RARE : Gas containing renal calculus

Click on images to view in full size

GAS CONTAINING RENAL CALCULUS : RARE !?

'Gas-containing renal stones are exceedingly rare, but have been linked to serious renal infections.'
 (Urology. 2006 Oct;68(4):890.e13-5).


The first case of a gas-containing stone was reported by Simpson et al. in 1998 in a 68-year-old non-diabetic man with a history of ipsilateral untreated uretero-pelvic junction obstruction !!!

'Gas-containing urinary stones are a rare entity, and are associated with anaerobic fermenting organisms such as  Escherichia coli and Klebsiella. Gas-containing renal stones are invariably associated with emphysematous pyelonephritis commonly caused by E. coli and Klebsiella. Contributing factors to gas-containing stone formation include urinary stasis, metabolic mineral derangement and, in a minority of the cases, diabetes.'

'Urinary stasis appears paramount in the formation of gas-containing urinary calculi. All patients in the literature had radiographic signs of obstruction at presentation '

In this case, even though the right kidney was slightly atrophic, there was no features of obstruction or active pyelonephritis or any gas in the PCS or perinephric region.On CT Urogram there was nephrogram at 1 minute and excretion of contrast without delay !!!.

 (Manny TB, Manny JS, Hemal AK. Transmesocolic robotic extended pyelolithotomy of a large gas-containing renal stone: Case report and review of the literature. Urol Ann [serial online] 2013 [cited 2015 Apr 3];5:126-8).

DV03042015

Incisive Canal Cyst (Nasopalatine Duct Cyst)

 Click on images to view in full-size

Patient is a 55yr old male, did CT for nasal obstruction, to look for sinusitis. Incidental cyst found in anterior maxilla between roots of central incisors. Multiple periapical lucencies are also seen in the maxillary molars of both sides.

 

Incisive Canal Cyst (Nasopalatine Duct Cyst)

A nasopalatine duct cyst (incisive canal cyst) is a nonodontogenic developmental cyst or fissural cyst arising in the nasopalatine duct near the anterior palatine papilla. It is the most common nonodontogenic cyst. The cysts probably arise from epithelial remnants in the incisive canal. They can occur at any age but are most frequently found in the fourth and sixth decades of life, with no sex predilection. These cysts are usually asymptomatic, but some patients note swelling in the palate, especially when the cyst is primarily in the incisive papilla. Alternatively, the anterior maxilla can be remodeled forward, elevating the columella of the nose.

It may be difficult on imaging to differentiate between an enlarged incisive fossa and an incisive canal cyst. The incisive canal cyst is always located at or close to the midline and usually is round or ovoid, although it may be heart-shaped. A condensed rim of cortical bone is often seen along the periphery, and the lesion may displace the roots of the central incisor teeth.

Reference : Head and Neck Imaging, by Peter.M.Som, 4th Edition.

Acute Pancreatitis with hemorrhage and Pancreas Divisum

Patient is a 40 year male patient, with h/o alcohol consumption 2 days back, presented with acute epigastric pain, and raised serum amylase. Non-contrast CT images showed features of acute pancreatitis with hyperdense attenuation in the peripancreatic region, superior to the distal D3 (horizontal) segment of duodenum.

Extravasated pancreatic enzymes are usually responsible for the capillary and venule disruption, which leads to hemorrhage. Bleeding is usually self limited, but marked hemorrhage can occur in 2-5% of cases.

Non-contrast images show fatty infiltration of liver (30-35HU).

Contrast images showed no enhancement of the hyperdense area.

Incidentally there was also Pancreas Divisum. There was no connection with the larger dorsal  duct (Duct of Santorini) and the smaller ventral duct (Duct of Wirsung). Dorsal duct drained into the minor papilla and ventral duct, joined the distal CBD and drained into the duodenum through the major papilla. Pancreas divisum may be seen in upto 10% of general population. The relationship of PD with Pancreatitis remains controversial.

DIAGNOSIS : Acute hemorrhagic pancreatitis with Pancreas Divisum.

Incidentally the patient had a right distal ureteric calculus close to the VUJ, which he was not symptomatic of, at the time.

Reference : 'The Bloody Pancreas', AJR,2009.

