Ecchymosis

Ecchymoses are discolourations of the skin =>10mm in diameter, caused by displacement of red blood cells or their products into the extravascular space, particularly the subcutaneous tissue. Ecchymoses can be traumatic or a sign of other underlying disease.

Traumatic vs. Non-traumatic Ecchymoses

Traumatic ecchymoses may arise from iatrogenic causes, i.e. venepuncture and cannulation, surgery, or otherwise. In these circumstances, the following mechanism takes place:

1. A vessel containing blood is punctured.
2. Prior to successful clotting, red blood cells escape the vein (which travels in the subcutaneous tissue and has tunica intima, media, and externa, just as arteries have).
3. Red blood cells continue to enter the subcutaneous tissue until a clot is formed at the perforation of the vessel.

Non-iatrogenic traumatic ecchymoses may arise anywhere around the body. Bruises in specific positions may be named and have deeper clinical meaning than meets the eye.

Ecchymoses may arise from non-traumatic causes too. These include but are not limited to clotting disorders, renal failure, cirrhosis, leukaemia, aplastic anaemia, and intraperitoneal or retroperitoneal organ haemorrhage. *Keep in mind that obviously abdominopelvic organ haemorrhage could be of traumatic origin.

Special Case: Basilar Skull Fracture

Background anatomy: the "base" of the skull consists of the usually unpaired frontal, ethmoid, sphenoid, and occipital bones, and paired temporal and parietal bones.

The skull base can be divided into three cranial fossae: anterior, middle, and posterior. 

• Anterior: floor consists of frontal, ethmoid, and part of sphenoid bone. It is bound posteriorly by the limbus of the sphenoid bone (medially), and lesser wings of the sphenoid bone (lateral aspects).

• Middle: floor consists of the body and greater wings of the sphenoid bone, and the squamous and petrous parts of the temporal bone. It is bound posteriorly by the dorsum sellae of the sphenoid bone (medially), and petrous part of the temporal bones laterally.

• Posterior: floor consists of mastoid part of the temporal bones and the majority of the occipital bone (squamous, condylar, and basilar parts).

Battle Sign

Battle sign is relatively late (1-2d) postauricular or mastoid ecchymoses, a sign of middle or posterior fossa basilar skull facture. The following mechanism is typically present:

1. High force impact leads to fracture of the petrous or mastoid part of the temporal bone.
2. Emissary veins (connecting the intracranial venous sinuses to the extracranial veins - bidirectional flow), and diploic veins (which connect the dural sinuses and diploic space within the bone) are torn.
3. Blood from these veins tracks into the subcutaneous tissue present behind the ear.

It should be noted that mastoid ecchymoses may arise from non-traumatic causes i.e. hepatic encephalopathy.

Raccoon Eyes

Just as with Battle sign, raccoon eyes are a relatively late (1-2d) sign of basilar skull fracture. However, raccoon eyes occur following an anterior fossa fracture, and generally present as unilateral OR bilateral ecchymoses around the eyes +/- oedema. True raccoon eyes (as opposed to traumatic black eye) will have tarsal plate sparing due to the presence of the orbital septum (think of preseptal cellulitis).

Just like Battle sign, raccoon eyes are not always traumatic in the usual sense - case reports exist of metastatic neuroblastoma in children, leukaemia, vigorous sneezing, coughing, vomiting, nose blowing causing raccoon eyes.

Special Case: Intra and Retroperitoneal Haemorrhage

Two well-known clinical signs are the Cullen and Grey-Turner signs. These are typically thought to represent haemorrhagic pancreatitis, but actually may be caused by any intra-peritoneal or retro-peritoneal haemorrhage.

Inside the peritoneum, think ischaemic or gangrenous bowel (including strangulating hernias), ruptured ectopic pregnancies, haemorrhagic ovarian cysts, liver trauma, and splenic rupture.

Retroperitoneally, think injuries to the SADPUCKERs. This includes ruptured aortic aneurysms, haemorrhagic pancreatitis, retroperitoneal necrotising fasciitis, and any vascular anomalies of the kidneys or adrenal glands.

Cullen Sign

The mechanism of Cullen sign is intriguing - intraperitoneally, blood tracks along the round ligament (of the liver), exiting the peritoneum, then traveling superficially to the anterolateral peritoneum, to the umbilicus. Remember, this ligament is also called ligamentum teres hepatis and was our umbilical vein at one point! Retroperitoneally, blood must track the gastrohepatic ligament until it reaches the falciform ligament, before it can finally enter the round ligament complex to the umbilicus.

Grey-Turner Sign

Grey-Turner sign sees blood from any retroperitoneal source diffuse to the lateral edge of the quadratus lumborum, where defects in the transversalis fascia allow the blood to track through the musculature of the abdominal wall and subsequently settle in subcutaneous tissue in the flank. See this great article for more detail on both Cullen and Grey-Turner signs (download full article).

Enough Anatomy... What's the Physiology of Ecchymoses?

Anyway, the whole reason I wanted to write this article was to describe the colour phases of a bruise. The following phases are loosely based on the Camps bruise age classification system.

Phase 1: Red

Some insult occurs, which sees red blood cells pour out of a vessel and into the extravascular space. Many of these RBCs burst (mechanical trauma, osmotic stress) releasing haemoglobin. It is a mix of RBC and haemoglobin in the subcutaneous tissue which causes the typical red hue of a new ecchymosis.

Phase 2: Bluey-Purple

As time passes, the RBCs and haemoglobin in the tissue will deoxygenate. Deoxygenated blood itself is not blue, rather, the lower oxygen content causes it to be a darker red. This causes red light to be absorbed more effectively, while pale skin reflects blue light. The absorption of red and reflection of blue light gives the appearance of a blue bruise (this is also the reason veins appear blue, not red).

Phase 3: Green

As part of the immune response, monocytes will be directed to the area and transform to macrophages in the tissue. These macrophages will phagocytose RBC and their breakdown products, churning haeme from the haemoglobin into biliverdin via haeme oxygenase. Biliverdin is green, hence why the bruise may have a green hue for a while. This will also produce Fe2+ and CO (plus convert 1 NADPH to NADP).

Phase 4: Yellow

Biliverdin will be further reduced to unconjugated bilirubin, via biliverdin reductase. Bilirubin has an orange-yellow hue, hence why the bruise will eventually turn yellow. This unconjugated bilirubin will exit the macrophages and return to the liver for conjugation and entrance to enterohepatic circulation.

Phase 5: Back to Usual ...or... Brown?

Remember in phase 3 that haeme oxygenase produces iron. This iron is stored in macrophages as haemosiderin. If there is sufficient venous return from the site of ecchymoses, these macrophages will eventually wash back out and you wouldn't be able to tell the region was ever bruised.

However, if venous return is insufficient, macrophages containing high concentrations of haemosiderin (and therefore iron) will remain in the tissue. This can cause the region to be stained brown, termed "haemosiderin staining". This is a sign of chronic venous insufficiency.