Severe Liver Injury Complicated by Portal Hypertension and Traumatic Arterioportal Shunt: A Case Report.

Rationale: The search for new ways to stop bleeding in severe liver injuries is an urgent task of modern surgery, due to the technical complexity of known hemostasis methods, the high frequency of postoperative complications and the need for relaparotomies. Objective: To improve the results of treatment of patients with severe traumatic liver injuries. Methods: A randomized controlled clinical trial was conducted, including 70 patients with severe traumatic liver injuries. In the main group (n = 35), the original “Method of hemostasis in severe traumatic liver injuries” was used (patent Russian Federation 2792914). The control group (n = 35) uses traditional surgical techniques of hemostasis. Results: The groups were comparable in terms of the main demographic indicators, the degree of liver damage, and the combination of injuries. In the main group, complications were biliary — 31.4%, inflammatory, requiring relaparotomy — 5.7%, liver failure — 11.4%, there were no recurrence of bleeding, relaparotomy — 2 was performed. In the control group, complications were biliary — 40.0%, inflammatory, requiring relaparotomy — 28.6%, liver failure — 31.4%, recurrent bleeding — 8.6%, relaparotomy — 19. Conclusion: The original method of hemostasis allows to improve the results of treatment of patients with severe liver injuries, by reducing the frequency of postoperative complications and the need for relaparotomies. The effectiveness of the technique is based on the absence of direct contact of gauze tampons with the liver, which prevents them from sticking to the wound surface, impregnation with biological fluids and, accordingly, secondary infection.

PurposeIn this study, we retrospectively investigated the prevalence of arterioportal (AP) shunts in hepatocellular carcinoma (HCC) patients with portal vein tumor thrombosis (PVTT) and evaluated the changes in AP shunts after chemoembolization followed by external beam radiation therapy (EBRT).Materials and MethodsWe analyzed 54 HCC patients with PVTT who were treated with chemoembolization followed by EBRT. EBRT was uniformly delivered at a total dose of 30 to 45 Gy (median, 35 Gy), with a daily dose of 2 to 4.5 Gy. Angiographic images of chemoembolization before and after radiation therapy (RT) were reviewed to investigate the AP shunt.ResultsDuring the initial session of chemoembolization, 33 of 54 patients (61%) had an AP shunt. After EBRT, 32 out of 33 patients had an additional session of chemoembolization and were evaluated for a change in the AP shunt. The AP shunt decreased in 20 of 32 patients (63%) after chemoembolization followed by EBRT. The 1-year calculated overall survival (OS) rate for all patients was 52.6% and the 2-year OS was 36.4%. The median OS in all patients was 13 months. Patients with AP shunt showed poorer median OS than those without AP shunt, but there was no statistically significant difference (median, 12 months vs. 17 months).ConclusionThe AP shunt frequently occurs in HCC patients with PVTT. This study suggests that a poor prognosis is associated with an AP shunt. Chemoembolization followed by RT may produce a decrease in AP shunts.

A 73-year-old woman with massive ascites associated with a giant hepatic mass accompanied by arterio-portal (AP) shunt was admitted to our hospital. Based on contrast-enhanced computed tomography (CT) and angiography findings, hepatic hemangioma with AP shunt and ascites due to portal hypertension was diagnosed. Transcatheter arterial embolization (TAE) by N-butyl-2-cyanoacrylate (NBCA) was performed without complications. The patient's ascites disappeared, and her liver function test results improved after the treatment. The patient has maintained a steady state for two years. This case indicates that TAE with NBCA is a safe and effective treatment for hepatic hemangioma accompanied by AP shunt.

