Category Archives: ABDOMEN




Primary and secondary liver tumors are a common cause of morbidity and
mortality around the world. While curative therapies for some of these cancers
exist – hepatocellular carcinoma (HCC) can be treated with partial hepatectomy
or liver transplantation – many patients are ineligible for curative liver resection
due to the advanced stage of their cancers; furthermore, widespread implementation of liver transplantation is prevented by a shortage of donor organs.

The same is true for patients with metastatic colorectal or neuroendocrine tumors. Due to these
shortcomings, various palliative therapies have been advanced in the management
of hepatic neoplasms.

These include systemic chemotherapy, radiation therapy, and local and regional percutaneous modalities. The latter group comprises both ablative techniques (chemical and thermal), and the intra-arterial monotherapies.

Unlike healthy hepatocytes, which are supplied largely by the portal venous circulation, both primary and secondary liver tumors receive their vascular supply principally from the hepatic artery.

Thus, occlusion of the hepatic artery would be expected to lead to ischemic necrosis of tumor cells while selectively sparing the native liver. This principle has been exploited in the development of bland transarterial embolization (TAE) and transarterial chemoembolization (TACE).

In both of these approaches, the branches of the hepatic artery that supplies the tumor are occluded with embolic particles.

For chemoembolization, chemotherapeutic agents are added to the embolization mixture for delivery directly into the tumor.

In principle, chemoembolization targets liver lesions by a multifaceted attack. First, embolization of the vascular supply triggers localized tissue ischemia. Second, since the chemotherapeutic agents are delivered directly into the ischemic tumor, their local concentrations and tissue dwell times can be significantly increased [1–5].

Equally importantly, the ischemia induced by chemoembolization may counteract
drug resistance by causing metabolically active cell membrane pumps to fail, thereby
increasing intracellular retention of the chemotherapeutic agents [3,6].

Technique of chemoembolization

Pretreatment assessment

Preoperative evaluation for chemoembolization includes imaging, serology, and counseling. A patient should have either a definitive tissue diagnosis or a compelling clinical diagnosis, such as a markedly elevated serum alpha-fetoprotein (AFP) level associated with an HCC-like mass in a cirrhotic liver [3].

The patient must have a dynamic gadolinium-enhanced MRI or triple-phase CT of the liver.

The extrahepatic disease should be excluded by a bone scan and cross-sectional imaging of the chest, abdomen, and pelvis. Serological studies should include CBC, PT,
PTT, creatinine, liver function tests, and AFP levels. Due to the demanding nature
of this palliative treatment, patients should receive thorough counseling about
their regimens. In particular, this discussion should mention the common postembolization syndrome, the 5–7% risk of serious complications, and the 1–4%
chance of periprocedural mortality. The patient and family members should clearly
understand that chemoembolization is a palliative regimen with the potential for
significant discomfort, risk, and expense.

Embolization procedure

Patients need not be routinely admitted until the morning of their procedure, but they should be advised to fast overnight.

On the morning of the procedure, patients are hydrated with 0.9% NSS at 200–300 cm3 h−1. Prophylactic medications are administered intravenously, including antibiotics (cefazolin 1 g, metronidazole 500 mg) and antiemetics (odansetron 24 mg, decadron 10 mg, diphenhydramine
50 mg).

The evidence for antibiotic prophylaxis is not compelling except for patients without a functioning sphincter of Oddi (e.g., post-Whipple or biliary stent), and not all practitioners administer them routinely.

The patient is sedated, prepped, and draped. Before any embolization is performed, diagnostic angiography of the celiac and superior mesenteric arteries is performed to determine the arterial supply to the liver and to confirm the patency of the portal vein.

Because non-target embolization of the gut or gallbladder is a significant cause of morbidity, the origins of the right gastric, supraduodenal, cystic, and other potential extrahepatic arteries must be clearly identified [7].

Once the arterial anatomy has been mapped, a catheter is advanced super selectively into a lobar or segmental branch of the right or left hepatic artery.

Typically, the lobe with the greatest tumor burden is embolized first, with subsequent treatments
targeting the contralateral side.

The chemo-embolic mixture is injected into the segmental artery until nearly complete stasis of blood flow is achieved. Intra-arterial lidocaine (30mg boluses, up to a total of 200mg) and intravenous fentanyl and midazolam should be used to alleviate discomfort during the procedure

Post-procedure care

Antibiotics, antiemetics, and intravenous hydration are continued after the embolization (3L of 0.9% NSS over 24h).

The common post-embolization syndrome must be managed aggressively with palliation of pain, nausea, and fever.

Specifically, narcotics, perchlorpromazine, odansetron, decadron, and acetaminophen should
be liberally administered.

The patient can be discharged with the resumption of oral intake and the cessation of parenteral narcotic therapy.

Typically, half of the patients are discharged on the first postoperative day, while most of the remainder leave after 2 days [3].

Oral home medications include antibiotics (5 days), antiemetics, and narcotics when needed. Laboratory studies are repeated in 3 weeks to ensure the normalization of liver enzymes. Depending upon the tumor burden and arterial anatomy, a cycle of chemoembolization will include between one and four procedures. Thus, the patient will return for the next embolization in about 4 weeks; treatments alternate between the left and right lobes, as well as any parasitized

Following completion of the treatment cycle, responseis assessed with repeat cross-sectional imaging and tumor marker serology. If the response has been inadequate, further rounds of chemoembolization can be administered.

Embolic materials

Choice of embolic particles

Variousembolicparticlesareavailableon the market.Thoughtheydifferinstructure, no agent has been conclusively demonstrated to be superior to any other.

The first embolic particle to be developed, the gelatin sponge (Gelfoam; Upjohn, Kalamazoo,
MI) has been used in the majority (71%) of chemoembolization trials [8].

Historically it has been available in various formulations – particles, cubes, pellet, powder,
fragments, and strips – the size of the particles determining how distal the embolization would take place [8].

Notably, use of the powder formulation has been discontinued because of an unfavorable side-effect profile. In all of these formulations, the gelatin causes only temporary devascularization, allowing recanalization to take place in about 2 weeks.

A similar temporary occlusion agent has also been developed from cross-linked bovine collagen (Angiostat; Regional Therapeutics, Pacific Palisades, CA).

More permanent embolic particles include polyvinyl alcohol (PVA; several vendors) and trisacryl gelatin spheres (Embosphere microspheres; BioSphere Medical, Rockland, MA).

Both of these come in a range of sizes (40–1000 μm), allowing the clinician to select the level of embolization. Less commonly, reports exist of the use of steel coils, starch microspheres, autologous blood clots, and even the herb Bletilla striata to embolize the hepatic artery [8]. Recent studies have begun to assess the feasibility of drug-eluting beads, a new approach that may
offer an improved pharmacokinetic profile compared to traditional chemoembolization [9].

Choice of chemotherapeutic agents

Several chemotherapeutic agents are available for chemoembolization, for use as monotherapy or in combination.

Doxorubicin and cisplatin are the most commonly used single agents [8]. Most reports from Europe and Asia use doxorubicin or epirubicin, whether alone or in combination with mitomycin-C.

Centers in the United States prefer cisplatin monotherapy or a combination of 100–150 mg
cisplatin, 40–60 mg doxorubicin, and 10–20 mg of mitomycin-C (CAM).

Although at least one case series suggested that cisplatin may confer a survival benefit over doxorubicin [10], no randomized trial has shown the superiority of any of these agents [8].

In fact, apparent differences between these agents may be driven by the ability to administer more embolizations in patients treated with cisplatin [10].In any case, no clear consensus has yet emerged for the superiority of any chemotherapeutic agent or combination.

Choice of emulsion: transarterial oily chemoembolization

The observation that iodized poppyseed oil (Ethiodol; Savage Laboratories, Melville, NY) selectively accumulated in hepatocellular carcinomas led to the incorporation of lipiodol (Guerbet, Aulnay-sous-Bois, France) into chemo-embolic regimens.

This technique, now known as transarterial oily chemoembolization, has the potential to more accurately target the chemotherapeutic drugs.

When iodized oil is injected into the hepatic artery, it travels to the distal arterioles, where it shunts
into the terminal portal venules at the pre-sinusoidal level.

From there, the oil slowly moves into the sinusoids and becomes trapped in the tumor vessels. In
theory, any chemotherapeutic agents suspended in this oily phase would thus be targeted to the liver.

Studies in rabbits [1] and humans [11] have demonstrated that the combination of oily chemoembolization with a particulate agent is superior to oily chemoembolization alone [11].

Such an effect is probably caused by the fact that most chemotherapeutic drugs remain in the aqueous phase of the emulsion. When chemoembolization is performed exclusively with an oily emulsion, continuous arterial inflow elutes out the aqueous drug, even though the oil itself remains
suspended in the liver.

Particulate-only chemoembolization causes relatively proximal occlusion, allowing continued inflow into the tumor from the portal venules, again diluting the chemotherapeutic drugs and resulting in reduced ischemia.

Thus the combination of oil and particles allows the occlusion of both distal arterioles and
portal venules – effectively sandwiching the drugs and maintaining tumor ischemia. Additionally, since this technique increases hepatic drug retention, it has the benefit of reduced systemic toxicity

Efficacy of chemoembolization

Historically, the efficacy of the transarterial embolo- therapies has been somewhat controversial. For example, early studies were inconclusive about the efficacy of chemoembolization in the treatment of hepatocellular carcinoma.

Nevertheless, evidence has emerged during this decade from several randomized trials that a role
exists for chemoembolization in the management of HCC.

Though the evidence is slightly less clear for the management of colorectal and neuroendocrine metastases, chemoembolization has nonetheless become established as an important palliative
therapy in the oncologist’s armamentarium.

