Hepatic Venous Congestion Research Articles

Doppler Sonography to Diagnose Venous Congestion in a Modified Right Lobe Graft After Living Donor Liver Transplantation

The objective of our study was to assess the value of Doppler sonography for the diagnosis of hepatic venous congestion in a modified right lobe graft during the early postoperative period after living donor liver transplantation. Doppler sonography examinations were prospectively performed in 54 patients within 24 hours after living donor liver transplantation with a modified right lobe graft in which large (> 5 mm) middle hepatic vein (MHV) tributaries were reconstructed. The number, flow direction, and waveform of the MHV tributaries; the echogenicity of the surrounding parenchyma; and the flow direction of the corresponding portal branch were evaluated. Hepatic venous congestion was diagnosed when there was no color flow or a monophasic waveform of an MHV tributary. The sensitivity of Doppler sonography for the detection of MHV tributaries was assessed using donors' preoperative CT scans and surgical records as references. The diagnostic values of Doppler sonography for hepatic venous congestion were assessed using recipients' postoperative CT scans as references. Differences in prevalence of Doppler sonography findings between the group with hepatic venous congestion and the non-hepatic venous congestion group were assessed. Doppler sonography enabled us to identify 90% (155/173) of all and 98% (129/131) of the large MHV tributaries. The sensitivity and specificity of Doppler sonography for hepatic venous congestion were 90% (28/31) and 77% (96/124), respectively, for all and 88% (15/17) and 85% (95/112), respectively, for large MHV tributaries. Parenchymal hyperechogenicity was more commonly seen in the hepatic venous congestion group (65%, 20/31) than in non-hepatic venous congestion group (6%, 7/124) (p < 0.01). All five MHV tributaries with reversed flow were seen in the non-hepatic venous congestion group. All five portal branches with hepatofugal flow were seen in the hepatic venous congestion group. Doppler sonography provides a reliable noninvasive surveillance tool for hepatic venous congestion in a modified right lobe graft during the early postoperative period after living donor liver transplantation.

Can matrix metalloproteinases be targeted in hepatic ischemia/reperfusion injury?

Can matrix metalloproteinases be targeted in hepatic ischemia/reperfusion injury?

Hepatic Venous Congestion After Right-lobe Living-donor Liver Transplantation

To describe and determine the additional value of delayed-phase imaging of hepatic venous congestion after living-donor liver transplantation. Twenty-eight patients who had surgical ligation of the middle hepatic vein (HV) in living-donor liver transplantation underwent 3-phase computed tomography scans. Two radiologists analyzed in consensus the presence and pattern of the hepatic attenuation difference and the opacification of the HV in the congested areas of the liver during each phase of the initial and follow-up computed tomography scanning. The imaging findings were correlated with the serum bilirubin level. Opacification of the HV was observed more frequently in 22 (92%) of 24 hyperattenuating areas on delayed-phase (DP) scans than in 2 (50%) of 4 hypoattenuating areas in the congested areas of the liver. Patients with persistent hypoattenuatation in the congested areas on all phases (14%) showed significantly persistent hyperbilirubinemia after postoperative 4 weeks and showed a higher mortality rate (50%) than did the other patients with hyperattenuation on DP scans. A hypoattenuating area of the liver during DP scans indicates severe hepatic congestion and is correlated with hyperbilirubinemia and a high mortality rate.

2415: Role of Doppler US for the diagnosis of hepatic venous congestion in the anterior segment of the modified right lobe graft after living donor liver transplantation: A prospective study of 40 patients

