Hemorrhage on MRI

Last revised by Daniel J Bell on 9 May 2023

Hemorrhage on MRI has highly variable imaging characteristics that depend on:

  • the age of the blood

  • the type of hemoglobin present: oxy-, deoxy- or met-

  • whether or not the red blood cell walls are intact: i.e. intra- vs extracellular

  • the MRI sequence

Although MRI is often regarded as being insensitive to acute hemorrhage, this is in fact untrue, particularly with more modern sequences 5,7. However, the appearance of hemorrhage will be different at different times and is not perfectly stereotyped. Caution should therefore be exercised when precisely aging hemorrhages. 

The oxygenation state of hemoglobin and its location (whether it is contained within red blood cells or diffused in the extracellular space) have a tremendous effect on the imaging effects of blood. The three hemoglobin states to be considered are oxyhemoglobin, deoxyhemoglobin and methemoglobin. 

Oxyhemoglobin accounts for 95% of hemoglobin in arterial blood and 70% in venous blood. It is only weakly diamagnetic, having little T2* effect and only mildly shortening T1 relaxation time 2,6. This is the result of the heme iron existing in its ferrous form (Fe2+) with no unpaired electrons 2.

Deoxyhemoglobin, in contrast, having lost its oxygen, has four unpaired electrons and is therefore strongly paramagnetic. This results in a substantial signal loss and blooming artefact on T2* weighted sequences such as susceptibility-weighted imaging 2

Methemoglobin results from oxidative denaturation of the heme molecule to the ferric (Fe3+) form. It has five unpaired electrons and is also strongly paramagnetic 2

Oxyhemoglobin and deoxyhemoglobin produce little effect on the T1 signal. The presence of blood proteins results in intermediate T1 signals in hyperacute and acute hemorrhages. 

T2* weighted sequences, such as susceptibility-weighted imaging and gradient-echo are primarily affected by the hemoglobin oxygenation state and whether or not cell lysis has occurred 2

While contained within red blood cells, resulting in uneven distribution of paramagnetic effects, both deoxyhemoglobin and methemoglobin result in signal loss. Once the cells lyse and methemoglobin is distributed evenly throughout the clot, the local magnetic field distortion is also lost and T2 signal loss fades 2

Eventually, hemosiderin and ferritin (both strongly paramagnetic) are ingested by monocytes and macrophages and results once more in unevenly distributed paramagnetic effects and signal loss 2

Apparent diffusion coefficient (ADC) maps demonstrate fairly stable values substantially lower than normal white matter in all stages except for chronic (see below), whereas isotropic/trace DWI images, due to the combination of T2 and diffusion effects, demonstrate high signal only on hyperacute and late subacute phases 8

In general, five stages of hematoma evolution are recognized 8:

  1. hyperacute (<1 day)

    • intracellular oxyhemoglobin

    • T1: isointense

    • T2: isointense to hyperintense

    • DWI: high

    • ADC: low

  2. acute (1 to 3 days)

    • intracellular deoxyhemoglobin

    • T1: remains isointense to hypointense

    • T2: signal intensity drops (T2 shortening) to become hypointense

    • DWI: low

    • ADC: low

  3. early subacute (3 to 7 days)

    • intracellular methemoglobin

    • T1: signal gradually increases (T1 shortening) to become hyperintense

    • T2: remains hypointense

    • DWI: low

    • ADC: low

  4. late subacute (7 to 14-28 days)

    • extracellular methemoglobin

    • T1: remains hyperintense

    • T2: signal gradually increases over the next few weeks as cells break down and extracellular methemoglobin increases

    • DWI: high

    • ADC: low

  5. chronic (>14-28 days)

    • periphery

      • intracellular hemosiderin

      • T1: hypointense

      • T2: hypointense

    • center

      • extracellular haemichromes

      • T1: isointense

      • T2: hyperintense

      • DWI: low

      • ADC: high

Remembering these may be facilitated by these aging blood on MRI mnemonics.

  • extracranial blood products age differently from intracranial blood products, and extracranial hematomas often have a heterogeneous appearance, confounding attempts at reliably dating the age of an extracranial hemorrhage 3,4

  • subacute and chronic blood appears hypointense and blooms on MRI T2* weighted sequences (e.g. susceptibility weighted imaging (SWI))

  • the presence of blood products in a cavity will result in low ADC values and therefore make the utility of diffusion restriction in diagnosing pus in an abscess useless

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