Role of chemoembolization in unresectable hepatocellular carcinoma

Initial retrospective cohort studies in the Orient, Europe, and the United States suggested that chemoembolization was effective in the palliation of unresectable  HCC: rates of tumor necrosis ranged from 60% to 100% [3].

Cumulative probability of survival in these studies was 54–88% at one year, 33–64% at 2 years, and 18–51% at 3 years, with the best results obtained by repeated embolizations with a combination
of iodized oil, gelfoam, and chemotherapeutic drugs.

Survival varied directly with oil uptake and retention, and inversely with tumor volume, stage, and Child class.

Nevertheless, early randomized controlled trials failed to demonstrate a survival benefit for patients with unresectable HCC. Chemoembolization with gelfoam/doxorubicin (n = 42 patients) [12], lipiodol/5-epidoxorubicin (n = 50) [13], and gelfoam/lipiodol (n = 96) [14] did not increase survival compared to control subjects who received only palliation of pain.

Interestingly, however, two of these studies [13,14] did demonstrate non-significant trends towards increased survival from chemoembolization, suggesting that they may have been underpowered to
answer this question.

Since that time, however, evidence has begun to mount in favor of chemoembolization in the management of unresectable HCC. In 2002, two randomized studies demonstrated a clear survival benefit from chemoembolization.

In the first study, of 80 patients from Hong Kong, survival in patients treated with cisplatin/
lipiodol/gelatin-sponge chemoembolization was 57%, 31%, and 26% at 1, 2, and 3
years, compared with 32%, 11%, and 3% in those receiving conservative management [15].

In the second study, of 112 patients from Barcelona, 1-year and 2-year survival was 82% and 63% in patients receiving doxorubicin/gelatin-sponge chemoembolization, 75% and 50% in those treated only with gelatin-sponge bland TAE, and 63% and 27% for those receiving conservative management [16].

The authors hypothesized that the results of these trials may have differed from earlier studies because of differences in patient demographics and tumor background [15].

In particular, the studies from Hong Kong and Barcelona were conducted in patients whose HCC arose in the presence of viral hepatitis in 80% of cases, compared to a higher preponderance of alcohol-induced liver disease in the earlier French studies [14].

The tolerance of patients with alcohol-induced cirrhosis for chemoembolization may have been lower than that of those with viral hepatitis [15].

A recent meta-analysis of 175 cohort studies and randomized controlled trials (RCTs) of chemoembolization in the treatment of unresectable HCC concluded that chemoembolization does provide a significant survival benefit when compared to conservative therapy (631 patients in nine RCTs, p = 0.0025) [8].

Interestingly, a sub-analysis of studies comparing chemoembolization to bland TAE (412 patients,
3 RCTs) failed to demonstrate a survival benefit for either methodology, though
chemoembolization trended towards an improved outcome (p = 0.052).

Lastly, chronologically later studies demonstrated improved outcomes in comparison to
earlier trials [8]; this finding could be partially explained as a result of the improving
proficiency of clinicians.

In summary, evidence indicates that patients with unresectable hepatocellular carcinomas benefit from transarterial chemoembolization, though the benefit of specific choices of chemoembolic combinations remains unproven.

Disagreements between early randomized trials of chemoembolization and newer studies may have
resulted from differences in the patient populations or from the improving proficiency of clinicians.

Role of chemoembolization as a neoadjuvant therapy in HCC

While chemoembolization has become well established as a palliative therapy in the management of unresectable hepatocellular carcinomas, its role as a neoadjuvant therapy for HCC has been more controversial.

In theory, chemoembolization could prevent tumor growth in patients awaiting orthotopic liver transplants, thus decreasing attrition from the transplant waiting list due to tumor progression: as
such, chemoembolization could serve as a bridge to transplantation.

Alternatively, preoperative chemoembolization might be expected to improve outcomes after
partial hepatic resection, and might even convert some unresectable lesions into resectable tumors.

Early support for the role of chemoembolization as a neoadjuvant came from retrospective cohort studies showing that neoadjuvant chemoembolization could induce a reduction in tumor size and thus a downstaging of HCC before hepatic resection or liver transplantation [17,18].

Similarly, while the 6-month drop-out rate from the transplant waiting list is typically between 23% and 46% [19], those patients who receive neoadjuvant chemoembolization have been reported to have a drop-out rate of only 15% [20].

Nevertheless, while such early studies were encouraging, it is unclear whether their conclusions can translate to improved outcomes.

For example, the aforementioned study [18] failed to demonstrate a statistically significant improvement in patient survival, thus calling into question the clinical relevance of the findings.

In fact, the results of later retrospective cohort studies of chemoembolization as a bridge to transplant have been contradictory [19,21], and no RCT has yet been conducted on the issue.

In fact, a recent systematic evidence-based review of the available studies concluded
that at present there is insufficient evidence to claim that chemoembolization could be used as a bridge to transplant, that it would decrease transplant waiting list drop-out rates, or that preoperative chemoembolization could improve posttransplant survival in patients with HCC [19].

Perhaps the most relevant confounding variable is wait times for listed patients. In regions with short wait times (< 3 months), the drop-out rate is low, so neoadjuvant therapy is not

When wait times are very long, approaching the median time to-progression after image-guided therapy, the benefit from neoadjuvant stabilization is lost.

The wide geographic and temporal variation in wait times makes analysis of the benefit of neoadjuvant therapy from prior literature difficult.

Nevertheless, in the absence of any randomized trials, chemoembolization continues to be used in a non-palliative role in the pre-transplant setting, largely because it at least has not been shown to increase postoperative complications in transplant patients [22].

The effectiveness of preoperative chemoembolization in patients receiving hepatic resection has been similarly controversial. In theory, the combination of chemoembolization with curative surgery might be expected to improve patient outcomes.

Moreover, since chemoembolization has been shown to be capable of downstaging tumors [18], it might be able to convert some patients with unresectable lesions into surgical candidates. Indeed, some studies have shown just this, with preoperative chemoembolization significantly improving the 5-year survival of patients undergoing hepatic resection from 19% to 39% [23].

These findings have been further supported by a large retrospective cohort analysis

However, other prospective trials have failed to show a benefit from neoadjuvant chemoembolization before hepatic resection; one prospective study actually demonstrated worsened actuarial survival in chemoembolized patients due to the delay in curative resection [25].

A review of various adjuvant and neoadjuvant therapies in HCC has concluded that there is insufficient evidence to claim that neoadjuvant chemoembolization improves patient survival before resection [26].

Still, in the absence of definitive randomized controlled trials, the issue remains unresolved.

In summary, the role of chemoembolization as a neoadjuvant before liver transplantation or hepatic resection has been rather controversial.

Despite positive findings from some studies, the preponderance of evidence has not yet supported
such an indication. In fact, where the administration of chemoembolization may delay a definitive therapy, chemoembolization may actually worsen patient survival [25].

Clearly, randomized controlled studies are needed to further clarify these questions.

Toxicity of Chemoembolization

Despite having a more favorable side-effect profile than conventional chemotherapy, chemoembolization is not free of complications.

Thirty-day mortality ranges from 1% to 4%; chemoembolization in the treatment of HCC had a median mortality of 2.4% in a recent meta-analysis of 2858 patients [8].

Severe complications of chemoembolization occur in 5–7% of subjects, though these rates can be
reduced to 3–4% when patients are properly selected.

Most patients suffer from a self-limited post-embolization syndrome. Major complications of chemoembolization include hepatic insufficiency, abscesses, ischemic complications (cholecystitis,
bile duct necrosis, perforation of the alimentary tract), and renal dysfunction.

Less commonly, chemoembolization can also lead to tumor rupture, occlusion of the hepatic artery, and clinically significant pancreatitis.

Post-embolization syndrome

The majority of patients (40–86%) [14,38] suffer from a condition termed post-embolization syndrome (PES).

This is generally characterized by fever (74% of patients), abdominal pain (45.2%), nausea/emesis (58.9%), and a transaminitis (54%) [39].

In most cases PES is self-limited, though its palliation does necessitate hospitalization. On average, patients defervesce within 3 days, their nausea and pain can be medically managed, and their hepatic function gradually returns to normal [39].

Though previously thought to be indicative of tumor necrosis and thus a successful treatment, neither the presence nor the severity of PES has been shown to correlate to positive patient outcomes [38].

While reliable clinical predictors of the severity of PES have not yet been identified,PES does trend towards a more indolent course when embolization of the gall bladder is avoided, and when the patient is receiving repeat embolization to previously treated territory [7].

Major complications

Acute irreversible hepatic decompensation has been reported to occur in 3% of patients [8,39]. It should be distinguished from the transient and self-limited transaminitis that occurs with post-embolization syndrome.

Irreversible decompensation is more common with the use of high doses of cisplatin and poor
pretreatment hepatic function (high bilirubin, prolonged PT, and advanced cirrhosis) [39].

Abscess formation affects between 0.2% and 2.5% [40,43] of patients receiving chemoembolization.

The majority of these infections occur in the liver, though 0.4% of patients may suffer from a splenic abscess [40].

While their proximate cause is an infectious process, their formation is ultimately permitted by local ischemic necrosis.

Abscesses present with localized pain, fever, and leukocytosis,and can be definitively diagnosed by ultrasound or CT [40].

The likelihood of abscess formation has been strongly linked to a history of a Whipple procedure:
the presence of a bilioenteric anastomosis increases the incidence of a hepatic abscess by an odds ratio of 894 [41].

