Hepatic veno-occlusive disease (sinusoidal obstruction syndrome) after hematopoietic stem cell transplantation in adult patients: Diagnosis, incidence, prophylaxis, and treatment.

Hepatic veno-occlusive disease/sinusoidal obstruction syndrome (VOD/SOS) affecting the liver is a rare, possibly life-threatening complication of hematopoietic stem cell transplantation (HSCT). Sinusoidal endothelial cell (SEC) damage triggered by various factors (especially conditioning regimen) results in post sinusoidal portal hypertension due to obstruction of the hepatic vein. Diagnosis is guided by traditional clinical diagnostic criteria; the modified Seattle criteria, the Baltimore and revised European Group for Blood and Marrow Transplantation (EBMT), specifically. While there are promising results of imaging techniques studies in the diagnosis of VOD/SOS, none of those imaging techniques are routinely utilized in diagnosis yet. However, risk stratification is essential; conflicting results have been shown in studies aiming to define risk factors for development of VOD/SOS conducted to date. The only approved drug for the treatment of VOD/SOS yet is defibrotide, with early treatment offering higher chances of survival. In this review, we will focus on pathogenesis, clinical presentation and diagnostic criteria, risk factors, prophylaxis, and treatment of the VOD/SOS occurring post-HSCT.

Influence of portal vein occlusion on portal flow and liver elasticity in an animal model.

Hepatic fibrosis causes an increase in liver stiffness, a parameter measured by elastography and widely used as a diagnosis method. The concomitant presence of portal vein thrombosis (PVT) implies a change in hepatic portal inflow that could also affect liver elasticity. The main objective of this study is to determine the extent to which the presence of portal occlusion can affect the mechanical properties of the liver and potentially lead to misdiagnosis of fibrosis and hepatic cirrhosis by elastography. Portal vein occlusion was generated by insertion and inflation of a balloon catheter in the portal vein of four swines. The portal flow parameters peak flow (PF) and peak velocity magnitude (PVM) and liver mechanical properties (shear modulus) were then investigated using 4D-flow MRI and MR elastography, respectively, for progressive obstructions of the portal vein. Experimental results indicate that the reduction of the intrahepatic venous blood flow (PF/PVM decreases of 29.3%/8.5%, 51.0%/32.3% and 83.3%/53.6%, respectively) measured with 50%, 80% and 100% obstruction of the portal vein section results in a decrease of liver stiffness by 0.8% ± 0.1%, 7.7% ± 0.4% and 12.3% ± 0.9%, respectively. While this vascular mechanism does not have sufficient influence on the elasticity of the liver to modify the diagnosis of severe fibrosis or cirrhosis (F4 METAVIR grade), it may be sufficient to attenuate the increase in stiffness due to moderate fibrosis (F2-F3 METAVIR grades) and consequently lead to false-negative diagnoses with elastography in the presence of PVT.

Venoocclusive Disease With Both Hepatic and Pulmonary Involvement.

Pulmonary venoocclusive disease (PVOD) is a rare form of pulmonary vascular disease with pulmonary hypertension characterized by preferential involvement of the pulmonary venous system. Hepatic venoocclusive disease (HVOD), also known as sinusoidal obstruction syndrome, is a condition that occurs in 13% to 15% of patients after hematopoietic stem cell transplantation (HSCT). Although hepatic and pulmonary venoocclusive diseases may share some pathologic features as well as some etiologies such as HSCT, these two disorders have never been described together in a single adult patient. We report the case of a patient who received HSCT and developed HVOD and PVOD within 9 months. Despite their differences, PVOD and HVOD share common risk factors and associated conditions, suggesting that in the context of HSCT, the two diseases share common pathophysiological mechanisms. Optimal treatment for HSCT-related PVOD remains to be determined.

Conservation of both hematocrit and liver regeneration in hepatectomies: a vascular occlusion approach in rats.

