Acute Cholecystitis with intrahepatic perforation of GB causing secondary liver abscess

Above image shows distended gall bladder with pericholecystic fat stranding (orange arrow) consistent with acute cholecystitis.

Above post contrast CECT portal venous phase images showed focal small defect (yellow arrow) in the GB wall suggesting GB perforation, with abscess formation in segment V of right lobe. Blue arrow points to a single calculus within the GB lumen.

Serial axial sections showing small air pocket (orange arrow) within the liver, with adjacent heterogenous hypodense areas (yellow arrow),  superior to the hepatic abscess in segment V. If looked carefully complete pancreatic atrophy, with smooth duct dilatation and intraductal calculi can also be seen, consistent with Chronic Calcific Pancreatitis.

Eventhough acute cholecystitis is a common entity, GB perforation is rare and rarer still is its intrahepatic perforation. GB perforation is commoner in males. Risk of perforation is more in acalculous cholecystitis due to sepsis and associated co-morbidities.

Obstruction of cystic duct causes increased intraluminal pressure which inturn results in impared lymphatic and venous drainage. This results in vascular impairement leading to wall necrosis and finally perforation.

Niemeier classfied GB perforations into 3 types,
Type 1: Acute : Perforation with generalized biliary peritonitis.
Type 2: Subacute : Perforation with pericholecystic abscess and localized peritonitis.
Type 3: Chronic : Perforation with cholecysto-enteric fistula (Original classification did not include intrahepatic perforation / internal fistulae).

Treatment is with antibiotics and percutaneous drainage initially, followed by interval cholecystectomy. Open drainage and cholecystectomy has also been performed.



References:

Date RS, Thrumurthy SG, Whiteside S et al. Gallbladder perforation: case series and systematic review. Int J Surg 2012; : 63–68

Bilateral basal ganglia T1 hyperintensity

Left image shows normal T1 signal intensity of Globus Pallidus, where as
right T1 axial image in a 54yr old male with known chronic liver disease
 shows bilateral globus pallidus T1 hyperintensity.

 

Right image: Another CLD patient with bilateral T1 hyperintensity of Globus Pallidus.

Common causes of bilateral T1 hyperintense basal ganglia include:
1. Physiologic calcification.
2. NF-1
3. Hepatic Encephalopathy.
4. Hyperalimentation (Patients undergoing parenteral feeding).

Less common causes:
1.HIE (Term HIE, Hypoxic cerebral infarction).
2. CO poisoning.
3. Kernicterus.
4. Wilson's Disease.

Rarely thyroid / parathyroid hormonal imbalances, hypoglycemia, Fahr's disease, Hallervorden-Spatz syndrome, JE, Congenital HIV etc. also may cause T1 hyperintensity of the basal ganglia.

In chronic liver disease / cirrhotic patients there is symmetrical T1 hyperintensity in Globus Pallidus and Substantia Nigra.


References:
1. Expert-DDx Brain.

Hibernomas

A hibernoma is a rare benign fatty tumor arising from the vestiges (remnant / trace) of fetal brown fat. It is predominantly seen in 20-40 yrs age group with a slight female predilection. It is named so because of resemblance to brown fat in hibernating animals.

Most often the lesion is located in subcutaneous regions of the back (periscapular /interscapular region), neck, axilla, shoulder, thorax, thigh and retroperitoneum. Rarely these are also seen in scalp, breast, peri-ureteric region and scrotum.

Hibernoma usually manifest as slowly growing painless soft-tissue mass. Sometimes patient can be symptomatic due to compression of adjacent neuro-vascular structures, for example sciatica in a posterior thigh lesion.

In ultrasound these usually appear as hyperechoic lesions. Angiography will reveal lesional vascularity with arterio-venous shunting. These can mislead due to increased uptake in 18-FDG-PET.

In CT these lesions show low attenuating lesion, slightly higher attenuating than the subcutaneous fat. Enhancing septae may be seen, with lesion showing mild enhancement. MRI usually demonstrate lesion to be isointense to subcutaneous fat in most cases, with intervening enhancing sepatations. Reduced T1 and T2 signal intensity is also described in few cases. Contrast enhancement need not be present in all cases.

Additionally prominent lesional vessels may be seen in the ultrasound or as T2 flow voids in MRI, with can cause torrential hemorrhage during biopsy, especially in deep seated lesions.

Case courtesy of Dr Matt A. Morgan, Radiopaedia.org. From the case rID: 37589

Above image shows an intermuscular lesion between the gluteus medius and maximus muscles, with intermediate attenuation between fat and muscle. Prominent feeding vessel is seen along the lateral margin of the lesion.

Pre-operatively differentiating from liposarcomas is difficult. Four histological subtypes have been defined: Typical (~80%), Myxoid (8%), Lipoma-like and spindle cell variant. 'Typical' variant has predominantly brown fat. Myxoid variant is seen more often in men with higher water content (increased T2 signal). Lipoma-like lesion is seen more commonly in thigh, more resembling adult fat.


References:
Imaging Findings of a Hibernoma of the Neck
A.C.B.S. da Motta, D.E. Tunkel, W.H. Westra and D.M. Yousem
American Journal of Neuroradiology September 2006, 27 (8) 1658-1659;

CT and MR characteristics of hibernoma: six cases
Dursun, Memduh et al.
Clinical Imaging , Volume 32 , Issue 1 , 42 - 47

From the Archives of the AFIP
Benign Musculoskeletal Lipomatous Lesions
Mark D. Murphey, John F. Carroll, Donald J. Flemming, Thomas L. Pope, Francis H. Gannon, and Mark J. Kransdorf. RadioGraphics 2004 24:5, 1433-1466