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 Table of Contents  
CASE REPORT
Year : 2021  |  Volume : 5  |  Issue : 3  |  Page : 135-137

Spontaneous rupture of hepatocellular carcinoma at first presentation


1 Department of Medical Education, Hamad Medical Corporation, Doha, Qatar
2 Department of Clinical Imaging, Hamad Medical Corporation, Doha, Qatar
3 Department of Internal Medicine, Hamad Medical Corporation, Doha, Qatar

Date of Submission23-May-2021
Date of Acceptance27-Aug-2021
Date of Web Publication11-Oct-2021

Correspondence Address:
Dr. Nedia Neffati
Department of Internal Medicine, Hamad Medical Corporation, Doha
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ljms.ljms_31_21

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  Abstract 


Hepatocellular carcinoma (HCC) is the leading primary malignancy of the liver and typically develops in the background of chronic liver disease, particularly those with cirrhosis due to viral hepatitis B and C. Ruptured tumor is the most serious complication of HCC primarily occurring in older patients with significant mortality rate. In this report, we present a case of acute abdomen with the features of impending shock as the first presentation of a spontaneously ruptured HCC in a previously healthy young man.

Keywords: Hepatic artery embolization, hepatocellular carcinoma, Philippines, postembolization syndrome, ruptured hepatocellular carcinoma


How to cite this article:
Ebrahim E, Ageila MA, Abdurabu M, Twair A, Ali R, Neffati N. Spontaneous rupture of hepatocellular carcinoma at first presentation. Libyan J Med Sci 2021;5:135-7

How to cite this URL:
Ebrahim E, Ageila MA, Abdurabu M, Twair A, Ali R, Neffati N. Spontaneous rupture of hepatocellular carcinoma at first presentation. Libyan J Med Sci [serial online] 2021 [cited 2021 Nov 29];5:135-7. Available from: https://www.ljmsonline.com/text.asp?2021/5/3/135/328085




  Introduction Top


Hepatic and intrahepatic bile duct cancers rank sixth most common primary malignant tumors in men.[1] Hepatocellular carcinoma (HCC) is the leading primary malignancy of the liver and typically develops in the background of chronic liver disease, particularly those with cirrhosis due to viral hepatitis B and C.[2],[3] Those who are >40 years of age and men are more likely to develop HCC than young patients and females [3:1] F:M ratio.[1],[4] Other risk factors for the development of HCC include cirrhosis of any etiology, aflatoxin, smoking, and others.[2],[3] Geographically, HCC cases from Asia pacific region appear to constitute 72% of the overall global burden.[1],[5]

Among the most serious and acute complications of HCC is the rupture of the tumor with intraperitoneal bleeding. This life-threatening complication has variable incidence from 3% in the Western regions to 26% in the East.[6] Unfortunately, the early mortality rate following rupture of HCC is high ranging between 25% and 75%.[7] Some risk factors for HCC rupture were described in the literature including cirrhotic liver, large tumor size >5 cm, hypertension, vascular thrombosis, and extrahepatic invasion.[7] In this report, we present a case of acute abdomen with impending shock in a previously healthy young man.


  Case Report Top


A 28-year-old male patient from the Philippines, unknown case of any chronic illness, presented to our emergency department (ED) with a complaint of increasing right upper abdominal and shoulder pain for 2 days. The patient is a smoker for the past 3 years and drinks alcohol in moderation. His pain started about 2 months ago, it was progressive in course, excruciating pain, located mainly to right hypochondrium, with radiation to the right shoulder, increased significantly in the past 2 days before presentation and is worst at the time of presentation to the ED. During the ED encounter, the patient was standing unable to lie down due to severe pain. The pain was not related to food intake throughout the illness course. There was no vomiting, fever, constipation, diarrhea, or melena. However, there was nausea and sensation of abdominal fullness. Review of other systems is overall negative except for dark urine, yellowish discoloration of the eyes, and recent unintentional weight loss of around 10 Kg over 3 months.

The patient had negative medical and surgical histories. He has not used long-term medications, herbals, or drugs of abuse. His family history was significant for diabetes in both parents but was negative for malignancies.