Acute Necrotizing Pancreatitis

 Patient : 30 years, female, presented with acute epigastric pain.

CT Diagnosis : Acute Necrotizing Pancreatitis (Modified CT Severity Index 10).

Mild (0-2 points) Moderate (4-6 points) and Severe (8-10 points).

There is no odd integer score in Modified CT severity index.

Even if there are multiple extra-pancreatic complications are present, the score given is only 2. For example, if there is both ascites and pleural effusion, score is not 2 +2 = 4, but only 2.

Reference : AJR article 2004.

Multiple Cavernomas in Brain

CT findings of Cavernomas or Cavernous Angiomas of Brain

NECT

Negative in 30-50%
Well-delineated round/ovoid hyperdense lesion, usually < 3 cm
40-60% Ca++
No mass effect unless recent hemorrhage
Surrounding brain usually appears normal

CECT: 

Little/no enhancement unless mixed with other lesion (e.g., DVA)

CTA: Usually negative

Reference : DI, Brain.

TAKAYASU ARTERITIS : A less common presentation

Patient is a 20 year old female, who presented with complaints of lower limb claudication.

CT ANGIOGRAM : CASE FINDINGS 

Click on the images to view in full-size

The branches of aortic arch showed no involvement. There was circumferential wall thickening of the thoracic aorta starting distal to the origin of left subclavian artery, extending in a contiguous fashion with increasing severity to involve the abdominal aorta. Involvement of iliac arteries were also seen.

The above image shows the progressive increase in the wall thickness of abdominal aorta, with maximal involvement of the infra-renal segment, where the lumen was almost a thread like / non-existent.

Celiac trunk, SMA, Bilateral renal arteries showed significant stenosis origin/ proximal portion. IMA origin was completely blocked, which got collateral blood supply from a large tortuous branch from SMA (meandering mesenteric artery / wandering artery of Drummond).

Above the 3D-VRT image shows the engorged Superior Epigastric arteries (branch of Internal Thoracic / Internal Mammary artery) bilaterally, with tortuous anastomosis within the bilateral rectus abdominis muscles - where it anastomose with the corresponding Inferior Epigastric Arteries.

3D- VRT images showing the gradual smooth tapering of abdominal aorta; Rat-tail appearance.

Coronal MPR images showing marked wall thickening of infra-renal Abdominal Aorta.

DIAGNOSIS :

Since the wall thickening is seen involving the descending thoracic aorta and abdominal aorta, but sparing the ascending aorta and arch, the diagnosis is more fitting into a Type III Takayasu Arteritis.

Midaortic dysplastic syndrome cannot be distinguished from late-phase Takayasu arteritis on the basis of radiologic findings alone. The two disease entities can be differentiated only by histopathologic exclusion of inflammatory change, which is present in Takayasu arteritis but not in midaortic dysplastic syndrome. (Radiographics, 2003).

TAKAYASU ARTERITIS 

Takayasu arteritis is a chronic, idiopathic, inflammatory disease that primarily affects large vessels, such as the aorta and its major branches and the pulmonary and coronary arteries. The non-specific inflammation of involved vessels usually leads to concentric wall thickening, fibrosis and thrombus formation. Diseased arteries become stenotic or occluded, undergo vascular remodelling or develop aneurysms.

Disease occurs primarily in young women with associated rheumatic complaints including arthritis, myalgia, pleuritis, pericarditis, fever and rash, none of which was present in any of our patients. The ESR is usually raised.

Sharma criteria for diagnosis of Takayasu arteritis

Major criteria

1. Left mid-subclavian artery lesion
2. Right mid-subclavian artery lesion
3. Characteristic signs and symptoms of at least one month duration [a]

Minor criteria

1.  High erythrocyte sedimentation [b]
2. Carotid artery tenderness
3. Hypertension [c]
4. Aortic regurgitation or annuloaortic ectasis
5. Pulmonary artery lesion
6. Left mid-common carotid lesion
7. Distal brachiocephalic trunk lesion
8. Descending thoracic aorta lesion
9. Abdominal aorta lesion
10. Coronary artery lesion

Presence of two major, or one major and two minor criteria, or four minor criteria suggests a high probability of Takayasu arteritis.

