Left Lobe Atrophy Research Articles

S2887 Stones, Strictures and Atrophy: Treating Sequelae of Infectious Hepatolithiasis

Introduction: Primary intrahepatic cholelithiasis has been well-associated with brown or pigmented stones and recurrent pyogenic cholangitis. However, other important potential chronic complications exist beyond cholangitis of which gastroenterologists should be aware. Case Description/Methods: We present a case of a 57 year-old man with history of diabetes who returned from a 13-month stay in Japan to be admitted to an outside facility with DKA and cholangitis. He was found to have a liver abscess and left hepatic duct stricture treated with sphincterotomy, biliary stenting via ERCP, abscess drainage, and cholecystectomy. He followed up externally for stent removal with normalization of liver chemistries however CT imaging 1 year later showed persistent left hepatic duct stricture with intrahepatic segmental dilation. He experienced no early satiety, weight loss, or jaundice. He was referred to our service for further evaluation of chronic indeterminate biliary stricture. Endoscopic ultrasound demonstrated extensive small and large left-sided hepatolithiasis (A). Cholangiography during ERCP demonstrated complete filling defect of the left intrahepatic biliary ductal system preventing selective guidewire passage. Cholangioscopy was performed with successful electrohydraulic lithotripsy (EHL) of stone burden in the left main hepatic system for selective wire passage and stenting of the left intrahepatic system with a plastic stent. Biliary epithelium appeared smooth and benign. The patient was given antibiotics with no complications. ERCP was repeated in 6 weeks with further cholangioscopy with EHL fragmentation and removal of stones in left intrahepatic ductal branches, however ductal disease remained throughout smaller distal branches of the left lobe on cholangiogram. The main duct was protected with a fully-covered metal stent and antibiotics were given. Follow-up MRI/MRCP demonstrated atrophic left liver lobe (C) in addition to our findings. Left partial hepatectomy was thus performed by Surgery for definitive therapy of the diseased lobe and the patient did well post-operatively with benign pathology. (Figure) Discussion: Even in the absence of a typical recurrent cholangitis clinical syndrome, treatment of other chronic sequelae of severe primary hepatolithiasis is important in the prevention of progression to cirrhosis. Multiple interventional endoscopic methods are available and should be utilized to establish the diagnosis and optimize therapy; which may include surgery in severe cases.Figure 1.: (A) Linear EUS view of left lobe intrahepatic cholelithiasis; (B) cholangioscopic view of intrahepatic cholelithiasis fragmented by electrohydraulic lithotripsy; (C) MRI with left lobe atrophy and hepatolithiasis.

Increased Prevalence of Left Lobe Atrophy in Long-standing Extrahepatic Portal Vein Obstruction.

The aim of this study was to describe long-term changes in standard blood tests and ultrasound (US) findings in pediatric patients with Extrahepatic Portal Vein Obstruction (EHPVO) who have not undergone Meso-Rex Bypass (MRB) surgery. US, laboratory, and endoscopic data of 77 patients were analyzed and compared at 2 different points in time: at initial workup and at most recent follow-up. Differences were assessed using McNemar and Wilcoxon tests, while correlations were evaluated using generalized estimating equations. Upper gastrointestinal bleeding was the most frequent initial manifestation of EHPVO, in 45.4% of subjects. The mean age at diagnosis was 4.3 years. Seventy-four percentage had a previous history of umbilical catheterization and/or neonatal sepsis. Over time, there was a significant increase in the prevalence of leukopenia, thrombocytopenia, and, interestingly, of left lobe atrophy (LLA), even though the number of esophageal varices and the need for endoscopic interventions reduced. A significant correlation was found between history of umbilical catheterization and LLA, splenomegaly and LLA, and gallbladder wall thickening and LLA. Overall, the number of patients with cholelithiasis at initial workup was low (and therefore, not analyzed with inferential statistics); however, we observed a relative increase over time. In this cohort of patients with EHPVO followed over more than 8 years without treatment with MRB, we report the novel finding of a significant increase in the prevalence of LLA over time. LLA correlated with past medical history of umbilical catheterization, and findings of splenomegaly and gallbladder wall thickening. We propose that that LLA should be further explored as a marker of portal hypertension, particularly in the context of a history of umbilical catheterization.

Budd-Chiari syndrome computed tomographic imaging: Elucidating the devil in the details.