Attempts at prophylaxis against the formation of abscesses have led many clinicians to treat patients with broadspectrum antibiotics peri- and postoperatively [8]; others have even advocated
the addition of antibiotics to the embolic mixture.

However, a recent prospective cohort study from Germany casts doubt on these practices: patients who  did not receive treatment with antibiotics had no more infections or other complications than those who received 3 days of intravenous and 7 days of oral broad-spectrum antibiotics [42].

Severe ischemic complications, other than abscesses, have been reported to occur in 2.1% of patients receiving chemoembolization: these consist of ischemic cholecystitis (1.1%), bile duct necrosis (1.1%) [40], and perforation of the duo denum (0.05%) [43].

However, several other studies have quoted the incidence of gastroduodenal erosions and ulcerations to be significantly higher: one retrospective analysis of 280 cases demonstrated an endoscopy-proven incidence of 5.3% [44].

Since such lesions can result from the reflux of embolic material into the gastric circulation, the importance of meticulous attention to anatomic variants and adherence to selective or superselective embolization is the primary safeguard against this possibility [44].

Alternatively, at least some of these lesions could be the result of stress ulceration. Similarly, embolization distal to the cystic artery is the primary way of avoiding ischemic cholecystitis [40].

Nevertheless, since chemoembolization purposefully causes tissue ischemia, some damage to structures that are dependent on the hepatic artery is unavoidable (e.g., the intrahepatic bile

Renal failure has also been documented as a complication of chemoembolization, though its reported incidence varies between 0.05% [43] and 13%, averaging 1.8% in the aforementioned meta-analysis [8].

A prospective cohort study revealed an incidence of 8.6%, with 2.9% developing irreversible renal impairment [45].

Independent risk factors for the development of acute renal failure are the number of chemoembolization sessions, high Child–Pugh class, and a severe course of post-embolization syndrome; irreversible renal dysfunction was predicted only by the presence of diabetes [45].

The proximate causes of such kidney damage may be
the use of arterial contrast agents, the nephrotoxicity of the chemotherapeutic drugs, and inflammatory factors released from tumor necrosis [8,45].

The less common complications of chemoembolization include tumor rupture, occlusion of the hepatic artery, and clinically significant pancreatitis.

Spontaneous rupture of the treated tumor occurs in 0.15% of patients, most often after the
embolization of a large neoplasm [43].

Occlusion of the hepatic artery is a complication of repeated embolizations, occurring in 2% of patients following their second or third round of chemoembolization [43].

Though clinically significant pancreatitis is generally considered a rare complication – Roullet et al. report an incidence of 1.7% [46] – subclinical elevations in pancreatic enzymes may occur in as many as 15.2% of patients [47].

Patient selection

The likelihood of suffering severe side effects from chemoembolization is attenuated by both meticulous technique and proper patient selection. In principle, patients must be selected to include only those who will both benefit and tolerate the embolization procedure.

Selecting patients for optimum efficacy

Patients with multiple or unresectable lesions located exclusively or predominantly in the liver are ideal candidates for chemoembolization.

Since liver embolization only targets intrahepatic lesions, patients whose hepatic tumor burden is the primary driver of their symptoms and survival are the most likely to benefit from chemoembolization.

Nevertheless, the presence of some extrahepatic disease is not an absolute contraindication to chemoembolization; some patients whose metastatic disease is minimal or indolent may still be candidates for this therapy.

Selecting patients for optimum tolerability

The fundamental principle underlying the intra-arterial embolo-therapies is the differential blood supply of the hepatic neoplasms (supplied via the hepatic artery) and hepatocytes (supplied via the portal vein). Thus, if the native hepatocytes were to become more dependent on the blood flow from the hepatic artery,embolization of this vessel would be expected to lead to increased side effects.

This has in fact been demonstrated. Conditions that predispose the healthy liver to injury by increasing the relative contribution of blood from the arterial circulation include portal vein thrombi and superimposed liver disease.

Thus, occlusion of the portal vein is a relative contraindication to chemoembolization, though small
case series suggest that patients with the significant collateral flow can still be embolized
safely [48].

Patients with significant liver disease, such as those of Child-Pugh class C, with tumor replacing > 50% of liver [49], alpha-fetoprotein > 400 U L−1 [49], lactate dehydrogenase > 425 IU L−1, aspartate aminotransferase > 100 IU L−1, or total bilirubin ≥ 2 mg dL−1, are also at increased risk. Severe liver disease, as indicated by hepatic encephalopathy or jaundice, is an absolute contraindication to embolization.

Biliary pathology is another relative contraindication. Biliary obstruction predisposes patients to biliary necrosis even in the absence of hyperbilirubinemia.

As discussed previously, a surgical biliary anastomosis or stent virtually guarantees the development of a hepatic abscess, at least in the absence of prophylactic antibiotics [41].

Last, since the chemoembolization procedure must include angiography, patients with contraindications to this procedure cannot be embolized. All of the contraindications for chemoembolization also apply to bland embolization.

New developments in chemoembolization technology

The latest generation of embolic particles are polyvinyl alcohol polymeric beads specifically designed to load chemotherapeutic drugs and elute them over time into the tumor tissue following embolization.

Preclinical bench-top and animal studies have confirmed the ability of these drug-eluting beads to provide enhanced local drug delivery over a prolonged period with minimal systemic exposure

Phase I/II clinical trials for hepatoma in Europe and Asia have shown promising 1-year and 2-year survivals in the 85–90% range, but a disturbing incidence of major complications at around 10%, with a surprising frequency of hepatic abscess [52,53].

Randomized trials against conventional oily chemoembolization have not been completed. These beads are available as bland embolics in the USA and can be loaded with one or more drugs, but such off-label use is discouraged until their safety and efficacy is established in clinical trials, particularly given their high cost.


Transarterial chemoembolization is a powerful and well-established tool in the palliative management of both primary and secondary liver tumors.

While future randomized trials are still needed to unequivocally prove the survival benefits of
chemoembolization in some cancers, its effects on the management of symptoms have been clearly demonstrated.

When performed with meticulous technique, chemoembolization can be efficacious while still maintaining a side-effect profile superior to that of conventional therapies.

Though patient selection remains crucial, the transarterial embolotherapies can be offered to many more patients than traditional hepatic resection or transplantation.

Therefore, familiarity with chemoembolization is essential for any clinician involved in the care of patients with primary or secondary liver tumors.


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Transarterial chemoembolization 91
High-intensity focused ultrasound (HIFU)
treatment of liver cancer



Pathology and clinical condition of HCC

This is a well-known medical truth that Hepatocellular carcinoma (HCC) now involving about the fifth of all malignant tumors in the world, and it’s one of the most common causes of deaths resulting from cancer in the world and USA (1).

It causes about 250.000 to 1000.000 deaths/year (2).

HCC develop mainly in the cirrhotic liver.

Liver damage which eventually leads to liver illness (cirrhosis or fibrosis ) can occur due to several causes.

We can numerate Viral infections, Alcoholism, Obesity, Toxic agents, metabolic function disease. In Asia and Africa (3), HCC has higher incidence more than other regions.

The main cause of HCC in there are endemic Hepatitis B, C, and Aflatoxins. In the USA and Europa HCC has a lower incidence (5), however, it still has a high incidence. Hepatitis C consider causing more than 30% of HCC in the state, either alone or with other cause like alcohol, others (4).

Another noncirrhotic cause is found to spread nowadays, especially in western countries. We can mention hemochromatosis,
Primary biliary cirrhosis, autoimmune hepatitis, and obesity with nonalcoholic steatohepatitis, or can also call (NASH) (4).

NASH now considered one of the most important causes of HCC in the states and Europe.the end result of NASH is called cryptogenic cirrhosis which increases HCC incidence. (4)

As the clinical presentation of HCC is variable and limited mainly to the underlying cause. so it’s mostly discovered late during the patient survey and that affects the disease prognosis. so the surveillance in cirrhotic and hepatitis patients is very important in reducing the incidence and deaths of HCC (2).

HCC has a male predominance(2). typical usual presentation of HCC is an old man with cirrhosis and Ascites with splenomegaly and weight loss, increase alpha-fetoprotein (2). However acute presentation of acute RUQ pain may occur due to rupture of liver capsule.(2)

In cirrhotic patients the pathology of HCC  evolute form necrosis and fibrosis of hepatocytes to the neoplasm. This evolution takes multiple steps from regeneration nodules to low-grade dysplastic nodules to high-grade dysplastic nodules to early HCC and finally advanced HCC (6).

This figure shows a high vascular heterogenous mass lesion which invades the adjacent portal vein in cirrhotic liver. (2)


MRI sequences of Localize and characterizations of HCC:

Hepatocellular Carcinoma is typically a hyper-vascular spherical heterogenous mass with contrast enhancement wash-out and portal vein invasion. The size of HCC may be small, less than 2 cm, or large, more than 5 cm.

The smaller ones are more liable to be cured by ablation or resection, or transplantation. While the larger ones especially if associated with venous invasion, those are more able to TACE (trans-arterial chemo-embolization) (2).

If HCC invades the portal vein, the following imaging signs are detected; first  the lumen of the portal vein is seen expanded, Second the tumor is seen enhanced within the vein, third the tumor and portal vein is fused with each other.(2)

Now let’s talk a look at sequences of MRI used to localize and characterize HCC, we should note that variable intensity of HCC depends mainly on necrosis, fibrosis and fatty changes degree:

T1 Weighted Image:

In this sequnce, HCC usually appears as a hypointense mass in compared to surroundings. As the cell increases in number, which means increase water amount. but in small HCC, it may appear hyper or iso  due to increase fat and glycogen content.(7)

T2 Weighted Image:

in T2 HCC is usually have a hyper-intense appearance to the liver density.

on the other side, the regenerative nodule usually appeared hypo-intense to the liver.

