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 Table of Contents  
ORIGINAL ARTICLE
Year : 2017  |  Volume : 5  |  Issue : 1  |  Page : 27-34

Ruptured hepatocellular carcinoma: Management options


1 Department of Surgery, Armed Forces Hospital-Southern Region-Khamis Mushait, Saudi Arabia
2 Department of Radiology, Armed Forces Hospital-Southern Region-Khamis Mushait, Saudi Arabia
3 Department of Medicine, Armed Forces Hospital-Southern Region-Khamis Mushait, Saudi Arabia

Date of Web Publication12-Apr-2017

Correspondence Address:
M Ezzedien Rabie
Department of Surgery, Armed Forces Hospital, Southern Region, P. O. Box 101, Khamis Mushait
Saudi Arabia
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ssj.ssj_68_16

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  Abstract 

Background: Hepatocellular carcinoma (HCC) has endemic proportions in some regions of the world, including the Sub-Saharan Africa, China, and the Far East. One of its known complications is tumor rupture, with a bleak prognosis.
Aim: This study aims to report on our experience with the management of ruptured HCC.
Materials and Methods: We reviewed our records to retrieve cases of ruptured HCC, from September 2013 to December 2015.
Results: We were able to identify five patients, all of them were males with a median age of 70 years (range 26). One patient had hepatitis B, three had Schistosoma, and the status of the fifth was undetermined. In one patient, who eventually died, an emergency laparotomy deemed necessary to control the bleeding. In the other four, who were stabilized to undergo computerized axial tomography scan, angioembolization of the tumor feeding vessels succeeded to arrest the bleeding. Unfortunately, two patients died shortly after the procedure, while the other two survived and were discharged for follow-up.
Conclusion: Spontaneous rupture of HCC is a grave event with a dismal prognosis. The optimal management should be individualized, based on the condition of the patient, the tumor characteristics, the facilities, and expertise available. Close collaboration between the interventional radiologist, gastroenterologist, oncologist, and surgeon is fundamental for success. The emergency laparotomy may be the appropriate action for the unstable patients. For those who could be stabilized, angioembolization with or without chemotherapy is an attractive option. Conservative treatment may be reserved for those with the worst prognosis.

Keywords: Angioembolization, hepatitis B, hepatocellular carcinoma, Schistosoma, spontaneous rupture


How to cite this article:
Rabie M E, Alqahtani SA, El Hakeem I, Al Qahtani AS, Alhagawi YA, Al Qahtani N, Al Qahtani SM. Ruptured hepatocellular carcinoma: Management options. Saudi Surg J 2017;5:27-34

How to cite this URL:
Rabie M E, Alqahtani SA, El Hakeem I, Al Qahtani AS, Alhagawi YA, Al Qahtani N, Al Qahtani SM. Ruptured hepatocellular carcinoma: Management options. Saudi Surg J [serial online] 2017 [cited 2017 Dec 15];5:27-34. Available from: http://www.saudisurgj.org/text.asp?2017/5/1/27/204420


  Introduction Top


Hepatocellular carcinoma (HCC) has endemic proportions in some regions of the world, including the Sub-Saharan Africa, China, and the Far East. It has a male:female ratio of 5:1, with a peak incidence in the third and fourth decades in endemic areas. In North America, where the disease is uncommon, the peak incidence is in the fifth and sixth decades of life.[1] Chronic hepatitis B and C virus are major causative factors.[1],[2] Other causative factors include alcoholic cirrhosis, bronzed diabetes, alpha-1 antitrypsin deficiency, certain chemical hepatotoxins and aflatoxin produced by the Aspergillus fungus.[1] In our country, HCC ranks 5th cancer in males and 11th in females.[3] In another study, hepatitis B virus appeared to play a more significant role in the causation of HCC than Hepatits C.[4]

Pathologically, the tumor may be a single mass, a multinodular growth or a diffuse infiltrative type.[1]

A known complication of HCC is tumor rupture which carries a dismal prognosis.


  Materials and Methods Top


We reviewed our records to retrieve cases of ruptured HCC, from September 2013 to December 2015. The patients' demographics, mode of presentation, associated viral hepatitis status, and management provided were collected.