Hepatic venous outflow obstruction, due to hepatic venous thrombosis is the hallmark of Budd-Chiari Syndrome (BCS), a relatively uncommon disorder. The aim of this study was to explore imaging details and causes, and define invasive and non-invasive interventions for achieving successful portosystemic shunting (PSS). The variations in imaging topology and associated risk factors in BCS cases, diagnosed during the past 20 months, were studied. Of the 53 cases (32 males, 21 females; mean age: 34.4±13.5 years), 5 (9%) were Hepatitis-B virus (HBV) positive, 12 (23%) were HCV positive and 6 (11%) were co-infected, rest were negative. Imaging features included mottled cirrhotic hepatic parenchyma, thrombosed hepatic and portal-vein with or without IVC thrombosis, left lobe atrophy, caudate hypertrophy, splenomegaly, portosystemic varices and ascites. Three cases had subacute onset; two had acute while the rest were chronic BCS. The aetiology was: protein C, S and anti-thrombin deficiency in 24 (45%), JAK2 mutation in 3 (6%), lupus antibody with increased homocysteine levels in 5 (9%) and cryptogenic in 21 (40%) cases. Twelve cases were planned for liver transplantation, 20 were prepared to undergo TIPS, and the rest were optimised medically.

2458 Autoimmune Hepatitis-Induced Hepatic Lobar Atrophy

INTRODUCTION: Lobar atrophy of the liver can be a morphologic manifestation of benign and malignant liver or biliary duct disease. Rarely has it been associated with autoimmune hepatitis (AIH). CASE DESCRIPTION/METHODS: A 26 year old woman presented with a 2 month history of severe RUQ abdominal pain associated with anorexia, 10 lb weight loss, pruritus, and scleral icterus. Physical exam was notable for cachexia, jaundice, abdominal distension and tender hepatomegaly. Initial labs revealed: hemoglobin 10.1 g/dl, MCV 80, platelets 107, AST 968 U/L, ALT 487 U/L, ALP 369 U/L, total bilirubin 12.0 mg/dl, DB 9.0 mg/dl, total protein 6.4 g/dL, albumin 2.1 g/dl and INR 1.65. Serological data were as follows: AMA <1:20; ANA 1:160; and anti-smooth muscle antibody 1:20. Viral markers for hepatitis A, B and C were negative. CT abdomen revealed a large area of infiltrative hypoattenuation of the right hepatic lobe. Abdominal MRI noted a diffuse edema within both hepatic lobes. N-acetylcysteine was started for impending acute liver failure and prednisone for AIH. She improved clinically. A liver biopsy done showed diffuse liver cell necrosis with lobular collapse, acute and chronic inflammation in the portal tracts, and in the interface. She was deemed stable for discharge to return to clinic but she was lost to follow up. A year later, she returned with worsening RUQ pain, further weight loss of 30 pounds. Her LFTs were within normal limits but a CT abdomen showed portal hypertension, hypoattenuation of the right lobe, and cirrhosis with left hepatic lobe atrophy. Azathioprine was started in addition to Prednisone. DISCUSSION: This patient's left lobar atrophy was not deemed to be congenital due to the presence of the left hepatic lobe on prior imaging studies. Hepatic neoplasms which can as well cause lobar atrophy was also ruled out with imaging. This is one of the few reported cases of hepatic lobar atrophy attributed to AIH which is a chronic disease characterized by increased autoantibodies in circulation and inflammation around the portal vein. This inflammation can result in lobar atrophy via occlusion of the portal vein resulting in impairment of liver blood flow as well as a reduction in the supply of hepatotrophic substances, particularly insulin. This may cause ischemia in certain areas of the liver and subsequently, atrophy secondary to necrosis and apoptosis. This patient also had significant cholestasis on initial presentation which could also contribute to cellular apoptosis through the Fas ligand pathway.

Changes in liver morphology in patients with extrahepatic portal venous obstruction: a retrospective magnetic resonance imaging study.

To investigate the liver parenchymal changes on MRI in patients with extrahepatic portal venous obstruction (EHPVO). This was a retrospective evaluation of the MRI studies in patients with EHPVO between January 2016 and April 2018. The diagnosis of EHPVO in each case had been established on the basis of clinical and Doppler parameters. Following findings were recorded on MRI: liver size; outline; overall volume redistribution; volume redistribution of caudate, right and left lobes; signal heterogeneity, intrahepatic biliary radicle dilatation, focal liver lesions, gallstones and ascites. A total of 164 MRI studies were evaluated. Median age was 27 years (range, 6-70). There were 90 (54.9%) males and 74 (45.1%) females. The median liver size was 14 cm (range 5-17). The median spleen size was 15.9 cm (range, 6-28). A spleen size ≥12 cm was seen in 136 (82.9%) patients. The liver outline was nodular in 32 (19.5%) patients. Volume redistribution was seen in 63 (38.4%) patients. Caudate lobe hypertrophy was seen in 49 (29.9%) patients. Right lobe atrophy and hypertrophy was seen in 4 (2.4%) and 1 (0.6%) patients respectively. Left lobe atrophy and hypertrophy was seen in 15 (9.1%) and 10 (6.1%) patients respectively. 30 MRI (18.3%) showed heterogeneous signal intensity. Focal lesions were seen in 22 (13.4%) patients. Intrahepatic biliary radicle dilatation, gallstones and ascites were seen in 120 (73.2%), 54 (32.9%) and 26 (15.9%) patients respectively. Liver morphological changes are common in EHPVO. The morphological changes in liver in patients with EHPVO have not been described previously. This information will prevent misdiagnosis of this condition as cirrhosis.