Objectives: To assess the value of Doppler US for the diagnosis of hepatic venous congestion (HVC) in anterior segment of the modified right-lobe graft (MRLG) after living donor liver transplantation (LDLT).Methods: Doppler US in 40 patients following LDLT with MRLG, in which middle hepatic vein tributaries(MHVT) larger than 5 mm were reconstituted with interposition vein graft, were prospectively evaluated. On color Doppler US, the number of MHVT of anterior segment of MRLG, their flow velocity and direction and reversal of segmental portal vein were evaluated. In addition, parenchymal echogenecity on grayscale US was recorded. HVC was diagnosed when there is dampened flow of MHVT in anterior segment of MRLG. Doppler US results were correlated to CT and angiographic findings.Results: Doppler US identified 100 of 103 MHVT larger than 5 mm (sensitivity 97%). The sensitivity and specificity of Doppler US for diagnosis of HVC was 89% (8/9) and 93% (85/91). Among 10 territories with HVC, increase of parenchymal echogenecity, reversed flow of MHVT and reversal of segmental portal vein was found in 7, 5 and 1, respectively.Conclusions: Doppler US provide excellent noninvasive screening for HVC in anterior segment of MRLG after LDLT. Dampened flow of MHVT larger than 5 mm may indicate HVC. Objectives: To assess the value of Doppler US for the diagnosis of hepatic venous congestion (HVC) in anterior segment of the modified right-lobe graft (MRLG) after living donor liver transplantation (LDLT). Methods: Doppler US in 40 patients following LDLT with MRLG, in which middle hepatic vein tributaries(MHVT) larger than 5 mm were reconstituted with interposition vein graft, were prospectively evaluated. On color Doppler US, the number of MHVT of anterior segment of MRLG, their flow velocity and direction and reversal of segmental portal vein were evaluated. In addition, parenchymal echogenecity on grayscale US was recorded. HVC was diagnosed when there is dampened flow of MHVT in anterior segment of MRLG. Doppler US results were correlated to CT and angiographic findings. Results: Doppler US identified 100 of 103 MHVT larger than 5 mm (sensitivity 97%). The sensitivity and specificity of Doppler US for diagnosis of HVC was 89% (8/9) and 93% (85/91). Among 10 territories with HVC, increase of parenchymal echogenecity, reversed flow of MHVT and reversal of segmental portal vein was found in 7, 5 and 1, respectively. Conclusions: Doppler US provide excellent noninvasive screening for HVC in anterior segment of MRLG after LDLT. Dampened flow of MHVT larger than 5 mm may indicate HVC.

Endovascular stent placement for interposed middle hepatic vein graft occlusion after living-donor liver transplantation using right-lobe graft

Middle hepatic vein (MHV) reconstruction is performed to drain the right paramedian sector to prevent hepatic venous congestion (HVC). The aim of the present study was to evaluate endovascular stent placement in patients with stenosed and/or occluded interposition vein graft (IVG) to segment V hepatic vein (V5) and segment VIII hepatic vein (V8) after living-donor liver transplantation (LDLT). The procedure was performed in 11 recipients; 7 underwent it within 24 hours of LDLT. The following parameters, including technical success, clinical success, complications, patient survival data, and serial computed tomography (CT) findings during follow-up, were documented retrospectively. Technical success was defined as both successful stent placement and resolution of stenosis or occlusion with copious flow of contrast medium through the stent, while clinical success was defined as both improvement of liver function tests (LFTs) and reduction or disappearance of hepatic low-attenuation areas on follow-up CT scans taken within 1 week of stent placement. Technical success was achieved in 10 of 11 patients (91%), and clinical success was achieved in 9 of 11 patients (82%). Acute thrombotic occlusion of the stent-inserted hepatic vein occurred in 1 patient 1 day following stent placement. During the mean follow-up period of 468 days (range, 13-891 days), 9 patients survived and 2 patients died. No death was directly related to stent placement or its related complications. The low-attenuation area in the involved hepatic segment V (S5) and/or VIII (S8) area prior to stent placement disappeared completely on follow-up CT scans performed at 3-12 days (mean, 5.4 days) after stent placement in all 9 patients with clinical success. No attenuation change occurred even in cases with chronic occlusion of the stent-inserted hepatic veins. In conclusion, though IVG to V5 and V8 remains controversial, the treatment of their stenosis or occlusion is safe and effective, even during their immediate postoperative period.

Jaundice as a Presentation of Heart Failure

On rare occasions the first manifestation of heart disease is jaundice, caused by passive congestion of the liver or acute ischaemic hepatitis. We looked for this presentation retrospectively in 661 patients referred over fifty-six months to a 'jaundice hotline' (rapid access) service. The protocol included a full clinical history, examination and abdominal ultrasound. Those with no evidence of biliary obstruction had a non-invasive liver screen for parenchymal liver disease and those with suspected heart disease had an electrocardiogram, chest X-ray and echocardiogram. 8 patients (1.2%), bilirubin 31-79 micromol/L, mean 46 micromol/L, had a primary cardiac cause for their jaundice. All had dyspnoea, an increased cardiothoracic ratio on chest X-ray and an abnormal electrocardiogram. The jugular venous pressure was raised in the 3 in whom it was recorded. In 6 patients the jaundice was attributed to hepatic congestion and in 2 to ischaemic hepatitis. All patients had severe cardiac dysfunction. Jaundice due to heart disease tends to be mild, and a key feature is breathlessness. The most common mechanism is hepatic venous congestion; ischaemic hepatitis is suggested by a high aminotransferase.

