imaging in acute nontrumatic solid organs injuries

Imaging in acute nontrumatic solid organs injuries

A. Norouzi MD

The 'acute abdomen' is a clinical condition characterized by severe abdominal pain, requiring the clinician to make an urgent therapeutic decision.

This may be challenging, because the differential diagnosis of an acute abdomen includes a wide spectrum of disorders, ranging from life-threatening diseases to benign self-limiting conditions (Table 1).

Table 1. Common causes of acute abdomen from life-threatening to self-limiting.

Indicated management may vary from emergency surgery to reassurance of the patient and misdiagnosis may easily result in delayed necessary treatment or unnecessary surgery.

Sonography and CT enable an accurate and rapid triage of patients with an acute abdomen.

Radiological strategy

Before you perform an examination, obtain relevant information from the referring clinician.

Don't let the clinician simply 'order' a sonogram or CT, but discuss the patient's age and posture, laboratory results and the number one clinical diagnosis and differential diagnosis.

Based on that information and your own degree of confidence with the modalities decide for yourself whether to perform sonography or CT.

Sonography has the advantage of close patient contact, enabling assessment of the spot of maximum tenderness and the severity of illness without ionizing radiation.

In general the diagnostic accuracy of CT is higher than sonography.

In patients with inconclusive US-results, CT can serve as an adjunct to sonography, and vice versa.

Clinics, laboratory, and plain abdominal film The clinical presentation of patients with an acute

abdomen is often nonspecific. Both surgical and nonsurgical diseases may present

with a similar clinical history and symptoms. Laboratory findings (leucocyte count, erythrocyte

sedimentation rate, CRP) are equally nonconclusive. Findings may be normal in patients who need

emergency surgery (such as appendicitis) and may be abnormal in patients without a surgical disease (like salpingitis).

A plain abdominal film has a limited value in the evaluation of abdominal pain.

A normal film does not exclude an ileus or other pathology and may falsely reassure the clinician.

An ileus may not be appreciated on a plain abdominal film if bowel loops are filled with fluid only without intraluminal air (figure).

Alternatively if a plain abdominal film does indicate an ileus then sonography or CT are usually needed to identify its cause.

Thus, a plain abdominal film is seldomly useful, with the exception of detection of kidney stones, bowel obstruction or a pneumoperitoneum.

For all other indications use sonography or CT.

LEFT: Plain abdominal film in a patient with an acute abdomen, showing no abnormalities.

RIGHT: Subsequent CT shows distended small bowel loops (arrowheads) that are not seen on plain abdominal film because they are filled with fluid only and do not contain intraluminal air.

Confirm or exclude the most common disease

Always remember: Commonest are the commonest

Many disorders may cause an acute abdomen, but fortunately only a few of these are common and clinically important.

Focus on confirming or excluding these frequent disorders:

Screen for general signs of pathology

After excluding these frequent disorders, search for signs of any other pathology, by systematically screening the whole abdomen.

Look for inflamed fat, bowel wall thickening, ileus, ascites and free air.

Inflamed fat Inflamed fat is

hyperechoic, space occupying and noncompressible at sonography.

Inflamed fat at sonography. Extended-view of the ventral abdomen depicting an area of hyperechoic noncompressible inflamed fat in the omentum (red arrows). Compare this to the echogenicity of normal abdominal or subcutaneous fat (green arrows). This patient had an omental infarction.

Same patient as above. Unenhanced CT depicts an area of fatty tissue with slightly increased density (arrowheads), in the right-upper quadrant. Compare this to normal low-density subcutaneous fat. Diagnosis: omental infarction.

Inflamed fat is shown as fat-stranding at CT. Inflamed fat usefully points out where and what the problem is.

As a rule, the organ or structure in the centre or nearest to the inflamed fat is the cause of the inflammation.

Bowel wall thickening Thickening of bowel wall indicates

inflammation or tumor, and has an extensive differential diagnosis.

Thickening of small bowel loops usually indicates regional inflammation, as small bowel tumors (carcinoid, lymphoma, GIST) are relatively infrequent.

In patients with local colonic wall thickening a carcinoma is a prime concern.

Diffuse thickening of bowel wall in a patient with colitis.

Ileus Pathologic distention of bowel loops

may be caused by obstruction or paralysis.

Firstly determine which parts of the gut are affected: small bowel, large bowel, or both.

Look for normal nondistended bowel loops, which, if present, strongly suggest an obstructive cause for the ileus.