  Results Top


Five patients were identified, they were all males with a median age of 70 years (range 26). The hepatitis status, Schistosoma status, and other comorbidities are shown in [Table 1]. The result of ultrasound (US) and computerized axial tomography in providing the diagnosis is shown in [Table 2]. The mode of presentation, management provided and its result is shown in [Table 3].
Table 1: Hepatitis and Schistosoma status and other comorbidities

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Table 2: Result of ultrasound/computed tomography scan

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Table 3: Mode of presentation, management, and its result

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In the first patient, an emergency laparotomy deemed necessary due to the unstable condition of the patient and upon the discretion of the surgeon. Unfortunately, the patient eventually died despite the initial success to arrest the bleeding. In the other four, who were stabilized, angioembolization of the tumor feeding vessels succeeded to arrest the bleeding. Unfortunately, two patients died shortly after the procedure, while the other two survived and were discharged for follow-up.

Case summaries

First case

A 93-year-old male a known case of diabetes mellitus, hypertension, and old cerebrovascular accident, presented to the emergency room in an unconscious and hypotensive state with shallow breathing. His blood pressure (BP) was 80/40 mmHg, and pulse was 123/min. The patient was intubated, ventilated, and resuscitation with intravenous (IV) fluids and inotropic support. The presence of coffee ground material in the nasogastric aspirate as well as a mildly distended tender abdomen with sluggish bowel sounds necessitated a surgical consultation. With resuscitation, his BP rose to 120/55, but the pulse remained rapid at 144 beat/min.

Investigations showed normal liver function, raised urea (9.9 mmol/L, reference range: 2.5–7.5) and creatinine (174 μmol/L, reference range: 62–106), and very low hemoglobin (Hb) (5.9 gm/dl, reference range: 14–18), for which reason blood transfusion was ordered.

Abdominal US showed a focal lesion in the right lobe of a cirrhotic shrunken liver with subhepatic heterogeneous collection and moderate amount of free fluid in the abdomen [Figure 1].
Figure 1: Ultrasound showing a mass in the right hepatic lobe 59 mm × 37 mm (white arrows), suggestive of hepatoceuuluar carcinoma (a), with free intraperitoneal fluid collection (black arrows) (b)

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The possibility of ruptured HCC was considered and upon the discretion of the surgeon, a decision for laparotomy was taken.

During surgery, about 3 L of blood and clots were evacuated from the abdomen, and a ruptured hepatic tumor was found in the lower edge of segment VI. The tumor within a margin of liver tissue was resected and hemostasis secured [Figure 2]. During the hemostatic maneuvers, the monopolar diathermy tip touched a metal retractor, and an electric spark was generated near the hepatic flexure of the colon, but no injury was observed. There were three other lesions in the left lobe and another one in the right hepatic lobe, which were intact.
Figure 2: Resected lower part of segment VI containing the tumor

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Postoperatively, the patient did will initially, but on the 6th postoperative day, he sustained a convulsive fit for which he was reintubated. On reassessment, his abdomen appeared distended and tender to touch. Because of the incidental sparking during surgery, which raised the fear of a possible bowel injury, reexploration was performed where <500 ml of serosanguineous fluid were found in the abdomen with no evident bowel injury.

On recovery from the second operation, his liver and renal values, as well as his coagulation profile, continued to deteriorate, and he needed maximum inotropes to support his circulation. Finally, he passed into adult respiratory distress syndrome which culminated into cardiorespiratory arrest.

Histopathology report showed well-differentiated HCC, and serological tests came positive to cytomegalovirus G and hepatitis B virus.

Second case

A 67-year-old male, a known case of hypertension, diabetes mellitus and chronic liver disease, presented with dizziness, vomiting, and decreased urine output for 2 days. There was no abdominal pain, hematemesis or melena, and no other urinary symptom.

His previous US showed coarse liver, splenomegaly with multiple calcification and no ascites.

On examination, he looked pale but oriented, with marked tachycardia. Initially, his BP was 74/55 mmHg, and after IV fluid boluses, it came up to 109/85 mmHg but dropped again to 85/65 mmHg. Cardiovascular and chest examinations were normal, and there was no focal neurological deficit. Abdominal examination showed no organomegaly or fluid thrill and no shifting dullness could be elicited that time. Hypovolemic shock versus septic shock was suspected and resuscitative measures with IV fluids and inotropes continued.

His blood works showed Hb of 10.8 gm/dl (previously 15.9, reference range: 14–18), normal electrolytes and deranged renal and liver functions. His blood urea was 11.5 mmol/L (reference range: 2.5–7.5), creatinine 332 μmol/L (reference range: 62–106), aspartate aminotransferase (AST) 110 μ/L (reference range: 10–42) alanine aminotransferase (ALT) 56 μ/L (reference range: 10–60), and total bilirubin (TB) 26 μmol/L (reference range: 3–17).

