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Case of the Week

Week of October 18, 2021: Ectopic Pancreatitis

History: A 40-year-old woman presented to the Emergency Department with one week of abdominal pain, nausea, and vomiting.  Labs were notable for elevated lipase.

Finding:

Axial and coronal images from the contrast-enhanced CT of the abdomen and pelvis demonstrated a lobulated focus of soft tissue posterior to the duodenal-jejunal junction.  It has the appearance of pancreatic tissue with interdigitating fat and measures approximately 2.5 cm in diameter. There is associated inflammation with surrounding fat stranding and adjacent lymph nodes.

Additional images of the same patient demonstrate that there is normal-appearing pancreatic tissue in the expected location without associated inflammation.

A follow-up CT after treatment of acute pancreatitis demonstrates a persistent soft tissue mass posterior to the duodenal-jejunal junction with a resolution of the adjacent fat stranding.  Note that this ectopic pancreatic tissue could easily be mistaken for an enlarged lymph node, bowel, or tumor when there is no surrounding fat stranding. 

Diagnosis:  Heterotopic pancreas with acute pancreatitis

Teaching Points:

Ectopic/heterotopic pancreatic tissue is defined as pancreatic tissue in the submucosal, muscularis, or subserosal layers of the luminal GI tract.  It lacks any ductal or vascular connection with the main pancreatic gland.  The most common locations for ectopic pancreas include the proximal duodenum, proximal jejunum, and gastric antrum.  Less common sites include the ileum, esophagus, and Meckel’s diverticulum. The cause of the ectopic pancreas is unknown, but it is embryological/developmental in etiology and is thought to be related to deposits of pancreatic tissue being “dropped” into the developing GI tract.

It is most commonly asymptomatic but can demonstrate any pathology that can be seen in the normal pancreas including pancreatitis or pancreatic tumors.  Most lesions are solitary and measure less than 3 cm.

There are multiple histologic subtypes of ectopic pancreatic tissue.  Type 1 heterotopic tissue contains acini, ducts, and islet cells similar to normal pancreatic tissue.  Type 2 contains only acini and ducts and Type 3 contains only ducts.

On fluoroscopic barium studies, ectopic pancreatic tissue has the appearance of an extramucosal intramural lesion with a broad base and smooth surface, and often contains a central barium-filled pit or umbilication.

On CT, the characteristic location, endoluminal growth pattern, microlobulated borders, and prominent enhancement of the overlying mucosa help to differentiate the ectopic pancreas from other tumors. 

On MRI, the heterotopic pancreatic tissue will have similar signal characteristics as the main pancreatic gland with a characteristic high intrinsic T1 signal.

References:

  1. Resvani M, et al. Heterotopic Pancreas: Histopathologic Features, Imaging Findings, and Complications. 2017; 37(2).
  2. Kim JY, et al. Ectopic Pancreas: CT Findings with Emphasis on Differentiation from Small Gastrointestinal Stromal Tumor and Leiomyoma. Radiology. 2009; 252(1).

Subramanian M, et al. Clinics in diagnostic imaging: duodenal ectopic pancreas.  Singapore Medical Journal. 2014; 55(12): 629-634.

Previous Cases

 Week of October 04, 2021: Oreo Cookie Sign of a Pericardial Effusion

History: 70-year-old male with a history of cardiac amyloidosis who presented to the Emergency Department with shortness of breath.

Findings:

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The PA chest radiograph demonstrates an enlarged cardiac silhouette. The cardiothoracic ratio is a measurement obtained on PA chest radiographs and is defined as the ratio of maximal horizontal cardiac diameter (top line) to maximal horizontal thoracic diameter measured from inner rib to inner rib (bottom line). When this ratio measures greater than 0.5, the cardiac silhouette is considered enlarged. This could be related to cardiomegaly or pericardial effusion.  Prominent epicardial fat pads can also sometimes lead to this ratio measuring enlarged when there is no true pathology involving the heart or pericardium.

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The lateral chest radiograph of the same patient demonstrates the “Oreo Cookie” sign.  This sign describes two vertical linear lucent lines (yellow arrows) separated by an opaque line (green arrow) on the lateral chest x-ray.  The most anterior lucent line (directly posterior to the sternum) represents paracardial fat and the most posterior lucent line represents epicardial fat.  In between these two fat layers is the opaque line (green arrow), which represents pericardial fluid.  When this sign is seen on a chest x-ray, it is highly suggestive of pericardial effusion. 

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A sagittal view from a PET/CT on the same patient confirms the presence of pericardial effusion. The two yellow arrows in the picture correspond to the two vertical lucent lines on the chest radiograph and are seen to represent paracardial fat and epicardial fat. The green arrow shows the moderate-sized pericardial effusion between the two fat layers, which corresponds to the opaque vertical line on the chest radiograph.

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A sagittal view from a cardiac MRI in the same patient shows similar findings, again confirming the presence of pericardial effusion as suggested on the chest radiograph.

Diagnosis: “Oreo Cookie” Sign of Pericardial Effusion"

Teaching Points:

Pericardial effusions are collections of excess fluid within the pericardial space. There are numerous etiologies for pericardial effusions, including idiopathic, uremia, malignancy, infection, systemic lupus erythematosus, rheumatoid arthritis, post-myocardial infarction (Dressler syndrome), traumatic, and pulmonary arterial hypertension, among many other causes.

In order for pericardial effusions to be visible on the chest radiograph, over 200 mL of fluid must be present.  On the PA view, the cardiac silhouette will be globally enlarged and often takes on a “water bottle” configuration.  The cardiothoracic ratio described above will be greater than 0.5.  The “oreo cookie” sign described above can be seen on the lateral radiograph.

If there are signs suggestive of pericardial effusion on chest radiograph, further evaluation with echocardiography should be recommended.

Symptoms from a pericardial effusion are related to the speed of fluid accumulation rather than the absolute volume.  If the fluid accumulates gradually, the pericardium can stretch and accommodate larger volumes.  However, if the fluid accumulates rapidly, even a small amount of fluid can impair cardiac function and potentially lead to cardiac tamponade. Echocardiography is the most reliable method to assess the hemodynamic impact of the effusion.