The portal-invasing hepatocellular carcinoma (HCC) and arterioportal (AP) shunting are not rare in patients with HCC. But a fatal complication of AP shunting and spontaneous partial regression of malignant portal vein thrombosis (PVT) are rely rare. In one patient, portal vein invasion of HCC was diagnosed by fine needle aspiration cytology. Computed tomography demonstrated portal vein thrombosis and angiography showed thread and streaks sign. Follow-up duplex Doppler studs 45 days later alter diagnosis revealed spontaneous partial regression of thrombus is with obvious arterioportal shunting and hepatofugal flow. Due to increased portal pressure from arterioportal shunting and regression of PVT, the patient suffered from ascites, hepatic encephalopathy, and episodic acute variceal bleeding. Transcatheter arterial embolization of arterioportal shunting and esophageal variceal banding ligation provided only temporary effect. Finally, he expired due to uncontrolled varices bleeding.

This Month in Gastroenterology

To compare the prevalence of arterioportal (AP) shunting associated with (a) small (< or =3 cm) hemangiomas and (b) hepatocellular carcinomas (HCCs) (< or =3 cm) at two-phase helical computed tomography (CT). Two-phase helical liver CT was performed in 107 patients (61 men, 46 women; age range, 25-73 years; mean, 48.6 years) with 169 small hemangiomas and in 384 patients (292 men, 92 women; age range, 18-82 years; mean, 58.3 years) with 598 HCCs 3 cm or smaller. Diagnosis of HCC was verified with histologic findings (n = 30) or typical imaging and clinical findings (n = 568); that of all hemangiomas was verified with typical imaging and clinical findings. Three radiologists retrospectively reviewed all CT images in consensus. Contrast material-enhanced CT scans were obtained during the hepatic arterial and portal venous phases. AP shunt was considered to be present when wedge-shaped or irregularly shaped homogeneous enhancement peripheral to tumor appeared at hepatic arterial phase CT and isoattenuation or slight hyperattenuation in that area appeared at portal phase CT. The prevalence of AP shunting associated with hemangiomas and that associated with HCCs were compared with multivariate model testing. Speed of lesion enhancement (rapid enhancement, when extent of intratumoral enhancement at hepatic arterial phase CT was >50%; slow enhancement, when extent of intratumoral enhancement was < or =50%) and presence of AP shunt were correlated with chi2 or Fisher exact testing. AP shunts were more frequently found in hemangiomas (36 lesions [21.3%]) than in HCCs (25 lesions [4.2%]) (P <.001). Twenty-four (38%) of the 64 hemangiomas with rapid enhancement had AP shunts, whereas only 12 (11.4%) of the 105 hemangiomas with slow enhancement had AP shunts (P <.001). There was no significant difference between prevalence of AP shunt in the 573 HCCs with rapid enhancement (24 lesions, 4.2%) and that in the 25 HCCs with slow enhancement (one lesion, 4.0%). AP shunts were more frequently seen at two-phase helical CT in small hepatic hemangiomas than in HCCs and thus represent a suggestive but not specific finding of hemangioma. Small hemangiomas with AP shunts tend to show rapid rather than slow enhancement.

A 44-year-old woman with multiple sclerosis (MS) receiving interferon (IFN)-beta-1a treatment was admitted to a local hospital for severe icterus and liver injury. She was transferred to our university hospital because fulminant hepatitis (FH) was suspected. She was diagnosed with acute-type FH based on hepatic coma, severe liver injury and liver failure, and she received plasma exchange and continuous hemodiafiltration therapy. On hospital day 6, she died from liver failure despite intensive care. An autopsy revealed histological findings consistent with FH. Physicians should monitor the hepatic function of MS patients receiving IFN-beta-1a treatment, as serious events can occur in rare cases.

