Summary
Background
Haematomas compromise flaps in the absence of a pressure effect and pedicle thrombosis.
While animal models confirmed the toxic effect of whole blood on adjacently sited
random pattern flaps, our understanding of this phenomenon remains incomplete. Our
aim was to identify mechanisms by which a subjacent haematoma leads to flap compromise
to inform clinical practice.
Methods
A literature review was conducted of all peer-reviewed publications relating haematoma
to tissue compromise including free transferred tissue, vascularised flap models and
brain injury. Clinical correlation was made with free vascularised flaps and rhytidectomy
skin flaps.
Results
Haematomas compromise around 2–4% of free tissue transfers and local flaps. We propose
that several mechanisms are responsible. Cytokines, generated by platelet degradation,
recruit neutrophils, releasing both reactive oxygen species and proteolytic enzymes.
Reactive oxygen species (ROS), including superoxide and hydroxyl (OH−) are also produced by ATP degradation, promoted by NAD+ sequestration.
Additionally, the complement cascade is triggered by thrombin. Ferrous ions, freed
by complement-mediated lysis of erythrocytes and degradation of haemoglobin also promote
generation of ROS. Reactive oxygen species, complement and activated neutrophils cause
endothelial cell disruption, leading to activation of pro-thrombotic mechanisms and
small vessel occlusion, with consequent tissue ischaemia, which in turn generates
further ROS.
Conclusion
Haematomas cause tissue injury by a complex sequence of inter-related biochemical
and cellular processes merging on a common pathway of local tissue ischaemia which
the overlying tissue is unable to regulate. Emergent evacuation of haematoma must
be considered irrespective of envelope tension.
Keywords
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Article info
Publication history
Published online: January 09, 2012
Accepted:
December 20,
2011
Received:
October 12,
2011
Identification
Copyright
© 2011 British Association of Plastic, Reconstructive and Aesthetic Surgeons. Published by Elsevier Inc. All rights reserved.
