DOCSLIB.ORG

Spontaneous Bacterial Peritonitis and Chylothorax Related to Brucella Infection in a Cirrhotic Patient

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Spontaneous Bacterial Peritonitis and Chylothorax Related to Brucella Infection in a Cirrhotic Patient SPONTANEOUS BACTERIAL PERITONITIS AND CHYLOTHORAX RELATED TO BRUCELLA INFECTION IN A CIRRHOTIC PATIENT Mustafa Güçlü1, Tolga Yakar1 , M Ali Habeoğlu2 Başkent University, Faculty of Medicine, Departments of Gastroenterology1 and Pulmonary Disease2, Adana Teaching and Medical Research Center, Adana, Turkey Brucellosis can affect almost all organ systems in humans. Digestive symptoms have been reported in several series. Brucella infection is a chronic systemic disease, particularly in which there is reticuloendotelial system involvement. It can cause rarely hepatitis, cholecystitis or pancreatitis in the gastrointestinal tractus. Brucella infection can rarely cause spontaneous bacterial peritonitis. Although a variety of clinical presentations and complications involving various organ systems has been reported, peritoneal involvement is a very rare presentation. There has been no reported case of massive chylothorax in a cirrhotic patient due to brucellosis in the literature. This report presents a case of spontaneous bacterial peritonitis and chylothorax caused by Brucella melitensis. Key words: Brucella melitensis, chylothorax, spontaneous bacterial peritonitis Eur J Gen Med 2007; 4(4):201-204 INTRODUCTION CASE Brucellosis, a common widespread A 60 year-old women was admitted to zoonosis, especially in countries of the our hospital with complaints of abdominal Mediterranean region, is a multisystemic pain, weakness, dyspnea, diffuse body infectious disease with a wide range of pain and abdominal distention. She had a clinical symptoms. It is known that Brucella history of cirrhosis for five years. Although infection is a systemic disease, but rarely, there was no history of animal keeping, it may also cause local infections in the eating fresh cheese and milk products were gastrointestinal system (i.e. hepatitis, identified. On physical examination, her body cholecystitis, pancreatitis or colitis) (1-2). temperature was 38.70C, pulse 96/minute, and Brucella infections present in two clinical blood pressure 120/80 mmHg. Pulmonary forms: acute and chronic brucellosis, which examination revealed dullness with decreased may resemble a number of diseases. The most breath sounds and fremitus over the right prominent symptoms of acute brucellosis are lung base. There was 2/6 systolic murmur. fever, chills, headache, backache and myalgia Diffuse dullness suggesting ascites was or arthralgia. Splenomegaly is usually present identified in the abdomen. On X-ray of chest and the liver may be palpable. A variety of we noticed pleural effusion in the medial and clinical presentations and complications of basal zones of the right lung and the shift of brucellosis involving various parts of the mediastinum to left. Diagnostic thoracentesis body have been reported. and paracentesis were performed. Bedside Spontaneous bacterial peritonitis (SBP) inoculation of blood culture bottles were is a serious complication of cirrhosis which performed. is seen in 15-20% of advanced cases. The Laboratory analyses were as follows: most common pathogenic organisms of hemoglobin 9.3 g/dL, white blood cell count SBP are Escherichia coli and Klebsiella 9600/mm3 and platelet count 81000/mm3. pneumonia. Brucella is an extremely rare Abnormal biochemical findings were blood cause of peritonitis. Herein, we report an urea nitrogen: 49 mg/dL, creatinine: 1.45 interesting case of cirrhosis complicated with mg/dL, albumin: 2.7 g/dL, total bilirubin: 2.8 chylothorax and ascites, from both of which mg/dL, direct bilirubin: 2.1 mg/dL, alkaline Brucella melitensis were isolated. phosphatase: 173 IU/L, gama-glutamyl