BACKGROUND: Hepatectomies promote considerable amount of blood loss and the need to administrate blood products, which are directly linked to higher morbimortality rates. The blood-conserving hepatectomy (BCH) is a modification of the selective vascular occlusion technique. It could be a surgical maneuver in order to avoid or to reduce the blood products utilization in the perioperative period. AIM: To evaluate in rats the BCH effects on the hematocrit (HT) variation, hemoglobin serum concentration (HB), and on liver regeneration. METHODS: Twelve Wistar rats were divided into two groups: control (n=6) and intervention (n=6). The ones in the control group had their livers partially removed according to the Higgins and Anderson technique, while the rats in the treatment group were submitted to BCH technique. HT and HB levels were measured at day D0, D1 and D7. The rate between the liver and rat weights was calculated in D0 and D7. Liver regeneration was quantitatively and qualitatively evaluated. RESULTS: The HT and HB levels were lower in the control group as of D1 onwards, reaching an 18% gap at D7 (p=0.01 and p=0.008, respectively); BCH resulted in the preservation of HT and HB levels to the intervention group rats. BCH did not alter liver regeneration in rats. CONCLUSION: The BCH led to beneficial effects over the postoperative HT and serum HB levels with no setbacks to liver regeneration. These data are the necessary proof of evidence for translational research into the surgical practice. A) Unresected liver; B) liver appearance after the partial hepatectomy (1=vena cava; 2=portal vein; 3=hepatic vein; 4=biliary drainage; 5=hepatic artery).

Ultrasound in Hepatic Veno-occlusive Disease (HVOD) after Pediatric Hematopoietic Stem Cell Transplantation (HSCT): Comparison of Diagnostic Criteria Including the Pediatric Criteria of European Society for Blood and Marrow Transplantation (EBMT).

The European Society for Blood and Marrow Transplantation (EBMT) has recently announced new diagnostic criteria for pediatric hepatic veno-occlusive disease (HVOD) after hematopoietic stem cell transplantation (HSCT). We retrospectively inspected 97 ultrasound exams of 60 pediatric HSCT patients, and compared its diagnostic value using the Baltimore, Seattle and pediatric EBMT criteria. Nine of the ten patients who were diagnosed as HVOD only in the EBMT criteria had severe or very severe HVOD. In the Seattle and EBMT criteria, portal vein velocity, peak systolic velocity and resistance index of hepatic artery, gallbladder wall thickening and ascites were statistically significant. No ultrasound variable showed significant association in the Baltimore criteria. All patients with portal vein velocity below 10 cm/s were in higher EBMT grade. A scoring system was developed, to evaluate the overall relationship of the ultrasound findings with the diagnosis of HVOD, showing fair (0.768 and 0.733) AUC in the ROC curve of EBMT and Seattle criteria.

The role of hepatic sinusoidal obstruction in the pathogenesis of the hepatic involvement in HELLP syndrome: Exploring the literature.

AIM: This study aims to determine, based on existing data, whether the mechanism resulting in liver dysfunction in HELLP syndrome resembles that in Sinusoidal Obstruction Syndrome (SOS). BACKGROUND: HELLP syndrome is a serious pregnancy disorder with high maternal and perinatal morbidity and mortality rates. Because of poor insight in its pathophysiology, particularly that of the liver involvement, clinical management is limited to symptomatic treatment, often followed by termination of pregnancy. SOS is a rare, potentially life-threatening complication of radio and/ or chemotherapy in the preparation of hematopoietic cell transplantation. The etiology of liver dysfunction in SOS is - unlike that in HELLP syndrome - better-understood and seems to be initiated by direct toxic damage and demise of endothelial cells, causing hepatic sinusoidal obstruction and ischemia. METHODS: We searched Pubmed, Embase and Cochrane for reports on the etiology of HELLP and SOS. This yielded 73 articles, with 14 additional reports from the references listed in these articles. RESULTS: The dysfunctional placenta in women developing HELLP initiates a cascade of events that eventually results in liver dysfunction. The placenta releases, besides anti-angiogenetic factors, also necrotic debris and cell-free DNA, a mixture that not only induces systemic endothelial dysfunction as in preeclampsia, but also a systemic inflammatory response. The latter aggravates the endothelio-toxic effects in the systemic cardiovascular bed, amplifying the already increased pro-thrombotic conditions. Particularly in microcirculations with extremely low shear forces, such as in the hepatic sinusoids, this will facilitate microthrombi formation and fibrin deposition eventually resulting in obstruction of the sinusoids similar as in SOS. The latter causes ischemic damage and progressive demise of hepatocytes. CONCLUSION: The available information supports the concept that the liver damage in HELLP and SOS results from sinusoidal ischemia, presumably resulting from partially overlapping pathophysiological mechanisms.