Treatment is most often conservative, but if the patient is symptomatic and there is evidence of hemodynamic compromise, then a pericardiocentesis can be performed for drainage.

References:

  1. Chiarenza A, et al. Chest imaging using signs, symbols, and naturalistic images: a practical guide for radiologists and non-radiologists. Insights into Imaging. 2019;10(114).
  2. Wang ZJ, Reddy GP, et al. CT and MR imaging of pericardial disease. 2003;23: S167-180.
  3. Weissman NJ, Adelmann GA. Cardiac imaging secrets.  Elsevier Health Sciences.  (2004) ISBN: 1560535156.

 Week of September 13 , 2021: Emphysematous Pyelonephritis

History: A 70-year-old female patient with a history of diabetes was admitted after a fall with a left femoral fracture and developed sepsis with leukocytosis and bacteremia while an inpatient.

Findings:

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Ultrasound images of the left kidney demonstrate an avascular, echogenic region in the lower pole of the left kidney with associated “dirty” posterior acoustic shadowing. Further evaluation with cross-sectional imaging was recommended.

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 September 07, 2021: Epiploic Appendagitis

History: A 50-year-old woman presented to the Emergency Room with acute left lower quadrant abdominal pain.

Findings:

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Axial, coronal, and sagittal views of the contrast-enhanced CT abdomen and pelvis demonstrate two adjacent ovoid-shaped, fat-density structures located anterior to the descending/proximal sigmoid colon.  These structures demonstrate thin enhancing rims and significant surrounding inflammatory fat stranding.  A central hyperdense “dot” is seen within the center of these structures.

Diagnosis: Epiploic appendagitis

Teaching Points: Epiploic appendagitis is a self-limiting inflammatory process involving an appendix epiploica of the colon.  There are approximately 50-100 appendices epiploicae located along the colon, the majority of which are located in the region of the rectosigmoid colon.  These appendages are peritoneal pouches arising from the serosal surface of the colon and are attached to the colon via a vascular stalk.  Epiploic appendagitis results when there is torsion or spontaneous thrombosis of the venous outflow to one or more of these appendices epiploicae.

Patients with epiploic appendagitis present with acute abdominal pain, which can often mimic diverticulitis or appendicitis.  There is a predilection for middle-aged women and obese patients.

On CT, epiploic appendagitis will appear as a fat-density, ovoid structure adjacent to the colon, most often along the anterior aspect of the sigmoid or descending colon.  They tend to have thin, hyperdense rims and surrounding inflammatory fat stranding.  Sometimes, a “central dot sign” can be seen (as in our case shown above), in which the thrombosed vascular pedicle appears as a punctate hyperdense dot within the fat-density structure.  Epiploic appendages are typically visible on CT only when they are inflamed.  There is usually no significant wall thickening of the adjacent bowel. In its chronic stage, the infarcted epiploic appendage can calcify and detach from the colon wall, forming an intraperitoneal loose body.

Epiploic appendagitis is self-limiting and usually responds well to NSAIDs.  Surgery is not necessary.  Symptoms resolve within 2 weeks for most patients, although CT findings can persist for several months. 

The main differential consideration is an omental infarct. Still, these are more often located adjacent to the cecum or ascending colon and are typically larger (greater than 3 cm, as opposed to epiploic appendagitis, which more often measures 1.5-3 cm).  Omental infarcts also lack the hyperdense rim seen with epiploic appendagitis.

References:

  1. Singh AK, et al. Acute Epiploic Appendagitis and Its Mimics. 2005; 25(6): 1521-1534.
  2. Nadida D, et al. Acute epiploic appendagitis: radiologic and clinical features in 12 patients.  Int J Surg Case Rep. 2016;28: 219-222.
  3. Giambelluca D, et al. CT imaging findings of epiploic appendagitis: an unusual cause of abdominal pain. Insights Imaging.  2019;10:26.

 September 01 , 2021: Area Postrema Syndrome

History: 30-year-old male with a history of neuromyelitis optica presented to the Emergency Department with intractable hiccups for 3 weeks, with associated intermittent nausea and vomiting.

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Post-contrast axial and sagittal MRI images of the brain shown above demonstrate a 3 mm focus of enhancement in the left dorsal aspect of the medulla in the region of the area postrema.

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Post-contrast axial and coronal MRI images through the orbits demonstrate enhancement of the right optic nerve.  Note the normal left optic nerve without enhancement.

Diagnosis:  Neuromyelitis Optica with Area Postrema Syndrome and Optic Neuritis 

Teaching Points:

Neuromyelitis Optica spectrum disorders (NMOSD) are a group of inflammatory, autoimmune, demyelinating diseases. The majority are associated with a pathologic antibody specific for the aquaporin-4 (AQP4) water channel.  In fact, the clinical diagnosis of NMOSD requires a positive AQP4-IgG and 1 core clinical characteristic, or 2 core clinical characteristics without the AQP4 antibody.  Core clinical characteristics of NMOSD include optic neuritis, transverse myelitis, area postrema syndrome, acute brainstem syndrome, and symptomatic narcolepsy.

Brain lesions in NMOSD tend to occur in areas rich in AQP4.  One of these areas is known as the area postrema, as seen in the top 2 pictures shown above.  The area postrema is located in the dorsal tegmentum of the medulla at the floor of the 4th ventricle and acts as an emetic reflex center and mediates hiccups due to its extensive network of chemo-sensitive neurons and connections with the hypothalamus, brainstem, and bloodstream.  Lesions in the dorsal medulla cause inflammation in this area and loss of AQP4 reactivity and therefore result in attacks of intractable nausea, vomiting, and hiccups lasting longer than 48 hours, known as Area Postrema Syndrome.  It is estimated that 30% of patients with NMOSD will have Area Postrema Syndrome during the course of their illness.  Symptomatic therapies such as antiemetics are typically ineffective, but steroids or plasmapheresis tend to result in rapid cessation of symptoms.

The main imaging feature of area postrema syndrome is an abnormal enhancement of the dorsal medulla in the correct clinical setting. An abnormal FLAIR signal in this region can also be seen.