transpeptidase: 123 IU/L. The prothrombin time was 18 seconds (INR: 1.5). Aspartate Correspondence: Mustafa Güçlü aminotransferases, Alanine aminotransferase, E-mail: [email protected] lactic dehydrogenase, serum total cholesterol, 202 Güçlü et al. triglyseride and urinary analysis were DISCUSSION normal. Creatinine clearence was 24 mL/ Defects in the host defense mechanism play minute. Uremia was investigated by the a major role in the pathogenesis of SBP. There nephrologists and attributed to prerenal are frequent infections in cirrhotic patients, azotemia. Erytrocyte sedimentation rate was as their defenses against infectious agents 90 mm/hour and C-reactive protein was 46 are altered, and bactericidal and opsonic mg/L (normal: 0-6 mg/L). activites in the ascites of cirrhotic patients are Ascitic fluid findings were as follows: gross reduced. Although E. coli and K. pneumonia appearance was transparent yellow, leukocytes are the most common etiological organisms, 380 /mm3 (with 65% lymphocytes), LDH: 13 a few unusual organisms such as Yersinia IU/L, triglyceride: 45 mg/dL, total protein: enterocolitica, Listeria monocytogenes and 0.33 gr/dL, albumin 0.22 gr/dL. Serum ascites Brucella melitensis may cause SBP (3-4). albumin gradient (SAAG) was 2.48 gr/dL. The Most cases were associated with chronic liver gross appearence of pleural fluid was milky disease or other underlying conditions such and the characteristics were as transuda. The as continuous ambulatory peritoneal dialysis leukocyte number was 6000/ml and there was (5). Brucellosis is a zoonosis and almost neutrophil dominancy in the pleural fluid. The all infections derive directly or indirectly Acid-fast bacillus (AFB) was negative. The from animal exposure. Human brucellosis is level of triglyceride was 161 mg/dl. In the diagnosed on the basis of epidemiological cytologic investigation of pleural fluid many and clinical findings and bacteriological and polymorphonuclear leukocytes, erythrocytes serological tests. Symptoms of the disease and small amounts of lymphocytes and may mimic many of the diseases and show mesothelial cells were identified. Because of varied manifestations of acute and chronic massive and symptomatic pleural effusion, the infection. Complications of brucellosis fluid was drained by thorax tube. In the sputum sometimes may lead to misdiagnosis. analysis AFB was negative and no culture was Brucellosis exists worldwide especially positive (including tuberculosis). Computed in the Mediterranean basin, the Arabian tomography of thorax did not demonstrate Peninsula, the Indian subcontinent, in parts of any pulmonary parenchymal pathology. The Mexico and Central and South America (6). HCV antibody was positive and the patient Brucellosis is endemic in some parts of our has been followed as cirrhosis for about country, especially in the central Anatolian five years. The hepatitis B virus serology, region. It is a multisystem infection that may autoimmune markers and other etiologies of present with a broad spectrum of clinical cirrhosis were negative. Esophagial varices presentations. The most frequent symptoms and severe portal hypertensive gastropathy are fever, chills or rigors, malaise, generalized were observed during upper GI endoscopy ache, headache and fatigue. Brucella is and abdominal ultrasonography revealed an usually caused by ingestion of unpasteurised atrophic nodular liver, splenomegaly and dairy products or infected raw liver. Once tense ascites with the portal vein thrombosis Brucella coccobacilli are ingested, they enter and cavernous transformation. the lymphatic system via the gastrointestinal Because of the diffuse body pain and fever system. A hematogenous dissemination Brucella agglutination test was performed. ensues and is then followed by colonization Brucella serology showed a positive slide of Brucella in reticuloendothelial cells of