenuated inversion recovery images demonstrate petechial hemorrhages that are isointense to the brain. The MRI can detect ischemic areas and changes associated with diffuse axonal injury. The MRI can also be used later for cognitive problems. The logistic barriers to acquiring and analyzing CT data are lower compared to MRI-based approaches in the acute phases of the cerebral contusions.[32]

Treatment / Management

A dictum is a stringent neurological assessment used to determine the level of consciousness. Assessment of pupillary size and GCS score is the most straightforward and effective approach for monitoring patients.[32] Preventing hypotension or hypoxia according to the Advanced Trauma Life Support guidelines is crucial. Optimising cerebral perfusion and monitoring intracranial pressure (ICP) is pivotal.[15] Tranexamic acid helps stabilise the contusions.

After the head CT scan is obtained, management is decided. In patients with no immediate neurosurgical lesions, the priority is managing ICP. Monitoring ICP is performed if the GCS is below 8. An external ventricular drain has the advantage of cerebrospinal fluid (CSF) drainage. Intraparenchymal devices can also be used. In patients with cerebral contusions, seizure prophylaxis is started for 7 days to prevent posttraumatic seizures. Cerebral perfusion pressure (CPP) is defined as the difference between the mean arterial pressure (MAP) and the ICP. CPP = MAP − ICP. The treatment goals are to maintain an ICP of under 20 mm Hg and a CPP of above 60 mm Hg. Patients with increased ICP are treated using sedation, diuresis, and hypertonic saline.

Some patients need immediate craniotomy for evacuation of the contusion; however, there is still debate about the value of removing intraparenchymal lesions. Indications for surgical removal include progressive neurological deterioration, signs of mass effect on brain CT, unresponsive increased ICP, midline deviation of more than 5 mm, cistern compression evidenced on brain CT, and temporal contusions of greater than 20 cc of volume.[33] In extreme cases, unresponsive to the usual mechanisms to reduce the ICP, decompressive craniectomy can be performed, resulting in lower mortality but also with more patients in a vegetative state.[34] 

Hemorrhage/contusion progression in up to 87% of the cases is a potential complication of decompressive craniectomy.[17][35] Corticosteroids are not recommended for the management of increased ICP. Early enteral nutritional support should be started within 72 hours. The Brain Trauma Foundation has specific guideline recommendations, along with the level of evidence for each one, that can be used to develop treatment protocols.[36][37](B2)

The American College of Surgeons published a three-tiered protocol in 2015 for managing increased ICP. 

Tier 1

• The head of the bed is elevated at a 30° angle.
• Sedation and analgesia using short-acting agents for intubated patients.
• External ventricular drain with intermittent drainage.
• Repeat head CT imaging if no improvement.
• If ICP remains ≥20 to 25 mm Hg, proceed to Tier 2.

Tier 2

• If using a parenchymal ICP device, change to an external ventricular drain.
• Hyperosmolar therapy (mannitol or hypertonic saline) is given intermittently.
• Mannitol is administered in intermittent boluses (0.25 to 1 g/kg body weight). Check the serum sodium and osmolality frequently; additional doses are held if the serum osmolality exceeds 320 mOsm/L.
• Hypertonic saline, a 3% sodium chloride solution, is administered in intermittent boluses of 250 mL over 0.5 hours (2-5 mL/kg over 10-20 minutes). Serum sodium and osmolality are monitored every 6 hours. Additional doses are held if the serum sodium level exceeds 160 mEq/L. A bolus of up to 23.4% sodium chloride solution can be given for refractory increased ICP.
• CPP no less than 50 mm Hg, with a target range of 60 to 70 mm Hg.
• PaCO₂ should be maintained between 30 and 35 mmHg.
• Repeat head CT imaging if no improvement.
• Administer a test bolus of neuromuscular paralytic agent if indicated.
• If ICP remains ≥20 to 25 mm Hg, proceed to the next tier.

Tier 3

• Decompressive hemicraniectomy or bilateral craniectomy.
• Neuromuscular paralysis through continuous infusion (titrated to maintain at least 2 twitches out of a train-of-four). Adequate sedation must be utilized.
• Barbiturate or propofol coma. Hypotension is a common adverse effect. Continuous EEG is used to achieve burst suppression.
• Hypothermia below 36 °C is not indicated as an initial TBI treatment. Use only as salvage therapy after all previous Tier 3 treatments have failed.

Evolution in the Management Strategies for Cerebral Contusions

In the early 20th century, techniques such as gentle dehydration using magnesium sulfate and sodium chloride administered rectally, along with the removal of CSF, were commonly practiced.[15] Later, in the 1950s, hyperosmolar compounds such as urea were introduced, followed by mannitol and hypertonic saline in the 1960s. In the same decade, Nils Lundberg pioneered the use of a ventricular catheter for monitoring ICP. In 1981, Galbraith and Teasdale established ICP-based management guidelines. Harvey Cushing performed a subtemporal decompressive craniectomy in 1908, and Polin recommended performing decompressive craniectomy within 48 hours if ICP exceeded 40 mm Hg.[15] Multimodal monitoring emerged in the early 2000s, and currently, algorithm-based ICP management is the recommended approach.