[a] Including limb claudication, pulselessness or pulse differences in limbs, an unobtainable or significant blood presence difference, fever, neck pain, transient amaurosis, blurred vision, syncope, dyspnea or palpitations.
[b] Higher than 20mm per hour (Westergren method).
[c] Higher than 140/90mmHg brachial or 160/90mmHg popliteal.

 Disease has two phases of progression:

The Early phase / Systemic phase / Pre-pulseless phase : where the steroid therapy can affect prognosis.

Late phase or Pulseless phase or Occlusive phase symptoms depend upon the site of occlusion. The interval between the early and late phase can vary between 1 to 8years.

Early-phase arteritis is limited to the arterial wall. Therefore, absence of stenotic or occlusive changes in the aorta, its branches, and the pulmonary artery on conventional angiograms of a young female patient with fever of unknown origin does not exclude the possibility of early phase Takayasu arteritis. So CT/MRI is required to assess the aortic wall to know the presence of inflammation in early phase.

According to the vessels involved, the most recently proposed angiographic classification divides TA into six types :- (See the image below)

Type I involves only the branches of the aortic arch.
Type IIa involves ascending aorta, aortic arch and its branches.
Type IIb affects ascending aorta, aortic arch and its branches, and thoracic descending aorta.
Type III involves the descending thoracic aorta, the abdominal aorta and/or the renal arteries. The ascending aorta, the aortic arch and its branches are not affected.
Type IV involves only the abdominal aorta and/or renal arteries.
Type V has combined features of Type IIb and IV.

Additionally, involvement of the coronary and pulmonary arteries should be indicated as C (+) or P (+), respectively. Type V has been documented as the most common type.

CT angiography features

1. Mural thickening

a. typical manifestation for Takayasu is the concentric mural thickening of the involved arteries.
b. Calcification (27%, Often transmural) in the thickened wall is another important sign of Takayasu.

c. Double ring enhancement pattern (See the above image) on CECT – inner hypodense rim – due to intimal edema and outer enhancing wall due to medial and adventitial inflammation.

2. Luminal changes

a. Stenosis is the most common finding associated with wall thickening (in 90%).
b. Abdominal and thoracic aorta stenosis in up to 60%.
c. Branches showing stenosis : Subclavian and Common carotids > Renal.
d. Occlusion, ectasis(ascending) and aneurysm(abdominal) formation seen less often.
e. Sometimes, the normal or dilated proximal vessels associated with tapered narrowing of distal segments exhibit a characteristic ‘‘rat tail’’-like configuration, especially in patients with both thoracic and abdominal aorta involved (as in this case).

3. Collateral vessels : (MIP is useful for assessment of collaterals.)

a. When the superior mesentenc artery is stenotic or occluded, excellent collateral flow via a meandering mesenteric artery reconstitutes the distal portion. Blood flow is retrogradely directed from the inferior mesenteric artery to the distal superior mesenteric artery branches via the meandering mesenteric artery.

b. When the infrarenal portion of the abdominal aorta is nearly or totally occluded, blood flow is directed antegradely from the superior mesenteric artery to the inferior mesenteric artery via the meandering mesenteric artery ( As in this case). In this situation, the meandering mesenteric artery is dilated as much as the aorta.[2]

4. Other findings

a. Pulmonary and coronary artery involvement can be seen in ~60% and ~40% of patients, respectively.

Differential diagnosis

 

1. Midaortic dysplastic syndrome.

2. Atherosclerosis : Atherosclerotic plaques are more common in patients aged 45 years and above, and not usually associated with long segment luminal stenosis.

3. Giant cell arteritis : >50yrs, branches of the external and internal carotid arteries are most frequently diseased.

4. Polyarteritis nodosa :30–50 years, males more than females, and it also more commonly affects patients with hepatitis B. Gastrointestinal and renal arteries are the primary sites diseased. Multiple small aneurysm formation in the involved artery is the characteristic manifestation on CTA.

Treatment

TA is a rare entity with poor prognosis.Corticosteroids have been considered to be the mainstay of treatment for TA, with a remission rate up to 60%. In patients with symptomatic stenotic or occlusive lesions, percutaneous transluminal angioplasty and stenting or bypass surgery is the most common palliative treatment



References :
[1]Takayasu arteritis: imaging spectrum at multidetector CT angiography, BJR -2012.
[2] Takayasu Arteritis – Radiographics,1997.