test, micro-agglutination titer of 1/1280. On liver, spleen, lymph nodes, bone marrow and the fourth day of admission, gram-negative kidney. Brucella rarely causes infections in coccobacilli were noted in blood culture the gastrointestinal system such as hepatitis, bottles inoculated from both ascites and cholecystitis, colitis and pancreatitis (7-8). pleural effusion and on the sixth day, they SBP due to Brucella is extremely rare (9-10). were identified as Brucella melitensis. The 20 Ten cases of brucella peritonitis are reported, mCi 99mTc-MDP radionuclide scans of whole 3 of which were culture negative. To our body bone were normal. knowledge, this is the 11th reported case Ciprofloxacin (500 mg bid) and rifampin ( of culture-proven SBP caused by Brucella 300 mg a daily) was prescribed for six weeks melitensis in a cirrhotic patient. Our patient for the treatment of Brucellosis. A week later, had not only cirrhosis and SBP caused by the patient’s condition had improved and she Brucella melitensis, but also had massive became afebrile. chylothorax (possibly hepatic hydrothorax) with positive culture for brucella. There has been no reported case of massive chylothorax Spontaneous bacterial peritonitis 203 in a cirrhotic patient due to brucellosis in the Brucella peritonitis is a rare clinical form of literature. brucellosis. It should be considered especially Pleural effusion (>500mL) in a cirrhotic in endemic regions, and appropriate patient without primary cardiac or pulmonary serological and microbiological tests should disease is defined as hepatic hydrothorax be performed to confirm the diagnosis. (HH) (11). Precipitating factors for HH are decreased colloid osmotic pressure due to REFERENCES hypoalbuminemia, increased azygous vein 1. Bauze E, Garcia de la Torre M, Parras F. pressure due to the collaterals between portal Brucella meningitis. Rev Infect Dis 1977; and azygous system, fluid leakage from 9: 810-22 thoracic duct by lymphatic flow, fluid oozing 2. Hall WH. Modern chemotherapy for from abdominal
Load more

Recommended publications
  • Intraperitoneal Haemorrhagefrom Anterior Abdominal
    490 CLINICAL REPORTS Postgrad Med J: first published as 10.1136/pgmj.69.812.490 on 1 June 1993. Downloaded from Postgrad Med J (1993) 69, 490-493 © The Fellowship of Postgraduate Medicine, 1993 Intraperitoneal haemorrhage from anterior abdominal wall varices J.B. Hunt, M. Appleyard, M. Thursz, P.D. Carey', P.J. Guillou' and H.C. Thomas Departments ofMedicine and 1Surgery, St Mary's Hospital Medical School, Imperial College, London W2 INY, UK Summary: Patients with oesophageal varices frequently present with gastrointestinal haemorrhage but bleeding from varices at other sites is rare. We present a patient with hepatitis C-induced cirrhosis and partial portal vein occlusion who developed spontaneous haemorrhage from anterior abdominal wall varices into the rectus abdominus muscle and peritoneal cavity. Introduction Portal hypertension is most often seen in patients abdominal pain of sudden onset. Over the pre- with chronic liver disease but may also occur in ceding 3 months he had noticed abdominal and those with portal vein occlusion. Thrombosis ofthe ankle Four years earlier chronic active swelling. by copyright. portal vein is recognized in both cirrhotic patients,' hepatitis had been diagnosed in Egypt and treated those with previous abdominal surgery, sepsis, with prednisolone and azathioprine. neoplasia, myeloproliferative disorders,2 protein Examination revealed a well nourished, jaun- C3 or protein S deficiency.4 diced man with stigmata of chronic liver disease Oesophageal varices develop when the portal who was anaemic and shocked with a pulse of pressure is maintained above 12 mmHg.5 Patients 100mm and blood pressure 60/20 mmHg. The with oesophageal varices often present with severe abdomen was distended, diffusely tender and there haematemesis.