Jaundice as a presentation of heart failure

On rare occasions the first manifestation of heart disease is jaundice, caused by passive congestion of the liver or acute ischaemic hepatitis. We looked for this presentation retrospectively in 661 patients referred over fifty-six months to a 'jaundice hotline' (rapid access) service. The protocol included a full clinical history, examination and abdominal ultrasound. Those with no evidence of biliary obstruction had a non-invasive liver screen for parenchymal liver disease and those with suspected heart disease had an electrocardiogram, chest X-ray and echocardiogram. 8 patients (1.2%), bilirubin 31-79 micromol/L, mean 46 micromol/L, had a primary cardiac cause for their jaundice. All had dyspnoea, an increased cardiothoracic ratio on chest X-ray and an abnormal electrocardiogram. The jugular venous pressure was raised in the 3 in whom it was recorded. In 6 patients the jaundice was attributed to hepatic congestion and in 2 to ischaemic hepatitis. All patients had severe cardiac dysfunction. Jaundice due to heart disease tends to be mild, and a key feature is breathlessness. The most common mechanism is hepatic venous congestion; ischaemic hepatitis is suggested by a high aminotransferase.

Hepatic vein anatomy of the medial segment for living donor liver transplantation using extended right lobe graft

Hepatic vein anatomy (V4) of the medial segment (S4) has been a matter of concern since introduction of extended right lobe (ERL) graft. To assess risk of hepatic venous congestion (HVC) in ERL donors, we tried to newly classify V4 anatomy. We analyzed V4 anatomy of 328 living donor livers by using 3-dimensional reconstruction (3-DR) and volumetry of computed tomography (CT). Variations of V4 were divided into type A (middle hepatic vein [MHV] dominant: n = 142, 43.3%), type B (MHV-dominant, but enabling preservation of dorsal V4 branch [V4b]: n = 40, 12.2%), type C (mixed: n = 92, 28%), and type D (left hepatic vein dominant: n = 54, 16.5%). We analyzed the amount of HVC at S4 in 143 donor livers of right lobe (RL) and ERL grafts. Occlusion of MHV trunk induced HVC equivalent to 85.2%, 85.4%, 55.2%, and 35.4% of S4 volume and 34%, 33.9%, 20.3%, and 14.2% of left liver volume in livers of types A, B, C, and D, respectively. Tailored V4b preservation reduced HVC significantly in type B livers. Considering that functional capability may be decreased in HVC portion, functional hepatic resection rate (FHRR) of ERL graft procurement ranged as follows: 62.3%-75% in type A; 62.2%-75% and 62.2%-68.7% in type B with and without V4b preservation, respectively; 63.2%-70.7% in type C; and 61.8%-67.2% in type D. These results support the theory that these categories of V4 types are closely correlated with potential amount of HVC at S4, reflect the possibility of V4b preservation, and are compatible with CT findings. We believe that this V4 classification is applicable to assess donor V4 anatomy in practice.

Composite clustered reconstruction of multiple middle hepatic vein branches in right lobe graft

Composite clustered reconstruction of multiple middle hepatic vein branches in right lobe graft

Intraoperative assessment of hepatic venous congestion with direct clamping of the hepatic vein trunk for living donor liver transplantation

We devised a hepatic vein clamping method to assess the amount of hepatic venous congestion (HVC) before liver transection. From February 2003 to May 2003, this method was applied to 5 of 58 living donor livers especially to assess donor safety. The left portal vein and proper hepatic artery as well as the middle hepatic vein (MHV)–left hepatic vein (LHV) trunk were clamped simultaneously to assess the HVC in the remnant right lobe before performing extended left lobectomy. As three donors demonstrated the extent of the HVC equivalent to about 40% of the right lobe volume (RLV), their operations proceeded according to the preoperative plan. The territory of HVC after liver transection was the same as that observed with direct clamping of the hepatic vein. However, one donor showed massive HVC more than 50% of RLV and the operative plan was adjusted to harvest only the left lobe without the MHV trunk for donor safety. To assess the HVC in the remnant left lobe, the isolated LHV trunk was occluded after clamping the donor's proper hepatic artery. The whole left lobe except for a small area at the anterior portion of the medial segment became discolored on LHV clamping: the opposite demarcation appeared on MHV clamping. The amount of HVC was so small that we harvested the right lobe with the MHV trunk. All donors and recipients recovered uneventfully. We believe that this direct clamping method makes the assessment of HVC feasible before parenchymal transection of a donor liver.