FRCR 1 ANATOMY QUESTION : 16

FRCR part 1 : Anatomy Review : Question -

What is the structure labelled?

CASE OF BILATERAL PYELONEPHRITIS

Case : Bilateral Pyelonephritis.

Discussion on : 

1. Appearance of Pyelonephritis on USG and CECT.

2. Acute Pyelonephritis Vs Renal Infarct.

Patient is a 35year old diabetic female, who presented with fever with chills, right upper quadrant and loin pain, with Urine examination showing plenty of pus cells, RBCs and Bacteria.

Clinical diagnosis was of acute right pyelonephritis.

USG showed only hypoechoic mildy enlarged kidneys bilaterally. No urolithiasis / hydroureteronephrosis was seen.

CECT was done, which showed areas with relative lack of enhancement in lower and posterior interpolar region of right kidney and upper pole of left kidney. Only  minimal perinephric fat stranding was seen. Minimal pararenal fascial thickening was seen on right side only.

No urolithiasis / hydroureteronephrosis was seen in CT.

Click on the images to view full size.

ACUTE PYELONEPHRITIS Vs SEGMENTAL RENAL INFARCTS

In segmental renal arterial infarcts, the peripheral most cortical supply gets derived from the capsular arteries, which shows an enhancing rim around the infarct - which is called as the Cortical Rim Sign. This is not seen in Pyelonephritis, in which case the entire thickness is involved. Rim sign is however only seen in approximately 50% cases of renal infarcts.

ACUTE PYELONEPHRITIS

Image courtesy of Dr Frank Gaillard From the case Acute pyelonephritis

Cortical Rim Sign : SEGMENTAL RENAL INFARCTS

Image courtesy of Dr Frank Gaillard, Radiopaedia.org. From the case Renal infarction

CECT findings of Acute Pyelonephritis (abnormal in 65-90%):

1. Perinephric fat stranding and pararenal fascial thickening.
2. Hypoattenuating (80-90 HU) wedge-shaped area of cortex extending from papilla to renal capsule
3. During nephrographic phase(= lobar segments of hypoperfusion +edema)
4. Striated nephrogram
5. Poor corticomedullary differentiation
6. Dense parenchymal staining on scan delayed 3-6 hr in area of earlier diminished enhancement(= functioning renal parenchyma)
7. Soft-tissue filling defect in collecting system (=papillary necrosis, inflammatory debris, blood clot) calyceal effacement.

CT is best for detecting presence of calculi, level of obstruction and complications.

 

 US findings in Acute Pyelonephritis (abnormal in <50%):

1. Swollen kidney of decreased echogenicity – (kidney becomes more globular, with increased AP dimension. The parenchymal thickness sometimes appears to be increased because of parenchymal edema.)
2. Loss of central sinus complex (Sometimes described as effacement of renal sinus fat)
3. Wedge-shaped hypo to isoechoic zones, rarely hyperechoic (due to hemorrhage)
4. Thickened sonolucent corticomedullary bands
5. Blurred corticomedullary junctions
6. Localized increase in size + echogenicity of perinephric fat ± fat within renal sinus
7. Localized perinephric exudate
8. Thickening of wall of renal pelvis
9. Focally decreased blood flow on power Doppler.

Ultrasound is often the first imaging study, and it is difficult to diagnose Pyelonephritis by USG.

Differentiating between Ascending and Hematogenous infection may not be possible, however these points might be of some help -

            'In acute bacterial nephritis, the alternating bands of hypo- and hyperattenuation, which correspond to differential enhancement of infected and noninfected parenchyma, are sharply defined. Over time, the differential enhancement becomes less distinct and ultimately will either completely normalize or evolve to scar, as evidenced by loss of parenchymal volume. When round, peripheral hypoattenuation renal lesions are seen in the clinical setting of pyelonephritis, hematogenous seeding should be considered'. [3]



References : 

• [1] Dahnert, Radiology Review Manual 7th Edition.
• [2] Radiopedia.org article on Cortical Rim Sign.
• [3]  Pyelonephritis: Radiologic-Pathologic Review, Radiographics.