Obstructive ileus. CT depicts distended small bowel loops, but part of the small bowel and the whole colon is nondistended. Therefore this must be an obstructive small bowel ileus, and in this case its cause can easily be identified: intussusception (arrowhead).

Alternatively, an ileus without any normal bowel loops strongly suggests a paralytic cause. This is usually a response to general peritonitis, which may have many possible causes of the inflammation.

Ascites Asymptomatic volunteers do not have a

detectable amount of free intraperitoneal fluid, with the exception of an incidental drop of fluid in Douglas in fertile women.

The presence of ascites is a nonspecific sign of abdominal pathology, indicating that 'something is wrong'.

You may want to perform a US-guided diagnostic puncture of the ascites, in order to investigate whether it is sterile reactive fluid, pus, blood, urine, or bile.

Clinically appendicitis. US only showed a little bit of ascites. A diagnostic puncture (arrow marks needletip) revealed blood. In a woman this finding is very suspicious of an EP.

Free air The presence of free intraperitoneal air is proof of

bowel perforation, and indicates a surgical emergency.

A pneumoperitoneum has only two frequent causes: Perforation of a gastric ulcer Perforation of colonic diverticulitis

Free air is usually not seen in perforated appendicitis.

Always examine the images in lung setting for better detection of free intraabdominal air (figure).

Intraperitoneal air in a patient suspected of having appendicitis. Air better seen on images with lung setting on the right.

Cholecystitis

Cholecystitis occurs when a calculus obstructs the cystic duct. The trapped bile causes inflammation of the gallbladder wall. 

As gallstones are often occult on CT, sonography is the preferred imaging method for the evaluation of cholecystitis, also allowing assesment of the compressiblity of the gallbladder. 

The diagnosis of a hydropic gall bladder is solely made on the non-compressability of the gall bladder. Do not rely on measurements. Some gall bladders happen to be small and others are large.

The imaging appearance of cholecystis consists of an enlarged hydropic (meaning non-compressible) gallbladder with a thickened wall in the region of maximum tenderness (the so-called 'Murphy sign')

Longitudinal and transverse US show thickened gallbladder wall. The gallbladder is noncompressible ('hydropic') and causes an impression in the anterior abdominal wall (arrowheads).

The inflamed gallbladder usually contains stones or sludge, whereas the obstructing calculus itself may or may not be identified because it is located deep within the gall bladder neck or cystic duct.

The gallbladder may be surrounded by inflamed fat, but on sonography this frequently is not seen, while CT sometimes does show fat-stranding. 

Potential pitfalls are pancreatitis, hepatitis or right-sided heart failure, which all may lead to thickening of the gallbladder wall without cholecystitis.

Therefore be certain that hydropic obstruction of the gallbladder is present before assigning the diagnosis of cholecystitis.

Gallbladder Wall Thickening

Thickening of the gallbladder wall is a relatively frequent finding at diagnostic imaging studies.

Historically, a thick-walled gallbladder has been regarded as proof of primary gallbladder disease, and it is a well-known hallmark feature of acute cholecystitis.

The finding itself, however, is non-specific and can be found in a wide range of gallbladder diseases and extracholecystic pathological conditions.

Sonography, CT and MRI all allow direct

visualization of the normal and thickened gallbladder wall.

Traditionally, sonography is used as the initial imaging technique for evaluating patients with suspected gallbladder disease, because of its high sensitivity in the detection of gallbladder stones, its real-time character, speed and portability

However, CT has become popular for evaluating the acute abdomen and often is the first modality to detect gallbladder wall thickening, or it may be used as an adjunct to an inconclusive sonography or for staging of disease.

The potential value of MRI in the evaluation of gallbladder pathology has been shown, but it still plays little role.

LEFT: US of a normal gallbladder after an overnight fast shows the wall as a pencil-thin echogenic line.RIGHT: US in the postprandial state shows pseudothickening of the gallbladder

The normal gallbladder wall appears as a pencil-thin echogenic line at sonography.

The thickness of the gallbladder wall depends on the degree of gallbladder distention and pseudothickening can occur in the postprandial state.

Contrast-enhanced CT shows the normal gallbladder wall as a thin rim of enhancing soft-tissue

The normal gallbladder wall is usually perceptible at CT as a thin rim of soft-tissue density that enhances after contrast injection.

Thickened gallbladder wall Thickening of the gallbladder wall is a

relatively frequent finding at diagnostic imaging studies.

A thickened gallbladder wall measures more than 3 mm, typically has a layered appearance at sonography, and at CT frequently contains a hypodense layer of subserosal oedema that mimics pericholecystic fluid.