    [Show full text]
  • Risk Factors of Portal Vein Thrombosis After Splenectomy in Patients with Liver Cirrhosis
    Yang et al. Hepatoma Res 2020;6:37 Hepatoma Research DOI: 10.20517/2394-5079.2020.09 Review Open Access Risk factors of portal vein thrombosis after splenectomy in patients with liver cirrhosis Ze-long Yang1, Ting Guo2, Dong-Lie Zhu1, Shi Zheng1, Dan-Dan Han1, Yong Chen1 1Department of Hepatobiliary Surgery, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, Shaanxi, China. 2Department of Obstetrics, Huaxi Hospital, Sichuan University, Cheng Du 610011, Si Chuan, China. Correspondence to: Yong Chen, PhD, Chief Physician, Department of Hepatobiliary Surgery, Xijing Hospital, Fourth Military Medical University, 127 West Changle Road, Xincheng District, Xi'an 710032, Shaanxi, China. E-mail: [email protected] How to cite this article: Yang ZL, Guo T, Zhu DL, Zheng S, Han DD, Chen Y. Risk factors of portal vein thrombosis after splenectomy in patients with liver cirrhosis. Hepatoma Res 2020;6:37. http://dx.doi.org/10.20517/2394-5079.2020.09 Received: 31 Jan 2020 First Decision: 13 Apr 2020 Revised: 4 May 2020 Accepted: 10 Jun 2020 Published: 10 Jul 2020 Academic Editor: Guang-Wen Cao, Guido Guenther Gerken Copy Editor: Cai-Hong Wang Production Editor: Tian Zhang Abstract Portal vein thrombosis (PVT) is a common complication after splenectomy, causing a possible negative impact on the prognosis of patients with liver cirrhosis. However, the risk factors of PVT are not completely clear. Many factors are related to the occurrence of postoperative PVT, such as hemodynamic changes, splenomegaly, splenectomy, coagulation and anticoagulation disorder, liver cirrhosis, platelet count, D-dimer level, infection, inflammation, and other factors.Hemodynamic changes are mainly caused by thicker portal and splenic vein diameters, larger spleen, slower portal vein blood flow rate, lower portal vein pressure before and after surgery, etc.
    [Show full text]
  • Portal Vein Thrombosis After Laparoscopic Sleeve Gastrectomy
    Surgery for Obesity and Related Diseases 12 (2016) 1787–1794 Original article Portal vein thrombosis after laparoscopic sleeve gastrectomy: presentation and management LeGrand Belnap, M.D.a, George M. Rodgers, M.D.b, Daniel Cottam, M.D.a,*, Hinali Zaveri, M.D.a, Cara Drury, P.A.a, Amit Surve, M.D.a aBariatric Medicine Institute, Salt Lake City, Utah bHuntsman Cancer Hospital, Hematology Clinic, Salt Lake City, Utah Received January 5, 2016; accepted March 4, 2016 Abstract Background: Portal vein thrombosis (PVT) is a serious problem with a high morbidity and mortality, often exceeding 40% of affected patients. Recently, PVT has been reported in patients after laparoscopic sleeve gastrectomy (LSG). The frequency is surprisingly high compared with other abdominal operations. Objective: We present a series of 5 patients with PVT after LSG. The treatment was not restricted simply to anticoagulation alone, but was determined by the extent of disease. A distinction is made among nonocclusive, high-grade nonocclusive, and occlusive PVT. We present evidence that sys- temic anticoagulation is insufficient in occlusive thrombosis and may also be insufficient in high- grade nonocclusive disease. Setting: Single private institution, United States. Methods: We present a retrospective analysis of 646 patients who underwent LSG between 2012 and 2015. In all patients, the diagnosis was established with an abdominal computed tomography (CT) scan as well as duplex ultrasound of the portal venous system. All patients received systemic anticoagulation. Depending on the extent of disease, thrombolytic therapy and portal vein throm- bectomy were utilized. All patients received long-term anticoagulation. Results: Four patients with PVT were identified.
    [Show full text]
  • (I): Diagnosis, Treatment and Prognosis of Budd-Chiari Syndrome
    rEViEW Vascular liver disorders (i): diagnosis, treatment and prognosis of budd-Chiari syndrome J. Hoekstra, H.L.A. Janssen* Department of Gastroenterology and Hepatology, Erasmus Medical Center, University Medical Center Rotterdam, PO Box 2040, 3000 CA Rotterdam, the Netherlands, *corresponding author: room Ha 206, tel.: +31 (0)10-703 59 42, fax: +31 (0)10-436 59 16, e-mail: [email protected] AbsTract IntroductioN budd-Chiari syndrome (bCs) is a venous outflow obstruction Thrombosis involving the liver vasculature is rare but of the liver that has a dismal outcome if left untreated. Most constitutes a potentially life-threatening situation. cases of bCs in the Western world are caused by thrombosis of Budd-Chiari syndrome (BCS) is characterised by the hepatic veins, sometimes in combination with thrombosis thrombosis of the hepatic outflow tract. It is defined of the inferior vena cava. Typical presentation consists as a venous obstruction that can be located from the of abdominal pain, hepatomegaly and ascites, although level of the small hepatic veins up to the junction of the symptoms may vary significantly. Currently, a prothrombotic inferior vena cava with the right atrium (figure 1).1 Hepatic risk factor, either inherited or acquired, can be identified in outflow obstruction related to right-sided cardiac failure the majority of patients. Moreover, in many patients with bCs or sinusoidal obstruction syndrome (SOS, also known as a combination of risk factors is present. Myeloproliferative veno-occlusive disease)2 is not included in the definition of disorders are the most frequent underlying cause, occurring BCS. The clinical symptoms of BCS were first described by in approximately half of the patients.