US and computed tomography (CT) scans showed cirrhotic liver with an ill-defined hypoechoic/heterogeneous mass in segment V of the right hepatic lobe with the irregularity of its inferomedial border and a large amount of hyperdense free fluid in the abdomen. These features were suggestive of ruptured HCC [Figure 3] and [Figure 4].
Figure 3: (a and b) Mass in the inferior part of the right lobe of the liver (red circle) with perihepatic fluid

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Figure 4: Free fluid surrounding the irregular surface of the right lobe of the liver

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After stabilization, angiographic embolization was done. The procedure started with selective catheterization of the hepatic artery, followed by super selective catheterization of two segmental branches supplying the tumor in segment V. Embolization of the two arteries using 500–700 then 700–900 mm particles followed by gel-foam was performed until cessation of tumor blush was achieved [Figure 5]. Following embolization, no complications were observed and the procedure was tolerated well.
Figure 5: Angiographic embolization of the tumor feeding vessel

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The patient tested positive to Schistosoma (titer 1:1024, reference range ≤1:32) but his hepatitis serology came negative, and in due time, he was discharged for follow-up.

Two months later, he presented with deep jaundice and upper gastrointestinal bleeding. Upper endoscopy showed esophageal varices Grade 4 with cherry red spot and rubber band ligation was done. Later, repeat endoscopy showed Grade 2 non bleeding esophageal varices, and he was treated conservatively and discharged for follow-up.

Third case

A 90-year-old diabetic male presented with sudden onset of severe abdominal pain mainly epigastric, and vomiting, for 1 day.

On examination, he was in pain and looked pale but alert with no jaundice or respiratory distress. His BP was 107/57 mmHg, pulse 89/min, temperature 36.4°C, and O2 saturation 88% on room air.

Chest examination showed good bilateral air entry, and his neurologic assessment was normal but his abdomen was diffusely tender with guarding.

Initially, his Hb was 10.3 gm/dl but then dropped to 8.9 gm/dl. His blood biochemistry showed alkaline phosphatase (ALP) 82 μ/L, (reference range: l36–126), ALT 205 μ/L (reference range: 10–60), AST 204 μ/L (reference range: 10–42), TB 12 μmol/L (reference range: 3–17), gamma-glutamyl transferase 95 μ/L (reference range: 5–64), blood urea 17.2 mmol/L (reference range: 2.5–7.5), and creatinine 366 μmol/L (reference range: 62–106).

His chest and abdominal X-rays were normal, and his abdominal US and CT scans showed enlarged liver (span 21 cm) with multiple heterogeneous masses in both liver lobes and free intraperitoneal fluid [Figure 6] and [Figure 7]. With these findings, supported by raised alpha fetoprotein of 129.4 μg/L (reference range: 0.0–15), the diagnosis of multifocal HCC with spontaneous rupture was established.
Figure 6: Abdominal ultrasound, showing a mass in the right lobe of the liver, measuring 10 cm × 6.6 cm (a), and in the left lobe measuring 6.5 cm × 5.4 cm (b)

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Figure 7: CT abdomen showing right and left hepatic masses (red arrows), with surrounding fluid (white arrows)

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After stabilization with fluid and blood transfusion, the patient underwent angioembolization of the tumor feeding vessel. He tolerated the procedure well with no complications. A couple of days later, he was discharged in a stable condition.

His serological examination tested positive for Schistosoma (1:2048, normal range <1:32) but hepatitis serology was negative.

Fourth case

A 67-year-old diabetic and hypertensive female, diagnosed in another hospital with decompensated liver cirrhosis and HCC 4 months earlier, presented to our emergency room with fever, shortness of breath, and abdominal distension for 1 week. There was no hematemesis or melena and systematic review was unremarkable.

On examination, she looked ill, confused, pale, and jaundiced. Her temperature was 36°C, pulse 117/min, BP 146/78 mmHg, respiratory rate 24/min, and O2 saturation 90% on room air.

Chest examination revealed central trachea and dullness in the right infrascapular region with diminished air entry.

Abdominal examination revealed distension of the abdomen with everted umbilicus, and there was generalized tenderness but no guarding or rigidity. The liver was enlarged with a span of 18 cm, and the spleen was impalpable. There was also massive ascites, and rectal examination showed no melena.

Her investigations showed Hb 6.3 gm/dl (reference range: 12–16), white blood count 21.000/mm 3 (reference range: 4.000–10.000), normal platelet count 139.000 (reference range: 140.000–400.000), international normalized ratio 2.3 (reference range: 1.1), and activated partial thromboplastin time 62.5 s (reference range: 25–29.9).