Additional typical areas of brain involvement in NMOSD at sites of AQP4 include the periependymal surface of the corpus callosum, hypothalamus, periaqueductal area, lateral ventricles, third ventricle, fourth ventricle, and optic chiasm.

More classic symptoms in NMOSD include optic neuritis and transverse myelitis, the other core clinical characteristics which meet the criteria for NMOSD diagnosis.  When area postrema syndrome does occur, it tends to precede involvement of the orbits or spinal cord and therefore can serve as a warning sign for progressive symptoms.  Treatment of area postrema syndrome not only helps relieve symptoms of vomiting and hiccups but can also prevent subsequent episodes of optic neuritis or transverse myelitis. 

Our patient also had optic neuritis, as shown in the bottom 2 pictures. Imaging features of optic neuritis include high T2 signal and abnormal enhancement of the optic nerve.  In NMOSD, optic neuritis tends to occur bilaterally, whereas it is more often unilateral in the case of multiple sclerosis (although our patient shown above only has unilateral involvement). 

References:

  1. Shosha E, Dubey D, et al. Area Postrema Syndrome: Frequency, Criteria, and Severity in AQP4-IgG positive NMOSD. 2018;91(17): e1642-1652.
  2. Hyun JW, Kwon YN, et al. Value of Area Postrema Syndrome in Differentiating Adults with AQP4 vs. MOG Antibodies. Frontiers in Neurology. 2020;11:396.
  3. Chan KH, Vorobeychick G. Area postrema syndrome: a neurological presentation of nausea, vomiting, and hiccups. BMJ Case Reports. 2020; 13: e238588.
  4. Dutra BG, et al. Neuromyelitis Optica Spectrum Disorders: Spectrum of MR Imaging Findings and Their Differential Diagnosis. 2018; 38(1): 169-193.

 August 25, 2021: Diagnosis Penetrating Atherosclerotic Ulcer (PAU)

History: A 70-year old male with a history of hypertension and COPD presented to the Emergency Department with acute onset chest pain and shortness of breath. 

Findings:

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The initial chest radiograph obtained in the Emergency Department showed hyperinflation of the lungs and flattening of the diaphragms, which can be seen with COPD/emphysema. In addition, a focal opacity in the left retrocardiac region was seen, which appeared to silhouette the contour of the distal descending thoracic aorta. Given the history of acute chest pain, further evaluation with a CT angiogram of the chest was recommended.

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Three images from the CT angiogram of the chest demonstrate an irregularly shaped, focal outpouching of the distal descending thoracic aorta. This outpouching is contrast-filled, directed anterolaterally to the left, and measures approximately 2.5 x 2.1 x 1.7 cm. It is associated with an area of calcified atherosclerotic plaque. Soft tissue attenuation areas along the margins of this outpouching that do not fill with contrast likely represent a component of mural thrombus.

Diagnosis: Penetrating Atherosclerotic Ulcer (PAU)

Teaching Points:

A penetrating atherosclerotic ulcer (PAU) describes an atherosclerotic plaque that erodes the internal elastic lamina into the media of the aortic wall. They occur in regions of advanced atherosclerosis.

Patients with PAU present with the classic symptoms of the acute aortic syndrome, most commonly acute tearing chest pain. They tend to occur in the older male population with a history of hypertension, smoking, coronary artery disease, peripheral artery disease, and COPD.

CT angiogram is the test of choice for PAUs. Our case described above is interesting because we can actually detect the focal outpouching of the aorta on the chest radiograph. On CTA, PAUs appear as contrast-filled outpouchings off the wall of the aorta. They most often involve the aortic arch or mid-distal thoracic aorta. They occur in areas of advanced atherosclerosis as evidenced by jagged, irregular aortic walls from atheroma and the presence of intimal calcification.

In general, PAUs can be classified according to the Stanford classification in the same way as aortic dissections. PAUs occurring in the ascending aorta proximal to the left subclavian artery origin (Stanford type A) have a higher risk of rupture and are treated with early surgical intervention. PAUs that do not involve the ascending aorta (Stanford type B) can be managed with antihypertensive medication and imaging follow-up if asymptomatic or with endovascular repair if symptomatic and/or progressing.

PAUs can rupture and lead to intramural hemorrhage, which can subsequently cause a limited intermedial dissection, saccular pseudoaneurysm, or aortic rupture. If associated with intramural hematoma, non-contrast CT will show a high-density hematoma surrounding the PAU. Intramural hematomas associated with PAU have a worse prognosis compared to intramural hematomas in the absence of PAUs. PAUs actually have an even higher incidence of aortic rupture when compared to aortic dissection. PAUs measuring greater than 10mm in depth or 20mm in diameter have a higher rate of progression. Persistent or recurrent pain, as well as new/increased pleural effusions, are also important predictors of disease progression.

It is important to distinguish PAU from irregular atherosclerotic plaque, a very common finding in which atheromatous plaque causes irregular margins of the aortic wall. Still, no contrast material extends beyond the level of the intima.

References:

1. Maddu KK, Shuaib W, et al. Nontraumatic Acute Aortic Emergencies: Part 1, Acute Aortic Syndrome. American Journal of Roentgenology. 2014;202: 656-665.

2. Hayashi H, Matsuoka Y, et al. Penetrating Atherosclerotic Ulcer of the Aorta: Imaging Features and Disease Concept. Radiographics. 2000;20(4): 995-1005.

3. Ganaha F, Miller DC, et al. Prognosis of Aortic Intramural Hematoma With and Without Penetrating Atherosclerotic Ulcer. Circulation. 2002;106(3).

4. Macura KJ, Corl FM, et al. Pathogenesis in Acute Aortic Syndromes: Aortic Dissection, Intramural Hematoma, and Penetrating Atherosclerotic Aortic Ulcer. American Journal of Roentgenology. 2003;181: 309-316.

 January 21, 2021: Uterine Didelphys

A pregnant woman in her 30's was noted to have a uterine anomaly during prenatal ultrasound. Patient now presents for MRI after successful delivery for further evaluation of this anomaly.