In this sequence, we can discriminate The HCC which arise inside the dysplastic nodule, as it has a pattern of (Nodule within the module) as it appears as small increase signal intensity focus within nodule of decreased intensity. (2)

T1 plus gadolinium contrast:

on this sequence, HCC appears as hyperintense heterogenous mass, associated with washout on delayed and venous phase.

To differentiate HCC from arterio-portal shunt, we should know that HCC takes fast central washout with residual capsular enhancement.(2)

A hepatobiliary contrast agent (gadoxetate):

the use of gadoxetate ( its trade names are Eovist, Primovist) after twenty minutes delay phase, reveal that Normal liver and some cirrhotic liver, brightly enhance m while HCC appears as hypo-intense masses.

some good differentiated HCC has proved to show persistent enhancement with gadoxetate. This technique is the most specific and sensitive technique for detection and location of HCC, it increases the incidence of small HCC diagnosis. (2)

Diffusion-weighted MR:

Diffusion restriction within HCC, usually detected as a bright signal in the focal lesion, it helps in increase MR sensitivity of HCC detection. (2)

Hepatocellular carcinoma (HCC) schematic diagram. HA, hepatic artery; HADP, hepatic artery–dominant phase; HBV, hepatitis B virus, IVC, inferior vena cava; PV, portal vein.(8) 

Large Complex HCC. A, The moderately T2-weighted image shows a large heterogeneously hyperintense lesion (arrow) bulging the liver capsule. The arterial phase (B) and delayed (C) images show variegated enhancement, often seen in large lesions.(8)

The Figure show DW MR of Cirrhotic liver. At dual-echo (a, b) and on T1-w.i (c), multiple nodules appear as iso- to hyperintense, while on T2-w.i (d) they show as slightly hypointense. On postcontrast dynamic study, no arterial nodular enhancement is detectable (e) as well as no wash-out is evident on the venous.and late phases (f, g). On hepatobiliary phase (h), acquired 20’ after contrast medium injection, all nodules show a significant uptake. (7)

This figure show : Different behavior of HCC and dysplastic nodule (DN) at MR. MR examination shows the oexistence of two differentiated nodules. At baseline (a, b), the HCC lesion (arrow) appears as hypointense on T1-w.i (a) and hyperintense in T2-w.i (b), while the DN (dotted arrow) shows the opposite signal behavior. At dynamic study (c–e), HCC presents the typical wash-in in arterial phase and wash-out in portal and late phases, while DN is iso–hypointense in all post-contrast phases. On hepatobiliary phase (f), HCC is hypointense due to the lack of intracellular contrast uptake, while DN is homogeneously hyperintense because of the
maintained hepatocyte function and cholestasis. (7)

Sequences are used to plan treatment, assess the completeness of treatment and detect a change in the lesion.

MR sequences have proved to be very effective in HCC treatment planning, monitoring the response of the lesion to treatment. Here we will enumerate the most important sequences used;

Diffusion-weighted MR:

has proven to be very effective in planning treatment either by surgical resection (ADC measurement before operations are very effective in measuring the risk of recurrence after surgery) or other treatment options as (TACE) transarterial chemo-embolization.(9.

In Trans-arterial Chemo-embolization (TACE), use of DWI to monitor ADC mapping measurements of the tumor response to treatment, as if poor response, it shows lower ADC measurements .(10)

ADC mapping can also together with venous enhancement of the lesion predict survival ration of the patient, by arranging them in survival classifications. (11)(12)

DWI, in general, is a very good factor in monitoring treatment effect and predicting survival rate as treatment cause local dynamic changes could be monitoring by DWI.(13)


MR Elastography.

In addition to its role in characterization of malignant liver tumors, as malignant tumor has higher stiffness than benign ones and it’s more viscous (14), the MR Elastography is very helpful in assessing the response of the tumor to chemotherapy and agents that cause vascular disruption. (15)

The technique of MR Elastography includes external vibrators that produce compression waves, that penetrate through tissue viscosity and elasticity of the tissues. This technique has been proved to be reliable in the liver in 22% for elasticity and 26% for viscosity.(16)


Dynamic contrast-enhanced MR imaging

in this sequence we use contrast to more visualization and detection of tumor response to treatment.

Usually, we use gadolinium contrast, then we take three phase of the liver: Arterial, Portal, and Delay (3-5 min after injection).

We can also use special hepatocyte contrast called Gadoxetate, in this case, we take additional hepato-biliary phase ( after 20 min of injection).

All phases (including arterial and portal and delayed phases) of Dynamic contrast-enhanced MR imaging should be done in routine to localize and tumor and detect its response to treatment.

so we use an especial contrast ( gadoxetate) , which in turn we get hepatobiliary phase, in which some HCC which is not good seen at classical phases of Dynamic MR imaging sequences .

and has low vascularity appears to be hypo-intense at hepato-biliary phase.Also, hyperintense lesion on these sequences predicts to prgnosed to HCC which has high vascularity. (17)

So we can say that Dynamic contrast-enhanced MR and DW MR  together can be used monitor intraarterial therapy.

There were noted survival differences between patients who their ADC level increase above 25%, their venous enhancement decrease. that’s like the difference between patients who are stable and patient who has single parameter respond, so the above text reveals the service could present the functional MR (multi-parameters) in evaluating treatment response.(18)

MRI Sequences used to grade HCC condition.

Diffusion-weighted MR:

also is useful in the grading of patients with HCC.

And almost considered the most useful sequence in this field. For example, if we had a patient with hypo-vascular liver nodule which is hyperintense on DWI. The studies proved that this nodule progress to be high vascularity HCC.

In addition, there is a correlation, but an inverse one between the level of ADC mapping and the grading of the tumor. The High differentiated tumor has more diffusion more than the poor differentiated one .(19) It’s also can predict other factors as VEGF (vascular endothelial growth factor)  (20)prognostic cell marker (21)and microvascular invasion. (22)


Tumor Grade ADC Potential association
High differentiation Good diffusion No reported association
Well differentiation Moderate diffusion No reported association
Poor differentiation Restricted diffusion presence of progenitor cell markers 1
Scarce differentiation Scarce diffusion presence of progenitor cell markers 1, vascular endothelial growth factor (VEGF) expression2-51, and microvascular invasion52.

Table, reveal the relation of ADC and HCC grading (23)

LI-RADS MR Grading system:  this system is the most common used and the most efficient to grade HCC.


This figure show LR-MR grading system of HCC. (24)

To get this we use these sequences :

MRI with extracellular contrast agents or gadobenate meglumine:

to make an HCC grading with an extra-cellular agent, we should use these sequence:

First, T1-W IP & OP sequences with no enhancement. Secondly, T2-WI (fat suppression per institutional preference).

Third Multiphase T1-WI.

Fourth Precontrast imaging.

Fifth Arterial phase, and recommended to be late.

Sixth Portal venous phase. Seventh Delayed phase.

Seventh Diffusion-weighted imaging.Eight Subtraction imaging and Multiplanar acquisition.

Lastly one to three hours hepatobiliary phase. (24)

MRI with gadoxetate disodium:

Sequenced performed with gadoxetate disodium to grade HCC.

First, T1-W IP & OP sequences with no enhancement.

Secondly, T2-WI (fat suppression per institutional preference).

Third Multiphase T1-WI.

Fourth Precontrast imaging.

Fifth Arterial phase, and recommended to be late.

Sixth Portal venous phase. Seventh Delayed phase.

Seventh Diffusion-weighted imaging.

Eight Subtraction imaging and Multiplanar acquisition.

Nine hepatobiliary phase .and we don’t forget transitional phase which we take two to five minutes after injection. (24)


Treatment options and outcomes for the patient

Treatment options of HCC vary according to the lesion and its nature and extent.

If the patient had a small HCC, localized peripherally and has no vascular invasion; this will be ideal for surgical resection.

So surgical resection id very optimal in previously described small peripheral avascular lesions, but its effect is limited to due to the hepatic reserve will be inadequate in the majority of patients. (2)

In patients who are not suitable for surgical resection and has an HCC isolated tumor less than 4 cm, these patients will be candidates for Radio-frequency Ablation.

On the other hand, Multi-centric HCC patients who are cannot undergo resection, they are ideal for Trans-arterial Chemo-embolization (TACE) (2).

But this procedure is limited as the hepatic reserve may be insufficient. So there is an alternative to it, The radio-embolization with Yttrium-90Y-tagged microspheres. Transplantation sill a very good choice for those who have nonmetastatic HCC tumor with no vascular invasion(2).

There are criteria called Milan Criteria used to the assessment of transplantation. these criteria are; first HCC tumor should be either solitary and less than 5 cm in diameter, or it’s more than one (up to 3 HCC nodules, each less than 3 cm in diameter).

Second, it must have no extra-hepatic metastasis and had no vascular invasion. Systemic treatment is still an option, sorafenib which is tyrosine kinase inhibitor, give good survival benefit. (2)


MRI Recurrence Monitoring sequences.

Diffusion-weighted MR:

It has proven to be very effective in monitoring recurrence of HCC.

As it offers a great service in distinguishing between the recurrence of the tumor, and the effect of the treatment.

The recurrent tumor gives a low ADM mapping measurements, while the necrotic tissue or the edematous area resulting as a response to treatment give high ADC mapping measurements.and as more increasing ADC level, the more successful treatment is. (25)(26)(27)

As tumor is mixed tissue components, the necrotic part could mix with the tumor part. So it can mix up in the evaluation of recurrence, so the used of Dynamic enhanced MRI with DWI is recommended to give the best precise assessment of the recurrence.(28)

Gadoxetate Disodium–Enhanced MRI:

this sequence has proved to be very effective in the assessment of recurrence of HCC after treatment especially after radio-frequency Ablation.