To evaluate the value of precontrast phase (PP) of quadriphasic CT for differentiation of small arterial enhancing hepatocellular carcinoma (HCC) from non-tumorous arterioportal (AP) shunt in patients with chronic liver disease. Forty-eight patients with 28 HCCs and 28 AP shunts were enrolled. All lesions (5-20mm) showed arterial hyperenhancement with isoattenuation on portal venous phase or delayed phase without typical features of AP shunt. We evaluated and analyzed the attenuation of the lesions with qualitative and quantitative methods in each phase. The size, location, shape, margin, and coexistent HCC were evaluated. Diagnostic performances were also compared with triphasic CT and quadriphasic CT including PP in prediction of AP shunts from HCCs. The round or oval shape and visually low attenuation on PP were independent predictors for differentiating HCCs from AP shunts in multivariate analysis. Our study also revealed significantly increased diagnostic performances for both observers when PP was added to the triphasic CT. PP can be helpful in differentiation of small arterial enhancing HCCs from AP shunts. Careful evaluation of PP may lower need for follow-up CT or MRI, and can possibly achieve earlier diagnosis of small HCCs.

Value of precontrast and portal venous phases for evaluating atypical hepatocellular carcinoma mimicking arterioportal shunt

Intrahepatic arterioportal fistula (APF) is a rare cause of portal hypertension. Although it may be congenital or acquired, most often it develops after trauma or iatrogenically after transhepatic interventions. Spontaneous APF may develop in patients with hepatocellular carcinoma or rupture of a hepatic artery aneurysm. Congenital lesions are rare. Isolated congenital APFs may have initial symptoms of portal hypertension, failure to thrive, diarrhea, and malabsorption. To date, all reported pediatric patients have had symptoms develop in the first year of life (1-10). We report the case of a 3-year-old patient with a congenital APF. CASE REPORT A 3-year-old boy had a 1-month history of weight loss and diarrhea and a 2-week history of fever. Initial blood, urine, and stool cultures were negative. Despite empirical treatment with amoxicillin, the fever persisted. Abdominal distension prompted an abdominal ultrasound, which revealed a vascular mass within the liver and mild splenomegaly. Abdominal computed tomographic scan suggested a mass originating from the adrenal gland. He was transferred to our institution with a provisional diagnosis of neuroblastoma. Medical history showed an unremarkable pregnancy and delivery. Birth weight was 3.3 kg. There was no history of trauma or surgery. the patient was admitted to a hospital for pneumonia at 3 months and 27 months of age. Results of a sweat test were positive but a second one and subsequent genetic testing for cystic fibrosis produced negative results. There was no history of hematemesis, rectal bleeding, or melena. During the month before admission, his stools were looser than usual, and his body weight decreased by approximately 2 kg. On physical examination, weight was 13.27 kg (25th percentile) and height 95.2 cm (50th percentile). Heart rate was 86 beats per minute, blood pressure was 104/56, respiratory rate was 24, and he was afebrile. Abdominal distension was noted. The liver was 3 cm below the right costal margin, and a continuous murmur was heard over the liver. The spleen was not palpable. Findings in cardiopulmonary examination were within normal limits. Laboratory results were: white blood cell count 4.5 × 103/mm3, hemoglobin 8.0 g/dl, and platelet count 547 × 103/mm3. Prothrombin and partial thromboplastin times were normal, and serum electrolytes, liver enzymes, and bilirubin were at normal levels. Serum proteins were 6.3 g/dl, and serum albumin was 3.4 g/dl. Abdominal ultrasound showed mild splenomegaly with an enlarged hepatic artery feeding a hypoechoic vascular liver lesion. The portal vein was enlarged and pulsatile with hepatofugal flow. Echocardiography showed a large patent ductus arteriosus (PDA), a small apical muscular ventricular septal defect, and left auricular and ventricular enlargement. The right ventricle was normal. Cardiac function was described as good. The patient was discharged home, and iron supplements were prescribed. He returned 6 weeks later for cardiac catheterization to occlude the PDA. He had lost 1.9 kg and had poor oral intake and markedly decreased activity. His resting heart rate was 160. He had cachexia and was dehydrated. After rehydration, hemoglobin was 6.6 g/dl, albumin was 2.8 g/dl, and prealbumin 13.6 mg/dl. An abdominal radiograph showed multiple dilated loops of bowel and air-fluid levels. After transfusion, he underwent cardiac catheterization. A small PDA was embolized. There was a small apical restrictive muscular ventricular septal defect. A diagnosis of large hepatic APF was made. The fistula was caused by a direct communication between a branch of the right hepatic artery and a venous structure with a large dilated aneurysm traversing toward the left branch of the portal vein and opening close to the entrance of the umbilical vein into the left portal branch. There was therefore a communication between the artery and the anomalous venous structure and communication of this structure with the left portal branch, similar to a long venous tract. The hepatic artery was enlarged, and there was hepatofugal flow in the portal vein (Figs. 1A, 1B, 1C). The portal vein