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The above pictures show two widely-spaced uterine corpora and edometrial cavities with separate, non-communicating divergent uterine horns and a large fundal cleft.

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The above picture shows two separate cervices.

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The above picture shows a partially duplicated vagina superiorly near the two cervices. The normal H-shaped appearance of the vagina is lost.

Diagnosis: Uterine Didelphys

Uterine didelphys is a type of Mullerian duct anomaly secondary to complete failure of ductal fusion. Normally, the Mullerian ducts fuse during the 6th to 11th weeks of gestation to form the uterus, Fallopian tubes, cervix, and upper 2/3 of the vagina. In uterine didelphys, however, the failed fusion resulted in complete duplication of the uterine horns and cervix.

Imaging findings include two widely-spaced uterine bodies and endometrial cavities, each with a single Fallopian tube. The divergent uterine horns are separated by a large fundal cleft. Two separate cervices are always present. In 75% of cases, there is also an upper vaginal septum.

Mullerian duct anomalies are commonly associated with renal anomalies, most commonly in the form of ipsilateral renal agenesis. Ectopia, hypoplasia, fusion, malrotation, and duplication are other renal anomalies that can be seen.

Vaginal septa may cause obstruction from one uterine horn and can result in subsequent hematometrocolpos (appearing on MRI as a markedly distended unilateral uterine horn with high T1 signal related to blood). In addition, vaginal septa can lead to retrograde menstrual flow and result in endometriosis, infection, and pelvic adhesions. In the absence of an obstructing vaginal septum, most patients with uterine didelphys are asymptomatic.

Successful pregnancy is possible in the setting of uterine didelphys, but remains relatively high risk in relation to the normal population. It most commonly occurs unilaterally. Breech presentation is common due to the reduced uterine volume. In addition, the nonpregnant uterus may block the pelvic inlet. For these reasons, cesarean sections are common in these patients.

Differential diagnosis includes bicornuate uterus and separate uterus. In a bicornuate uterus, only the uterine horns are separated and there is communication between them. In a separate uterus, a midline uterine septum is seen.

References

1) Behr SC, Courtier JL, Qayyum A. Imaging of Mullerian duct anomalies. Radiographics. 2012;32:233-50.

2) Dykes TM, et al. Imaging of Congenital Uterine Anomalies: Review and Self-Assessment Module. American Journal of Roentgenology. 2007; 189:S1-S10.

3) Felker EA. Uterus Didelphys and Pregnancy. Journal of Diagnostic Medical Sonograph. 2004; 20:131-133.

 April 14, 2020: COVID-19 in Lung Screening

An older male with multiple comorbidities presented with nonspecific shortness of breath, found to be in florid heart failure. COVID-19 testing returned positive. Here’s what we are seeing on imaging throughout the admission.

Prior comparison CXR: clear, without significant evidence of underlying lung disease on radiographs. 

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Admission CXR: Patchy bilateral airspace opacities with mild consolidation in the right lower lobe. 

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CXR 2 days later: florid progression of disease with extensive patchy airspace opacities throughout both lungs. Denser areas of consolidation are also seen more pronounced in the lower lobes. 

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CT Chest (same day as above): Progressive ground-glass opacities with dense consolidation in the bilateral lower lobes, suspicious for pneumonia including atypical etiologies such as coronavirus. No pleural effusions.

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Follow-up CT Chest (almost 2 weeks after above exam): Progression of extensive ground-glass opacities throughout the lungs with a slight peripheral predominance, as well as progressive dense consolidation of the lower lobes. No pleural effusions.

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Clinical Bullet Points

  •  Nonspecific clinical presentation delays or precludes diagnosis in many cases.
  •  Clinical diagnosis is by RT-PCR, with a known significant false negative rate. New rapid testing is being developed with goals of higher sensitivity.
  •  Complications include ARDS, acute cardiac injury, secondary infection (bacterial pneumonia), sepsis, AKI, multiorgan failure.

Imaging Bullet Points:

  •  Here’s a summary of what the Fleischner Society consensus published 7 April 2020:
    •  Imaging is not indicated in patients with suspected COVID-19 and mild clinical symptoms
    •  Imaging is indicated in a COVID-19 patient with worsening respiratory symptoms
    •  In the setting of resource limitations, imaging is indicated for medical triage of patients with suspected COVID-19 presenting with moderate-severe clinical features and high pretest probability.
  •  Key Imaging features: findings of atypical pneumonia or organizing pneumonia in the setting of clinical suspicion for COVID-19:
    •  Plain Radiograph: airspace opacities (consolidation or ground-glass opacities); bilateral, peripheral, lower lung predominant; pleural effusion is rare.
      •  May be normal in early disease
      •  Findings are most extensive 10-12 days after symptom onset
    •  Chest CT: 
      •  Ground-glass opacities (GGOs) - bilateral, peripheral/subpleural
      •  Crazy paving (GGOs with interlobular septal thickening)
      •  Air space consolidation
      •  Bronchovascular thickening
      •  Traction bronchiectasis
    •  Many asymptomatic patients may have CT abnormalities.

Take home point: Peripheral distribution, predominantly ground-glass opacities without pleural effusions should raise suspicion for COVID-19 in the appropriate clinical setting

 April 20, 2020: Identifying an Abnormal Enhancement Pattern

This week, we have a younger gentleman with multiple comorbidities. On the supplied image we see hyperenhancement of the liver - specifically in segment IV as well as multiple abnormal collateral vessels throughout the abdominal wall.

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Hot quadrate sign refers to a focal area of increased enhancement in the medial segment of the left hepatic lobe (segment IV). This finding is classically due to obstruction of the superior vena cava with portosystemic venous shunting between the SVC and left portal vein (via the internal thoracic and paraumbilical veins). This is contrasted with the Budd-Chiari syndrome which causes hypervascularity of the caudate lobe due to differential venous outflow.

Key point: Identifying the abnormal enhancement in this specific location as well as the collaterals suggests pathology elsewhere (in the SVC).

 April 25, 2020: Hand Joint Swelling Without Joint Space Destruction

A middle-aged man came in with hand pain and swelling.