HCC usually when occurring as a recurrence it appears as nodular abnormal signal intensity areas or has enhanced margins especially the ablated tumor.(29)

This figure shows  70-year-old man with locally recurrent hepatocellular carcinoma after radiofrequency ablation in an anterosuperior segment of the right liver lobe.
A T2-weighted image (TR/TE, 1600/80) shows multiple areas of nodular hyperintensity (arrows) adjacent to the ablated area (arrowhead), which was hypointense on the fat-suppressed image.
B, MR image obtained during hepatic arterial phase shows area of nodular enhancement (arrow), corresponding to one of the hyperintense areas in A, adjacent to ablated
tumor. This area of enhancement showed mild washout during the portal venous phase and was due to local tumor recurrence.
C, 3D T1-weighted gradient-echo image (TR/TR, 4.0/2.1) obtained during hepatocyte phase shows area of hypointensity (solid arrow) adjacent to ablated tumor
(arrowhead), corresponding to the area of enhancement in B. This local tumor recurrence had a signal intensity ratio of 0.61. Another area of faint hypointensity (open arrow)
corresponding to a hyperintense area in A was observed adjacent to ablate the tumor. This lesion was found to be caused by reactive response to therapy and had signal
The intensity ratio of 1.65. Note area of hypointensity (asterisk) showing another ablated tumor.(30)





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24 MR-LIRADS grading system 2017 by Mostafa Bashir and Victoria Chernyak and others published at American college of Radiology , available at:


25. Mannelli L, Kim S, Hajdu CH, Babb JS, Clark TW, Taouli B. Assessment of tumor necrosis of hepatocellular carcinoma after chemoembolization: diffusion-weighted and contrast-enhanced MRI with histopathologic correlation of the explanted liver. AJR American journal of roentgenology. 2009;193:1044-52.


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28. Goshima S, Kanematsu M, Kondo H. et al. Evaluating local hepatocellular carcinoma recurrence post-transcatheter arterial chemoembolization: is diffusion-weighted MRI reliable as an indicator?. Journal of magnetic resonance imaging: JMRI. ;27:834-9.


29. Gadoxetate Disodium–Enhanced MRI Useful for Detecting Local Recurrence of Hepatocellular Carcinoma After Radiofrequency Ablation Therapy , Haruo Watanabe1, Masayuki Kanematsu1 2, Satoshi Goshima1, Mariko Yoshida1, Hiroshi Kawada1, Hiroshi Kondo1 and Noriyuki Moriyama at: American Journal of Roentgenology. 2012;198: 589-595. 10.2214/AJR.11.6844.


30. Fig 1: Gadoxetate Disodium–Enhanced MRI Useful for Detecting Local Recurrence of Hepatocellular Carcinoma After Radiofrequency Ablation Therapy?

Haruo Watanabe1, Masayuki Kanematsu1 2, Satoshi Goshima1, Mariko Yoshida1, Hiroshi Kawada1, Hiroshi Kondo1 and Noriyuki Moriyama, at: American Journal of Roentgenology. 2012;198: 589-595. 10.2214/AJR.11.6844.



























This is a well known medical truth that The Pancreas is one of the largest and most important mixed (exocrine and endocrine) Gland in the body.

It lies behind Stomach and next to Small Intestine. It is considered as endocrine gland as it releases insulin and glucagon to control blood sugar level .

It acts as exocrine gland as it releases digestive enzymes that help the small intestine to do a good job in food digestion (1).

Acute Pancreatitis can be defined as Acute inflammation of the pancreas, it may be caused by reflux of the bile and pancreatic enzymes into the pancreatic parenchyma (2).

In another way, we can define pancreatitis as Pancreatic inflammation be caused by multiple etiologies that result in a final common pathway of premature activation of pancreatic enzymes that result in autodigestion of pancreatic parenchyma (3).

Acute Pancreatitis is considered a potential life threating condition.

Effective utilization of imaging in patients with acute pancreatitis needs a profound information of the natural course of disease and familiarity with the subtypes and complications of acute pancreatitis.

Imaging, primarily computerized tomography (CT), in acute pancreatitis has numerous aims. CT will ensure the diagnosing or give an alternate diagnosing, determine the etiology of pancreatitis, observe native duct gland and extrapancreatic complications, provide prognostic data, and guide therapeutic interventions.

Conventional radiography, ultrasound (US), endoscopic retrograde cholangiopancreatography (ERCP), and resonance imaging (MRI) have necessary complementary roles within the assessment and management of patients with acute pancreatitis.

This Article discusses the role of imaging in the assessment of etiology of acute pancreatitis. Also, imaging characteristics of these with expected severe disease and people with duct gland and extrapancreatic complications directly influencing individual patient management are going to be self-addressed.


Among all gastrointestinal tract diseases, Acute Pancreatitis remains a commonly encountered clinical entity, with an incidence of 44 cases per 100,000 adults per year (4).

In the United States, in 2009, Acute Pancreatitis was the most common gastroenterology discharge diagnosis with a cost of 2.6 billion dollars. An increase in the annual incidence of Acute pancreatitis has been observed in most recent studies.

Epidemiologic review data from the 1988 to 2003 National Hospital Discharge Survey showed that hospital admissions increased from 40 per 100,000 in 1998 to 70 per 100,000 in 2002.

Although the case fatality rate has decreased over time, the overall population mortality rate has remained unchanged (5).


Before CT was widely used in cases of abdominal pain, the main cornerstone of diagnosis of Pancreatitis is clinical criteria of acute pancreatitis and by the exclusion of other causes.

X-ray signs especially cut-off signs of the pancreas could be helpfull. Detected edematous pancreas in the ultrasound and confirmation of peripancreatic fluid was a great imaging help in the diagnosis of acute pancreatitis.

The value of imaging in pancreatitis:

Using different Imaging modalities in the diagnosis of Acute Pancreatitis is very helpful in the determination of the severity of disease, the extent of involvement, local complication. It’s useful for the evaluation of fluid collection. Accompanying MRCP may help to determine the cause of pancreatitis (stone, stricture, mass, pancreatic divisum).

Radiological Anatomy:

The pancreas is mixed accessory GIT gland, it has Exocrine Function as Pancreatic acinar cells secrete pancreatic Juice that passes throughout pancreatic duct to the second part of Duodenum. It has the endocrine function as pancreatic cells of Langerhans secrete insulin, glucagon & other polypeptides reaching portal venous system (6).

The Pancreas is a retroperitoneal gland. it lies transversely across the upper part of the posterior abdominal wall, extending from concavity of duodenum on the right to the spleen on the left (7).

The Pancreas Consists of four main parts: Head, Neck, Body, Tail.

The Head of the pancreas lies in the curve of the duodenum with pylorus and duodenal bulb overlapping its upper surface, the uncinate process projects posteriorly and to the left from its lower part to lie posterior to superior mesenteric vessels.

The common bile duct passes posteriorly to pancreatic head in a tunnel till its termination in the second part of the duodenum (8).

The Pancreatic neck extends from the upper part of the anterior portion of the head . it lies just anterior to the union of the superior mesenteric vein and splenic vein to make portal lies anterior to left kidney and adrenal gland.

The splenic artery runs along the upper surface of the pancreas in the sinuously intermittent course.

Finally the pancreatic’s related to splenic hilum where it lies in the splenorenal ligament.

Pancreatic duct begins at the tail and runs to head, it ‘s mainly located in the anterior half of the pancreas. It joins CBD at the ampulla of Vater. Its accessory duct of Santorini arises from the pancreatic head and drains via the minor papilla into the duodenum, it lies 2 cm proximal to the ampulla of Vater. It usually communicates with the main duct and it may be absent in some individuals.(9)

Figure (1) shows anatomy of pancreatic ducts and its drainage (10)

The Pancreas receives its blood supply from the Pancreatico-duodenal artery that receives its blood supply from Gastroduodenal Artery.

Also the inferior pancreaticoduodenal artery (from SMA). There are multiple anastomoses between these two vessels.The remainder of

The pancreas is supplied from the splenic artery via multiple small direct branches and arterial pancreatic manga. Another arterial supply is from the dorsal pancreatic artery, which arises from the coeliac or proximal splenic artery.

Venous drainage from the pancreatic head is to SMV and portal veins and to the splenic vein from the rest of the pancreas (11).
The Variations in Pancreatic Anatomy has wide variations:

Pancreas divisum: failure of fusion of the dorsal and ventral moieties results in the anterosuperior part of the head and the body and tail draining via the accessory papilla, while the posteroinferior part of the head drains to the ampulla; this is the commonest variation, affecting 4 – 10% population

Annular pancreas is a rare condition where the ventral pancreatic bud rotates incompletely leaving a segment of pancreatic tissue surrounding the second part of the duodenum

Agenesis of the dorsal pancreatic moiety: this results in a pancreas with a head but no body or tail and is very rare.

Figure (2) shows variation in the anatomy of the pancreatic ducts (12):

(A) atrophic accessory duct persists as a tiny accessory duct in 60%;
(B) accessory (upper) duct atrophies completely – no connection with the duodenum (20%);
(C) major and minor ducts open separately and do not communicate (pancreas divisum) (10%);
(D) both ducts persist, communicate and open separately (10%)

Pancreatic rests/ectopic pancreas (accessory nodules of pancreatic tissue) may occur in the wall of the stomach, the duodenum, the small intestine or within a Meckel ’ s diverticulum The most common site is on the wall of the duodenum closest to the pancreas and close to the opening of the pancreatic duct (13).