Her liver and renal values were deranged, and her alpha-fetoprotein was very high (10.342 μg/L, reference range: 0.0–15).

Resuscitative measures, including blood transfusion commenced and the patient was prepared for abdominal CT scan, which showed a cirrhotic liver studded with multiple irregular hypodense lesions, mainly in the right lobe with the largest measuring 10 cm × 13 cm, and there was apparent breaching of the overlying liver tissue with extensive free fluid in the abdomen [Figure 8], features suggestive of ruptured hepatic tumor.
Figure 8: (a and b) Large hepatic tumor occupying almost the entire right lobe (white arrow) with breaching of the overlying liver capsule (white arrowhead) and surrounding free fluid (black arrow)

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After stabilization, transarterial embolization (TAE) was successfully performed and bleeding was arrested [Figure 9]. Unfortunately, after a short period of initial improvement with stabilization of the Hb level, the patient passed into multiorgan failure, disseminated intravascular coagulation, sepsis, and finally died.
Figure 9: Angiographic embolization of the tumor feeding vessels ([a] before and [b] after embolization)

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Fifth case

A 70-year-old male, previously diagnosed with bilharzial liver disease a year earlier and lost to follow-up, presented to our emergency room with abdominal pain, vomiting, and jaundice.

His laboratory investigations showed normal hemogram (Hb 12.7 g - reference range: 12–16), renal values, international normalized ratio, and alpha-fetoprotein.

His liver functions were deranged, with a TB of 201 μmol/L (reference range: 3–17), ALT 49 μ/L (reference range: 10–60), AST 101 μ/L (reference range: 10–42), ALP 201 μ/L (reference range: l36–126).

Abdominal US and triphasic CT scan showed multiple liver masses, with the largest at the caudate lobe. However, CT scan did not show the specific contrast enhancement of HCC and dynamic magnetic imaging (magnetic resonance imaging) was inconclusive for the nature of the masses.

True cut biopsy of the liver masses was planned, but unfortunately, the patient developed hypotension, and his Hb dropped to 8 gm/dl. Massive transfusion was activated, and the patient was shifted to the Intensive Care Unit. Surgical consultation was sought and repeat CT scan showed a newly appearing large amount of intra-abdominal fluid collection, along with the liver masses, features suggestive of ruptured HCC.

Urgent angiography was performed and the feeding vessels to the big mass in the caudate lobe were embolized [Figure 10].
Figure 10: Hepatic angiography before (a) and after (b) embolization

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Resuscitative efforts including repeat blood transfusions continued, and due to the extent of the liver masses and the very poor condition of the patient, surgery as an option was excluded. Finally, the patient succumbed to his illness.


  Discussion Top


In several occasions, HCC may remain unsuspected till it declares itself once it ruptures.[5] This was seen in our patients, in whom hepatitis B infection was present in one patient and schistosomiasis in three others with their known for the malignant transformation. In the fifth patient, this association remained obscure.

In contrast to the well-established association between viral hepatitis and HCC, the association between schistosomiasis and HCC has not been fully defined, and it has been suggested that Schistosoma potentiates, rather than initiates, the carcinogenic effect of known risk factors, such as hepatitis C and B infection.[6],[7]

The incidence of spontaneous rupture of HCC has been estimated at 2.87%;[8] and definitely it carries a poor prognostic impact on survival.[9] A 6-month median survival time and a 4% 5 years survival rate have been reported.[10] Moreover, patients who survive the primary event may present several months later with intraperitoneal metastases from tumor seedling.[11]

Risk factors for tumor rupture have been defined. In a case–control study, Zhu et al. compared 200 patients with ruptured HCC with 202 control group without rupture. In their multivariate logistic regression analysis, risk factors were: Coexistent hypertension, liver cirrhosis, tumor size >5 cm, vascular thrombus, and extrahepatic invasion.[10]

To overcome the problem of sudden presentation with ruptured HCC, as seen in our patients, it has been suggested that patients with stable liver cirrhosis should be investigated once they show up with any of the following conditions: Newly developed ascites, deterioration of liver functions, increasing jaundice or weight loss,[12] signs which herald the development of HCC.