Spontaneous Retroperitoneal Hemorrhage

A middle aged male patient, was undergoing hemodialysis ( with anticoagulation), developed sudden drop of Hemoglobin 10 to 6g/dL.

Ultrasound scan showed right retroperitoneal hemorrhage. CT images showed a large right sided retroperitoneal hematoma, measuring ~10cm x12.5cm x 13cm.

Another smaller intramuscular hematoma was also seen along the right Iliacus muscle, reaching upto it's insertion.

Diabetic patients on hemodialysis are susceptible to develop spontaneous retroperitoneal hemorrhage. 'In patients receiving anticoagulant therapy in whom progressive anemia and unstable vital signs are present, spontaneous retroperitoneal bleeding should be considered as a possible cause.'[1].

'The presenting common symptoms and signs of retroperitoneal bleeding included sudden and progressive abdominal pain with blood pressure drop and subsequent development of an abdominal mass. These symptoms were associated with a falling hematocrit without any documented external blood loss and with suggestive X-ray changes, including absence of psoas shadow with soft tissue density.[2]

References :
[1] :  Spontaneous retroperitoneal bleeding: a case series : Hitoshi Yamamura. Sep 2014.
[2] : Ann Intern Med. 1977 Feb;86(2):189-92. Spontaneous retroperitoneal bleeding in patients on chronic hemodialysis.

FRCR 1 ANATOMY QUESTION : 15

 Name the 5 structures labelled A to E.

NB : This was the old model FRCR question, where 5 structures were asked from a single image x 20 images in total, which as of now, changed to 100 images, with single question from each image.

FRCR 1 ANATOMY QUESTION : 14

FRCR 1 ANATOMY QUESTION : 13

Name the structure labelled..

FRCR 1 ANATOMY QUESTION : 12

Name the labelled structure?

Orbital Blow-out Fractures

The CLASSIC BLOWOUT FRACTURE involves the floor of the orbit, usually sparing the orbital rim. Frequently, orbital tissues are trapped in the fracture site and ocular motility disturbances have been ascribed to entrapment of one or both inferior EOMs, but may be also due to orbital hematoma / inflammation.

The term orbital blow-out fracture describes the injury that results from a blow to the orbit by an object that is too large to enter the orbit (fist, baseball, etc.). The force of the blow is absorbed by the orbital rim and is transmitted to the thinner orbital floor, which shatters, usually in the middle third near the infraorbital canal. As the eye is pushed back into the conical orbital apex, it increases intraorbital pressure and this ‘‘blows out’’ the fractured floor into the maxillary sinus.

Pure blow-out Vs. Impure blow-out fractures

Usually the orbital rim is not fractured (pure blow-out fracture) and the globe remains undamaged. Less commonly the inferior orbital rim also is fractured; this is referred to as an impure blow-out fracture. 

Herniation of orbital fat, inferior rectus muscle, and inferior oblique muscle can occur with occasional muscle entrapment in the fracture line, resulting in diplopia on upward gaze.

Diplopia is the most frequent complaint in all patients with blow-out fractures and may occur solely because of periorbital edema and hemorrhage, which exert pressure on the globe. This type of diplopia resolves in several days, whereas entrapment diplopia remains.

Ref : Head and Neck Imaging, 4^th Edition, Peter.N.Som.

Terms 'Blow-out / Blow-in' fractures can also be used in cases of Medial wall or rarely roof fractures also. Medial wall fractures are more likely to cause diplopia than a floor blow-out. Roof fractures might require an intracranial approach of treatment because of the breach of dura.

Sometimes the fractured floor, can sprang back into place, after the inferior rectus has herniated, trapping the muscle, this is called as a 'Trapdoor Fracture' (See the image below)

CT coronal section (soft tissue window) showing the entrapped inferior rectus, with the fractured floor back into anatomical position -- TRAPDOOR fracture.

Ref : RG 2006; 26:783-793 - 'Diagnosis of Midface fractures with CT'.

 
The extra-ocular muscle that herniates in the floor blow-out fracure is almost always the Inferior Rectus - Oblique. But below is a rare case, where the medial rectus has herniated through the floor defect into the maxillary sinus.

Click on the image to view in full-size