LEFT: US in a 59-year-old woman with acute cholecystitis shows the layered appearance of a thickened gallbladder wall, with a hypoechoic region between echogenic linesRIGHT: At contrast-enhanced CT the thick-walled gallbladder contains a hypodense outer layer (arrow) due to subserosal oedema

Differential diagnosis of gallbladder wall thickening The differential diagnosis of gallbladder

wall thickening is listed on the table 2. Diffuse gallbladder wall thickening may

produce a diagnostic problem, as it occurs in symptomatic and asymptomatic patients, and in patients with and without an indication for a cholecystectomy.

Diffuse thickening of the gallbladder wall may occur in patients who do not have a primary gallbladder disease, but in whom the gallbladder is secondarily involved in an extrinsic pathological condition.

In these patients a cholecystectomy is unwarranted, and gallbladder abnormalities will usually return to normal after correction of its extrinsic cause.

What is your diagnosis

43-year-old woman with acute calculous cholecystitis.

What is your diagnosis

Chronic cholecystitis

What is your diagnosis

Xanthogranulomatous cholecystitis. LEFT: US shows marked wall thickening with intramural hypoechoic

nodules (arrowheads), and an intraluminal stone (arrow). RIGHT: Contrast-enhanced CT shows a deformed and thickened

gallbladder wall containing hypoattenuating nodules

What is your diagnosis

Porcelain gallbladder.

What is your diagnosis

LEFT: Gallbladder carcinoma. US shows marked generalized wall thickening (arrowheads), replacing the gallbladder lumen. Multiple

gallbladder stones (arrow) indicate the probable location of the filled lumen.

RIGHT: Contrast-enhanced CT depicts a thick-walled gallbladder (arrowhead), with local infiltration of the mass in the adjacent liver

(arrow).

What is your diagnosis

Adenomyomatosis in a 39-year-old woman. US shows mural thickening with calcifications with the characteristic 'comet-tail' reverberation artifact (arrow) due to small cholesterol crystals

within Rokitansky-Aschoff sinuses.

What is your diagnosis

56-year-old man with liver cirrhosisLEFT: US depicts wall thickening (arrow), surrounded by ascites. Note the irregular cirrhotic liver parenchyma. 

RIGHT: At contrast-enhanced CT the wall of the gallbladder (arrow) appears nearly normal, because subserosal oedema can not be well differentiated from surrounding ascites at CT.

What is your diagnosis

Diffuse gallbladder wall thickening in congestive

right heart failure

What is your diagnosis

Pancreatitis in a 56-year-old manContrast-enhanced CT shows peripancreatic

inflammatory changes (arrowheads), and thickening of the wall of the gallbladder (arrow) which is

secondarily involved in the pancreatic inflammation.

Acute Pancreatitis

Introduction Acute pancreatitis

varies from a mild uneventful disease to a severe life-threatening illness with multisystemic organ failure (MOF) with shock, renal failure, respiratory failure and death.

Illustration of acute pancreatitis with necrosis of the pancreatic body

Imaging of Acute Pancreatitis In the diagnosis and staging of acute

pancreatitis and its complications CT is the imaging modality of choice.

Ultrasound is important in determining whether gallstones are the cause of the acute pancreatitis (i.e. biliary pancreatitis).

ERCP with sphincterotomy and stone extraction should only be used if a patient has biliary pancreatitis and signs of biliary obstruction.

MRI is as sensitive as CT, but not as practical or accessible.

In certain cases it can be of additional value.

There is no additional value of an early CT (within 72 hours) in patients with acute pancreatitis.

The diagnosis is usually made on clinical and laboratory findings.

An early CT may be misleading concerning the severity of the pancreatitis, since it can underestimate the presence and amount of necrosis.

Early CT is only recommended when the diagnosis is uncertain, or in case of suspected early complications such as perforation or ischemia.

Severe pancreatic necrosis, but normal enhancing pancreas on day 1.

The case on the left shows a normally enhancing pancreas with enhancement comparable to that of the spleen on day 1.

As the patient's condition worsened, a second CT was performed on day 3.

Notice how the majority of the pancreatic body and tail no longer enhance - in fact only a small part of the pancreatic head enhances.

Classification of Acute Pancreatitis CT Severity Index (CTSI) It is critical to identify patients who are at

high risk for severe disease, since they require close monitoring and possible intervention.

Early staging is based on the presence and degree of systemic organ failure (cardiovascular, pulmonary, renal) and on the presence and extend of pancreatic necrosis.