was enlarged. The catheter was placed in the hepatic artery, then through the fistula into the portal vein, and a pressure of 30 mmHg was obtained in the portal vein. The cardiologist attempted an embolization of the APF with two 12-mm × 8-cm 0.038 Gianturco coils (Wilson-Cook Medical, Inc., Winston-Salem, NC, U.S.A.).FIG. 1: (A) Image from an abdominal aortogram, frontal projection, obtained during cardiac catheterization. Arterial phase showing an enlarged hepatic artery communicating with the portal venous system through a large arterioportal fistula. Arrow indicates the rent of the fistula. Arrowheads indicate direction of the flow. (B) Venous phase showing filling of the portal system from the fistula. Arrowheads indicate direction of flow. (C) Late venous phase showing filling of the splenic vein and the superior mesenteric vein. Arrowheads indicate direction of flow.Two days later, the patient returned to the cardiac catheterization laboratory to undergo embolization of the remainder of the APF. The fistula was still patent, and the flow in the portal vein was hepatofugal. Portal pressure was 34 mmHg. Occlusion of the APF at the communication between the long venous tract and the left portal branch, away from the fistulous rent, was mistakenly performed with nine 12-mm × 8-cm 0.038 Gianturco coils. A small branch of the portal vein in the right posterolateral lobe was also occluded with three 3-mm × 2-cm 0.038 Gianturco coils. The embolization was thought to be adequate, but a Doppler study the next day showed persistent hepatofugal pulsatile flow in the portal vein and a markedly enlarged hepatic artery feeding the APF. Despite these findings, he was sent home. The patient's nutritional status deteriorated, and he was admitted 2 weeks later to a peripheral hospital for institution of nasogastric feedings. Emesis soon developed and became bloody, with melena. He was transferred to our center. On admission, his weight was 12 kg. He had tachycardia, cachexia, and mild dehydration. The liver was palpated at 2 cm below the right costal margin with no thrill or bruit. The spleen was not palpable. Gastric lavage produced coffee ground-like material. Laboratory values were white blood cell count 18.6 × 103/mm3, hemoglobin 9.9 g/dl, platelet count 611 × 103/mm3, normal prothrombin and partial thromboplastin times, serum sodium 120 mmol/l, potassium 6.2 mmol/l, chloride 80 mmol/l, CO2 22 mmol/l, urea 26 mg/dl, creatinine 0.5 mg/dl, aspartate aminotransferase 105 U/l, alanine aminotransferase 65 U/l, alkaline phosphatase 248 U/l, γ-glutamyl transferase 167 U/l, total bilirubin 0.8 mg/dl, serum proteins 7.9 g/dl, and albumin 4.6 g/dl. An abdominal radiograph was within normal limits, except for the metal coils. Abdominal ultrasound showed persistence of the APF, with hepatofugal and pulsatile flow in the portal vein. The patient continued to have bloody emesis and melena. A transfusion was administered, and an octreotide drip was initiated. The Department of Interventional Radiology was then consulted. Hepatic angiography revealed a communication between segment VIII of the right hepatic artery and a right branch of the portal vein extending into an anomalous portal branch draining into the left portal trunk. The previously placed coils were identified in the outlet of the fistula; at the communication with the left branch of the portal vein and into a smaller peripheral radicle of the right branch of the portal vein. The APF was open with a single artery feeding a large venous aneurysm (Fig. 2A). Flow in the portal vein was hepatofugal, and there was retrograde filling of esophageal varices through the left gastric vein (Fig. 2B). Embolization of the right arterial branch that fed the APF was performed using two 5-mm × 5-cm and three 2-mm × 3-cm Gianturco coils.FIG. 2: (A) Injection of the hepatic artery showing the previously placed coils in the left branch of the portal vein (open arrow) and in a small branch of the right portal vein. The fistula is indicated with a filled arrow. (B) Venous phase showing retrograde filling of the portal venous system. Arrows indicate direction of flow. (C) Images obtained after embolization of the arterial feeder (filled arrow) showing no further communication between the hepatic artery and the portal venous system. Open arrow indicates previous embolization. (D) Arterial portogram shows hepatopetal flow in the portal vein. Arrows indicate direction of flow. Arrowhead indicates catheter in the superior mesenteric artery.An aortogram after the embolization showed no residual filling of the APF, confirming complete occlusion of the fistula, with no further filling of the portal vein (Fig. 2C). Injection of the superior mesenteric artery showed that hepatopetal flow was reestablished in the portal system (Fig. 2D). Gastroscopy performed concurrently revealed four grade II to grade III-IV esophageal varices, one exhibiting a clot; the antrum showed features consistent with portal hypertension gastropathy. There was no active bleeding. No intervention was undertaken, because it was likely that the therapeutic embolization had relieved the portal hypertension. Antral biopsy showed vascular ectasia and some increased fibrosis in the lamina propria. After arteriography, the patient had no further bleeding, and the hemoglobin remained stable. Biweekly Doppler evaluation showed no residual fistula. Flow was hepatopetal in the portal vein, but there was suspicion of an occult fistula. Persistently