Traumatic intracerebral hemorrhage expansion

J.Sales-Llopis

Neurosurgery Department, General University Hospital Alicante, Spain.

• Evaluating the Utility of Repeat Computed Tomography Scans in Patients with Isolated Mild Traumatic Subarachnoid Hemorrhage
• Scalp incision technique for decompressive hemicraniectomy: comparative systematic review and meta-analysis of the reverse question mark versus alternative retroauricular and Kempe incision techniques
• Predicting Hematoma Expansion and Prognosis in Cerebral Contusions: A Radiomics-Clinical Approach
• Andexanet alfa versus non-specific treatments for intracerebral hemorrhage in patients taking factor Xa inhibitors - Individual patient data analysis of ANNEXA-4 and TICH-NOAC
• Assessment of Midline Shift in Postdecompressive Craniectomy Patients in Neurocritical Care: Comparison between Transcranial Ultrasonography and Computerized Tomography
• Haemostatic therapies for stroke due to acute, spontaneous intracerebral haemorrhage
• Prognostic Neuroimaging Biomarkers in Acute Vascular Brain Injury and Traumatic Brain Injury
• Dual-energy computed tomography material decomposition improves prediction accuracy of hematoma expansion in traumatic intracranial hemorrhage

see also Spontaneous intracerebral hemorrhage expansion.

Traumatic intracerebral hemorrhage (ICH) expansion refers to the enlargement or growth of the hemorrhage within the brain following a traumatic brain injury (TBI).

Traumatic ICH expansion can have significant implications for the patient's outcome and is an important consideration in the management of traumatic brain injuries.

Several factors can contribute to the expansion of intracerebral hemorrhage after a traumatic injury:

Secondary Injury Mechanisms: Traumatic brain injuries can trigger secondary injury mechanisms, such as inflammation, edema, and increased intracranial pressure. These processes can exacerbate the initial bleeding and contribute to the expansion of the hemorrhage.

Coagulopathy: Disruption of blood vessels during a traumatic event can lead to coagulopathy, a condition where the blood's ability to clot is impaired. This can result in ongoing bleeding and contribute to the expansion of the intracerebral hemorrhage.

Vascular Injury: Damage to blood vessels within the brain can occur during a traumatic event. The compromised vascular integrity may lead to ongoing bleeding and hematoma expansion.

Rebleeding: In some cases, the initial traumatic injury may not lead to immediate hemorrhage expansion, but rebleeding can occur in the subsequent hours or days. This delayed bleeding can contribute to the enlargement of the intracerebral hemorrhage.

Shear Injury: Shearing forces during the traumatic event can cause additional damage to blood vessels and surrounding tissues, leading to further bleeding and expansion of the hemorrhage.

Management of traumatic intracerebral hemorrhage and its potential expansion involves a multidisciplinary approach, including close monitoring, medical interventions to control intracranial pressure, and, in some cases, surgical interventions to evacuate the hematoma. Early detection and prompt management are crucial to improving outcomes for patients with traumatic brain injuries and intracerebral hemorrhage.

Traumatic intracerebral hemorrhage, like spontaneous hemorrhage, often expands over time. The contrast extravasation, on multidetector CT angiography, is a strong and independent predictor of hematoma expansion, poor outcome, and increased risk of in-hospital mortality.

Genetic abnormalities have been identified as a risk factor for hematoma expansion in patients with traumatic brain injury. Trials targeting these genes are currently ongoing, and they may open avenues for targeted treatment.

Data showed that 51% of the subjects demonstrated an increase in tICH volume and that most of the increase occurred early. In addition, larger hematomas exhibited the greatest expansion. Thromboembolic complications were identified in 13% of subjects. This study demonstrates that tICH expansion between the baseline and 24-hour CT scans occurred in approximately half of the subjects. The earlier after injury that the initial CT scan is obtained, the greater is the likelihood that the hematoma will expand on subsequent scans. The time frame during which hemorrhagic expansion occurs provides an opportunity for early intervention to limit a process with adverse prognostic implications ¹⁾

Several noncontrast CT (NCCT) signs of heterogeneous density and irregular shape have been identified as predictors of hematoma expansion in ICH. The blend sign, black hole sign, swirl sign, fluid level, and hypodensities are signs of heterogeneous density; another, the island sign, reflects irregular shape ^{2) 3) 4) 5) 6) 7)}

Antoni et al. retrospectively analyzed data on patients with head trauma and antithrombotic therapy without pathologies on their initial CT. During the observation period, we followed a protocol of routine repeat CT before discharge for patients using vitamin K antagonists, clopidogrel, or direct oral anticoagulants.

793 patients fulfilled the inclusion criteria. Acetylsalicylic acid (ASA) was the most common antithrombotic therapy (46.4%), followed by vitamin K antagonists (VKA) (32.2%) and Clopidogrel (10.8%). We observed 11 delayed hemorrhages (1.2%) in total. The group of 390 patients receiving routine repeat CT showed nine delayed hemorrhages (2.3%). VKA was used in 6 of these 11 patients. One patient needed an urgent decompressive craniectomy while the other patients were discharged after an extended observation period. The patient requiring surgical intervention due to delayed hemorrhage showed neurological deterioration during the observation period.

CRoutine repeat CT scans without neurological deterioration are not necessary if patients are observed in a clinical setting. Patients using ASA as a single antithrombotic therapy do not require in-hospital observation after a negative CT scan ⁸⁾

85-year-old man with frontal traumatic brain injury under treatment with Apixaban.

Left frontal and right temporal subarachnoid hemorrhage (SAH) foci with ipsilateral post-traumatic contamination of the Sylvian fissure.

5 days later

Considerable increase in previous hemorrhages: Appearance of a left frontal intraparenchymal hematoma measuring 4.4 cm, causing a moderate mass effect expanding the sulci of the left frontal lobe and compressing the left frontal horn of the lateral ventricle. N The emergence of a voluminous subarachnoid hemorrhage filling the entire right Sylvian cistern, sulci of the right temporal convexity, and extending into the right side of the suprasellar cistern. In subcutaneous soft tissues, a discreet increase in the right frontal subcutaneous hematoma is observed. A complementary angio-CT of the Willis polygon is performed: No aneurysms are observed in the area of the subarachnoid hemorrhage.

Hemorrhagic progression of contusion (HPC) often occurs early in cerebral contusions (CC) patients, significantly impacting their prognosis. It is vital to promptly assess HPC and predict outcomes for effective tailored interventions, thereby enhancing prognosis in CC patients