According to the Brain Trauma Foundation guidelines and expert opinion from the Scandinavian Neurotrauma Committee, surgery is indicated under the following conditions:

• Contusion volume greater than 50 cm³
• GCS score of 6 to 8 with frontal or temporal contusions greater than 20 cm³, a midline shift greater than 5 mm, and cisternal compression
• Neurological deterioration and refractory high ICP [15]

Surgical strategies include focal lesionectomy and decompressive craniectomy.

Venous Thromboembolism Prophylaxis in Cerebral Contusion

Patients with TBI, particularly those with cerebral contusions, face a substantially elevated risk of venous thromboembolism with reported incidence rates approaching 25% in moderate-to-severe cases and exceeding 30% in specific high-risk cohorts.[36] This predisposition stems from a hypercoagulable state triggered by the release of tissue factor, endothelial injury, and prolonged immobilization, which collectively amplify thrombogenic mechanisms.[38][39] Current guidelines strongly advocate early initiation of pharmacological prophylaxis, barring contraindications, such as active intracranial hemorrhage or coagulopathy. Low-molecular-weight heparin has demonstrated superiority over unfractionated heparin for venous thromboembolism prevention in trauma populations, including those with TBI, due to its more predictable pharmacokinetics, reduced bleeding complications, and lower failure rates.[36] The optimal timing for chemoprophylaxis initiation remains nuanced, although contemporary evidence supports administration within 24 to 72 hours post injury, provided follow-up neuroimaging confirms hematoma stability. Mechanical prophylaxis, including intermittent pneumatic compression, should be employed during periods when pharmacological agents are contraindicated; however, its efficacy as monotherapy remains inferior to that of anticoagulant-based approaches. Geriatric patients and those with obesity or polytrauma warrant heightened vigilance given their compounded thrombotic risks. In contrast, paediatric protocols now preferentially recommend direct oral anticoagulants, such as dabigatran or rivaroxaban, over traditional agents based on 2025 guideline updates.[38] Critically underutilization persists with nearly 50% of eligible patients receiving delayed or suboptimal prophylaxis, contributing to preventable morbidity, including fatal pulmonary embolism, which frequently manifests within 5 to 7 days post injury.[40](B2)

Differential Diagnosis

After a traumatic event, cerebral contusions are typically distinguishable from other conditions. However, in rare instances, a patient may first have a nontraumatic hemorrhage, which then provokes a traumatic event, including:

• Traumatic intracerebral hemorrhage
• Hypertensive hemorrhagic stroke
• Lobar bleed from amyloid angiopathy
• Cerebral venous thrombosis with hemorrhagic transformation
• Intraparenchymal hemorrhage from a ruptured aneurysm
• Reperfusion injury in strokes
• Diffuse axonal injury
• Cerebral cavernoma
• Acute intratumoral bleed
• Hemorrhagic metastasis

Prognosis

Mortality increases as the GCS decreases. The most critical factors in the outcome are the patient's age and mechanism of injury.[41] A prolonged duration of coma is a strong predictor of long-term disability. For moderate head injuries, approximately 60% of the patients make a positive recovery, but 25% have a residual moderate degree of disability. In severe head injury cases, only 25% to 33% have positive outcomes. Patients may experience impaired concentration, attention, and memory. Cognitive deficits and personality changes may persist. A brain contusion is an essential factor in the development of posttraumatic seizures.[42]

The number of non-reactive pupils (0-2) has recently been used as a prognostic indicator in TBI.[43] A commonly used formula subtracts the number of non-reactive pupils from GCS. In patients with a GCS of 3 and no reactive pupils, the mortality rate 6 months after injury is 74%, and the unfavorable outcome is 90%. If one pupil is reactive, the mortality rate 6 months after injury is 47%, and the unfavorable outcome is 70%. If both pupils are reactive, the mortality rate 6 months after injury is 28%, and the unfavorable outcome is 50%. Very similar results are found in patients with a GCS of 4. For patients with a GCS of 5 and no reactive pupil, the mortality rate 6 months after injury is 54%, and the unfavorable outcome rate is 82%.

Increasing age is a significant factor for mortality and unfavorable recovery 6 months after TBI.[44] The same study found that the outcomes based on single CT findings, such as hematoma, cisterns, or subarachnoid hemorrhage, are very similar among patients. However, when the 3 findings are combined, a progression toward an unfavorable outcome is observed, based on the number of abnormalities present in the study.