Abstract P6-02-18: Hepatic complications of breast cancer

Abstract Background Breast cancer is the most common malignancy and the leading cause of cancer death in women in the United States. Nearly 30% of women with metastatic breast cancer will have liver metastases, with a median survival from time of 4.23 months from time of metastatic diagnosis. Hepatic involvement of breast cancer is common and can result from metastatic tumor burden or treatment with chemotherapy or radiation. Being able to recognize and diagnose hepatic involvement of breast cancer is of utmost importance, as it has a dramatic effect on patient prognosis and management. Learning Objectives To familiarize multidisciplinary clinical team members with the radiographic presentations of hepatic complications of breast cancer in a variety of imaging modalities including computed tomography, dual-energy computed tomography, ultrasound, and MR. This will facilitate accurate and prompt diagnosis and treatment of hepatic involvement of breast cancer. Abstract Our educational pictorial essay demonstrates the typical appearance of hepatic metastases on multiple imaging modalities, as well as atypical presentations such as hyperdense, hypervascular, or hypoechoic lesions and pseudoprogression. We will show examples of hepatic metastases presenting as pseudocirrhosis, left lobar atrophy, capsular retraction, as well as sequelae of pseudocirrhosis such as malignant ascites, varices, portal vein thrombosis, and biliary obstruction. We will discuss the radiographic appearance of the liver after being treated with locoregional liver-directed techniques such as surgical resection, ablation, and chemoembolization. Importantly, we will illustrate examples of hepatic complications from systemic therapy including steatohepatitis from tamoxifen, as well as hepatic fibrosis from gemcitabine. Conclusion Clinicians must have a thorough understanding of the hepatic complications of cancer to ensure excellent diagnostic accuracy and management.

Liver resection for perihilar cholangiocarcinoma – why left is sometimes right

IntroductionLeft-sided liver resection (LLR) for perihilar cholangiocarcinoma (PHC) may require right hepatic artery (RHA) resection and reconstruction because of its intimate relationship with the biliary confluence. Consequently right-sided resections (RLR) are preferred for Bismuth-Corlette IIIb tumours, and resections avoided in Bismuth-Corlette IV tumours with left lobar atrophy when the RHA is involved by tumour. MethodsA retrospective analysis of patients with PHC who presented between December 2009 and June 2015. ResultsThirty-six patients underwent resection for PHC (23 LLR, 13 RLR). The number of Bismuth-Corlette IV patients undergoing LLR was significantly greater than those undergoing RLR (8/23 vs 0/13, p = 0.032). The need for arterial reconstruction (AR) was significantly greater during LLR than RLR (10/23 vs 0/13, p = 0.006). Postoperative liver dysfunction was greater after RLR (5/13 vs 0/23, p = 0.003), and hospital stay was shorter after LLR (10 vs 15 days, p = 0.013). ConclusionsSafe AR increases the ability to perform potentially curative LLR for PHC. This improves the resectability rate for PHC, particularly for Bismuth-Corlette Type IV tumours. The larger liver remnant after LLR results in less postoperative liver dysfunction and shorter hospital stay without increased operating time, blood loss or morbidity.

Perdas econômicas pela condenação em matadouro frigorífico de fígados de bovino por fibrose causada por ingestão de Braquiaria spp

Resumo: A ingestão crônica de braquiária induz lesões hepáticas em bovinos caracterizadas por fibrose, atrofia do lobo esquerdo, hipertrofia compensatória do lobo direito e proliferação de ductos biliares. Tipicamente, essas lesões são associadas com agregados de macrófagos espumosos no parênquima hepático. Nesse trabalho foram estudados fígados com essas lesões num abatedouro frigorífico do Brasil Central e as perdas econômicas causadas pela condenação de tais fígados afetados foram estimadas. Durante o período estudado, 488.476 bovinos foram abatidos nesse matadouro frigorífico, dos quais 5.295 fígados foram condenados devido à fibrose, e 192 com lesão hepática foram estudados. Cálculos econômicos permitiram inferir que essas condenações representaram uma perda de R$ 108.817,60. Conclui-se que a condenação de fígados em razão de fibrose induzida pela ingestão de braquiária causa uma perda significativa para a indústria de carne e produtos bovinos devido à condenação de 23,6 toneladas de fígado em um ano em apenas um frigorífico, com perdas estimadas acima de R$ 100.000,00.

