LETTERS TO THE EDITOR

 

Acute pancreatitis as fatal complication after chemoembolization of hepatocellular carcinoma

Pancreatitis aguda como complicación fatal de la quimioembolización de un carcinoma hepatocelular

 

 

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Key words: Acute pancreatitis. Embolization. Transcatheter arterial chemoembolization. Hepatocellular carcinoma. Complication. DC Bead.

Palabras clave: Pancreatitis aguda. Embolización. Quimioembolización arterial transcatéter. Carcinoma hepatocelular. Complicación. DC Bead.

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Dear Editor,

The transarterial chemoembolization (TACE) of hepatocellular carcinomas (HCC) is performed as treatment, also palliative for these patients with stage B tumors of Barcelona Clinic Liver Cancer (BCLC), as well as a treatment during the waiting period towards the liver transplantation(1,2).

 

Case report

We report the case of an 82-years-old man with a history of hypertension, smoker and drinker of alcohol who was diagnosed with cirrhosis by abdominal ultrasound for hypertransaminasemia. In the same test, three hepatic lesions were observed, and by computerized tomography a multicenter HCC was diagnosed, being the largest of these lesions 55mm in size.

The patient had compensated cirrhosis (Child-Pugh A5) and he was found in the BCLC intermediate stage, so he underwent palliative treatment through TACE.

Arteriography of the celiac trunk and superior mesenteric artery (SMA) was carried out. The left hepatic artery was a branch of the celiac trunk and the right hepatic artery of the SMA. The TACE was done through a superselective way with a microcatheter to the branch from the segment II of the celiac trunk. Thirty milligrams of adriamycin charged in DC Beads particles between 300 and 500microns were administered. Micro-catheterization of the artery of segment VII was also done from the branch of the SMA and twenty milligrams of adriamycin charged in the same particles were injected.

It was a procedure without incidents and no immediate complications. A good result of the embolization through posterior catheterism was obtained.

The patient remained in good general state for 24hours and he was discharged.

Ten days later he returned with nausea, vomiting and fever of a week of evolution. In the physical examination, the regular general state was observed, and the abdomen was painful with decreased bowel sounds. The blood analysis showed a clotting alteration, mild hypertransaminasemia and leukocytosis with neutrophil prevalence. He was admitted and treated with a wide spectrum antibiotic. In the computerized tomography hypodense and hypervascular small lesions were observed and the largest of segment II with air in its interior which could correspond to necrosis or abscesses. There was also bilateral pleural effusion and large peripancreatic collections which extended to the transverse mesocolon, hepatic hilum and right anterior pararenal space. There was alteration in the structure of the gland and pancreatic necrosis, basically in the head and neck of the pancreas, all of the data demonstrating a serious acute pancreatitis (AP) (Fig. 1). The patient suffered respiratory insufficiency, renal failure and sepsis, causing death four weeks after.

 

 

Discussion

There are few studies evaluating the incidence of AP after TACE (3-7). It is an invasive treatment, which can give rise to complications, the most frequent of them have been the post embolization syndrome (3) which symptoms consists in abdominal pain, fever, nausea, vomiting and malaise. Between 2 to 7% of the procedures have serious complications and a mortality rate of 1-2% has been described (8). The incidence of this rare complication is low, from 1.7% to 2% of all the patients submitted to this treatment but there is elevation of pancreatic enzymes in up to 40% (4).

The ischemic lesion of the pancreatic gland has been postulated as the most probable etiopathogenic mechanism of this complication, producing an escape or regurgitation of a part of the emboligenic material through the nutritional vascular branches of the pancreas. It is probable that AP after TACE can have multifactorial etiology, toxic (5,9) or due to vasospasm, more frequent in case of arteriosclerosis. It is also possible that a relation exists between the frequency of this complication and the type of particles that are used for the embolization or the volume of the same (5) and the size of the tumor (3). Another risk factor could be the presence of vascular abnormalities or anatomical variants, as occurred in the case of the patient that we present.

By the very fact, it is probable that this complication was under-diagnosed due to the clinical similarities with the post embolization syndrome.

We recommend that in all those patients submitted to this technique who developed abdominal pain, vomiting, fever or paralytic ileum their pancreatic enzymes should be determined or carried out by a pertinent test to achieve the diagnosis, so adequate therapeutic measures can be taken.

 

M.^a Carmen Rodríguez-Grau¹, Vanesa Jusué¹,
Alfonsa Fiera², Carlos Castaño¹
and Luisa C. García-Buey¹
Department of Gastroenterology and Hepatology.
Hospital Universitario de La Princesa.
Instituto de Investigación Sanitaria Princesa. Madrid, Spain
²Department of Interventional Radiology. Hospital Universitario de La Princesa. Madrid, Spain

 

References

1. Bruix J, Sherman M. Management of hepatocellular carcinoma: An update. Hepatology 2011;53:1020-2.         [ Links ]

2. Llovet JM, Real MI, Montana X, Planas R, Coll S, Aponte J, et al. Arterial embolisation or chemoembolisation versus symptomatic treatment in patients with unresectable hepatocellular carcinoma: A randomized controlled trial. Lancet 2002;359:1734-9.         [ Links ]

3. Malagari K, Pomoni M, Spyridopoulos TN, Moschouris H, Kelekis A, Dourakis S, et al. Safety profile of sequential transcatheter chemoembolization with DC Bead^TM: Results of 237 hepatocellular carcinoma (HCC) patients. Cardiovasc Intervent Radiol 2011;34:774-85.         [ Links ]

4. Roullet MH, Denys A, Sauvanet A, Farges O, Vilgrain V, Belghiti J. Acute clinical pancreatitis following selective transcatheter arterial chemoembolization of hepatocellular carcinoma (in French). Ann Chir 2002;127:779-82.         [ Links ]

5. López-Benítez R, Radeleff BA, Barragán-Campos HM, Noeldge G, Grenacher L, Richter GM, et al. Acute pancreatitis after embolization of liver tumors: Frequency and associated risk factors. Pancreatology 2007;7:53-62.         [ Links ]

6. Hiraki T, Sakurai J, Gobara H, Kawamoto H, Mukai T, Hase S, et al. Sloughing of intraductal tumor thrombus of hepatocellular carcinoma after transcatheter chemoembolization causing obstructive jaundice and acute pancreatitis. J Vasc Interv Radiol 2006;17:583-5.         [ Links ]

7. Addario L, Di Costanzo GG, Tritto G, Cavaglià E, Angrisani B, Ascione A. Fatal ischemic acute pancreatitis complicating trans-catheter arterial embolization of small hepatocellular carcinoma: Do the risks outweigh the benefits? J Hepatol 2008;49:149-52.         [ Links ]

8. Marelli L, Stigliano R, Triantos C, Senzolo M, Cholongitas E, Davies N, et al. Transarterial therapy for hepatocellular carcinoma: Which technique is more effective? A systematic review of cohort and randomized studies. Cardiovasc Intervent Radiol 2007;30:6-25.         [ Links ]

9. Kumar DM, Sundar S, Vasanthan S. A case of paclitaxel-induced pancreatitis. Clin Oncol (R Coll Radiol) 2003;15:35.         [ Links ]