Hepatic venous congestion after living donor liver transplantation with right lobe graft: two-phase CT findings.

To describe and determine clinical importance of two-phase computed tomographic (CT) findings of hepatic venous congestion after living donor liver transplantation (LDLT) with right lobe graft. Forty-eight patients underwent two-phase (hepatic arterial phase and portal venous phase [PVP]) CT at 1, 2, and 4 weeks after LDLT. Images were evaluated for hepatic attenuation difference in areas of hepatic venous congestion, opacification of hepatic and peripheral portal veins in those areas, and changes in findings at follow-up CT. CT findings were correlated with serum bilirubin level. Fisher exact test and mixed model were applied. Histopathologic specimens were obtained in six patients. Thirty patients (62%) had attenuation difference in segments V and VIII of right lobe transplant at initial CT scanning. Opacification of hepatic or peripheral portal veins was seen in 17 (63%) and 27 (100%) hyperattenuating areas of congestion during PVP and in none and three (19%) of 16 hypoattenuating areas, respectively. At 4-week follow-up CT, attenuation difference decreased in volume in 11 of 16 patients with hypoattenuation during PVP. All 14 patients with hyperattenuation showed no change in volume, but attenuation difference had decreased or disappeared. Histopathologic specimens showed evidence of hepatic venous congestion in all six patients. Hypoattenuation was seen at PVP CT in all three patients with severe hepatic venous congestion at histopathologic examination. Serum bilirubin level was significantly different between patients with hypoattenuation and those with hyperattenuation during PVP (P =.035) and between patients with hypoattenuation and those without attenuation difference (P =.009). Areas possibly related to hepatic venous congestion after LDLT have variable attenuation at CT; decreased enhancement during PVP correlates with increased postoperative serum bilirubin level, which indicates severity of hepatic venous congestion.

Quilt venoplasty using recipient saphenous vein graft for reconstruction of multiple short hepatic veins in right liver grafts

Major short hepatic veins (SHV) are indicated for vascular reconstruction to prevent excessive hepatic venous congestion of right liver grafts. As separate anastomoses of multiple small SHVs are vulnerable to stenosis or regeneration-related torsion, a conjoined large opening of SHVs may be better than multiple separate anastomoses. We devised an innovative method to reconstruct SHVs through a patchwork quilt using autologous greater saphenous vein (GSV). We applied this method to 3 different configurations of multiple SHVs. For double SHVs in alignment, 2 GSV fragments were stitched longitudinally to wrap 2 SHVs, forming the cuff shape of an ovoid bowl. For double SHVs not in alignment, a central patch of GSV was placed between 2 SHVs to offset the alignment gap, and the outer fence of a long GSV fragment was anastomosed to make a common cuff. For complex anatomy of quadruple SHVs, the central patch was designed to contact with 4 SHVs altogether and the outer fence was similarly created. Although this method was applied to only 4 right liver grafts, there was no disturbance of SHV drainage during 4 months of follow-up. In conclusion, we think that this quilt venoplasty technique using autologous GSV may be applicable for reconstruction of multiple or variant SHVs.

Total Hepatic Vascular Occlusion For Difficult Right Adrenalectomy

A new approach to resect a functioning malignant pheochromocytoma originating from the right adrenal gland and large enough to encircle the retrohepatic inferior vena cava is reported. The adrenal vein in this situation is difficult to expose and ligate in the initial phase of the dissection and in order to occlude venous outflow from the tumor and prevent a catecholamine surge while handling the tumor. The inferior vena cava (IVC) was controlled above and below the liver. This report describes the value of Total Hepatic Vascular Exclusion ( THVE) in this situation. The IVC is controlled by encircling it above the liver and also just above the junction of the renal vein where the approach is unrestricted by the adrenal tumor. Pringle's maneuver of occluding the hepatic vascular inflow is also used to prevent acute hepatic venous congestion. Following this maneuver in our patient, the adrenal tumor was separated from the retrohepatic IVC with minimal bleeding and no recurrence of precipitous rise in blood pressure that resulted from handling the tumor prior to control of the IVC.