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There is nodular soft tissue swelling of several fingers and mild osteoarthritis (joint space narrowing and osteophytosis) of several joins in a distal distribution, favoring DIPs. There are few erosions which are characterized as juxtaarticular erosions, meaning the lucencies are not actually along the join but outside of the synovial covering of the joint space. (See the small arrows.) A few areas of mineralization are seen in the soft tissues as well.

A notable negative is that the MCPs are essentially unaffected.

Diagnosis: Gouty arthritis.

Key takeaways: This case is an example of a bunch of gouty tophi around the joints. The swelling around the joins is classic due to the urate crystal deposits around the joint. These can calcify (see the mineralization around the radial side of the second MCP on the left hand). The urate deposits cause an inflammatory reaction that can result in bone resorption and lytic foci in the juxtaarticular bone. This is not within the synovial joint, hence why we're not seeing joint space destruction.

 May 4, 2020: Diagnosing Inflammatory Breast Cancer

A middle-aged woman with a palpable abnormality. She noted her skin has been red and tender on her left breast.

Findings: The first image shows the initial evaluation demonstrating a mass in the outer left breast with mild skin thickening. Remaining images are a follow-up diagnostic mammogram workup months after.

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This case shows a large irregular mass in the upper-outer left breast (2 o'clock position), with remarkable skin thickening throughout the left breast. There's a trabecular thickening and slightly increased density of the left breast overall.

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If you look closely, there's a small calcification associated with the mass as well as a biopsy clip -- a finding that should should raise the radiologist's suspcions for cancer. Other findings include multiple enlarged left axiliar nodes in the LMO projection. US shows a large irregular hypoechoic mass without shadowing.

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Diagnosis: Inflammatory breast cancer - a clear case for BIRADS 5.

Inflammatory breast cancer is a diagnosis that requires both tissue biopsy and clinical evidence of inflammatory disease. It is a common occurrence for a middle-aged woman to come in having developed a hot, swollen breast very rapidly, sometimes showing the peau d'orange appearance clinically. This appearance is due to tumor invasion of the skin lymphatics so tissue sparing surgeries are generally not performed. Up to 30% of these cancers are metastatic at presentation. Inflammatory breast cancer itself is considered stage IIIb at presentation due to skin invasion so immediate action is required.

An important distinction: DDX is mastitis clinically. Mastitis is usually related to breast feeding so the patient can be younger. This should be resolved with therapy. Inflammatory breast cancer can also be associated with pregnancy, which is something to look out for.

 June 1, 2020: Left Lower Lobe Atelectasis On Chest X-ray

A 50 year-old female presented to the hospital with shortness of breath. She had a history of breast cancer. A chest X-ray was ordered. 

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A PA view of the chest demonstrates the classic findings of left lower lobe atelectasis. The retrocardiac sail sign describes a triangular opacity in the posteromedial aspect of the left lung (shown with the yellow arrow). The flat waist sign describes flattening of the left heart border as is also shown in this example. There is also slight inferior displacement of the left hilum. On this example, the hila are approximately level with eachother whereas the left hilum is normally slightly superior to the right hilum. 

A repeat chest radiograph the following day demonstrates persistent left lower lobe atelectasis with suggestion of an abnormal density within the left mainstem bronchus. CT was recommended for further evaluation. 

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The CT showed a 2.6m mass in the left hilar region that completely obstructs the left lower lobe bronchus and results in complete collapse of the left lower lobe. Bronchoscopic biopsy was recommended for further evaluation. 

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Diagnosis: The left hilar mass resulting in obstruction of the left lower lobe bronchus. Differential includes primary lung or bronchogenic malignancy, as well as metastasis. Bronchoscopic biopsy in this case confirmed a primary squamous cell carcinoma. 

This case shows typical findings for left lower lobe atelectasis on chest X-ray. It is important to be aware of the radiographic appearance of all types of lobar atelectasis. 

It is also a good example of the satisfaction of search phenomenon. On the second X-ray, it would be easy to call this persistent left lower lobe atelectasis. However, you should always look further for the cause of the lobar collapse as seen in this instance. 

The differential for an endobronchial lesion is broad. In children, central obstruction is most often due to a mucus plug or foreign body. In young adults, a low-grade endobronchial tumor such as carcinoid or adenoma enters the differential. After age 40, bronchogenic carcinoma is a common cause. 

 June 15, 2020: Ultrasound Diagnosis of Median Arcuate Ligament Syndrome

A 30 year-old female presented with epigastric pain and nausea after eating. An epigastric bruit was noted on the physical exam. Ultrasound was ordered to look for abdominal aortic aneurysm.

Findings show, during expiration there is narrowing of the origin of the celiac artery with a fish-hook configuration. 

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With inspiration, the celiac artery assumes a more vertical orientation with decreased narrowing at its origin. 

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A side-by-sie view demonstrates the difference in orientation of the celiac artery during expiration and inspiration. 

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During expiration, there is elevation of the peak systolic velocity of the celiac artery to 297 cm/ sec. There is also focal aliasing at the origin of the celiac artery, indicative of turublent high-velocity flow. 

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During inspiration, there is normalization of the peak systolic velocity to 171 cm/ sec and resolution of the focal aliasing at the origin of the celiac artery.

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Diagnosis: Median arcuate ligament syndrome

Median arcuate ligament syndrome, also known as celiac artery compression syndrome, is a condition in which the proximal part of the celiac trunk is compressed by the median arcuate ligament of the diaphragm during expiration. This ligament is a fibrous arch that connects the diaphragmatic crura on either side of the aortic hiatus. 

During inspiration, the celiac artery descends in the abdomen and the artery assumes a more vertical orientation, relieving the compression. For this reason, the symptoms associated with MALS are also relieved during standing as the celiac artery descends further in the abdominal cavity on standing. 

On ultrasound, this can be diagnosed when there is narrowing at the origin of the celiac artery (often with a fish-hook orientation) and a peak systolic velocity in the compressed segment of the celiac artery >200 cm/ sec during expiration. There should also be a >3:1 ratio of peak systolic velocity in the celiac artery during expiration compared to the peak systolic velocity in the abdominal aorta immediately below the diaphragm. Normalization of the velocity on inspiration and standing is classic. 