    [Show full text]
  • Portal Vein Thrombosis: an Unexpected Finding in a 28-Year-Old Male with Abdominal Pain
    J Am Board Fam Med: first published as 10.3122/jabfm.2008.03.070157 on 8 May 2008. Downloaded from BRIEF REPORT Portal Vein Thrombosis: An Unexpected Finding in a 28-Year-Old Male With Abdominal Pain Jason L. Ferguson, DO, and Duane R. Hennion, MD Background: Abdominal pain is a common primary care complaint. Portal vein thrombosis (PVT) is a rare cause of abdominal pain, typically associated with cirrhosis or thrombophilia. The following de- scribes the presentation of PVT in a young male, the search for risk factors and underlying etiology, and the debate of anticoagulation therapy. Case: A 28-year-old male presented with periumbilical pain, post-prandial nausea, and sporadic he- matemesis for 3 weeks. The diagnosis was confirmed with a triphasic liver computerized tomography after obtaining an abnormal right upper quadrant ultrasound. This unexpected finding prompted inves- tigation for intrinsic hepatic disease and potential hypercoagulable disorders. Laboratory analysis re- vealed a heterozygous genotype for the prothrombin 20210G/A mutation, an identified risk factor for venous thrombosis. Discussion: Recommendations concerning anticoagulation for PVT in the absence of cirrhosis are not clearly defined. Current literature describes the following factors as indications for anticoagulation: acute thrombus, lack of cavernous transformation, absence of esophageal varices, and mesenteric ve- nous thrombosis. This patient had clinical indications both for and against anticoagulation. Weighing this individual’s clinical circumstances, we concluded the risk of thrombus in the setting of a hypercoag- ulable disorder outweighed the risk of variceal bleeding. A minimum of 6 months of anticoagulation was initiated. copyright. Conclusion: PVT is an uncommon cause of abdominal pain, and the absence of hepatic disease should raise the index of suspicion for an underlying thrombophilia.
    [Show full text]
  • Chylous Vs. Pseudochylous Effusions
    Chylous Effusions subclavian vein superior vena cava Pleural chylous effusions develop due to transec- tion of the duct or block- age by tumor (typically lymphoma) thoracic duct Peritoneal chylous effusions develop due to cirrhosis, or portal vein thrombosis cysterna chyli lymph nodes Chylous effusions are rich in triglyc- Chylous vs. Pseudochylous erides and chylomicrons, with normal levels of cholesterol; lymphocytes Effusions may also be found. The thoracic duct runs along the spinal column, carrying lymph from the legs, gut, and chest. It Accumulations of fluid in body cavities are broadly neutral fat using stains such as Oil Red O or Sudan III. is a fluid rich in lymphocytes and chylomicrons. grouped into the two categories of transudates and ex- Chylous effusions occur in the pleural and peritoneal Chylous effusions of the peritoneal and pleural udates based on total protein, albumin, and LDH levels cavities. Causes of chylous ascites include obstruction cavities develop when the flow is obstructed. (see page 78). Many additional parameters, such as of lymphatic drainage by cirrhosis or portal vein throm- glucose, cell count and differential, and microbiologic bosis, and rare cases of congenital lymphatic anomalies culture, are often evaluated as well. Transudates are may be the cause in children. Chylous pleural effusions usually benign and are commonly the result of conges- are usually due to thoracic duct transection by trauma Pseudochylous Effusions tive heart failure or cirrhosis with hypoalbuminemia. or surgery, or obstruction of the thoracic duct by a ma- Exudates often signify serious abnormalities such as in- lignancy, often lymphoma. fection or malignancy. Most lipid-rich effusions, particularly those from Lymph from the lower extremities, abdomen, and the pleural and peritoneal cavities, are chylous.