L’hépatite ischémique

Ischemic hepatitis is defined as an acute reversible elevation in either the serum alanine or aspartate aminotransferase level of at least 20 times the upper normal limit, excluding known causes of acute hepatitis or hepatocellular injury (viral or toxic). Histopathologic examination reveals a centrolobular liver cell necrosis. The pathophysiology of ischemic hepatitis is poorly understood. At present, the pathophysiologic hypotheses most often proposed are an ischemic/reperfusion injury of the liver and a selective hypersensitivity of the mesenteric vasculature to the renin–angiotensin axis. In ischemic hepatitis an hepatic venous congestion and a hypoxia hepatitis should be present. An underlying cardiac disease is the factor that often leads to hepatic venous congestion. The hepatic hypoxia is the result of the decrease in systemic blood pressure leading to a reduction in hepatic blood pressure or the result of a severe arterial hypoxemia. The causes of a low cardiac output are more often cardiogenic, but hypovolemia or toxic causes are possible. More rarely, a hypoxemia, without shock, is responsible for ischemic hepatitis. The incidence of ischemic hepatitis in patients admitted to intensive care unit is unknown. The mortality rate, six months after the ischemic hepatitis is 50%. The prognosis is primarily related to cardiac function.

Viral cirrhosis with chronic right heart failure and cardiac liver sclerosis: a hypothesis on the differentiation between the two diseases through pulsed Doppler sonography examination

Chronic right heart failure determines cardiac liver sclerosis as a consequence of the hepatic venous congestion that is easily detectable with pulsed Doppler sonography measuring hepatic venous pulsatility. These Doppler parameters profoundly change on the basis of the causative agent of the liver sclerosis. In fact, on pulsed Doppler examination, we detected a flat waveform in hepatic veins of subjects with viral liver cirrhosis whereas we only observed biphasic waveforms in subjects with cardiac liver sclerosis. On the contrary, a pulsed Doppler sonography pattern in subjects with viral cirrhosis and associated chronic right heart failure is unknown. We suppose that splanchnic pulsed Doppler sonography has an important role both in differentiating cardiac liver sclerosis from viral cirrhosis with chronic right heart failure and in the follow-up of the seriousness of the right ventricular failure.

Epidemic dropsy: observations on pathophysiology and clinical features during the Delhi epidemic of 1998.

Epidemic dropsy results from the consumption of edible oils adulterated with Argemone mexicana oil by unscrupulous traders. Twenty consecutive 'in-door' patients of dropsy were intensively studied during the recent Delhi epidemic. Samples of edible oil used by them, their urine and their serum samples tested positive for sanguinarine on thin layer chromatography. The illness starts as a gastro-enteric illness followed by oliguria and pedal oedema. The following are often observed: cutaneous erythema with blanching and tenderness on pressure; violacious pigmentation of the skin; shortness of breath with orthopnoea; right-sided heart failure with normal left ventricle (LV) functions; as well as severe anaemia and hypoalbuminaemia. Renal function tests showed: bland urinary sediments; decreased glomerular filtration rate (GFR); mild to moderate azotaemia; acute tubular necrosis; patchy pneumonitis; moderate hypoxia with respiratory alkalosis; and restrictive ventilatory defects on blood gas analysis; and spirometry suggestive of interstitial pulmonary oedema of non-cardiogenic origin. 99mTc colloid sulphur liver scans showed colloid shift. There was marked dilatation and proliferation of dermal capillaries in the absence of significant inflammation in the biopsy specimens. Toxic alkaloids of Argemone mexicana oil induce widespread capillary dilatation and permeability causing leakage of protein rich plasma into the interstitial tissues of various organs. A hypovolaemic state is thus induced producing renal hypoperfusion which may progress to acute tubular necrosis. Interstitial fluid in alveoli causes restrictive ventilatory dysfunction with hypertension and right-sided failure with well-preserved LV function. The hepatic venous congestion induces Kupffer's cell dysfunction, which results in colloid shift on a radionuclide liver scan.