Essentially, there are three treatment options for ruptured HCC: Conservative treatment, TAE and tumor resection.[10],[13],[14]

An essential step in the management is the maintenance of hemodynamic stability by appropriate measures including blood transfusion. This not only preserves the life of the patient, but also preserves the already deteriorating liver functions, and consequently improves the prognosis. Initially, the patient's general condition, as well as his liver status and tumor characteristics, should be evaluated to choose the appropriate option. In those with advanced liver disease and poor prognosis, a conservative treatment may be reasonable. In stable patients, TAE, especially chemoembolization, may be appropriate as a sole treatment [13],[14] or in preparation for liver resection (two stage procedure).[14],[15],[16] If TAE is unavailable or fails or if the patient is not stable enough, emergency surgery may be considered. During surgery, careful assessment of the liver status and tumor characteristics should be done. Immediate hepatic resection,[5],[14],[17] selective ligation of the hepatic artery and portal vein of the tumor carrying lobe followed by resection several days later [18] or damage control laparotomy with perihepatic packing which may be followed by TAE,[19] are all valid options. As an extreme variant of surgery, laparoscopic resection of ruptured hepatic tumors has been described,[20] a highly controversial and ill-advised option to the vast majority of surgeons.

In an effort to define the best course, several studies have been conducted. In a retrospective multicenter study, patients received one of two treatment options, conservative treatment or TAE. The median survival time for the conservative treatment group was 13.1 days, which compared poorly to that of TAE group with 244.8 days.[13] In another study comprising 54 patients, 6 received conservative treatment, 19 received emergency hepatectomy, and 29 received TAE, either as a definitive treatment or followed by hepatectomy. In this series, conservative treatment was associated with increased 30 days mortality, while hepatectomy had higher survival rates (85.2% at 1 month and 62.2% at 1 year).[14]

In these tight situations, the optimal treatment for the individual patient is difficult to foresee, and in the absence of randomized controlled trials, which are difficult to conduct, the choice of treatment depends merely on the judgment of the treating team.

In the patients presented here, the choice of treatment was governed essentially by the condition of the patient on presentation and decisions were taken conjointly be the treating team members. Our first patient presented in an unconscious state and the US suggested the diagnosis. Due to the circulatory instability as well as the preference of the surgeon, exploratory laparotomy was performed. Intraoperatively, the condition was confirmed, and the bleeding tumor was resected, thus controlling the situation. However, the second laparotomy performed for a suspected bowel perforation was negative and, unfortunately, led to deterioration and patient's death.

On the other hand, the other four patients presented in a more stable condition, probably due to the slow trickling of blood from the tumor, and this allowed for radiologic confirmation of the diagnosis and TAE to be performed. Unfortunately, despite its success to control the bleeding, two patients succumbed shortly thereafter.

In this regard, the close collaboration between the surgeon, interventional radiologist, oncologist, gastroenterologist, and intensivist is invaluable. To this end, we suggest the algorithm shown in [Figure 11].
Figure 11: Suggested management algorithm for ruptured hepatocellular carcinoma

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  Conclusion Top


Spontaneous rupture of HCC is a grave event with a dismal prognosis. The optimal management should be individualized, based on the condition of the patient, the tumor characteristics, the facilities, and expertise available. Close collaboration between the interventional radiologist, gastroenterologist, oncologist, and surgeon is fundamental for success. Emergency laparotomy may be the appropriate action for the unstable patients. For those who could be stabilized, TAE with or without chemotherapy is an attractive option. Conservative treatment may be reserved for those with the worst prognosis.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.
Debas HT. Gastrointestinal Surgery: Pathophysiology and Management. 1st ed. New York: Springer-Verlag; 2004.  Back to cited text no. 1
    
2.
Alswat KA, Sanai FM, Altuwaijri M, Albenmousa A, Almadi M, Al-Hamoudi WK, et al. Clinical characteristics of patients with hepatocellular carcinoma in a middle Eastern population. Hepat Mon 2013;13:e7612.  Back to cited text no. 2
    
3.
Kingdom of Saudi Arabia. Ministry of Health. Saudi Cancer Registry. Cancer Incidence Report. Saudi Arabia; 2004.  Back to cited text no. 3
    
4.
Ayoola EA, Gadour MO. Hepatocellular carcinoma in Saudi Arabia: Role of hepatitis B and C infection. J Gastroenterol Hepatol 2004;19:665-9.  Back to cited text no. 4
    
5.
Polat KY, Akçay MN, Aydinli B, Erdogan F, Kantarci M, Oztürk G, et al. Spontaneous rupture of hepatocellular carcinoma: A case report and review of literature. Int J Clin Pract Suppl 2005;147:103-5.  Back to cited text no. 5
    