Conservation of both hematocrit and liver regeneration in hepatectomies: a vascular occlusion approach in rats / Hepatectomia hemoconservadora no rato: preservação do hematócrito e da regeneração hepática

ABSTRACT Background: Hepatectomies promote considerable amount of blood loss and the need to administrate blood products, which are directly linked to higher morbimortality rates. The blood-conserving hepatectomy (BCH) is a modification of the selective vascular occlusion technique. It could be a surgical maneuver in order to avoid or to reduce the blood products utilization in the perioperative period. Aim: To evaluate in rats the BCH effects on the hematocrit (HT) variation, hemoglobin serum concentration (HB), and on liver regeneration. Methods: Twelve Wistar rats were divided into two groups: control (n=6) and intervention (n=6). The ones in the control group had their livers partially removed according to the Higgins and Anderson technique, while the rats in the treatment group were submitted to BCH technique. HT and HB levels were measured at day D0, D1 and D7. The rate between the liver and rat weights was calculated in D0 and D7. Liver regeneration was quantitatively and qualitatively evaluated. Results: The HT and HB levels were lower in the control group as of D1 onwards, reaching an 18% gap at D7 (p=0.01 and p=0.008, respectively); BCH resulted in the preservation of HT and HB levels to the intervention group rats. BCH did not alter liver regeneration in rats. Conclusion: The BCH led to beneficial effects over the postoperative HT and serum HB levels with no setbacks to liver regeneration. These data are the necessary proof of evidence for translational research into the surgical practice.

RESUMO Racional: As hepatectomias compreendem considerável perda sanguínea e utilização de hemoderivados, o que diretamente estão relacionados com maior morbimortalidade. A hepatectomia hemoconservadora (HH) é modificação da técnica de oclusão vascular seletiva em hepatectomia. Ela pode ser alternativa cirúrgica para evitar ou diminuir o uso de hemoderivados no perioperatório. Objetivo: Avaliar os efeitos da HH sobre o volume globular (VG), concentração de hemoglobina (HB) e sobre a regeneração hepática em ratos. Métodos: Dois grupos de ratos Wistar foram constituídos: controle (n=6) e intervenção (n=6). Os do grupo controle foram submetidos à hepatectomia parcial de Higgins e Anderson e os do grupo Intervenção à HH. VG e HB foram medidos nos dias D0, D1 e D7. A relação peso do fígado/peso do rato foi calculada em D0 e D7. A regeneração hepática foi analisada qualitativamente e quantitativamente. Resultados: Houve diminuição dos níveis de VG e HB nos ratos do grupo controle a partir de D1, atingindo decréscimo de 18% em D7 (p=0,01 e p=0,008 respectivamente); a HH permitiu a manutenção dos níveis de VG e HB nos ratos do grupo intervenção. A HH não alterou a regeneração hepática. Conclusão: HH resultou em níveis maiores de VG e HB pós-operatórios sem alterar a regeneração hepática. Pode-se considerar estes dados como a prova necessária para a translação à pesquisa clinicocirúrgica.