Ischemic hepatitis: clinical presentation and pathogenesis

BACKGROUND: The pathophysiology of ischemic hepatitis, otherwise known as “shock liver,” is poorly understood, although it is believed to be the result of a reduction in systemic blood flow as typically occurs in shock. The aim of this study was to investigate the importance of this phenomenon as well as other clinical features in patients with ischemic hepatitis. METHODS: We identified a cohort of 31 patients (case group) who met the most commonly accepted definition of ischemic hepatitis (an acute reversible elevation in either the serum alanine or aspartate aminotransferase level of at least 20 times the upper limit of normal, excluding known causes of acute hepatitis or hepatocellular injury, in an appropriate clinical setting). We also evaluated the clinical features and serum aminotransferase levels in a cohort (the control group) of 31 previously healthy patients who sustained major nonhepatic trauma at San Francisco General Hospital, a major trauma center. Both groups of patients had documented systolic blood pressures <75 mm Hg for at least 15 minutes. Clinical and hemodynamic (invasive and noninvasive) data were recorded. RESULTS: Despite the marked reduction in blood pressure, no patient in the control group developed ischemic hepatitis. The mean (± SD) peak serum aspartate aminotransferase level in the control group was only 78 ± 72 IU, in contrast with a mean peak of 2,088 ± 2,165 IU in the case group. All 31 patients with ischemic hepatitis had evidence of underlying organic heart disease, 29 (94%) of whom had right-sided heart failure. CONCLUSIONS: Systemic hypotension or shock alone did not lead to ischemic hepatitis in any patient. The vast majority of patients with ischemic hepatitis had severe underlying cardiac disease that had often led to passive congestion of the liver. These data lead us to propose that right-sided heart failure, with resultant hepatic venous congestion, may predispose the liver to hepatic injury induced by a hypotensive event.

Hypoxic hepatitis in patients with cardiac failure: incidence in a coronary care unit and measurement of hepatic blood flow

The incidence of hypoxic hepatitis was prospectively studied for 1 year in a group of high-risk patients suffering from low cardiac output in a coronary care unit. Hypoxic hepatitis, defined as an increase in serum aminotransferase activity of at least 20 times the upper limit of normal without any other cause for hepatic necrosis, was observed in 20 patients. This represents 2.6% of the 766 patients admitted to the unit during this period and 21.9% of the 91 patients suffering from low cardiac output. Clinical, biological and hemodynamic data were compared between 20 patients with low cardiac output and hypoxic hepatitis, and 48 patients with low cardiac output but without hypoxic hepatitis who survived more than 24 h. In these two groups of patients, hepatic blood flow was measured by galactose clearance at low concentration. Patients with hypoxic hepatitis exhibited a higher central venous pressure (90% versus 38%-p < 0.001) as well as a lower hepatic blood flow (867 +/- 377 ml/min versus 1429 +/- 644 ml/min-p = 0.001). In conclusion, although it is considered a rare hepatic disorder, hypoxic hepatitis is frequent in patients with low cardiac output admitted to the coronary care unit, and is associated with a decrease in hepatic blood flow and passive hepatic venous congestion.

HEMODYNAMIC AND BIOCHEMICAL CHANGES DURING NORMOTHERMIC AND HYPOTHERMIC SANGUINOUS PERFUSION OF THE PORCINE HEPATIC GRAFT

Using an ex vivo liver sanguinous perfusion system, hemodynamic and biochemical changes of the porcine livers were studied, which were preserved cold (4 degrees C) for 24 hr in University of Wisconsin solution and reperfused with normothermic (37 degrees C) (n = 8) or hypothermic (32 degrees C) (n = 8) blood for 3 hr. Six more livers were reperfused with normothermic blood (37 degrees C) immediately after procurement as controls. The total hepatic blood flow was adjusted to 1 ml/min/g liver weight, in which hepatic artery and portal vein flows were administered at a 1:2 ratio. In livers stored cold for 24 hr in UW solution and perfused normothermically, a statistically higher hepatic artery resistance was exhibited at 30 and 60 min after reperfusion (P less than 0.05), and there was lower bile output (P less than 0.05) at 90 and 120 min as compared to the controls. In livers stored cold for 24 hr in UW solution and perfused hypothermically, as compared to ones perfused normothermically, statistically higher hepatic-artery and portal-vein resistances (P less than 0.05) were observed throughout the perfusion period and 60 min after reperfusion, respectively. In addition, bile output and oxygen consumption of these livers were statistically lower than those of ones perfused normothermically (P less than 0.05). In contrast, chemistries of the perfusate of livers perfused hypothermically were comparable to ones perfused normothermically. Histologic examination of the liver perfused hypothermically demonstrated hepatic arterial and/or portal venous congestion and mild-to-moderate hemorrhage in the portal triads. This study suggests that livers preserved for a prolonged period of time demonstrate a high hepatic arterial resistance shortly after revascularization, and that recipient hypothermia after revascularization may be a risk factor for the development of hepatic arterial thrombosis following liver transplantation.

Hepatocellular carcinoma with cardiac cirrhosis

Hepatocellular carcinoma is a recognized complication of hepatic cirrhosis, most commonly associated with alcohol excess, haemochromatosis and chronic hepatitis B infection. Long-standing hepatic venous congestion may cause cirrhosis. A search of the literature has not revealed a case of hepatocellular carcinoma complicating cardiac cirrhosis. A case is described and the association is discussed.