Haemorrhage on MRI

Last revised by Lam Van Le on 11 Jan 2025

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

  • the age of the blood

  • the type of haemoglobin 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 haemorrhage, this is untrue, particularly with more modern sequences 5,7. However, the appearance of haemorrhage will be different at different times and is not perfectly stereotyped. Caution should therefore be exercised when precisely ageing haemorrhages. 

The oxygenation state of haemoglobin and its location (whether it is contained within red blood cells or diffused in the extracellular space) has a tremendous effect on the imaging effects of blood. The three haemoglobin states to be considered are oxyhaemoglobin, deoxyhaemoglobin and methaemoglobin. 

Oxyhaemoglobin accounts for 95% of haemoglobin 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 haem iron existing in its ferrous form (Fe2+) with no unpaired electrons 2.

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

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

Oxyhaemoglobin and deoxyhaemoglobin produce little effect on the T1 signal. The presence of blood proteins results in intermediate T1 signals in hyperacute and acute haemorrhages. 

T2* weighted sequences, such as susceptibility-weighted imaging and gradient-echo are primarily affected by the haemoglobin 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 deoxyhaemoglobin and methaemoglobin result in signal loss. Once the cells lyse and methaemoglobin is distributed evenly throughout the clot, the local magnetic field distortion is also lost and T2 signal loss fades 2

Eventually, haemosiderin and ferritin (both strongly paramagnetic) are ingested by monocytes and macrophages andresults 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 haematoma evolution are recognised 8:

  1. hyperacute (<1 day)

    • intracellular oxyhaemoglobin

    • T1: isointense

    • T2: isointense to hyperintense

    • DWI: high

    • ADC: low

    • SWI: hyperintense, with thin hypointense rim

  2. acute (1 to 3 days)

    • intracellular deoxyhaemoglobin

    • T1: remains isointense to hypointense

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

    • DWI: low

    • ADC: low

    • SWI: hypointense

  3. early subacute (3 to 7 days)

    • intracellular methaemoglobin

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

    • T2: remains hypointense

    • DWI: low

    • ADC: low

    • SWI: hypointense

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

    • extracellular methaemoglobin

    • T1: remains hyperintense

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

    • DWI: high

    • ADC: low

    • SWI: hyperintense, with thin hypointense rim

  5. chronic (>14-28 days)

    • periphery

      • intracellular haemosiderin

      • T1: hypointense

      • T2: hypointense

      • SWI: hypointense rim

    • centre

      • extracellular hemichromes

      • T1: isointense

      • T2: hyperintense

      • DWI: low

      • ADC: high

      • SWI: variable

Remembering these may be facilitated by the ageing blood on MRI mnemonics.

  • extracranial blood products age differently from intracranial blood products, and extracranial haematomas often have a heterogeneous appearance, confounding attempts at reliably dating the age of an extracranial haemorrhage 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

Cases and figures

  • Figure 1: ageing blood on MRI
  • Case 1: hyperacute
  • Figure 2: MRI and CT characteristics
  • Case 2: late subacute extradural
  • Case 3: subacute sudural haematoma
  • Case 4: acute on chronic
  • Case 5: chronic
  • Case 6: early and late subacute
  • Case 7: subacute
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