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El-Tonsy MM, Hussein HM, Helal Tel-S, Tawfik RA, Koriem KM, Hussein HM. Schistosoma mansoni infection: Is it a risk factor for development of hepatocellular carcinoma? Acta Trop 2013;128:542-7.  Back to cited text no. 6
    
7.
Chou YH, Chiou HJ, Tiu CM, Chiou SY, Lee SD, Hung GS, et al. Duplex Doppler ultrasound of hepatic Schistosomiasis japonica: A study of 47 patients. Am J Trop Med Hyg 2003;68:18-23.  Back to cited text no. 7
    
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Bassi N, Caratozzolo E, Bonariol L, Ruffolo C, Bridda A, Padoan L, et al. Management of ruptured hepatocellular carcinoma: Implications for therapy. World J Gastroenterol 2010;16:1221-5.  Back to cited text no. 8
    
9.
Aoki T, Kokudo N, Matsuyama Y, Izumi N, Ichida T, Kudo M, et al. Prognostic impact of spontaneous tumor rupture in patients with hepatocellular carcinoma: An analysis of 1160 cases from a nationwide survey. Ann Surg 2014;259:532-42.  Back to cited text no. 9
    
10.
Zhu Q, Li J, Yan JJ, Huang L, Wu MC, Yan YQ. Predictors and clinical outcomes for spontaneous rupture of hepatocellular carcinoma. World J Gastroenterol 2012;18:7302-7.  Back to cited text no. 10
    
11.
Hung MC, Wu HS, Lee YT, Hsu CH, Chou DA, Huang MH. Intraperitoneal metastasis of hepatocellular carcinoma after spontaneous rupture: A case report. World J Gastroenterol 2008;14:3927-31.  Back to cited text no. 11
    
12.
Abdo AA, Hassanain M, AlJumah A, Al Olayan A, Sanai FM, Alsuhaibani HA, et al. Saudi guidelines for the diagnosis and management of hepatocellular carcinoma: Technical review and practice guidelines. Ann Saudi Med 2012;32:174-99.  Back to cited text no. 12
    
13.
Kirikoshi H, Saito S, Yoneda M, Fujita K, Mawatari H, Uchiyama T, et al. Outcomes and factors influencing survival in cirrhotic cases with spontaneous rupture of hepatocellular carcinoma: A multicenter study. BMC Gastroenterol 2009;9:29.  Back to cited text no. 13
    
14.
Hsueh KC, Fan HL, Chen TW, Chan DC, Yu JC, Tsou SS, et al. Management of spontaneously ruptured hepatocellular carcinoma and hemoperitoneum manifested as acute abdomen in the emergency room. World J Surg 2012;36:2670-6.  Back to cited text no. 14
    
15.
Yoshida H, Onda M, Tajiri T, Umehara M, Mamada Y, Matsumoto S, et al. Treatment of spontaneous ruptured hepatocellular carcinoma. Hepatogastroenterology 1999;46:2451-3.  Back to cited text no. 15
    
16.
Shimada R, Imamura H, Makuuchi M, Soeda J, Kobayashi A, Noike T, et al. Staged hepatectomy after emergency transcatheter arterial embolization for ruptured hepatocellular carcinoma. Surgery 1998;124:526-35.  Back to cited text no. 16
    
17.
Vergara V, Muratore A, Bouzari H, Polastri R, Ferrero A, Galatola G, et al. Spontaneous rupture of hepatocelluar carcinoma: Surgical resection and long-term survival. Eur J Surg Oncol 2000;26:770-2.  Back to cited text no. 17
    
18.
Tanaka H, Honna T, Muto M, Fujino A, Kasahara M, Kitano Y, et al. Selective ligation of portal vein and hepatic artery for ruptured hepatocellular carcinoma in a 13-year-old boy. J Pediatr Surg 2011;46:973-7.  Back to cited text no. 18
    
19.
Spaziani E, Briganti M, Saltarelli A, Iozzino M, Notarianni E, Cianni R, et al. Massive haemoperitoneum due to traumatic rupture of multifocal hepatocarcinoma in the right hepatic lobe. Case report. G Chir 2009;30:21-5.  Back to cited text no. 19
    
20.
Belgaumkar A, Carswell KA, Patel AG. Laparoscopic resection of ruptured liver tumors. J Laparoendosc Adv Surg Tech A 2009;19:641-5.  Back to cited text no. 20
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9], [Figure 10], [Figure 11]
 
 
    Tables

  [Table 1], [Table 2], [Table 3]



 

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