Gadoxetic Acid-Enhanced Hepatobiliary-Phase Magnetic Resonance Imaging for Pyrrolizidine Alkaloid-Induced Hepatic Sinusoidal Obstruction Syndrome and Association with Liver Function.

Hepatic sinusoidal obstruction syndrome (HSOS) can be caused by pyrrolizidine alkaloids(PAs)-containing herbals. In this study, the aim of our study was to investigate the imaging features of PAs-induced HSOS on gadoxetic acid-enhanced magnetic resonance imaging (MRI), susceptibility-weighted imaging(SWI) and T2* weighted imaging (T2* WI). We analyzed medical records and MR images of 28 PAs-induced HSOS patients enrolled from Feb, 2013, to Apr, 2017. Abnormal liver function was observed in most of the PAs-induced HSOS patients. Heterogeneity of liver parenchyma in hepatobillary phase (HBP) of gadoxetic acid-enhanced MR scan was observed in 100% of the PAs-induced HSOS patients. Distributional patterns of heterogeneous hypointensity were multifocal distribution (mild) in 4 patients (14.29%), multifocal distribution (severe) in 15 cases (53.57%), and diffuse distribution in 9 patients (32.14%). Hypointense in SWI and T2*WI was observed in the patients of PAs-induced HSOS, and the distribution of hypointense in SWI and T2*WI was similar to that of portal-venous phase of MR scan. The severity of heterogeneous hypointensity scored by volume fraction in hepatobillary phase of gadoxetic acid-enhanced MRI was positively correlated with PT and INR, the severity of hypointensity in HBP was a risk factor of death events. In conclusion: Heterogenous hypointensity of liver parenchyma was an imaging sign of hepatobillary phase in gadoxetic acid-enhanced MRI; thus, it will provide evidences for the diagnosis of PA-induced HSOS.

Quantitative Analysis of CT Images in Patients with Pyrrolizidine Alkaloid-Induced Sinusoidal Obstruction Syndrome.

This study evaluated hepatic lesion volumes on contrast-enhanced computed tomography (CT) images in patients with pyrrolizidine alkaloid-induced sinusoidal obstruction syndrome (PA-SOS) and the association of lesion volume with the clinical severity and prognosis of the disease. Twenty-five patients with PA-SOS were included in this study, and all patients were subjected to a complete CT imaging series. The imaging results were quantitatively analyzed by a threshold-based region growing algorithm. The liver volumes and hepatic lesion volumes of the patients were estimated. Based on clinical presentations, PA-SOS was classified into three categories: mild, moderate and severe. The associations of hepatic lesion volumes with liver function test parameters and the clinical severity and prognosis of the disease were analyzed. Based on estimations using the threshold-based region growing algorithm, hepatic lesion volumes in patients with mild PA-SOS were significantly lower than those in patients with moderate and severe PA-SOS (P < 0.05). The ratio of hepatic lesion volume to liver volume (Ratio) varied based on alanine aminotransferase (ALT), aspartate aminotransferase (AST) and serum total bilirubine levels; clinical severity; and disease prognosis, and the differences were statistically significant (P < 0.05). In conclusion, the threshold-based region growing algorithm can be employed to quantitatively analyze enhanced CT images of PA-SOS patients. And the ratio of hepatic lesion volume to liver volume in patients with PA-SOS is associated with a more serious clinical course and a poorer outcome.

Expert consensus on the clinical management of pyrrolizidine alkaloid-induced hepatic sinusoidal obstruction syndrome.