hemocult-positive stools prompted angiographic and endoscopic reevaluation. Celiac arteriogram revealed no evidence of APF or early venous filling that would suggest residual arterioportal communication, and there were no esophageal varices. The left hepatic artery, the splenic artery, and the inferior mesenteric artery were normal. Superior mesenteric artery injection and portal venous return showed filling of enlarged paraduodenal veins. The left branch of the portal vein was not opacified, suggesting occlusion at the site of the previous embolization by the cardiology service. Gastroscopy revealed three grade II to IV esophageal varices with no signs of bleeding. The stomach and the duodenum appeared normal. A colonoscopy to the cecum produced normal findings. Results of all biopsy specimen studies were normal. The patient was then discharged receiving nasogastric feedings, H2 blockers, and iron supplements. Two weeks later, an ultrasound examination showed no evidence of APF, decreased size of the spleen, thrombosis of the left branch of the portal vein, and the appearance of large veins in the porta hepatis. Hemoglobin, serum proteins, albumin, and liver enzymes were normal. The patient was asymptomatic and weighed 15.18 kg. Four months after the definitive embolization, his weight was 16.9 kg (75th percentile), and his height was 96.5 cm (25th percentile). He was asymptomatic, and his stools were negative for occult blood. Abdominal ultrasound again showed no evidence of residual fistula, and the size of the prominent veins in the porta hepatis had decreased. One year after the embolization, he remained well. DISCUSSION Arterioportal fistulas can be intrahepatic or extrahepatic (11-13). Although they may be congenital (1-10), they are usually acquired after blunt or penetrating trauma (14-19), percutaneous liver biopsy (19-22), transhepatic cholangiography (14,21), gastrectomy (23,24), or biliary surgery (25). They can also result from a ruptured hepatic artery aneurysm (23,26,27) or hepatocellular carcinoma (28). They may be associated with Rendu-Osler-Weber syndrome (29) or Ehlers-Danlos syndrome (14). The literature describes two common ages for presentation of congenital APFs: before the first year of life or after the fourth decade. It is often difficult to determine whether the late-onset fistulas are congenital or acquired (23). Congenital APF of the liver is rare and should be differentiated from the more common hemangioendothelioma, a vascular tumor that progresses in the first year of life and then regresses spontaneously. Hemangioendotheliomas typically have initial symptoms of high-output heart failure or isolated hepatomegaly and may be accompanied by consumption coagulopathy. Rarely, there will be shunting in the portal system. The angiographic appearance is extremely variable, ranging from relatively low-flow lesions with contrast "puddling," lesions with dense capillary blush, and lesions with direct arteriovenous or arterioportal shunting. Arteriovenous fistulas or APFs are single-hole arteriovenous communications, whereas arteriovenous malformations usually have a complex plexiform vascular nidus with multiple feeding arteries and draining veins, with or without multiple smaller arteriovenous fistulas within the nidus. Embolization of an arteriovenous fistula requires occlusion of the rent of the fistula or tract between the artery and the vein. Arteriovenous malformations are more difficult to treat, usually requiring multiple procedures, and are more prone to collateralization and recurrence after embolization. Symptoms of APF Hemodynamic Consequences Arterioportal fistula in infancy usually has an initial symptom of portal hypertension (1-3,5-7,9). Hepatofugal flow in the portal vein develops as the portal flow is arterialized. Splenomegaly, hypersplenism, esophageal varices, bleeding episodes, and ascites develop. The retrograde flow in the portal system can result in a "steal" of the flow from the superior mesenteric artery, leading to intestinal angina (1). When compared with other arteriovenous shunts, APFs are unique in that they lack propensity to result in high-output heart failure. This is thought to be related to the buffering effect of the hepatic sinusoids interposed between the lesion and the right heart (5,9,13,19,25,30,31). Occasionally, congestive heart failure may occur in infants because of associated patency of the ductus venosus. Intestinal Dysfunction Malabsorption occurs commonly (1-3,5-7,9). Intestinal dysfunction is multifactorial, in part because of venous congestion and stasis secondary to reversal of flow in the portal and superior mesenteric veins (1,2,8). High flow in the hepatic artery may compromise blood flow distal to its origin, resulting in steal of blood flow from the superior mesenteric artery if both the superior mesenteric artery and hepatic arteries originate from a common trunk. This phenomenon can result in small-bowel infarction (1). Finally, superimposed dehydration and anemia can lead to a further decrease in the mesenteric circulation, adding to the intestinal damage. Some intraoperative descriptions of the small bowel mention its congestive and cyanotic aspect (1,2,8,10). Radiologic images show edema with air-fluid levels and a malabsorptive pattern. In some cases, intestinal obstruction may be suspected (1,2,8,10). Pancreatic hypofunction, described in patients with extrahepatic portal venous obstruction, may contribute to malabsorption (32). Hepatic Dysfunction