CT is the more common method to diagnose this condition. On CT, you will see proximal celiac stenosis with the classic fish-hook configuration. You may also see post-stenoic dilation and prominent collaterals as seen int he example below obtained from Dr. Mahmoud Yacout Alabd on Radiopaedia.org

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This is often treated surgically with laparoscopic division of the median arcuate ligament. 

 June 22, 2020: Dysphagia lusoria

A 70 year-old male reported dysphagia and sensation of food getting stuck at the level of the suprasternal notch. A fluoroscopic esophagram was ordered for further evaluation. 

Frontal and lateral views show a mild posterior and lateral impression on the upper thoracic esophagus at the level of the aortic arch. Note that there is also laryngeal penetration and a small amount of tracheal aspiration in the second picture due to the patient's difficulty swallowing. 

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There is also a cricopharyngeal bar at the C5-C6 level causing greater than 50% impression on the posterior cervical esophagus. 

 

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Subsequent CT of the chest demonstrates an aberrant right subclavian artery which courses posterior to the esophagus and causes posterior compression on the esophagus. Note the calcific atherosclerosis at the origin of the aberrant right subclavian artery. 

 

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Diagnosis: Dysphagia lusoria and cricopharyngeal bar

Dysphagia lusoria is impairment in swallowing due to an aberrant right subclavian artery. Fluoroscopy will show an indentation in the posterior wall of the esophagus at the level of the aortic arch. Cross-sectional imaging is necessary to confirm the presence of the aberrant vessel. It is important to note that most patients with an aberrant right subclavian artery do not have symptoms. As in this case, the presence of atherosclerosis or aneurysm in the aberrant artery will often lead to worse symptoms. 

A cricopharyngeal bar will appear on lateral fluoroscopic images as a smooth posterior indentation of the cervical esophagus at the C5-C6 level - which is the level of the cricopharyngeus muscle. It can be idiopathic or related to cricopharyngeus muscle spasm or hypertrophy. It is usually an incidental finding. However, some patients complain of dysphagia. It can result in a Zenker diverticulum so be sure to look for that as well. 

 July 13, 2020: Golden S-Sign

This week, an older gentleman reported progressive shortness of breath. 

What we are seeing in the CXR is the Golden S-sign or S-sign of Golden. Here, the right upper lobe collapse is related to a mass in the hilum. As the right upper lobe collapses, it pulls the minor fissure upwards and the hilar mass impresses on the fissure downwards resulting in the S-shape. 

 

 

This is one of the signs residents learn about but don't often see. This, like many radiologic signs, were really important in the days before CT. Radiologists at that time were amazing at plain film interpretation. 

In this case, we have an image of a quick scan through the CT showing the mass and the right upper lung bronchus that's almost collapsed. The presenting X-ray a few months after the CT shows a complete collapse. The other image is the prior X-ray before the right upper lung collapse. 

 

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 July 27, 2020: Testicular Torsion

A man in his 60s with a history of right inguinal hernia repair within the past year is now presenting with several weeks of right testicular pain. 

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The echotexture of the right testicle is heterogeneous when compared to the normal homogenous echotexture of the left testicle. The hypoechoic (dark) regions within the testicle represent areas of necrosis. Note also the large complex hydrocele surrounding the necrotic right testicle with multiple septations, which is reactive in the setting of testicular torsion.

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Doppler images of the right testicle demonstrate no evidence of arterial or venous blood flow. Absence of blood flow within the testicle is a sign of complete torsion. 

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Compare the absent arterial and venous waveforms of the right testicle shown above to this normal arterial waveform in the left testicle. Note the arterial waveforms with sharp systolic upstrokes -- a normal finding.

 

The cine clip shown above shows the classic "whirlpool sign" of twisting of the right spermatic cord including the vascular pedicle. 

Diagnosis: Testicular Torsion with Necrosis

This is a classic case of complete testicular torsion with necrosis. This occurs when the spermatic cord and vascular pedicle twist and cut off blood supply to the testicle. Initially, the twisting is less than 360 degrees and only obstructs the venous outflow (incomplete torsion). Over time, as the twisting becomes greater than 360 degrees, the arterial inflow is also obstructed (complete torsion) and the testicular necrosis occurs. 

These patients usually present with acute testicular pain. Early diagnosis is important so that the testicle can be salvaged before testicular necrosis or infarction occurs. The time between onset of pain and detorsion is directly related to testicular salvage with nearly 100% salvage if the detorsion occurs within six hours. Only 20% salvage is expected if there is a delay of 12-24 hours. Treatment involves orchiectomy in order to prevent subsequent infection of the necrosed testicle. 

A review of the typical ultrasound findings, many of which are shown above: 

  • Twisting of the spermatic cord or "whirlpool sign" (the most sensitive and specific finding)
  • Absence of blood flow in complete torsion; elevated resistive indices or to-and-fro flow in incomplete torsion
  • Homogenous texture early on before necrosis occurs; heterogeneous echotexture with areas of necrosis in late presentations
  • Reactive hydrocele
  • Reactive thickening of scrotal skin

 August 3, 2020: Subdural Hematoma

A male in his 60s presents to the Emergency Department with acute onset of slurred speech. Stroke code was activated.

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Findings show a large, mixed attenuation subdural hematoma overlying the left frontoparietal cerebral convexity with hyperdense (bright) components with acute blood products.

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The large subdural collection results in significant effect with effacement/ flattening of the underlying cerebral gyri and 1.4 cm of left-to-right midline shift at the level of the septum pellucidum. The coronal image above nicely demonstrates subfalcine herniation and the axial image demonstrates mild effacement of the left aspect of the suprasellar cistern, indicative of developing uncal herniation.

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There is also effacement of the atrium of the left lateral ventricle (shown on the left) and asymmetric dilatation of the temporal horn of the left lateral ventricle (shown on the right). These findings are related to ventricular trapping from mass effect by the large subdural collection.

