Multisystemic Review of Calcifications Part 2
Part 2 board review of all things calcifications in radiology for the ABR Core Exam. Prepare to succeed.
Show Notes/Study Guide:
In hepatic echinococcal disease what is the significance of complete rim calcifications of the hydatid cysts?
With hepatic echinococcal disease you often get a “cyst within a cyst” or large cyst with multiple daughter cyst appearance. You can also have the “water lily sign” which is the ruptured cyst envelope floating within the fluid filled cystic space. The cysts often get peripheral calcifications and if the peripheral calcification is complete, so you have complete rim calcification that often denotes inactive hydatid disease. On a plain film you can see large curvilinear or rounded calcification(s) that should make you consider hepatic hydatid disease. Random fact is that hydatid disease is endemic in countries with lots of sheep.
What is the main difference in internal calcifications between an immature and mature teratoma?
Calcifications in an immature teratoma are often irregular and amorphous. Calcifications in a mature teratoma are coarser and tooth-like. Both mature and immature teratoma have macroscopic fat which are smaller and more scattered in an immature teratoma, and larger collections of fat are often seen in a mature teratoma.
If you have a renal cyst with a few thin septa under 1 cm in thickness with thin calcifications, internal blood products or protein, and the cyst is less than 3 cm in size what Bosniak classification is this?
Bosniak II (benign, minimally complex)
If you have a renal cyst with the above features but the septa contain thick calcifications, septa are increased in number, and cyst is larger than 3 cm what Bosniak classification is this?
Bosniak IIF (minimally complex, warrants follow-up, often in 6 months). F=follow-up.
Tip with Bosniak is a 1 is a simple cyst, 2 is benign with no follow-up, 2F is most likely benign but needs follow-up, 3 starts to have thickened walls and mural nodules, 4 has an overt mass associated with the cyst. Bosniak 3 and 4 need an MRI and urology consultation. Treatment is often with something like radiofrequency ablation for a Bosniak 3 and partial/total nephrectomy for a Bosniak 4 lesion.
What percentage of pheochromocytomas are calcified?
Remember 10%. With pheochromocytomas there are lots of 10% associations to include 10% bilateral, 10% extra-adrenal, 10% malignant, 10% pediatric, 10% clinically silent, 10% autosomal dominant, 10% are calcified. Pheochromocytoma—rule of 10s. If they ask you a pheochromocytoma asking about the percentage likelihood of an association, 10% is statistically likely to be the answer.
How can calcifications help differentiate the true from the false lumen in the setting of aortic dissection?
The true lumen has calcifications around the lumen. This makes sense because we know on CT scans that calcifications, when present, are seen circumferentially in the wall of the aortic lumen. The false lumen opens in the potential space in the aortic wall, not within the existing lumen with atherosclerotic calcifications.
Bonus question: What are other ways to tell the true from the false lumen in aortic dissection?
The false lumen is usually larger than the true lumen, enhances later than the true lumen. Thrombosis is more common in the false rather than the true lumen. The true lumen more often contains the celiac, superior mesenteric artery and right renal artery. Two facts to know: 1. The left renal artery usually arises from the false lumen. 2. If you are unsure which is the true or false lumen, the larger of the two lumen is more likely to be the false lumen.
What is the significance of atherosclerosis calcifications of the ascending aorta?
Atherosclerosis typically spares the ascending aorta so if you see atherosclerotic calcifications of the ascending aorta, consider a non-atherosclerotic process such as Takayasu and Syphilis.
What are differential considerations for urinary bladder wall and/or urinary lumen calcifications?
Top differential considerations include bladder calculi, schistosomiasis, and tuberculosis. Less common entities include things like amyloidosis and alkaptonuria.
What cancer is associated with urinary bladder schistosomiasis?
Squamous cell carcinoma of the urinary bladder.
Rapid fire CNS calcification questions:
What stage of neurocysticercosis is calcified?
Stage 4 nodular calcified neurocysticercosis. This is the quiescent stage with a calcified remnant of the prior viable parasite.
Bonus: What is the most symptomatic stage of neurocysticercosis?
Stage 2: colloidal vesicular stage which is the stage at which the parasite dies, the cyst membrane becomes leaky, and there is prominent edema and enhancement.
What is the significance of calcifications in neurotoxoplasmosis?
Calcifications denote non-active treated lesions.
Bonus: In the setting of uncertainty regarding toxoplasmosis vs CNS lymphoma, thallium uptake supports which entity?
Thallium uptake would typically be seen with primary CNS lymphoma with no uptake in neurotoxoplasmosis.
What are characteristic imaging features of Fahr syndrome?
The primary imaging feature of Fahr syndrome is extensive and symmetric calcifications of the basal ganglia and thalami and calcifications can also be seen elsewhere in the white matter. Some say Fahr disease is related to the genetic form of the disease and Fahr syndrome is the secondary form of the disease which can be due to things like parathyroid hormone dysregulation, infections like HIV, and carbon monoxide poisoning.
What is a description of the calcifications in the brain associated with Sturge Weber Syndrome?
Characteristic tram-track calcifications with gyriform cortical and subcortical parenchymal calcifications. Associated features include the classic facial port wine stain in a V1 ophthalmic division of the trigeminal nerve distribution. Childhood seizures are common.
What are some intracranial lesions that frequently calcify in tuberous sclerosis?
Cortical and subcortical tubers and subependymal hamartomas are common lesions in tuberous sclerosis that commonly calcify. Note that calcification of these lesions typically starts in childhood with the cortical and subcortical tubers often showing calcification by age 2.