    [Show full text]
  • Coexistence of Chylous Ascites and Thrombosis of the Portal Vein: Case Report and Literature Review
    CASE REPORT Coexistence of chylous ascites and thrombosis of the portal vein: case report and literature review Coexistência de ascite quilosa e trombose da veia porta: relato de caso e revisão da literatura Lennon da Costa Santos¹, Lucas Resende Lucinda¹, Guilherme Canabrava Rodrigues Silva¹, Anamaria Teixeira Gallo Rocha¹, Rosangela Teixeira2, Luciana Diniz Silva3 DOI: 10.5935/2238-3182.20150022 ABSTRACT 1 Medical School student at the Federal University of Chylous ascites (QA) is a rare condition, being characterized by the accumulation Minas Gerais – UFMG. Belo Horizonte, MG – Brazil. 2 MD. PhD in Infectious Diseases and Tropical Medicine. of lymph in the abdominal cavity. In adults, lymphomas constitute its most frequent Associate Professor in the Medical Clinical Department of cause; while cirrhosis and/or thrombosis of the portal vein are especially rare. This the Medical School of UFMG. Belo Horizonte, MG – Brazil. 3 MD. PhD in Gastroenterology. Associate Professor in the report presents a male patient, 36 years old, with chronic hepatitis C-related cirrhosis Medical Clinical Department of UFMG. and alcoholism, 15 kg weight loss, and milky ascites with a predominance of triglycer- Belo Horizonte, MG – Brazil. ides (1,500 mg/dL). The imaging methods identified the concomitance of thrombosis of the portal vein and cavernoma. The significant clinical improvement was obtained with the administration of total parenteral nutrition associated with octreotide. Alcohol abstinence was not achieved resulting in QA reappearance and deterioration of the clinical condition. The prognosis of QA in term of liver cirrhosis is bad. The treat- ment should be individualized according to the underlying clinical condition.
    [Show full text]
  • Diagnosis, Development, and Treatment of Portal Vein Thrombosis in Patients with and Without Cirrhosis Nicolas M
    Gastroenterology 2019;156:1582–1599 PERSPECTIVES REVIEWS AND REVIEWS IN BASIC AND CLINICAL GASTROENTEROLOGY AND HEPATOLOGY Douglas J. Robertson and Vincent W. Yang, Section Editors Diagnosis, Development, and Treatment of Portal Vein Thrombosis in Patients With and Without Cirrhosis Nicolas M. Intagliata,1 Stephen H. Caldwell,1 and Armando Tripodi2 1Division of Gastroenterology and Hepatology, University of Virginia Medical CenterCharlottesville, Virginia; and 2Fondazione Istituto di Ricovero e Cura a Carattere Scientifico Cà Granda Ospedale Maggiore Policlinico, Angelo Bianchi Bonomi Hemophilia and Thrombosis Center and Fondazione Luigi Villa, Milano, Italy Portal vein thrombosis unrelated to solid malignancy is also central to estimating prognosis and to aid therapeutic common in patients with cirrhosis, but less frequently decision-making. observed in patients without cirrhosis. Prompt diagnosis and management of acute symptomatic portal vein throm- bosis are essential. Failure to detect and treat thromboses Pathophysiology and Risk Factors of can result in mesenteric ischemia, chronic cavernous Cirrhotic and Non-Cirrhotic Portal Vein transformation, and complications of portal hypertension. Thrombosis In patients with cirrhosis, development of portal vein The low-pressure, slow-flow, and high-volume hemody- thrombosis is often insidious and remains undetected until its incidental detection. Management of portal vein throm- namics of the portal venous system results in a unique bosis in patients with cirrhosis is more controversial. vascular environment. All venous thromboses are ’ — However, there are data to support treatment of specific multifactorial due to components of Virchow s triad patients with anticoagulation agents. We review the com- hypercoagulability, endothelial injury, and reduced blood mon and distinct features of portal vein thromboses in pa- flow.