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Due to the significant mass effect and developing herniation, the patient underwent emergent craniotomy for decompression. On the left, you can see the postsurgical changes including a subdural drain that was left in place for drainage of the large hematoma. On the right, you can see the significantly decreased mass effect after surgery including decreased midline shift and decreased effacement of the atrium of the left lateral ventricle.

Diagnosis: Subdural hematoma requiring emergent decompressive craniotomy

Subdural hematomas are collections of blood located between the dura and arachnoid mater. They occur from tearing of the bridging cortical veins as they cross the subdural space before draining into a dural venous sinus. They are often crescent-shaped and are not limited by cranial sutures, which is why the subdural collection in this case extends across nearly the entirety of the left cerebral convexity.

This is in opposition to epidural hematomas, which are often secondary to tearing of the middle meningal artery in the presence of a skull fracture. They appear lens-shaped and are limited by cranial sutures.

On CT, the appearance of the subdural hematoma changes with time. In the first hour (hyperacute stage), the collection often has a swirling appearance due to mixing of clot and ongoing unclotted blood. In the acute stage, they key imaging feature is hyperdense (bright) blood as seen in our case here. In rare cases, acute SDH can appear isodense to the brain due to anticoagulation/ coagulopathy or severe anemia. In the subacute phase (3-21 days), the collection becomes isodense to the underlying cortex. In the chronic phase (beyond 3 weeks), the collection becomes hypodense (dark) relative to the cortex. An acute-on-chronic SDH will often appear with a hematocrit level, with a hyperdense component layering posteriorly.

Treatment depends on the degree of mass effect. Small subdural collections are often managed with serial CT scans to exclude enlargement. Symptomatic cases with a large amount of mass effect, as seen in our case, require surgery to evacuate the collection.

 August 28, 2020: Imaging Sign for Acute Infarct

A patient presented at the hospital after experiencing a few hours of left-sided weakness following trauma. 

The initial non-contrast CT was mostly unremarkable without any bleed or big infarct visible on CT. What can be seen adjacent to the suprasellar cistern is a hyperdense curvilinear structure in the region where one would normally expect the M1 segment of the right MCA. Typically, these vessels can be visualized on a few slices on noncontrast CT but the appearance here is far more dense. 

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This finding should raise suspicions for an obstructing thrombus in the vessel - the so-called "hyperdense MCA sign." Oftentimes, clinicians reviewing imaging will think they see a dense MCA but it's usually just an artifact. If the appearance is for hyperdense MCA - if the clinical picture fits and if the patient is within the window for treatment - vascular imaging is a must. 

Here, we got a CTA which shows complete occlusion of the distal M1 segment of the right MCA in the same region as the hyperdense MCA. This finding confirms our suspicion that the patient was taken for mechanical thrombectomy. 

Also shown was complete occlusion of the internal carotid artery on the same side due to a bad acute dissection. 

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The following MRI shows a large right MCA territory infarct with increased signal on DWI and corresponding low ADC signal (diffusion-restriction). A tiny infarct in the left frontal lobe suggests this is all related to showering emboli from the ICA dissection. 

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Follow-up vascular imaging post-thrombectomy shows reconstitution of the right ICA AND MCA. 

The hyperdense MCA sign is the earliest visible sign of MCA infarction - seen within 90 minutes after the event. The sensitivity is very low, however, at 30%, the absence of this sign doesn't rule out pathology. 

The finding is, as it sounds, just hyperdensity of the MCA relative to the other side and basilar artery. Be careful not to overcall this on just thick axial slices as there can be asymmetry. Use thin-section CT and multiplanar reformats to confirm in addition to vascular imaging. 

References:

Chayhan GB, Shroff MM. Twenty classic signs in neuroradiology: A pictoral essay. Indian J Radiol Imaging. 19 (2): 135-45. doi: 10.4103/0971-3026.50835

Tomsick T, Brott W, Broderick J, Haley EC, Spilker J, Khoury J. Prognostic value of the hyperdense middle cerebral artery sign and stroke scale score before ultraearly thrombolytic therapy. (1996) AJNR. American journal of neuroradiology. 17 (1): 79-85. 

 

 

 

 

 

 

 

 

 

 

 December 7, 2020: Active Inflammatory Crohn's Disease

A female in her 40s presented at the Emergency Department with acute-on-chronic abdominal pain and diarrhea. CT abdomen and pelvis was ordered. 

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The pictures above show a long segment of markedly thickened, inflamed bowel most prominently involving the mid-distal and terminal ileum. There is associated mucosal hyperenhancement of the thickened bowel loops. Some of the involved bowel loops show mural stratification with low attenuation of the thickened wall relating to submucosal edema juxtaposed with mucosal hyperenhancement. 

 

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Multiple strictures with areas of focal luminal narrowing and interposing regions of relative dilation are seen throughout the involved bowel segments, representing sites of fibrosis from prior bouts of active inflammation. 

 

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The picture above shows a pseudosacculation or pseudodiverticulum, which is a broad outpouching of normal bowel wall along the anti-mesenteric side, secondary to retraction / scarring of the opposite bowel wall from chronic ulcers. 

 

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The involved bowel segments demonstrate intramural fat deposition, shown as thin, hypodense (fat density) layers within the bowel wall. This is known as "fat halo" sign. 

 

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In addition to the bowel findings described above, this patient also has engorgement of the vasa recta ("comb sign") and mesenteric hyperemia. 

 

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The picture above shows fibrofatty proliferation of the mesenteric fat ("creeping fat") along the mesenteric border of the involved bowel segments. 

Diagnosis: Active Crohn-related bowel inflammation

Teaching points:

Crohn disease is an idiopathic chronic granulomatous inflammatory bowel disease. It is most common in young adults, and often presents wtih abdominal pain and diarrhea. 