Hepatic sinusoidal obstruction syndrome (HSOS) is a hepatic vascular disease presenting with abdominal distension, pain in the hepatic region, ascites, jaundice, and hepatomegaly. In China, this disease is often associated with the oral intake of plants that contain pyrrolidine alkaloids. The existing guidelines are limited to HSOS associated with hematopoietic stem cell transplantation in Western countries. The Hepatobiliary Diseases Committee of the Chinese Society of Gastroenterology convened an expert consensus conference on the diagnosis and treatment of PA-HSOS to evaluate current research in China and abroad. The "Nanjing criteria" developed by the committee to diagnose PA-HSOS include a confirmed history of PA-containing plant use and (i) abdominal distention and/or pain in the hepatic region, hepatomegaly, and ascites; (ii) elevation of serum total bilirubin or abnormal laboratory liver tests; (iii) evidence on enhanced computed tomography or magnetic resonance imaging; or (iv) pathological evidence that rules out other known causes of liver injury. Supportive symptomatic treatment, anticoagulant therapy, and placement of a transjugular intrahepatic portosystemic shunt for patients who do not respond to medical treatment are effective for the treatment of PA-HSOS. The benefits of glucocorticoids and prostaglandin E1 in PA-HSOS are not clear.

Sinusoidal Obstruction Syndrome (Veno-occlusive Disease) Following Hematopoietic Stem Cell Transplant: Insights and Therapeutic Advances.

Hepatic sinusoidal obstruction syndrome (SOS) is a rare fatal clinical entity seen following hematopoietic stem cell transplant (HSCT). It is more commonly reported to occur following allogeneic HSCT compared to autologous HSCT. Historically, it is known as hepatitis following HSCT. It is thought that endothelial damage to the hepatic venules leading to occlusion of the terminal hepatic venules and hepatic sinusoids is the trigger for the development of SOS. Several risk factors have been associated with this condition. Some of these risk factors are patient related while others are transplant process related. Given the high mortality of this condition, early identification of high-risk patients with severe disease is of utmost importance. The management of SOS varies depending on the severity of the disease. Mild to moderate disease has a good outcome with supportive measures alone, while severe presentation of the disease requires a more aggressive management. Defibrotide is the only Food and Drug Administration-approved therapy and it is reserved for severe cases of SOS. The role of defibrotide as a prophylactic therapy remains under investigation.

Noninvasive assessment of hepatic sinusoidal obstructive syndrome using acoustic radiation force impulse elastography imaging: A proof-of-concept study in rat models.

OBJECTIVES: To determine the feasibility of acoustic radiation force impulse (ARFI) elastography in the evaluation of hepatic sinusoidal obstruction syndrome (SOS) in rat models. METHODS: Rat SOS models of various severities were created by monocrotaline gavage (n = 40) or by intraperitoneal injection of 5-fluorouracil, leucovorin and oxaliplatin (FOLFOX) (n = 16). Liver shear-wave velocity (SWV) was measured using ARFI elastography. Liver samples were analysed for the SOS score, steatosis, lobular inflammation and fibrosis. RESULTS: The liver SWV was significantly elevated in the SOS models (1.29-2.24 m/s) compared with that of the matched control rats (1.01-1.09; p≤.09; veFor seven FOLFOX-treated rats which were longitudinally followed-up, the liver SWV significantly increased at 7 weeks (1.32±0.13 m/s) compared with the baseline (1.08±0.1 m/s, p=.015) and then significantly declined after a 2-week, treatment-free period (1.15±0.13 m/s; p=.048). Multivariate analysis revealed that the SOS score (p<.001) and lobular inflammation (p=.044) were independently correlated with the liver SWV. CONCLUSION: Liver SWV is elevated in SOS in proportion to the degree of sinusoidal injury and lobular inflammation in rat SOS models. ARFI elastography has potential as an examination for diagnosis, severity assessment and follow-up of SOS. KEY POINTS: • Liver SWV using ARFI elastography was significantly elevated in SOS rat. • Sinusoidal injury and lobular inflammation grades had correlation with liver SWV. • ARFI elastography has potential for diagnosis, severity assessment, and follow-up of SOS.

Severe Hepatic Sinusoidal Obstruction Syndrome in a Child Receiving Vincristine, Actinomycin-D, and Cyclophosphamide for Rhabdomyosarcoma: Successful Treatment with Defibrotide.