The neck, body, and tail of the pancreas drain to the splenic vein and the head drains to the superior mesenteric and portal veins.

Lymphatic drainage is to nodes along the course of the supplying arteries to preaortic coeliac nodes.

Now we will begin to discuss the radiological features of the pancreas in different imaging modalities:-

Plain X-ray Abdomen:

We will look First how the pancreas appears in Plain Film plain imaging of the abdomen. it’s not visible unless it’s calcified which occur mostly in chronic pancreatitis and seen as a transverse structure at first lumbar vertebrae level, with a larger head on the right side and a body and tail extending to the left and upwards.

Here we should note that acute pancreatitis may cause Ileus in the nearby intestine that will be visible in Plain Film. Another note, Acute Pancreatitis may cause fluid collection in the lesser sac which causes displacement of Stomach Gas anteriorly, visible on lateral film of the abdomen.

Figure (3) shows: Plain X-ray abdominal film of pancreatic calcification due to chronic pancreatitis (14)


Then we will discuss an important imaging module the Ultrasound. Although Ultrasound is very important in the diagnosis of abdominal Organ Pathology, Normal Pancreas seen only in 60% of abdominal ultrasound studies, this because it’s obscured by overlying Stomach and transverse colon Gas.

On transverse section, the pancreas appears anterior to the Splenic vein. Hepatic artery and bile duct are seen anterior to the portal vein and cephalad to pancreatic head.

Anteriorly we can see Stomach antrum, with the pylorus and duodenum above and be curving around the right side of the head In the upper part of the head.

Pancreatic head and neck are seen in the midline anterior to the confluence of splenic and superior mesenteric veins Just posterior to this, the left renal vein is usually seen crossing the aorta to drain into the IVC.The uncinate process is seen posterior to superior mesenteric vessels.

Pancreatic Tail can be seen by angling the transducer superolateral from midline towards the splenic hilum, or by oblique views through the spleen.

The pancreatic duct is seen within the gland closer to its anterior surface. It is seen in over 80% of cases and It is best seen in the central portion of the body where it is perpendicular to the plane of imaging. It measures approximately 1 5 mm in the tail, 2 mm in the body and 3 mm in the head(15).

Figure (4) shows : Axial ultrasound images through the pancreas centered on (A) the head and (B) the body.

The pancreas may initially be difficult to visualize but can be identifieded as it lies immediately anterior to the splenic vein. The pancreas is at least as echogenic as the liver and is more echogenic with increasing age and body fat (16).

Computed Tomography (C.T):

Before we finishing the radiological anatomy of the pancreas we should take a look at how it looks like at Computed tomography.

We should note that the pancreas lie in the abdomen at oblique position as the tail lies in a higher plane than the head . so the pancreas should be scanned in sequential thin CT slices . as we see the pancreas in the CT Cranio-caudal, on the highest slices we can see the pancreatic tail in the splenic hilum, then body.

The head and uncinate process can be seen in the lowest slices. The normal thickness of the head is 2 cm, the neck about 0 5 – 1 cm and the body and tail 1 – 2 cm.The height of the head is very variable and may measure up to 8 cm. The body and tail may measure 3 – 4 cm in height (17).

Figure (5) shows: The head of the pancreas lies lateral to the superior mesenteric vein (SMV) or SMV-portal vein confluence,while the uncinate process lies dorsal to the SMV (18).

Figure (6) shows: The uncinate process is that portion of the pancreas that extends dorsally to the superior mesenteric vein (SMV)(19).


Finally, we have to get a look at the MRI of the pancreas. The pancreas has the shortest T1 of the abdominal organs, so it has a higher signal intensity on T1-weighted imaging, equivalent to or slightly higher than that of normal liver.

The pancreas is also well seen on T2-weighted imaging, and faster sequences, including breath-hold sequences, reduce artifact from breathing.

The pancreas is highly vascular so it enhances markedly during the arterial phase of a gadolinium bolus.

Figure (7) shows Axial T2 Image of the pancreas (20).

Figure (8) shows Coronal T2 Image of the pancreas (21).

Figure (9) shows Axial T1 Image of the pancreas (22).

Figure (10) shows Opposed Phase Axial T1 Image of the pancreas (23).

Acute Pancreatitis

By imaging, Acute Pancreatitis can be seen as enlarged edematous pancreas with or without necrosis, with pre-pancreatic fat stranding and fluid collection.

We can classify acute pancreatitis into two main sub-types: the first subtype is mild Acute pancreatitis or Interstitial Edematous Pancreatitis, the second subtype is severe acute pancreatitis or Necrotizing Pancreatitis. (24).

Interstitial Edematous Pancreatitis: It’s characterized by Enlargement and edema of the pancreas with loss of normal fatty lobulation. this type shows no necrosis .it can be associated with peri-pancreatic fat standing and fluid collection. it’s the predominant type in about 70-80 % of cases.

Necrotizing Pancreatitis: It’s characterized by parenchymal necrosis. it occurs in 20-30 % of’s associated with pancreatic and peripancreatic necrosis. at this type, complications are more liable to occur.

Embryology of the Pancreas

The pancreas Develops among the dorsal part of dorsal mesentery, that typically fuse’s with the posterior abdominal wall. It leaves solely a brief splenorenal ligament .it Carries splenic vessels and tail of pancreas and Forms left a posterior wall of lesser sac.So pancreas becomes a retroperitoneal organ.

Causes of Acute pancreatitis

The most comm Cause is Gallstones (about 50% of cases) including occult stones, microlithesis, and mud(25), large stones are more likely to cause pancreatitis as it lodges into sphincter of Oddi.

Alcohol came in the second with about 25% of cases especially if associated with the long history of alcohol drinking.
metabolic causes include hypercalcemia, hypertriglyceridemia. Trauma also can cause’s common cause of pancreatitis in children. Endoscopic Maneuvers like ERCP, Pancreatitis one of its famous complications.Other causes include Malignancy, toxicity.

Finally, Pancreatitis Occurs without any cause, in this situation we called it (idiopathic).


pathogenesis of acute pancreatitis vary according to the cause: it includes reflux of pancreatic enzymes, bile, and duodenal contents into the pancreatic duct.

It may be due to the increase in ductal pressure due to ampullary obstruction, or activation of intracellular/extracellular homeostatic factors.

Another important one is activation of pancreatic enzymes and released into surrounding soft tissues causing inflammation and autodigestive injury to pancreas

These are two phases of acute pancreatitis: Early and late: Early phase over a week and is characterized by systemic inflammatory response syndrome (SIRS).

Late phase (only seen in severe cases) occurs after 1st week and is characterized by local complications and persistent systemic inflammation

Clinical Presentation

Patients with acute Pancreatitis presented with more or less characteristic symptoms, even so, the clinical diagnosis of acute pancreatitis can he extremely difficult and, in the initial stages, other acute abdominal conditions such as a perforated peptic ulcer or acute cholecystitis have to be included in the differential diagnosis (26).

He/She is presented with Epigastric Pain radiating to the back, Vomiting while holding his belly with leaning forward and his pain increases when he/she takes a supine position.

Severe acute pancreatitis patients presented by more dramatic symptoms and signs of shock, pulmonary insufficiency, renal failure, GIT age, metabolic abnormalities. flank ecchymosis (Grey Turner’s sign), and/or periumbilical ecchymosis (Cullen’s sign) (27).

Laboratory Findings

Increase Serum Amylase and Lipase levels are specific (Lipase is more sensitive and specific) for diagnosis of Acute Pancreatitis. Increased ALT suggests biliary etiology (usually gallstones).

Clinical outcome

Identification of the severity of acute pancreatitis is incredibly helpful in the treatment of the patients.

First of all mild pancreatitis, These patients haven’t any organ failure and even several of them haven’t any fluid collections and definitely no necrosis.These patients typically recover by the end of the primary week.

Moderate or severe pancreatitis, Patient condition depend upon their body responds to the pathological process, protein cascades lead to a general inflammatory response syndrome (SIRS), that will increase the chance of organ failure. The presence of organ failure is decided by respiratory (pO2↓), urinary organ (creatinine↑) and cardiovascular failure (blood pressure↓).

The extent of morphologic changes like necrosis and fluid collections isn’t directly proportional to the severity of organ failure. several of those patients, however, can have necrotizing pancreatitis and also the mortality will increase once the necrosis becomes infected(28).

Complications of Acute Pancreatitis

Acute pancreatitis is considered a and emergency life threating condition that may progress to the variation of complications, including the following:

1. Infected Pancreatic necrosis: in which Gas enter inside the gland and result in infection necrosis.

2. Central Necrosis: in which necrosis occurs in the center portion of the pancreas and spare the rest of the gland.

3. Pancreatic Pseudocyst: it’s encapsulated fluid collection, it’s more likely to occur in lesser sac region, its capsule may be indistinguishable. it occurs in about 40% of cases. It can resolve in 50% of patients, but unlucky 20% of the patient can proceed to more complications as Peritonitis if rupture, Abscess if infected and Obstruction of duodenum and bile duct.
4. Pancreatic Abscess: it’s pus collection near or adjacent to the inflamed pancreas.

Figure (11) shows: Pancreatic abscess. The above CT image shows enhanced thick walled fluid collection. (arrowheads). Aspiration was done and reveals Pus (29).

5.Pseudoaneurysm: it occurs most commonly in splenic and gastroduodenal arteries, but can occur at any vessel, it occurs mostly due to autodigestion of arterial wall by pancreatic enzymes that result in pulsatile mass.