On physical examination, the patient was ill-looking, conscious, oriented, apyrexial, but in pain. There was pallor, and jaundice but no lower limb edema or lymphadenopathy. The patient had a 92 b\min regular pulse, a respiratory rate of 19 c\min, temperature of 36.6o, blood pressure of 117\79 mmHg, and oxygen saturation of 99%. Cardiac and chest auscultation reveals normal heart sounds with no added sounds and normal vesicular breathing. His abdomen was distended, guarded, and tender to palpation all over. No ascites or organomegalies appreciated. Other systems examination was entirely normal.

Paraclinical work-up including laboratory tests and ultrasound imaging were requested. [Table 1] shows the laboratory findings. Abdominal ultrasound showed enlarged liver measuring 19 cm, with coarse parenchymal echotexture. There were multiple mostly hyperechoic nodular lesions, the largest measures 9 cm × 8 cm. A cyst was seen measuring 11 mm in diameter. Intrahepatic bile ducts were prominent. The liver showed cirrhotic features with multiple nodular lesions concerning for sinister pathology. There were moderate turbid ascites and a left pleural effusion. Chest and abdominal X-rays were normal except for an elevated right hemidiaphragm. An abdominal computed tomography (CT) scan was followed and is shown in [Figure 1] and [Figure 3].
Table 1: Laboratory test results on day of presentation

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Figure 1: Venus phase computed tomography axial (a) and coronal reformatted (b) images demonstrating a large heterogeneously enhancing mass occupying most of the right lobe of the liver. The mass is partially exophytic from the anterior aspect of the liver with evidence of discontinuity at its inferior margin (yellow arrows) suggestive of its rupture with a large amount of high-density ascites. There is a tumor extension into the middle hepatic vein and inferior vena cava (white arrow). Furthermore, note the liver surface nodularity with hypertrophy of its caudate and left lobes suggestive of the background liver cirrhosis

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Figure 2: Arterial phase computed tomography MIP coronal reformatted image demonstrating high ar terial vascularity of the tumor with 3 intratumoral arterial pseudoaneurysms (arrows)

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Figure 3: Fat saturated T1 postcontrast subtracted magnetic resonance image demonstrating extensive necrosis of the tumor postembolization

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Seven hours over the night during ED time, the patient developed tachycardia, tachypnea, and dropping hemoglobin. He received fluid resuscitation and transfusion followed by urgent percutaneous right hepatic artery embolization in the morning with satisfactory stagnation of forward arterial flow [Figure 2]. Additional screening and follow-up laboratory tests 24 h following embolization showed negative viral markers, increasing alanine aminotransferase and aspartate aminotransferase (413 and 782, respectively), prolonging prothrombin time and international normalized ratio (20 and 1.9, respectively), lowering albumin of 26, and a 1228 IU\ml high alpha-fetoprotein. After stabilization and frequent assessment by ED physician, medical registrar, and surgical registrar a decision to proceed for admission under medical team for further evaluation and discussion with hepatobiliary surgery and oncology for final management plan was carried out. Persistent spiking fever and chills developed with negative septic work-up consistent with the postembolization syndrome.

Multidisciplinary meetings recommended hepatic biopsy which provided inconclusive results followed by abdominal magnetic resonance imaging and magnetic resonance cholangiopancreatography [Figure 2] and [Figure 3]. Radioembolization was decided and agreed with the patient with poor prognosis and 1-year survival.


  Discussion Top


HCC is the most common malignancy of the liver, and seventh cancer causes worldwide.[1] It is a hypervascular tumor that often complicates chronic liver disease particularly secondary to hepatitis infection.[2],[3]