The Glasgow Outcome Scale is used for outcome assessment, employing a 5-point scale.[45]

• Score 5—Good recovery: Minor disabilities may be present, but the individual can resume everyday daily life
• Score 4—Moderate disability: More significant disabilities are present, but the individual is still able to live independently. Individuals can use public transportation and work in an assisted situation.
• Score 3—Severe disability: The individual is conscious but dependent on others for daily care, often requiring institutional support.
• Score 2—Persistent vegetative state: The individual is not conscious, though eyes may be open and may track movement
• Score 1—Death

Classifications to predict outcomes on TBI have been developed and published. The Marshall CT classification evaluates midline shift, cistern patency, hematoma size, and whether surgery was performed.[46] The Rotterdam CT score assesses midline shift, cistern patency, presence of an epidural mass, and the presence of intraventricular or subarachnoid blood.[47][48] The Rotterdam CT score has been validated recently in the literature.[49]

The largest temporal contusions impose higher odds of dependency and mortality compared to similarly sized frontal contusions, due to the early risk of central descending transtentorial herniation.[32] Machine learning algorithms have also been devised to prognosticate clinical outcomes.[50] The outcome of surgery in cerebral contusions is derived from the Surgical Trial in Traumatic Intracerebral Hemorrhage (STITCH) randomized controlled trial and the CENTER-TBI study.[15] DECRA and RESCUEicp trials have shown increased dependency, though improved survival rates among cohorts undergoing decompressive surgery.[15]

Complications

Hemorrhagic Progression of Contusion

The reported prevalence of hemorrhagic progression of contusion (HPC) ranges from 16% to 75%, with up to 20% of the same requiring surgery, conferring high rates of morbidity and mortality.[51] This discrepancy may be due to the lack of a standardized definition of HPC, which ranges from a 5% to 50% increase in diameter to a 1 cm increase, and a 12.5 mL increase in volume. Various methods are employed for assessing contusion volume, including the ABC/2 formula, manual segmentation, and automated image segmentation. Additionally, some authors refer to this phenomenon as progressive hemorrhagic injury, encompassing any hemorrhagic lesions, such as subarachnoid hemorrhage and subdural hematoma, in conjunction with contusions.[52] HPC typically occurs within the first 24 hours and may last for up to 1 week.[50][52]

Pathophysiology of progression: Initially, it was believed that the progression of contusions resulted from fractured microvessels, which can be exacerbated by coagulopathy. Recently, the concept of traumatic penumbra surrounding the contusion core has been postulated, involving specificity protein 1 and nuclear factor kappa B.[52]

Risk variables and predictors for progression:

• Advanced age: Due to microvasculature fragility and reduced resting cerebral blood flow
• Low GCS at presentation
• Male sex: Estrogen and progesterone in females confer membrane stability (inhibiting lipid peroxidation) and decrease apoptosis (through Bcl-2 upregulation)
• Hypertension: Increased blood-brain barrier permeability. Chronic hypertension increases the lower limit of autoregulation through a rightward shift of the cerebral autoregulatory curve 
• Smoking increases vessel fragility and reduces cerebral blood flow through vasospasm
• Alcohol impairs platelet function and minimizes vascular tone
• Hypoxia
• Coagulopathy: The most determining variables are the international normalized ratio and platelet count
• Low triglyceride levels (<150 mg/dL): Cholesterol is an essential constituent of the cell membrane
• Timing of the initial CT
• Baseline contusion characteristics:
  • Volume ≤4 mL is unlikely to progress
  • Location: Frontal contusions have a high predilection for progression
  • Bilateral or multiple contusions can coalesce

• Coexisting lesions: Subdural hematoma, subarachnoid hemorrhage, or skull fractures involving cortical veins, bridging veins, and venous sinuses
• A Rotterdam score of 5 or higher 
• Basal cistern compression, midline shift ≥5 mm
• Leakage sign in CTA
• Decompressive craniectomy: Loss of the tamponade effect
• Multihematoma fuzzy sign
• Low monocyte-to-lymphocyte ratio in CSF
• Low glucose-to-lactate ratio in CSF
• Use of antiplatelets [15][50][53][54]

Dual-energy CT (190 keV) is ideal for assessing the HPC.[52][55] HPC increases the length of surgical intervention, intensive care unit stay, ventilatory support, hospital stay, nosocomial infections, unfavorable clinical outcomes, and short- and long-term mortality.[52]

Other Complications

• Seizures: Early seizures are due to bleeding. The involved regions are later replaced with cavitated regions of gliosis and retracted plaque of hemosiderosis (plaque jaune), both of which are epileptogenic.
• Trauma-induced coagulopathy
• Acute and chronic hydrocephalus
• Dysautonomia
• Dyselectrolyetemia: Cerebral salt wasting and syndrome of inappropriate antidiuretic hormone secretion
• Superficial siderosis
• Persistent neurological deficits
• Pseudoaneurysm
• Vasospsam
• Dependency
• Coma
• Death
• Employment disability
• Impaired concentration, attention, and memory
• Cognitive deficits
• Personality changes
• Posttraumatic stress disorder and other mental health issues
• Chronic traumatic encephalopathy
• Complications related to chronic ICU stay
• Complications related to general anesthesia and surgery [15][53]