Hemorrhage on MRI

Haemorrhage on MRI has highly variable imaging characteristics that depend on both the age of the blood, the type of haemoglobin present (oxy- deoxy- or met-), on whether or not the red blood cell walls are intact and the specifics of the MRI sequence. Although MRI is often thought of as not being sensitive to acute haemorrhage, this is not, in fact, true particularly with more modern sequences ^5,7.

The appearance of haemorrhage will, however, be different at different times and is not perfectly stereotyped, as such caution should be exercised in precisely ageing haemorrhages. 

Physiology

The factors that affect the appearance of haemorrhage on MRI vary according to the sequence. The oxygenation state of haemoglobin and the location of either contained within red blood cells or diffused in the extracellular space have a tremendous effect on the imaging effects of blood. The three haemoglobin states to be considered are oxyhaemoglobin, deoxyhaemoglobin and methaemoglobin. 

Oxyhaemoglobin, accounting for 95% of haemoglobin in arterial blood and 70% in venous blood, is only weakly diamagnetic, having little T2* and only mildly shortening T1 relaxation time ^2,6. This is the result of heme iron is in ferrous form (Fe2+) and has no unpaired electrons ². 

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

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

T1 weighted sequences

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

T2* weighted sequences

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 lotlost and T2 signal loss fades ². 

Eventually hemosiderin and ferritin (both paramagnetic) are then injestedingested by monocytes and macrophages and result once more in unevenly distributed paramagenic effects and signal loss ². 

Stages

In general, five stages of haematoma evolution are recognised:

1. hyperacute (<1day)
   • intracellular oxyhaemoglobin
   • isointense on T1
   • isointense to hyperintense on T2
2. acute (1 to 23 days)
   • intracellular deoxyhaemoglobin
   • T2 signal intensity drops (T2 shortening)
   • T1 remains intermediate-to-low
3. early subacute (2(3 to 7 days)
   • intracellular methaemoglobin
   • T1 signal gradually increases (T1 shortening) to become hyperintense
4. late subacute (7 to 14-28 days)
   • extracellular methaemoglobin: over the next few weeks, as cells break down, extracellular methaemoglobin leads to an increase in T2 signal 
5. chronic (>14-28 days)
   • periphery
     • intracellular haemosiderin
     • low on both T1 and T2
   • centre
     • extracellular haemichromes
     • isointense on T1, hyperintense on T2

Remembering these may be facilitated by this ageing blood on MRI mnemonic.

Practical points

• 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))