Spontaneous rupture of HCC is a life-threatening condition and occurs in variable incidence according to regions, ranging from 3% in Western countries to 26% in the East.[6] Many factors contribute to this complication, but no clear mechanism has been elucidated yet; artery and vein thrombosis, tumor size, rapid growth of the tumor, and necrosis.[7],[8],[9] The common presentation of spontaneous rupture of HCC is acute abdominal pain, mainly in the right upper quadrant, that can be associated with signs of hypovolemic shock and peritoneal irritation.[9] The diagnosis of ruptured HCC is confirmed by the presence of hemoperitoneum, with evidence of liver tumor by US or CT of the abdomen.[10] Conventional angiography is another modality that can reveal contrast extravasation from the tumor.[9] Management of HCC rupture has two main components: Hemostasis and treatment of the tumor. Surgical and nonsurgical interventions can be offered: Transarterial embolization, hepatic resection (one stage or staged), perihepatic packing, hepatic artery ligation, and radiofrequency ablation.[11],[12] Conservative management is preferred in patients who are hemodynamically stable or with advanced disease and inoperable tumors. Survival after HCC rupture is influenced by the stage of the disease, hospital course and complications (LFTliver function tests, infections, thromboembolic events, respiratory failure, etc.).[7] Patients with advanced disease and severe rupture carry a high mortality rate.


  Conclusion Top


In summary, ruptured HCC in patients without a prior diagnosis of tumor is rare and challenging, it should be considered in the setting of acute abdomen, and imaging of hemoperitoneum and liver lesion.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Bray F, Ferlay J, Soerjomataram I, Siegel RL, Torre LA, Jemal A. Global cancer statistics 2018: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries. CA Cancer J Clin 2018;68:394-424.  Back to cited text no. 1
    
2.
Jafri W, Kamran M. Hepatocellular carcinoma in Asia: A challenging situation. Euroasian J Hepatogastroenterol 2019;9:27-33.  Back to cited text no. 2
    
3.
Zhu RX, Seto WK, Lai CL, Yuen MF. Epidemiology of hepatocellular carcinoma in the Asia-Pacific Region. Gut Liver 2016;10:332-9.  Back to cited text no. 3
    
4.
Global Burden of Disease Liver Cancer Collaboration, Akinyemiju T, Abera S, Ahmed M, Alam N, Alemayohu MA, et al. The burden of primary liver cancer and underlying etiologies from 1990 to 2015 at the global, regional, and national level: Results from the Global Burden of Disease Study 2015. JAMA Oncol 2017;3:1683-91.  Back to cited text no. 4
    
5.
Singal AG, Lampertico P, Nahon P. Epidemiology and surveillance for hepatocellular carcinoma: New trends. J Hepatol 2020;72:250-61.  Back to cited text no. 5
    
6.
Moris D, Chakedis J, Sun SH, Spolverato G, Tsilimigras DI, Ntanasis-Stathopoulos I, et al. Management, outcomes, and prognostic factors of ruptured hepatocellular carcinoma: A systematic review. J Surg Oncol 2018;117:341-53.  Back to cited text no. 6
    
7.
Lai EC, Lau WY. Spontaneous rupture of hepatocellular carcinoma: A systematic review. Arch Surg 2006;141:191-8.  Back to cited text no. 7
    
8.
Pinal-García DF, Nuño-Guzmán CM, Gómez-Abarca A, Corona JL, Espejo I. Spontaneous rupture of hepatocellular carcinoma in a young patient with fatal outcome. Case Rep Gastroenterol 2018;12:19-26.  Back to cited text no. 8
    
9.
Bialecki ES, Di Bisceglie AM. Diagnosis of hepatocellular carcinoma HPB (Oxford) 2005;7:26-34.  Back to cited text no. 9
    
10.
Battula N, Madanur M, Priest O, Srinivasan P, O'Grady J, Heneghan MA, et al. Spontaneous rupture of hepatocellular carcinoma: A western experience. Am J Surg 2009;197:164-7.  Back to cited text no. 10
    
11.
Yeh CN, Lee WC, Jeng LB, Chen MF, Yu MC. Spontaneous tumour rupture and prognosis in patients with hepatocellular carcinoma. Br J Surg 2002;89:1125-9.   Back to cited text no. 11
    
12.
Jin YJ, Lee JW, Park SW, Lee JI, Lee DH, Kim YS, et al. Survival outcome of patients with spontaneously ruptured hepatocellular carcinoma treated surgically or by transarterial embolization. World J Gastroenterol 2013;19:4537-44.  Back to cited text no. 12
    


    Figures

  [Figure 1], [Figure 2], [Figure 3]
 
 
    Tables

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