Characteristic features include:

  • Discontinuous involvement of the entire gastrointestinal tract from mouth to anus ("skip lesions")
  • Usually involves the small bowel, and almost always involves the terminal ileum
  • When involving the stomach, it favors the gastric antrum
  • When involving the colon, it favors the right side / ascending colon and often spares the rectosigmoid colon
  • Forms strictures secondary to chronic fibrotic change (marked narrowing at the terminal ileum / ileocecal valve, often termed "string sign")
  • Transmural inflammation with linear longitudinal and circumferential ulcers extending deep into bowel wall lead to formation of fistulae
  • Mesenteric abscess formation
  • Perianal abscesses and fistulae
  • Increased risk of small bowel and colonic adenocarcinoma and lymphoma, preferentially involving the distal and terminal ileum

Many of the most standard CT findings are shown above. CT findings indicative of active Crohn inflammation include:

  • Bowel wall thickening
  • Mucosal hyperenhancement
  • Mural stratification: juxtaposition of mucosal hyperenhancement with hypodense submucosal edema in the thickened bowel wall
  • Engorgement of the vasa recta ("comb sign") and mesenteric hyperemia

CT findings of chronic Crohn disease include:

  • Intramural fat deposition: This is a nonspecific finding. In patients with acute symptoms and preferential involvement of the terminal ileum, it may be related to Crohn disease. If preferentially involving the duodenum and proximal jejunum, it may relate to celiac disease. However, in a patient without a history of inflammatory bowel disease, it is most often related to obesity. 
  • Strictures representing sites of fibrosis from prior bouts of active inflammation. These strictures can lead to true bowel obstructions.
  • Fibrofatty proliferation of mesenteric fat along mesenteric border of involved bowel segments ("creeping fat")
  • Pseudosacculation / pseudodiverticulum on anti-mesenteric border of bowel wall secondary to scarring of opposite bowel wall from chronic ulcers
  • Abscesses and fistulae

Extraintestinal features of Crohn disease include: gallstones, hepatic abscesses, pancreatitis, sacroiliitis, erythema nodosum, uveitis, oxalate renal stones, and many more. 

Treatment includes medical management with steroids and immunomodulating agents. Surgery is often necessary in cases with strictures, bowel obstructions, fistulae, and perianal disease. 

References:

  1. Raman SP, Horton KM, Fishman EK. Computed tomography of Crohn's disease: The role of three dimensional technique. World J Radiol, 2013; 5(5):193-201. doi:10.4329/wir.v5.i5.193
  2. Furukawa A, Saotome T, Yamasaki M et al. Cross-sectional imaging in Crohn disease. Radiographics 2004;24(3):689-702.
  3. Gore RM, Balthazar EJ, Ghahremani GG et al. CT features of ulcerative colitis and Crohn's disease. AJR Am J Roengenol. 1996;167 (1):3-15.
  4. Lee SS, Kim AY, Yang SK et al. Crohn disease of the small bowel: comparison of CT enterography, MR enterography, and small-bowel follow-through as diagnostic techniques. Radiology. 2009;251 (3): 751-61.

 

 

 December 14, 2020: Acute Cholecystitis with Perforated Gallbladder

A man in his 60s presented at the Emergency Department with right upper quadrant pain and leukocytosis. Right upper quadrant ultrasound was obtained followed by a CT abdomen and pelvis. 

 

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The green arrows point to echogenic foci within the gallbladder lumen with associated posterior acoustic shadowing compatible with cholelithiasis. The yellow arrows point to a markedly thickened and edematous gallbladder wall with associated gallbladder wall hyperemia (increased flow on color Doppler images). In addition, there is pericholecystic fluid and the patient reported severe abdominal pain from pressure of the ultrasound probe over the gallbladder (positive sonic Murphy sign). 

 

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The ultrasound study also shows a focus of gallbladder wall discontinuity with a complex fluid collection between the gallbladder and liver. CT was recommended for further evaluation.

 

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CT redemonstrates a markedly thickened gallbladder wall with pericholecystic free fluid and surrounding fat stranding (green arrows). There is focal discontinuity of the gallbladder wall with a complex fluid collection in the subhepatic space between the liver and gallbladder (yellow arrows).

Diagnosis: Acute cholecystitis with type 2 gallbladder perforation and subhepatic abscess formation

Gallbladder perforation is a severe complication of acute cholecystitis that occurs in less than 5% of cases but increase morbidity and mortality. It tends to occur in elderly patients or patients with underlying chronic medical conditions. It presents with right upper quadrant pain. 

Acute cholecystitis is most often caused by a gallstone obstructing the cystic duct, which leads to retention of secretions within the gallbladder and resultant gallbladder distention. Eventually, the intraluminal pressure exceeds the arterial perfusion pressure and obstructs venous drainage causing ischemia / necrosis of the gallbladder wall with subsequent perforation. The gallbladder fundus is the most common site of perforation as it receives the terminal blood supply. Perforation can also occur in the setting of trauma. 

Perforation can occur between two days to several weeks after the onset of acute cholecystitis. There are four types of perforation according to the Neimeier classification:

  • Type 1: Acute free perforation of the gallbladder with generalized peritonitis
  • Type 2: Subacute perforation of the gallbladder with localized pericholecystic abscess and phlegmon (the most common type)
  • Type 3: Chronic perforation of the gallbladder with choecystoenteric fistula formation
  • Type 4: Perforation into the biliary tree with cholecystobiliary fistula formation

Additional complications include intraperitoneal free air, bile leak, hepatic abscess (via direct extension or hematogenous dissemination), and small bowel obstruction among others. 

Treatment includes cholecystectomy and abscess drainage with or without preceding percutaneous cholecystostomy tube placement to relieve the infection and inflammation prior to surgery. Additional procedures such as fistula repair may be necessary. 

References: 

  1. Anderson BB, Nazem A. Perforations of the gallbladder and cholecystobiliary fistulae: a review of management and a new classification. J Natl Med Assoc. 1987; 79(4): 393-9.
  2. Derici H, Kara C, Bozdag AD et-al. Diagnosis and treatment of gallbladder perforation. World J. Gastroenterol. 2006;12 (48): 7832-6.
  3. Patel NB, Aytekin O, Thomas S. Multidetector CT of emergent biliary pathologic conditions. Radiographics. 2013;33:1867-88.
  4. Madrazo BL, Francis I, Hricak H, Sandler MA, Hudak S, Gitschlag K. Sonographic findings in perforation of gallbladder. AJR Am J Roentgenol 1982;139(3):491-496.

 

 

 

 

 

 

 

 

 

 

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