    [Show full text]
  • Budd-Chiari Syndrome: a Rare and Life-Threatening Complication of Crohn’S Disease Camila C Simoes,1 Yezaz a Ghouri,2 Shehzad N Merwat,2 Heather L Stevenson1
    Unusual association of diseases/symptoms BMJ Case Reports: first published as 10.1136/bcr-2017-222946 on 17 January 2018. Downloaded from CASE REPORT Budd-Chiari syndrome: a rare and life-threatening complication of Crohn’s disease Camila C Simoes,1 Yezaz A Ghouri,2 Shehzad N Merwat,2 Heather L Stevenson1 1Department of Pathology, SUMMARY CASE PRESENTATION University of Texas Medical Budd-Chiari syndrome (BCS) is characterised by A 27-year-old African-American man was admitted Branch, Galveston, Texas, USA 2 obstruction of hepatic venous outflow and may be to our institution as a transfer from an outside Department of Internal triggered by the prothrombotic state associated with hospital to receive a higher level of care due to Medicine, University of Texas Medical Branch, Galveston, inflammatory bowel disease (IBD). We reported a case new-onset ascites and bilateral lower extremity Texas, USA of Crohn’s disease (CD) that presented with anasarca, oedema for the previous 2 weeks. He had a history ascites, symptomatic hepatomegaly, elevated liver of intermittent abdominal pain, haematochezia and Correspondence to enzymes, increased prothrombin time and low albumin. diarrhoea for the past year, when he was diagnosed Dr Heather L Stevenson, Oesophagogastroduodenoscopy and colonoscopy with IBD at an outside hospital. At that time, he hlsteven@ utmb. edu confirmed active CD.A bdominal CT showed hepatic vein was prescribed mesalamine and steroids, which he thrombosis. Liver biopsy revealed severe perivenular CCS and YAG contributed took for a short period with improvement in his equally. sinusoidal dilation with areas of hepatocyte dropout, diarrhoea although he never achieved complete bands of hepatocyte atrophy and centrizonal fibrosis, remission.
    [Show full text]
  • Extrahepatic Portal Vein Thrombosis, an Important Cause of Portal Hypertension in Children
    Journal of Clinical Medicine Article Extrahepatic Portal Vein Thrombosis, an Important Cause of Portal Hypertension in Children Alina Grama 1,2,†, Alexandru Pîrvan 1,2,†, Claudia Sîrbe 1,*, Lucia Burac 2, Horia ¸Stefănescu 3,4, Otilia Fufezan 5, Mădălina Adriana Bordea 6 and Tudor Lucian Pop 1,2,* 1 2nd Pediatric Discipline, Department of Mother and Child, Iuliu Hat, ieganu University of Medicine and Pharmacy, 400112 Cluj-Napoca, Romania; [email protected] (A.G.); [email protected] (A.P.) 2 Centre for Expertise in Pediatric Liver Rare Diseases, 2nd Pediatric Clinic, Emergency Clinical Hospital for Children, 400177 Cluj-Napoca, Romania; [email protected] 3 Hepatology Department, Regional Institute of Gastroenterology and Hepatology, 400162 Cluj-Napoca, Romania; [email protected] 4 Liver Research Club, 400162 Cluj-Napoca, Romania 5 Department of Imaging, Emergency Clinical Hospital for Children, 400078 Cluj-Napoca, Romania; [email protected] 6 Department of Microbiology, Iuliu Hatieganu University of Medicine and Pharmacy, 400151 Cluj-Napoca, Romania; [email protected] * Correspondence: [email protected] (C.S.); [email protected] (T.L.P.) † Both authors contributed equally to this paper and share the first authorship. Abstract: One of the most important causes of portal hypertension among children is extrahepatic portal vein thrombosis (EHPVT). The most common risk factors for EHPVT are neonatal umbilical vein catheterization, transfusions, bacterial infections, dehydration, and thrombophilia. Our study aimed to describe the clinical manifestations, treatment, evolution, and risk factors of children with Citation: Grama, A.; Pîrvan, A.; EHPVT. Methods: We analyzed retrospectively all children admitted and followed in our hospital Sîrbe, C.; Burac, L.; ¸Stef˘anescu,H.; with EHPVT between January 2011–December 2020.