Some interesting morphological features of liver lobes in Mumbai population

Introduction: Liver is the largest gland in the body mainly situated in the right upper quadrant of the abdomen. Abnormalities of liver are rare. Common abnormalities are irregularities in form, occurrence of one or more accessory lobes, fissures or abnormal ligaments. Rare abnormalities include atrophy, or complete absence of one of the lobes. Although the segmental anatomy of the liver has been extensively researched, very few studies have dealt with the surface variations of the liver. Accessory lobe may be confused with tumour. Accessory fissure may mimic internal trauma at the time of the post-mortem study. Aim: Present study was carried to find out the morphological variations of liver lobes occurring in Mumbai population. Methods & Materials: The materials used for present study comprised of formalin fixed 50 adult livers. Results & conclusion: In the present study we found accessory liver lobes in 3 cadavers i.e. 6 %, atrophy of left lobe in 15 cadavers i.e. 30 %, accessory fissures in 21 cases i.e.42%.There is also abnormal connection between left lobe and quadrate lobe in 14% cases. The findings of study may be helpful to radiologist and surgeons respectively, to avoid possible errors in interpretations and subsequent misdiagnosis, and for planning appropriate surgical approaches.

Childhood outcomes of neonates diagnosed with portal vein thrombosis

The study aims to determine childhood outcomes of neonates diagnosed with portal vein thrombosis (PVT). A retrospective chart review of neonates diagnosed with PVT who had documented follow up (physical examination, laboratory tests or ultrasonographic examination) at the age of 2 years or beyond was conducted. Data were available for 70 children (71% of eligible neonates) at a median age of 5 years (range 2-8 years). Physical examination was unremarkable in all who were examined (n= 68). Twenty-five children had liver functions assessed and only mild abnormalities were detected in nine children. Six of 25 patients tested for thrombophilia showed abnormalities. Thirty-seven children had ultrasonographic follow up. Left lobar atrophy (LLA) was noted in 20 children (16 had isolated LLA, two had LLA and splenomegaly, and two had LLA and portal hypertension). Five children who had normal ultrasound examinations at discharge had splenomegaly (two with additional finding of LLA) at follow up. Two children with portal hypertension diagnosed during neonatal period needed porta-caval shunting. Our results show that among patients, who had PVT as neonates, 28% still had asymptomatic LLA in childhood, 7% had slowly progressive splenomegaly and 3% required shunting because of progression of portal hypertension. Ultrasonographic follow up was the most sensitive method in detecting progression associated with neonatal PVT. Until more data are available, periodic long-term ultrasonographic follow up should be considered for neonates diagnosed with PVT.

A 56-Year-Old Man with Sudden Onset of Portosystemic Encephalopathy Years after Severe Electrocution Trauma

A 56-year-old white male painter, with a history of major electrocution and deep thermal injury, developed mental status changes initially ascribed to an acute neurological event. Unexpectedly, magnetic resonance imaging (MRI) of the head showed areas of high signal intensity in the basal ganglia, which can be observed in advanced liver disease. An electroencephalogram (EEG) suggested metabolic encephalopathy and coexistent elevation of ammonia, indicative of significant liver disease. The patient had had a long history of right upper quadrant pain and fluctuation in liver tests following the electrocution trauma. For these symptoms, he underwent surgery 7 years prior to his current presentation of portosystemic encephalopathy, and was found to have a gangrenous acalculous cholecystitis. Intraoperative cholangiogram suggested possible strictures within the right hepatic ducts. Multiple liver biopsies, however, showed only steatosis. Current evaluation including liver biopsy, MRI, magnetic resonance angiography (MRA), and magnetic resonance cholangiopancreatography (MRCP), revealed progression to biliary cirrhosis with large bile duct obstruction, and hepatic artery thrombosis/occlusion with evidence of left lobe atrophy and right lobe compensatory hypertrophy. The pathobiology of ischemic bile duct injury is discussed herein. The case is an example of serious late sequelae of an occupational injury.