Hepatic sinusoidal obstruction syndrome (SOS) is a life-threatening syndrome that generally occurs as a complication after hematopoietic stem cell transplantation or, less commonly, after conventional chemotherapy. Regarding SOS in rhabdomyosarcoma patients who received conventional chemotherapy, the doses of chemotherapeutic agents are associated with the development of SOS. Several cases of SOS in rhabdomyosarcoma patients after receiving chemotherapy with escalated doses of cyclophosphamide have been reported. Here, we report on a 9-year-old female with rhabdomyosarcoma who developed severe SOS after receiving chemotherapy consisting of vincristine, actinomycin-D, and a moderate dose of cyclophosphamide. She was treated successfully with defibrotide without sequelae to the liver.

Long-term outcome of endovascular intervention in hepatic venous outflow obstruction following pediatric liver transplantation.

The purpose of our study was to address the long-term outcome of angioplasty and stent placement for hepatic venous outflow obstruction following pediatric liver transplantation. From October 1999 to December 2011, 20 stenotic lesions were confirmed to constitute hepatic venous outflow obstruction in 18 pediatric patients (13 boys, 5 girls) among 152 pediatric patients following liver transplantation and were managed with endovascular intervention. Stent placement was favored over additional angioplasty in patients of preadolescent or adolescent age (>8 years old), after 1 or 2 sessions of balloon angioplasty. The primary patency and assisted primary patency were estimated using the Kaplan-Meier method. A total of 32 procedures (24 balloon angioplasties, 8 stent placements) were conducted. The technical success rate was 90.6% (29/32). Clinical success was achieved in 15 of 18 patients (clinical success rate of 83.3%). Major complications did not occur in our study. Median follow-up was 91.5 months (interquartile range, 54.7-137.3 months) for the 18 patients. The 1-year, 3-year, 5-year, and 10-year primary patencies of the 20 treated lesions were 63.5%, 57.8%, 57.8%, and 57.8%, respectively. The 1-year, 3-year, 5-year, and 10-year assisted-primary patencies of the lesions were 100%, 100%, 100%, and 100%, respectively. Of the 6 patients of preadolescent or adolescent age, 5 patients underwent stent placement procedures, and the stents were patent during the follow-up period of 57.3-162.5 months (median, 72.7 months). In conclusion, endovascular intervention is very effective in hepatic venous outflow obstruction following pediatric liver transplantation. In addition, early stent placement in patients of preadolescent or adolescent age can provide a safe and favorable long-term outcome.

The significance of nonobstructive sinusoidal dilatation of the liver: Impaired portal perfusion or inflammatory reaction syndrome.

UNLABELLED: Sinusoidal dilatation found in the absence of an impaired sinusoidal blood outflow has been so far of unclear significance. Sinusoidal dilatation may actually be a nonspecific feature of impaired portal venous blood inflow, whatever the cause, or a feature of severe systemic inflammatory reaction syndrome, whatever the cause. Sinusoidal dilatation is mainly located in the centrilobular area even in the absence of an outflow block. A predominantly periportal location is specifically found in oral contraceptive users, associated with an inflammatory condition. There is strong evidence for the association of sinusoidal dilatation and oxaliplatin-based chemotherapy but not for estroprogestative steroids or thiopurine derivatives. Exposure to anabolic androgen steroids appears to cause sinusoidal changes different from a mere sinusoidal dilatation. CONCLUSION: There is evidence of activation of the interleukin-6 and vascular endothelial growth factor pathways in sinusoidal dilatation, but the mechanisms linking the activation of these pathways with the microvascular changes must be identified.

Retrograde detection of the intrahepatic portal vein in primary biliary cirrhosis: is sinusoidal blockage the underlying pathophysiology?

