Acute stage and signs of active bleeding
On non-contrast CT, a typical acute subdural hematoma appears as a hyperdense (bright) collection of blood. However, its radiologic density may be atypical. In some cases, a fresh hematoma appears only slightly hyperdense or completely isodense relative to the adjacent brain parenchyma. This occurs for two reasons:
- The patient has a low hematocrit (severe anemia).
- The injury is accompanied by a tear of the arachnoid mater, allowing cerebrospinal fluid (CSF) to enter the subdural space and dilute the blood.
A critically important finding on CT is the presence of hypodense areas (low-density zones) within the main hyperdense mass of an acute SDH. This indicates active bleeding and ongoing enlargement of the hematoma volume. If such a patient shows clinical deterioration, a very low threshold for repeat (follow-up) imaging is required.
Hematoma evolution: subacute and chronic stages
Over time, the blood clot degrades, which is reflected on CT as a gradual decrease in radiologic density:
- Subacute stage (ranging from several days to a few weeks). Hematoma density varies from slightly hyperdense to isodense. At this stage, SDH may visually blend with the density of the adjacent cerebral cortex (e.g., the parietal lobe), requiring careful analysis of the scans.
- Chronic stage (several weeks and beyond). Density continues to decrease, and the hematoma becomes hypodense (dark).
A key distinction between subacute and chronic hematomas and acute ones is the formation of reactive granulation tissue membranes within the subdural space. On CT scans, especially following surgical drainage (e.g., via a burr hole), these membranes are clearly visible as partitions (septa) within the hematoma cavity.
Acute hemorrhage into a chronic hematoma
Special attention should be paid to the phenomenon of repeat hemorrhage into a pre-existing chronic SDH (acute-on-chronic), which is often accompanied by acute neurological deterioration and requires re-hospitalization.
On non-contrast CT, this condition appears as the emergence of fresh, hyperdense (acute) blood against the background of an old, hypodense (chronic) hematoma. The distribution of the fresh blood exhibits a characteristic layered or septated pattern. This unusual spread is caused by the presence of previously formed multiple septa and membranes that mechanically restrict the propagation of the new blood portion within the subdural space.
Associated traumatic injuries
Subdural hematoma rarely occurs in isolation. The goal of primary CT is not only to identify the SDH itself but also to evaluate associated injuries (contusions, epidural hematomas, hydrocephalus).
- Cerebral contusions: The most common type of parenchymal injury. Contusion foci are localized in the cortex and subcortical white matter (most often in the anterior-inferior parts of the frontal lobes and the anterior parts of the temporal lobes). Contre-coup contusions on the side opposite to the impact are possible.
- Traumatic subarachnoid hemorrhage (SAH): Blood accumulates in the sulci on the convexity, the Sylvian fissure, the interpeduncular cistern, or the ambient cistern. Focal SAH in the ambient cistern may indicate contusion of the brainstem against the tentorium cerebelli.
- Edema dynamics: In the early post-traumatic period, contusions often increase due to the progression of the hemorrhagic component, with worsening pericontusional edema and parenchymal swelling, leading to effacement of the cerebral sulci.
Briefly: answers to topical questions
Rupture of which blood vessels is the primary source of hemorrhage in the formation of a subdural hematoma?
The primary source of bleeding in a subdural hematoma is the rupture of bridging veins of the brain connecting the cortex to the venous sinuses.
- Bridging veins (cerebral bridging veins) — their thrombosis secondary to rupture underlies the primary injury in SDH formation.
- The bleeding is predominantly of a venous nature, unlike the arterial bleeding in epidural hematoma.
- Some cases are associated with the rupture of pial vessels on the brain surface.
How does a subdural hematoma spread within the cranial cavity in relation to cranial sutures and dural reflections?
A subdural hematoma spreads extensively across the surface of the brain and may abut the falx cerebri and tentorium cerebelli.
Evolution of SDH density on CT: hyperdense (acute) → isodense (subacute) → hypodense (chronic).
Class and exam questions
Why does an acute subdural hematoma sometimes not appear bright (hyperdense) on CT?
Acute SDH can be isodense (blending with brain tissue) if the patient has low hematocrit due to anemia, or if the arachnoid mater was torn during trauma and the blood was diluted by CSF.
How to determine from a CT scan that bleeding into the hematoma is still ongoing?
Active bleeding is indicated by lower-density areas (hypodense zones) located within a fresh hyperdense subdural (or epidural) hematoma.
What is the acute-on-chronic phenomenon in subdural hematoma?
This is a situation where fresh (acute) hemorrhage occurs into a pre-existing chronic hematoma. CT shows foci of bright fresh blood inside the dark chronic hematoma, with blood layering due to the presence of septated membranes.
How to differentiate traumatic subarachnoid hemorrhage from aneurysm rupture?
Aneurysmal SAH typically presents with a moderate or large volume of blood in the basal cisterns. Traumatic SAH is confirmed by the presence of other TBI markers (SDH, contusions); if in doubt, CT angiography is ordered.
What else to study on this topic
- Traumatic subarachnoid hemorrhage (SAH) and its differential diagnosis
- Cerebral contusion: direct impact zones and contre-coup injuries
- Evolution of contusion foci and pericontusional edema on follow-up CT scans
- Diffuse axonal injury (DAI) in high-velocity trauma
- Depressed skull fractures and their association with underlying parenchymal injury
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