Balthazar et al constructed a CT severity index (CTSI) for acute pancreatitis that combines the grade of pancreatitis (A-E) with the extent of pancreatic necrosis.

The CTSI assigns points to patients according to their grade of acute pancreatitis - which can be determined on a non-contrast CT as well as a contrast-enhanced CT - as well as the degree of pancreatic necrosis - which requires the use of intravenous contrast material.

More points are given for a higher grade of pancreatitis and for more extensive necrosis.

Mild pancreatitis Patients with pancreatitis but no

collections or necrosis (i.e. Balthazar grade A-C) have a mild pancreatitis.

This is also called 'edematous or interstitial pancreatitis' (no pancreatic necrosis).

It is a self-limiting disease with an uneventfull recovery occurring in 80% of patients with acute pancreatitis.

There is an intermediate form of pancreatitis without pancreatic necrosis with an intermediate clinical course.

This is called extrapancreatic necrosis (EXPN). Sometimes the term exudative pancreatitis is used. These patients have Balthazar grade D or E. These patients have a relatively mild course

because there is no pancreatic necrosis, but there is higher morbidity than in interstitial pancreatitis, because they have peripancreatic collections, that can become infected.

Severe pancreatitis, also called 'necrotizing pancreatitis' occurs in 20% of patients.

It is characterized by a protacted clinical course, a high incidence of local complications and a high mortality rate.

Interstitial pancreatitis On the left there is

normal enhancement of the entire pancreatic gland with only mild surrounding fatty infiltration.

There are no fluid collections or necrosis

(Balthazar grade C, CTSI: 2).

Exudative Pancreatitis In exudative pancreatitis, or better called

EXPN, there is normal enhancement of the entire pancreas associated with extensive peripancreatic collections.

These are often heterogeneous in appearance and may be progressive.

EXPN consists of necrosis of peripancreatic fat, extravasated pancreatic fluid and inflammatory and hemorrhagic components.

When peripancreatic collections persist or increase, it is usually due to the presence of fat necrosis (i.e. EXPN).

Since fat does not enhance on CT, we cannot diagnose fat necrosis.

In the case on the next on day 18 there is expansion of the peripancreatic collections.

There are two or more collections, but no pancreatic necrosis.

(Balthazar grade E, CTSI: 4)

Necrotizing Pancreatitis On the next a patient with acute

necrotizing pancreatitis. The detection of pancreatic necrosis in

clinical practice is important because most life-threatening complications occur in patients with pancreatic necrosis (1,2).

Necrotizing pancreatitis: only enhancement of a part of the pancreatic headThere are 2 or more fluid collections and more than 50% of the gland does not enhance (Balthazar grade E, CTSI :10).

Necrotizing Pancreatitis In the case on the left

the body and tail of the pancreas do not enhance after i.v. contrast (blue arrows).

There is however normal enhancement of the pancreatic head (yellow arrow).

More than 50% of the pancreas is necrotic and there are at least two collections (CTSI : 10).

Central gland necrosis Central gland necrosis is a subtype of necrotizing

pancreatitis. It represents necrosis between the pancreatic head and

tail and is nearly always associated with disruption of the pancreatic duct.

This leads to persistent collections as the viable pancreatic tail continues to secrete pancreatic juices.

These collections react poorly to endoscopic or percutaneous drainage.

Definitive treatment often requires distal pancreatectomy.

The images on the next illustrate a case of central gland necrosis.

There is a fluid collection in the omental bursa, adjacent to the stomach.

Notice the normal enhancement of the pancreatic head and tail, but the lack of enhancement of the majority of the pancreatic body.

Two weeks later the collection in the omental bursa and pancreatic body has increased significantly.

The pancreatic tail still enhances and so does the pancreatic head (arrows).

This patient developed septicaemia and underwent surgery.

Peripancreatic Collections Intraabdominal fluid collections and

collections of necrotic tissue are common in acute pancreatitis.

These collections develop early in the course of acute pancreatitis.

In the early stage such a collection does not have a wall or capsule.

Preferred locations are the omental bursa and the retroperitoneal space (anterior and posterior pararenal space).

50% of these collections show spontaneous regression (image on the left).

The other 50% either remain stable or increase and undergo organization and demarcation with liquefaction.

They may remain sterile or develop infection.

Based on imaging alone it is often not possible to determine whether these collections contain fluid or necrotic tissue and whether they are infected or not.

Consequently, instead of naming them as 'pseudocysts', 'abscesses' or 'necrosis', it is better to describe them as 'peripancreatic collections'.