Little is known about the long-term effect on the liver of arterialized portal blood flow. Liver enzymes are usually at normal levels. The increased flow in the portal venous system may lead to the ultimate development of disease in the liver and portal vessels exposed to high-pressure flow (9,12,13,24,33). This may result in portal hypertension, despite adequate treatment. Studies, using a canine model with chronic arterialized portal circulation, have shown a variety of obliterative changes in the intrahepatic portal microvasculature, such as thickening of the walls of the portal vein, fibrosis, scarring of the portal triad, and hypertrophy of the muscularis of the portal venous radicles (34). In 1969, Donovan et al. (12) reported two patients who had hepatoportal sclerosis with portal fibrosis and thick-walled veins after chronic arterialization of the portal flow. Portal vein thrombosis after successful eradication of APFs could be secondary to the damage to the portal system induced by longstanding arterialized flow (7). Diagnosis The diagnosis of APF should be suspected in patients with unexplained portal hypertension early in life, especially when associated with malabsorption and failure to thrive, even if liver function test results appear normal. Ultrasonography with Doppler study is a noninvasive, fast, reliable diagnostic tool (3,7,8,10,30,35). The roles of computed tomographic scan and magnetic resonance imaging are still to be defined (7). Arteriography should be performed early for diagnostic purposes and possible therapy. Treatment The treatment should be aimed at occlusion of the fistula. Spontaneous closure of small acquired fistulas, has been reported (15,17-21,30) but a large congenital fistula should not be expected to close. Portosystemic shunts to relieve portal hypertension should not be part of the therapy, because they may precipitate heart failure by redirecting arterialized portal blood into the systemic venous circulation (17,18,23). Embolization is the treatment of choice in first instance (4,5,18,20,22,30,31,35-37). If necessary, it may be repeated or followed by surgical ligation of the arterial feeder. Surgical resection should be considered only when other forms of therapy fail or when the fistula is extrahepatic (2,20,30). Review There are only 11 pediatric cases of congenital APF reported in the literature (1-10) (Table 1). The present case is the 12th. Initial symptoms usually occur early in life. In the 12 cases, all except the present patient had onset of symptoms in the first year of life. Nine of 12 (75%) patients had symptoms in the first 6 months. Consequences of portal hypertension, manifested as overt gastrointestinal bleeding, were present in 11 patients (91.6%); the remaining one had only anemia and hemepositive stools. Malabsorption syndrome with diarrhea and/or failure to thrive occurred in 9 patients (75%) (1-3,5-9). Steatorrhea that resolved after ligation of the hepatic artery was documented in one case (3), and an abnormal level of D-xylose in another (6). Assessment of intestinal specimens produced normal findings in one case (3) and showed edema and increased fibrosis of the lamina propria in another (6). Intestinal symptoms can mimic intestinal obstruction, as has been reported in four cases (33.3%) (1,2,8,10). One patient (8.3%) had an initial symptom of postprandial irritability and died of small bowel ischemia secondary to steal of flow from the superior mesenteric artery (1), and one (8.3%) had heart failure (8).TABLE 1: Reported pediatric cases of arterioportal fistulaOn physical examination, hepatomegaly was noted in nine patients (75%), splenomegaly in six (50%) (1,3,5,7,9), and ascites in only two (16.6%) (3,9). A bruit or a thrill was present over the right upper quadrant in seven patients (58.3%) (2,3,5,7,8,10). Embolization alone was successful in only two patients (16.6%) (4), including the present one, but in both cases two sessions were required. Two (16.6%) had embolization followed by surgical ligation (2,9). Three (25%) had surgical ligation alone (3,8,10). One patient had surgical ligation followed by embolization (5), and one required a left hepatectomy after surgical ligation and embolization failed (7). One had resection alone (6), and one had embolization followed by left hepatectomy and subsequent ligation (9). One died without treatment. Portal vein thrombosis occurred in two patients besides ours 5 months and 2 years after definitive therapy (5,7). Our patient is unique in that the symptoms occurred late; he was asymptomatic for the first 3 years of his life. The first embolization was unsuccessful because it was directed at the outflow system of the fistula instead of the arterial feeder. Subsequent embolization of this arterial feeder resulted in complete occlusion of the fistula. The only other case in which embolization was successful required embolization of the arterial feeder and subsequent embolization of the portal outflow (4). In our case, left portal vein thrombosis resulted, which may have been related to embolization of the outflow. Embolization of the feeder artery can be curative. However it is important to continue to observe patients, because the fistula can recur through arterial collateralization. There is a risk of portal vein thrombosis with recurrence of symptoms of portal hypertension after successful eradication of the APF (5,7), and therefore, the option of posttreatment anticoagulotherapy should perhaps be raised.