    [Show full text]
  • Post-Transplant Complications Portal Vein Thrombosis After Hematopoietic Cell Transplantation: Frequency, Treatment and Outcome
    Bone Marrow Transplantation (2002) 29, 329–333 2002 Nature Publishing Group All rights reserved 0268–3369/02 $25.00 www.nature.com/bmt Post-transplant complications Portal vein thrombosis after hematopoietic cell transplantation: frequency, treatment and outcome K Kikuchi, R Rudolph, C Murakami, K Kowdley and GB McDonald Gastroenterology/Hepatology Section and the Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, and the University of Washington School of Medicine, Seattle, WA, USA Summary: reported as risk factors for PVT. Decreased levels of the naturally occurring anticoagulants protein C and antithrom- Patients who develop veno-occlusive disease (VOD) of bin III have been observed in patients undergoing hemato- the liver may have low plasma levels of the natural anti- poietic cell transplantation, usually after the development coagulants protein C and antithrombin III, but large of veno-occlusive disease (VOD) of the liver,5–7 although vessel thromboses are not commonly reported in these a cause–effect relationship between decreased plasma lev- patients. We reviewed the records of 1847 consecutive els of protein C and antithrombin III and hypercoaguability patients for evidence of portal vein thrombosis. Eight has not been proven in the transplant setting. Some clinical patients (0.4%) developed portal vein thrombosis (PVT) and histologic data suggest that low plasma levels of these at a median of day +28 (range 3–58). All patients had natural anticoagulant proteins promote thrombosis after clinical evidence of VOD with ascites, a median total hematopoietic cell transplantation. For example, patients serum bilirubin 11.9 mg/dl, and median weight gain with hepatic VOD often develop deposition of fibrin in the from baseline of 7.9%.
    [Show full text]
  • Cancer-Associated Thrombosis in Cirrhotic Patients with Hepatocellular Carcinoma
    cancers Review Cancer-Associated Thrombosis in Cirrhotic Patients with Hepatocellular Carcinoma Alberto Zanetto 1,† , Elena Campello 2,† , Luca Spiezia 2 , Patrizia Burra 1, Paolo Simioni 2,* and Francesco Paolo Russo 1 1 Gastroenterology and Multivisceral Transplant Unit, Department of Surgery, Oncology and Gastroenterology, Padua University Hospital, 35128 Padua, Italy; [email protected] (A.Z.); [email protected] (P.B.); [email protected] (F.P.R.) 2 Thrombotic and Hemorrhagic Diseases Unit, Department of Medicine, Padua University Hospital, 35128 Padua, Italy; [email protected] (E.C.); [email protected] (L.S.) * Correspondence: [email protected]; Tel.: +39-049-821-2667; Fax: +39-049-821-2651 † These Authors equally contributed to the manuscript. Received: 15 October 2018; Accepted: 13 November 2018; Published: 16 November 2018 Abstract: It is common knowledge that cancer patients are more prone to develop venous thromboembolic complications (VTE). It is therefore not surprising that patients with hepatocellular carcinoma (HCC) present with a significant risk of VTE, with the portal vein being the most frequent site (PVT). However, patients with HCC are peculiar as both cancer and liver cirrhosis are conditions that can perturb the hemostatic balance towards a prothrombotic state. Because HCC-related hypercoagulability is not clarified at all, the aim of the present review is to summarize the currently available knowledge on epidemiology and pathogenesis of non-malignant thrombotic complications in patients with liver cirrhosis and HCC. They are at increased risk to develop both PVT and non-splanchnic VTE, indicating that both local and systemic factors can foster the development of site-specific thrombosis.
    [Show full text]