Figure (12) shows: CECT that shows high-density contrast collection (arrow) within a small retro-gastric pseudocyst.Angiogram was done and Pseudo-aneurysm was confirmed and embolized successfully(30).

6.Venous Thrombosis: mostly occurs in splenic, portal, SMV veins

7.hemorrhage: resulting from erosion of blood vessels and tissue necrosis

8.Fistula formation with pancreatic ascites: leakage of pancreatic secretions into the peritoneal cavity. .(31)

Acute Pancreatitis, how the imaging can show it

On X-Ray

On Abdominal X-ray erect, the film show gasless abdomen, with plus or minus ascites or intrapancreatic gas bubbles.

The Abdominal X-ray may also show dilated transverse colon with an abrupt transition to the gaseous descending colon, this is known as ‘colon cut off‘ sign.The film may also show localized segment of gas containing duodenum which known as ‘sentinel loop‘ sign (32).

As Pancreatitis cause fluid collection, a sympathetic pleural effusion may occur which appear on Chest X-ray as Pleural effusion more commonly to occur on the left side.

Figure (13) shows: Colon Cutoff Sign. White arrow on conventional radiograph points to air in colon which abruptly terminates at the splenic flexure (33).

On Ultrasound

Although CT is the technique of choice in evaluating patients with suspected acute pancreatitis, Ultrasound is often the initial test in patients presenting with abdominal pain – it may be possible to assess the inflamed pancreas or any fluid collections.

The Pancreas can be directly imaged with ultrasound, but the full length of the organ cannot be visualized in all patients either due to obesity or overlying gas.

Patient with interstitial edematous pancreatitis with mild Pancreatitis Signs may be subtle, but mostly patients presented on Ultrasound by oedematous enlarged hypoechoic spleen with blurred margins and peri-pancreatic exudates, Hypoechoic change may be diffuse or focal, the latter mimicking a tumor mass.

Accompanying dilated Pancreatic Duct may be seen due to compression or mass effect by surrounding lesion.The peripancreatic inflammatory process also can be seen.

Patients with Necrotizing Pancreatitis, imaging become more difficult because of severe tenderness and agonizing pain, but it appears on ultrasound as the Enlarged heterogeneous pancreas.

Also, we can see the cause of pancreatitis on ultrasound such as Gallstone or intraductal calculi, masses, others.

If pancreatitis is advance to complications, it can be seen as Pancreatic pseudocyst, it appears as well-circumscribed, unilocular cystic lesion within pancreas or peripancreatic tissue, it may need further follow-up ultrasound.

Pancreatic abscess can be seen as Thick-walled, mostly anechoic fluid collection with internal echoes and debris

Vascular complications as Pseudoaneurysm formation and port splenic venous thrombosis can be diagnosed by Doppler (34).Also, Portal Vein thrombosis can be seen on Color doppler Ultrasound.

Biliary pathology including common bile duct obstruction or dilatation can be seen with ultrasonography.

Figure (14) shows ultrasound of a pteint with mild interstitial edematous pancreatitis (35):

(Left) Transverse US demonstrates mild diffuse enlargement of the pancreas. The pancreatic duct is normal in size . The main sign of acute pancreatitis is fluid anterior to the pancreas as well as fluid anterior to splenic vein .

(Right) Longitudinal US of the body of the pancreas demonstrates peripancreatic fluid tracking caudally down the superior mesenteric vein . There is also fluid noted anterior to the body of the pancreas , a strong clue to the diagnosis of acute pancreatitis.


Contrast Enhanced CT is the diagnostic method of choice in acute pancreatitis, According to the main two sub-types, Acute pancreatitis can appear on Ct as the following:

Interstitial edematous pancreatitis,

in this type the pancreas appears enlarged and edematous with the loss of normal fatty lobulations. Peripancreatic fat edema and inflammation can be noted.

Fluid collection in the peripancreatic region mostly localized to Lesser sac, anterior pararenal spaces, and paracolic gutters.

normal enhancement of the gland with no necrosis is detected in this type.

Here we should mention important note that normal appearance of pancreas does not exclude pancreatitis as a mild type of pancreatitis presented with minimally elevated lipase levels can appear normal on imaging.

Figure (15) shows: CECT of a patient with Mild acute pancreatitis (36).

(A) Mild swelling of the gland that enhances uniformly but has indistinct margins because of peripancreatic edema. There is inflammatory tissue around the coeliac axis (arrow)

(B) The image at the level of the pancreatic head showing infiltration of the peripancreatic fat and fluid anterior to Gerota’s fascia (arrows).

(C) Different patient. Peripancreatic fluid with normally enhancing gland.

On the more severe type Necrotizing pancreatitis:

in this type, the necrosis in the pancreatic tissue appear as non-enhancing or severe hypoenhanced areas. Usually, it is accompanied by a greater amount of peripancreatic fluid and more sever inflammatory process (37).

Figure (16) show a patient with acute necrotizing pancreatitis. This is contrast enhanced CT image show pancreatic head enlargement with ascites and perirenal fluid collections. large necrotic nonenhancing pancreatic body and tail is noted (38).

CT technique of Pancreatitis.

Contrast-enhanced CT offers the broad spectrum of information in the diagnosis of pancreatic diseases, Thin-section spiral, and multislice CT have increased the sensitivity of CT for the detection of small lesions.

CT can be used in pancreatitis in Differentiation of exudative and necrotizing forms; and also can be used in Pretherapeutic CT to determine the extent of inflammatory spread.

It’s also used for detection and identification of pancreatic pseudocysts and in evaluation for a suspected abscess.

For pancreatitis, most Technicians perform only a contrast-enhanced scan in the parenchyma or the portal phase of enhancement.

A contrast dose of 70-100 ml is sufficient to differentiate between exudative and necrotizing pancreatitis (scan delay 40-60 s).

Thicker sections (7-8 mm) can be used for evaluation of the entire abdomen to detect spread of exudates or necrosis Because it
is a benign disease and pathology is often gross, dose reduction may be considered.

Even so that the overuse of CT in all acute pancreatitis patients can even harm rather than help the patient.So proper guidance of the clinical doctor is very helpful.


Mild interstitial edematous pancreatitis

appears resembling normal pancreas as slightly high intensity on T1 WI and gadolinium homogenous enhancement.

Diagnostic features are stranding of peripancreatic fat tissue, which is low in signal intensity on T1-WI without fat suppression and high in signal intensity on (fat-suppressed) T2-WI.

In necrotizing pancreatitis

contrast-enhanced images, similar to the CT protocol for pancreatitis, are mandatory to define necrotic areas.

Patients with necrotizing pancreatitis may develop complications, such as abscess, bleeding, and vascular complications such as thrombosis or an aneurysm.

The assessment of pancreatitis requires a comprehensive MR protocol with MRI and MRCP, and is more difficult to perform than CT in severely ill patients.

Therefore, the most important indication for MRI in acute pancreatitis is suspected choledocholithiasis (“biliary pancreatitis”) (39).

Figure (17) shows:Axial non-enhanced magnetic resonance T1-weighted with fat-suppression image.
(A) and axial T2-weighted with fat-suppression image.
(B) show that the parenchyma of the pancreatic head, body and part of the tail is hypointense (arrows in A) and hyperintense (arrows in B) relative to the liver , it’s a case of Acute oedematous Pancreatitis(40).

PET/CT has is role in Acute Pancreatitis

The Journal of Nuclear Medicine has published a study on August 6, 2014, that say that PET/CT with FDG-labeled leukocytes has a role in detecting infection in acute pancreatitis.

A team of researchers from Chandigarh and from Postgraduate Institute of Medical Education has done a study that includes 41 patients (28 men and 13 women, ages 21-69) with acute pancreatitis and radiological evidence of fluid collection in or around the pancreas.

They separate WBCs from patients blood, labeled with FDG, and reinjected intravenously. PET/CT imaging was performed two hours later.

They make A final diagnosis of infection based on the microbiological culture of fluid aspirated from the collection. Patients were managed with supportive care and antibiotics, and percutaneous drainage was performed when indicated.

They collected LAB results and notice increased FDG uptake in the collection in 12 (29%) of the 41 patients; 10 had a culture-proven infection and underwent percutaneous drainage, and aspiration was unsuccessful in two patients.

the result of PET/CT was negative for infection in 29 patients (71%) Of the 29 patients, 25 had negative fluid cultures, and aspiration was unsuccessful in four. Sensitivity, specificity, and accuracy of the scan were 100% in the 35 patients for whom fluid culture reports were available.

Dr. Anish Bhattacharya Said that this new technique can be used to diagnose infection in patients with the pancreatic fluid collection, individuals are spared empiric antibiotic therapy or radiological intervention followed by time-consuming microbiological workup. It also could be very useful in detecting or ruling out active infection of any part of the body (41).

The Overuse of imaging modalities in Acute Pancreatitis

Acute Pancreatitis is an emergency case, so should we request a lot of imaging modalities to every patient presented with symptoms of acute pancreatitis.

According to a study published online in Radiology from researchers at Brigham and Women’s Hospital in Boston. They found that clinical assessment of acute pancreatitis, rather than advanced imaging, works just fine for most patients.

Koenraad Mortele, MD, and his colleague have done the research and his colleagues have done the study. They wrote that “Studying imaging utilization in patients with Acute Pancreatitis is appealing because of the high estimated total healthcare cost associated with the disease, the presence of well-established practice guidelines for managing the disease, and the vast array of radiologic modalities that are available to image these patients,”.

Koenraad Mortele and his team have record data of 252 adult patients admitted to the hospital with a diagnosis of acute pancreatitis between June 2005 and December 2007.