OBJECTIVE: The aim of this study was to explore the underlying pathophysiological mechanism for portal hypertension in primary biliary cirrhosis (PBC) using radiological findings. PATIENTS AND METHODS: The study included 10 patients with PBC (Scheuer stage I, one patient; stage II, two patients; and cirrhosis, seven patients) and 29 patients with viral cirrhosis. Both groups underwent Doppler ultrasound and hepatic venous catheterization. The Doppler data, pressure data, and vascular enhancement findings were compared between the groups. RESULTS: Hemodynamics in the portal trunk and hepatic vein upon Doppler sonography did not differ between patients with viral cirrhosis, cirrhotic PBC, and noncirrhotic PBC. The hepatic venous pressure gradient (mean±SD) was 225.5±77.1 mmH2O (range 125-445 mmH2O) in viral cirrhosis, 224.6±39.5 mmH2O (range 170-262 mmH2O) in cirrhotic PBC, and 41.3±7.4 mmH2O (range 33-47 mmH2O) in noncirrhotic PBC, being significantly higher in viral cirrhosis and cirrhotic PBC than noncirrhotic PBC (P=0.0005). The intrahepatic portal vein was detected in a retrograde manner on the hepatic venogram in 29/29 (100%) patients with viral cirrhosis (all with gastroesophageal varices), 7/7 (100%) patients with cirrhotic PBC (5/7 with gastroesophageal varices), and 3/3 (100%) patients with noncirrhotic PBC (none with gastroesophageal varices). The presence of veno-venous communication was found in 15/29 (51.7%) patients with viral cirrhosis, 6/7 (85.7%) patients with cirrhotic PBC, and 3/3 (100%) patients with noncirrhotic PBC. CONCLUSION: The study suggested that sinusoidal blockage is the underlying pathophysiology even in the early-stage PBC, proved by the visible intrahepatic portal vein in three noncirrhotic PBC patients, and veno-venous communication in the liver is responsible for alleviated hepatic venous pressure gradient.

Peritoneal Patch for an Occluded Venous Conduit of a Right Lobe During a Living-Donor Liver Transplant.

Drainage of segments V and VIII venous tributaries usually is mandatory to avoid congestion of the anterior segment of right lobe during a living-donor liver transplant. Extension of the venous tributaries to the vena cava can be done with several vascular materials. Here, we describe using an 8 × 3 cm vascular patch from the peritoneum over the venous conduit (which had become kinked) that drained segments V and VIII veins. Peritoneal reconstruction worked well during the early postoperative period and avoided congestion of the right anterior liver segment. During the late postoperative period, the conduit became occluded as do other grafts used to extend tributaries; however, the collaterals that developed prevented congestion of the anterior liver segment. Using part of the peritoneum as a venous graft during living-donor liver transplant can be a good alternative to the other vascular grafting options. Peritoneal grafting provides temporary drainage of the liver lobe, prevents congestion of the anterior section, and saves time creating venous collaterals.

How I manage sinusoidal obstruction syndrome after haematopoietic cell transplantation.

Sinusoidal obstruction syndrome (SOS), also called veno-occlusive disease of the liver, is one of the most relevant complications of endothelial origin that appears early after haematopoietic cell transplantation (HCT). Despite its relatively low incidence and the fact that most cases of SOS resolve spontaneously, the cases that evolve to multi-organ failure (MOF; severe SOS) have a mortality rate higher than 80% and represent one of the major clinical problems after HCT. For this reason, transplantation teams must have a pre-established policy regarding preventive measures in high-risk patients, strict daily control of weight and fluid balance during HCT, homogeneous diagnostic criteria, appropriate complementary studies for a correct differential diagnosis and measures to prevent and manage hepatorenal syndrome; in addition they must also be ready to start early treatment with defibrotide in patients with a possible severe SOS. Due to the lack of definitive evidence to enable the establishment of general recommendations in the management of SOS, this review analyses all of these aspects based on the author's personal experience.