Subdural Hematoma

A Clinical Imaging Primer

A subdural hematoma (SDH) is a collection of blood accumulating in the potential space between the dura mater and the arachnoid mater of the meninges. It is typically caused by the tearing of bridging veins that cross the subdural space to drain into the dural venous sinuses.

Because venous bleeding occurs at low pressure, an SDH often develops more slowly than an epidural hematoma (which is usually of arterial origin). The appearance of an SDH on a cranial Computed Tomography (CT) scan evolves sequentially as the blood products degrade over time.

Radiological Hallmarks

Key Characteristic: A subdural hematoma typically assumes a crescentic (sickle-shaped) morphology. It crosses cranial suture lines but is bounded by and cannot cross dural reflections (e.g., the falx cerebri or the tentorium cerebelli).

When evaluating a potential SDH, non-contrast CT of the head is the initial modality of choice. The density of the hematoma relative to the adjacent brain cortex signifies the age of the hemorrhage.

CT Appearance by Age

Acute

< 3 days

Freshly extravasated clotted blood acts as a high-density area. It appears hyperdense (bright white) compared to the adjacent cortex.

Subacute

3 days to 3 weeks

As protein degrades, the density decreases. It becomes isodense (grey) to the cortex, making it notoriously difficult to see. Key clues: sulcal effacement, grey-white matter junction buckling, or medial displacement of the superficial cortical veins.

Chronic

> 3 weeks

Fully liquefied protein/cellular degradation leaves a serous fluid. The hematoma becomes hypodense (dark), approaching the density of cerebrospinal fluid (CSF).

Special Situations on CT

Acute-on-Chronic: A common scenario where re-bleeding occurs into a chronic SDH. The CT shows mixed attenuation—typically a hypodense collection containing regions of hyperdensity, where heavier fresh red blood cells settle dependently (e.g., creating a hematocrit effect).
Anemic Patients: In patients with severe anemia (Hb < 10 g/dL), an acute SDH may appear isodense rather than hyperdense because the reduced protein concentration lowers the overall x-ray attenuation.

Magnetic Resonance Imaging (MRI)

While CT is faster and superior for detecting fresh hemorrhage and evaluating for surgical intervention, MRI is much more sensitive for detecting small subdural collections, subacute blood (when isodense on CT), and for delineating the exact age of the blood products based on the biochemical evolution of hemoglobin.

The MRI appearance of hemorrhage follows the reliable progression of hemoglobin degradation:

Age	State of Hemoglobin	T1 Signal	T2 Signal	Mnemonic
Hyperacute (< 24h)	Intracellular Oxyhemoglobin	Isointense	Hyperintense	I Be (Iso / Bright)
Acute (1-3 days)	Intracellular Deoxyhemoglobin	Isointense	Hypointense	I Dity (Iso / Dark)
Early Subacute (3+ days)	Intracellular Methemoglobin	Hyperintense	Hypointense	BleeD (Bright / Dark)
Late Subacute (1+ week)	Extracellular Methemoglobin	Hyperintense	Hyperintense	B B (Bright / Bright)
Chronic (> 14 days)	Hemosiderin / Ferritin	Hypointense	Hypointense	D D (Dark / Dark)

*The mnemonic (IBe IDity BleeD BB DD) is a classic radiology tool for recalling the MRI signal intensities of blood products over time.

Acute-on-Chronic Hemorrhage on MRI

Just as with CT, recurrent bleeding into a pre-existing chronic subdural hematoma (acute-on-chronic) is a frequent clinical entity. The fragility of the neo-vasculature that forms along the encapsulating membranes of a chronic SDH predisposes the collection to repeated bleeding episodes.

On MRI, an acute-on-chronic SDH will present with a distinctly heterogeneous appearance. The key diagnostic feature is the presence of multiple compartments containing blood products of different evolutionary ages within the same subdural space. Findings often include:

Multiple Signal Compartments: Regions demonstrating characteristics of chronic blood (e.g., T1 and T2 hypointense due to hemosiderin/ferritin) interspersed with areas showing signals typical of acute or subacute blood (e.g., T1 hyperintense methemoglobin or T2 hypointense deoxyhemoglobin).
Septations: The organizing membrane of the chronic collection may form internal septations, creating loculated pockets that bleed independently, further complicating the signal heterogeneity.
Fluid-Fluid Levels (Hematocrit Effect): Perhaps the most striking feature on MRI. The heavier cellular components containing fresh, acute blood (intracellular deoxyhemoglobin: T1 iso, T2 dark) will settle dependently beneath the lighter, serous fluid of the chronic hematoma (T1 dark, T2 bright). This creates a distinct, gravity-dependent horizontal line separating the different signal intensities.

Secondary Mass Effects

The severity of an SDH is typically not just defined by its thickness but by its mechanical effect on the brain parenchyma. In imaging reports, always evaluate for:

Midline Shift: Displacement of structures like the septum pellucidum and pineal gland across the median plane.
Sulcal Effacement: Compression of the cortical sulci on the ipsilateral hemi-cranium.
Ventricular Compression: Compression of the ipsilateral lateral ventricle, occasionally with dilatation of the contralateral ventricle (due to Monro foramen obstruction).
Herniation: Watch for subfalcine, uncal (transtentorial), or tonsillar herniation, which are neurosurgical emergencies.

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