Patients who had been transferred from other hospitals or those with a history of chronic pancreatitis were not included.

The researchers defined acute pancreatitis as two or more of the following characteristics:
– Severe upper abdominal pain
– Serum amylase and/or lipase levels three or more times higher than normal
– CT or MR imaging results that demonstrated changes consistent with AP

The research team gathers all the hospital’s database of all imaging modules done with these patients and every imaging studies for each patient.

then they classify them according to modality and technique. they also gather a database of all U.S. Centers for Medicare and Medicaid Services (CMS) 2009 relative value units (RVUs) for each study to have a consistent scale with which to assess differences across exam types.

They found that among 1,324 radiologic studies were performed during the study time, the mean imaging utilization rate was 5.3 studies per patient during initial hospitalization, with an RVU of 3.9; the mean utilization rate was 9.9 exams per patient, in the one-year period after the initial admission, with an RVU of 7.8. Overall, 53% of the total imaging use occurred during a patient’s initial hospitalization.

They found that the most common imaging module done with patients with acute pancreatitis was Chest radiography, Abdomen and Pelvis Computed Tomography and Abdominal ultrasound. they make a chart of imaging modality used during the one-year period following initial hospitalization is detailed in the following chart:

Figure (18) shows: Imaging use by modality for acute pancreatitis ,Data courtesy of the Radiological Society of North America. (42)

The researchers found a 2.5-fold increase in the use of high-cost imaging modalities and a 1.4-fold increase in imaging RVUs (per case-mix-adjusted admissions), without significant improvement of patient condition.

The researcher’s team wrote “In this analysis, patient outcomes were relatively stable during the study period. … Therefore, although it remains difficult to analyze the effect of imaging utilization on patient outcomes, it can probably be inferred that in our institution the increasing use of cross-sectional imaging did not result in detectable improvement in outcomes for patients with AP,”

The researchers were surprised to know that even though 90% of the patients in the study had mild disease, CT and MR use surpassed recommended Appropriateness Criteria of the American College of Radiology’s.

Despite that, there is no confirmatory evidence in existing literature that says that CT scans in patients with the milder disease would result in upstaging of disease in a significant number of patients, according to the researchers.

And there’s no value to perform early un-necessary Radiological exams to predict the clinical severity of acute pancreatitis rather than just using a clinical evaluation, they noted.

Finally, Mortele and his team wrote, “If a diagnosis of Acute Pancreatitis is established with abdominal pain and increased serum amylase and lipase activity and no systemic signs of severe disease exist, CT may not be necessary”.

So CT should be Only for Patients with an equivocal diagnosis, those who have already been established as having severe acute pancreatitis, or those who don’t improve despite conservative measures, they concluded(43).

Staging and grading

These are two ways of grading and staging of Acute Pancreatitis.

Balthazar Grading System,

in this grading system we can classify pancreatitis into

A: Normal-appearing pancreas.

B: Focal or diffuse pancreatic enlargement

C: Mild degree of inflammation in the peripancreatic area.

D: Collection of fluid Only E: Two or more fluid collections

the mortality rate is 0%, , morbidity rate is 4% for grades A, B, and C.
the mortality is 14%, the morbidity rate is 54% for grades D and E (a fluid collection is a poor prognostic indicator).

Another Grading is CT severity index (CTSI),

it integrates the Balthazar grading system with the degree of necrosis:

Assigns 0–4 points for Balthazar A–E, with 0 points for Balthazar A and 4 points for Balthazar E.

Adds 0–6 points for necrosis to create a total score from 0-10.

0 points: 0% necrosis
2 points: <30% necrosis
4 points: 30–50% necrosis
6 points: >50% necrosis
CTSI 0–3: 3% mortality, 8% morbidity
CTSI 7–10: 17% mortality, 92% morbidity (44).

Atlanta Classification of Fluid Collections

The 2012 Revised Atlanta Classification discerns 4 types of peripancreatic fluid collections in acute pancreatitis depends on the content, degree of encapsulation and time.

1.Content: it contains only fluid in the acute peripancreatic fluid collection (APFC) and Pseudocyst.A mixture of fluid and necrotic material in the acute necrotic collection (ANC) and walled-off-necrosis (WON).

2.The degree of encapsulation: None or partial wall in APFC and ANC. Complete encapsulation in pseudocyst and WON.

3.Time: Within 4 weeks: APFC and ANC.After 4 weeks: pseudocysts and WON. It takes about 4 weeks for a capsule to form.

On CT, the discrimination between an APFC and ANC may be difficult, especially in the first weeks and the term “indeterminate peripancreatic collections” can be used.Fluid collections could remain sterile or become infected. Infection is rare during the first week.

Differential Diagnosis of Acute Pancreatitis

Even so, pancreatitis has characteristic imaging appearance, it may mimic a lot of other pathologies, here are some examples:
Heterogeneous, hip enhancing mass with abrupt obstruction of the upstream pancreatic duct and upstream pancreatic atrophy. Pancreatic cancer may present with pancreatitis in about 5% of cases.

Focal pancreatitis can appear mass-like and mimic malignancy. Presence of dilated pancreatic duct or biliary obstruction should prompt further investigation for underlying mass

Pancreatic cancer infiltrates dorsally into retroperitoneum, unlike pancreatitis, which infiltrates anteriorly and laterally.other signs of malignancy, including vascular encasement, metastatic disease (most often liver), etc.

Perforated Duodenal Ulcer can cause fat stranding and edema in anterior pararenal space and mimic pancreatitis. Pancreatic head may be edematous due to adjacent inflammation which primarily centered around duodenum, not pancreas (often more apparent on coronal reformations) < 50% show extraluminal gas or contrast extravasation “Shock” Pancreas which can include infiltration of peripancreatic fat planes with pancreatic edema (similar to pancreatitis) but usually associated with the clinical history of hypotension and other imaging stigmata of shock, such as “shock bowel”. It Quickly resolves following resuscitation

Lymphoma: Lymphoma can rarely diffusely infiltrate and enlarge pancreas, superficially mimicking pancreatitis. Usually associated with regional lymphadenopathy and pancreatic involvement appears mass-like. No evidence of pancreatic or biliary ductal dilatation. Vessels encased, but not narrowed or occluded (45).


The first line of treatment of acute pancreatitis is Conservative which includes Fluid resuscitation, Analgesics, Nothing per mouth . then nutritional support.In patient with gallstone ERCP and sphincterotomy will be helpful

Mild interstitial edematous pancreatitis patients will resolve with conservative measures alone

Severe pancreatitis with necrosis may require intensive care due to high risk of multiorgan failure and Infected pancreatic necrosis will require surgical debridement

Aspiration is used to distinguish sterile necrosis from infected necrosis if infection suspected and no response to antibiotics

Asymptomatic fluid collections do not need intervention. Symptomatic fluid collections (due to mass effect, infection, pain, etc.) need to be drained, with walled-off necrosis requiring large-bore catheter or necrosectomy (due to debris and solid components), while simpler fluid collections can be drained with standard catheters

Angiographic embolization is used for pseudoaneurysms, and anticoagulation is used for venous thrombosis either in portal vein or SMV


Pancreatitis has an overall mortality rate of 1-3%, even so, it has an excellent prognosis with interstitial edematous pancreatitis and Poor prognosis with Necrotizing Pancreatitis.

Mortality rate: reach up to 25% with multiorgan failure or 30% for infected necrosis (even with surgical debridement).


From the previous information we have listed in this long articles, we can say that acute pancreatitis is an emergency disease that needs to be well evaluated by clinical doctors and guide the patients to the appropriate radiological examination.

we can say that plain radiography, even so, it is of less value imaging modality in the confirmatory diagnosis of acute pancreatitis. Colon “cut off” sign and “Sentinal Loop” sign can be useful to help clinical doctors to diagnosis Acute pancreatitis without the need to cost the patient more radiological examinations (ultrasound will be very useful of course especially in detected peri-pancreatic fluid).

Ultrasound, I can say that ultrasound is the cornerstone here in imaging diagnosis of acute pancreatitis, as it’s low cost and is harmful the patients so it would no upgrade the condition.

Ultrasound is very useful to detect parenchymal changes of the pancreas (edema, necrosis, or any signs of inflammation), even so in mild type pancreas may appear normal, but peri-pancreatic fluid won’t’ be missed.

Also, Ultrasound is the best imaging module to detect fluid collection.The main problem of ultrasound sound in the diagnosis of acute pancreatitis is overlying gasses of the colon, this is a major problem that makes ultrasound in many cases no dependable in the diagnosis of acute pancreatitis.

Contrat Enhanced CT is the imaging modality of choice in the diagnosis of Acute Pancreatitis. CT can detect every pancreatic tissue changes either edema or necrosis or anti-inflammatory sign.

CT also can detect fluid collection. CT can overcome colonic gasses problem of the ultrasound. And it’s very accurate in detecting extension of the pathology and grading of the condition.

But even so, it has a major disadvantage, high radiation dose, and the cost makes the situation not accessible to every suspected acute pancreatitis case to perform CT scan, studies have done say that using CT in mild condition may even upgrading the condition.

So CT is recommended to use only in equivocal patients which are not confirmed by other imaging modalities and for complicated patients and finally for those who don’t respond to treatment to evaluate the cause of the problem.

MRI has been proven to be useful in the diagnosis of acute pancreatitis especially in detecting necrotic parts of the pancreas in necrotic pancreatitis. it’s very helpful when we suspect choledocholithiasis (“biliary pancreatitis”).

Finally, PET/CT is a new technique that has proved himself to become very helpful in diagnosing infection in patients with the pancreatic fluid collection.


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