03/08/2022 at 9:44 pm #39784
Sorry to bug you with what is likely a stupid question, but I’ve always struggled somewhat when it comes to classifying and differentiating echogenic foci in tendons. I can appreciate acute hydroxyapetite deposition but struggle to differentiate areas of chronic calcific scarring, from possible small avulsion fragments in the setting of an acute injury. Any tips on how to nut these buggers out would be most appreciated! Thanks also for putting this brilliant site together, it’s an amazing resource. Cheers,
03/08/2022 at 10:11 pm #39785Stephen BirdKeymaster
This is a great question, but requires a long answer!
If you see an echogenic area in a tendon there are a few options:
Gout is monosodium urate and has an access all areas pass as it is blood borne. It can accumulate anywhere, but it does have its favourite locations. These include the 1st TMT and popliteus fossa in the knee.
Gout typically has a fine crystal appearance and is red, tender, and warm to touch.
It comes often with a previous history of gout episodes.
On the radiograph the gout crystals are hard to see as they are not particularly radio opaque.
If it is inside a joint, it accumulates on the surface of the cartilage and forms what we call the “double contour sign” or “uric acid snow sign”
Gout crystals are not particularly attenuative on ultrasound so you can normally see the structures deep to the crystals with some degree of acoustic attenuation but rarely a dense acoustic shadow.
Hydroxyapatite (Calcific Tendinosis)
Hydroxyapatite is a bone salt and by definition, must have an enthesis to migrate from the bone into a tendon, ligament, joint capsule, retinaculum etc.
It is a fine-grained bone salt and forms what looks like a cumulous cloud of echogenic material within the tendon. It starts of quite liquid in nature and with transducer pressure you can see it sloshing about, and at this stage it is amenable for aspiration with a wide gauge needle.
The location of the crystal deposition is always adjacent to an enthesis.
It can occur at any enthesis, however the supraspinatus and infraspinatus tendons are very common locations.
The migration of the bone salt can be bidirectional where the hydroxyapatite migrates from the bone into the tendon and then it may migrate back the other way or be metabolized and disappear. Hence it is a dynamic phenomenon and I have seen deposits grow rapidly and also may disappear rapidly.
It starts out liquid and at this stage it is “slushy” and has good through transmission properties. As it matures it becomes more “cheese like” and the attenuation increases progressively as it hardens.
If it remains for a protracted period of time, it can burn out into a dense hard calcification resembling a hard piece of stone in the tendon,. At this stage it cannot be aspirated, but it is rarely symptomatic at this stage. At this stage the acoustic attenuation is marked, and it casts a dense acoustic shadow blocking visualisation of structures deep to it.
In the liquid and cheese like stages it is very tender, and the patient will often guard the area. Once it matures into the rock-hard state it is rarely symptomatic.
On plain radiographs it is much denser than gout and easily seen in all stages of the life cycle (liquid, cheese like, hard)
This is a good differentiator from gout
Calcium Pyrophosphate Dihydrate (CPPD / pseudogout)
This is another crystal deposition disease in the rheumatology spectrum.
It appears like echogenic crystal deposition on ultrasound and has a medium attenuation pattern.
It is easily seen on plain x-rays, much like hydroxyapatite.
The feature that sets it apart is the location.
It likes to follow ligamentous structures like joint capsules.
It also really loves fibrocartilage structures, so you see it very commonly in the meniscus of the knee and hp, as well as the TFCC of the wrist.
When it gets inside a joint it has a different pattern to gout. As I mentioned gout likes to sit on the surface of the hyaline cartilage and CPPD is licated typically in the center of the hyaline cartilage. It looks like it is buried deep in the cartilage. This distribution is not a hard and fast rule as there is a little cross over, however as a rule of thumb it is pretty good.
You will also often see other evidence of CPPD on old x-rays of other joints.
Dystrophic calcification is calcification within a tendon where there has been a prior tendinosis or tear event and the calcification has been deposited as part of the healing response. It often starts out not as calcium, but rather fibrosis / scar tissue and you will see this commonly in the supraspinatus for example as an echogenic linear line which is indeed fibrosis and may go on to form dystrophic calcification.
So it is not a bone salt, it is not a rheumatoid crystal deposition disease, it is simply a natural scarring up response to trauma or degeneration.
You will see them for example in the mid portion of an old degenerative Achilles tendon or in the distal patella tendon.
On plain x-ray it is invisible if it is only fibrosis, however once it calcifies it can look as dense as bone.
Capsule or Tendon Avulsion Fracture
This is where a joint capsule or tendon attachment is forcefully disrupted and the bone the tendon or joint capsule is attached to breaks off, staying connected to the tendon or the joint capsule. You could see the same with a retinaculum.
The patient will have a history of trauma and be point tender.
The avulsed fragment will be dense and attenuative on ultrasound. An exception to this is when the tendon or more commonly a joint capsule tear off the periosteum and no real cortical bone. In these periosteal stripping events, you will see a fine white line attached to the disrupted joint capsule collagen.
The pain x-rays are very helpful as they will often show where the avulsed fragment has been torn from the skeleton confirming the diagnosis.
Don’t be fooled by these, they are normal variants, and we see them commonly in locations such as the tibialis posterior insertion and the peroneus longus as it goes around the cuboid.
The plain x-ray will conform a well corticated piece of bone in a typical location for a normal variant.
They can be a source of pain if they are large and make a synchondrosis with the adjacent bone, and they can be a source of localised tendinosis and tenosynovitis.
This is heterotopic bone formation which occurs inside a muscle that has had a traumatic (usually crush) injury and then bleeds inside itself until it tamponades. What is often called a “corky”.
When this blood product is being reabsorbed, heterotopic bone may rapidly form disabling the muscle repair.
On ultrasound it appears as a dense, shadowing calcification within the muscle and on plain x-ray it appears as heterotopic bone.
This covers the common range of echogenic things you will see inside soft tissue. It is not an exhaustive list and there are other rarer conditions which may occur like xanthomas in the Achilles for example.
If you follow my logic and use a combination of clinical history / plain radiographs and ultrasound assessment you will arrive at the correct answer most of the time.
04/08/2022 at 12:48 pm #39795
Wow Steve, what an unbelievably thorough and well explained reply. Thank you so much for taking the time to go through all of that. My biggest stumbling area is in cases of acute on chronic tendon or ligament injuries, where I find it hard to differentiate chronic changes like those seen with distrophic calcification from acute avulsed bony fragments. I guess when in doubt, look to the X-ray! Thanks again Steve, your help is much appreciated. Cheers,
04/08/2022 at 1:30 pm #39799Stephen BirdKeymaster
Yes, ultrasound in isolation does not work.
Correlation with plain radiographs makes all the difference in these cases.
I will try and find time to convert my answer into a “tips and tricks” presentation for the website so everyone seed it.
04/08/2022 at 5:57 pm #39820
Thanks again Steve, you’re a wizard!
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