BackgroundThe damage control approach is known to reduce the mortality rate in severely injured patients and has now become a common practice. Transcatheter arterial embolization (TAE) has been shown to be useful with combining with damage control laparotomy in identifying and controlling active arterial hemorrhage. Hybrid operating room (OR) allows both damaged control surgery and TAE in the same location in minimal time. We report a case of a patient with three cardiac arrests who was saved by early intervention using damage control surgery (DCS) with interventional radiology (IVR) in the hybrid OR.Case presentationA 46-year-old woman was injured in a collision with a tree while snowboarding. She was eventually transported to hybrid operating room in our hospital with the diagnosis of significant liver laceration and hemorrhagic shock. Damage control surgery was performed with perihepatic packing (PHP) and TAE was conducted to stop active bleeding from right hepatic artery. She experienced 3 times of cardiopulmonary arrest, which was successfully resuscitated on each occasion. Although she had total of 3 times of laparotomy but tolerated well. She was discharged on day 82 of hospitalization and showed no neurological sequelae.ConclusionSaving the life of a patient with severe trauma requires a multidisciplinary approach with cooperation and early information sharing among trauma team members. Sharing treatment strategy with the trauma team and early intervention using DCS with IVR in the hybrid operating room could save the patient’s life.

Significant elevations in liver transaminases were noted in some patients during pre-marketing clinical trials with lumiracoxib, a selective COX-2 inhibitor. It was withdrawn from the Australian market in August 2007, because of an association with severe liver injury. We describe in detail three cases of severe liver injury in patients taking lumiracoxib Three patients admitted to our hospital with severe liver injury and taking lumiracoxib are described in detail, together with information on a further six cases reported to the Australian Therapeutics Goods Administration (TGA), none of whom had pre-existing liver disease or obvious risk factors for liver disease. Liver histology showed severe hepatic necrosis. One patient required liver transplantation and another died. Autoantibodies were detected in all three patients. As with the other six cases reported to the TGA, all were females who had been taking lumiracoxib 200-400 mg daily, typically for a few months, for osteoarthritis. Lumiracoxib can be associated with severe liver injury. The presence of a variety of positive auto-antibodies suggests an altered immune response may be contributory.