Infected necrosis Infected necrosis is:

Infection of necrotic pancreatic parenchyma And/or necrotic extrapancreatic fatty tissue

Usually occurs in the 2nd-3rd week. Most severe local complication of acute

pancreatitis Most common cause of death in patients with

acute pancreatitis Air bubbles are seen in 20% of cases with

infected necrosis.

On day 3 there is no enhancement of the pancreas, consistent with necrosis (compare to enhancing spleen).On follow up the peripancreatic collections increase in size and finally there are air bubbles in the heterogeneous collection, consistent with infected pancreatic necrosis.

Pseudocyst Collection of pancreatic juice enclosed by a wall of

fibrous tissue Absence of necrotic tissue is imperative for its

diagnosis Often communication with the pancreatic duct Requires 4 or more weeks to develop On CT we cannot diagnose a collection with certainty

as a pseudocyst, since it is usually not possible to determine what the content of a collection is.

Differential diagnosis includes abscess, necrosis and sometimes also pseudoaneurysm or cystic tumor.

There is a large, homogeneous, well-demarcated peripancreatic collection which abuts the stomach and the pancreas.

These cases illustrate that CT cannot reliably differentiate between collections that consist of pure fluid and those that contain fluid and solid debris with or without infection.

MRI is superior to CT in differentiating between fluid and solid debris.

On the left a patient with several homogeneous peripancreatic collections on CT.

Since these collections show homogeneous high signal intensity on a fat-suppressed T2 MRI sequence, they must be fluid-filled.

On the left another patient 2 months after an episode of acute exudative pancreatitis with also a homogeneous peripancreatic collection in the transverse mesocolon (arrow).

A T2-weighted MRI sequence however, shows that the collection has low signal intensity (arrow), and is therefore mainly solid.

This patient had no fever or signs of sepsis. If endoscopic or percutaneous drainage were attempted in this patient, there would be little or no effect on its size.

The only result would be an increased risk of infection when the collection is colonized following drain placement.

Aortic aneurysm rupture

Primary signs of Aortic Aneurysm rupture

Aortic aneurysm rupture is the most important diagnosis you want to be able to exclude in patients with acute abdominal pain especially when they present with back or flank pain.

The primary signs of AAA rupture are periaortic stranding, retroperitoneal hematoma and extravasation of IV contrast.

LEFT: Subtle periaortic stranding, MIDDLE: Hemorrhage into posterior pararenal and perirenal compartment, RIGHT: Extravasation of iv. contrast

On the next a classical case in a patient

with an aneurysm of the abdominal aorta and a large hyperdense retroperitoneal hematoma due to rupture.

The majority of these cases show posterior periaortic hemorrhage and in cases of massive hemorrhage, the posterior pararenal and perirenal compartments are the most frequently involved sites.

Signs of Pending Aneurysm Rupture

The CT features of contained leak or pending rupture of an aortic aneurysm may be subtle and easily overlooked.

High-attenuating crescent The high attenuating crescent represents an acute

hematoma within either the mural thrombus or the aneurysmal wall.

This sign is strongly associated with AAA rupture. Sensitivity of the high-attenuating crescent sign as an

indication of complicated aneurysm is 77%; specificity, 93%; and positive predictive value of 53%.

So even if there are no primary signs of rupture, we need to indicate to the referring physician, that this patient is at very high risk for aneurysm rupture within the next few days.

High-attenuating crescent sign in a patient with subtle evidence of leak adjacent to the right psoas muscle (broad arrow).

Focal discontinuity of intimal calcification Another sign of impending rupture or

contained leakage is focal discontinuity of intimal calcification.

In most of these cases we can also identify the tangential calcium sign.

In these cases it looks as if the calcium is pointing out away from the expected circumference of the aneurysm.

Tangential calcium sign

Tangential calcium sign (small arrow) and hemorrhage (broad arrow)

On the left we see another example of the tangential calcium sign.

The intimal calcification points away from the aneurysm and there is retroperitoneal leakage.

Draped Aorta A positive aortic drape sign is

considered to be present when the following features are seen:

area in which the posterior aortic wall is unidentifiable as a distinct line.

the posterior aorta follows the contour of the spine on one or both sides.

LEFT: draped aorta sign. RIGHT: two weeks later there is a rupture

On the next another patient who presented with backpain. There was no evidence of aneurysm leakage, but we see a draped aorta.

The posterior contour of the aorta follows the contour of the spine as if the aorta is draped over the vertebral body.

There is no imaging follow up in this patient, but three hours after this image was taken, this patient exsanguinated from a ruptured AAA.

The leakage was probably where the bulge was (arrow).