The purpose of this study was to assess the clinical effects of transcatheter arterial chemoembolization (TACE) during the corresponding portal vein occlusion (TACE-PVO) in patients with hepatocellular carcinoma (HCC) and marked arterioportal (AP) shunts. This was a prospective, nonrandomized study of TACE-PVO in patients with HCC who had marked AP shunts. The subjects were 21 patients with unresectable HCC and marked AP shunts who underwent shunt embolization with the use of coils and/or gelatin-sponge particles (group A: n = 7) or by TACE-PVO (group B: n = 14). Clinical parameters and data on embolization of AP shunts and on tumor response were assessed prospectively. No major procedure-related complication occurred in either group. Effectiveness of AP-shunt treatment was significantly better in group B than in group A in terms of both immediate results (P = 0.009) and subsequent results (P = 0.028). Tumor response in the therapeutic target area was significantly (P = 0.002) better in group B than in group A. Survival was significantly better in group B than in group A (P = 0.008). TACE-PVO may be a safe and useful therapy for selected patients with unresectable HCC and marked AP shunts.

Fístula arterioportal sintomática resuelta mediante tratamiento conservador

Although transcatheter arterial chemoembolization is one of the established treatments for hepatocellular carcinoma (HCC), it is difficult to treat HCCs with prominent arterioportal (AP) shunts because anticancer drugs and embolic materials migrate into the non-tumorous liver through the AP shunts and may cause liver infarction. We developed a novel method of balloon-assisted chemoembolization using a micro-balloon catheter alongside a microcatheter simultaneously inserted through a single 4.5-Fr guiding sheath, comprising proximal chemoembolization with distal arterial balloon occlusion. We applied this method to treat an HCC with a prominent distal AP shunt induced by previous proton beam therapy and achieved successful chemoembolization without non-tumorous liver infarction under temporal balloon occlusion of a distal AP shunt.