DOCSLIB.ORG

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

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read 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. Due to the cost of the medications, Accepted 28 December 2017 suggestive of BCS. The patient was treated with steroids he discontinued them and was lost to follow-up for CD and systemic anticoagulants for BCS. His liver for approximately 6 months. On admission, he function and enzymes normalised, and he reported complained of new onset of dyspnoea on exertion, symptomatic improvement. The precise mechanism fatigue and abdominal swelling. He had developed responsible for increased hypercoagulability in IBD severe bloody diarrhoea over the last 1 month, remains unclear. Early recognition and treatment for suggestive of an acute flare in the setting of chron- possible thrombotic complications of CD is critical to ically uncontrolled disease. His physical examina- prevent potentially fatal events like pulmonary embolism tion revealed an alert and oriented individual with or liver failure. pale conjunctiva and no signs of icterus. He had prominent tachycardia (heart rate 124/min), bilat- eral pitting pedal oedema and a distended abdomen BACKGROUND with the presence of shifting dullness, suggestive of http://casereports.bmj.com/ Crohn’s disease (CD) is a type of inflammatory ascites. The remainder of his physical examination bowel disease (IBD) that can involve any part of the was normal with no changes noted on the skin and gastrointestinal tract. It causes a systemic inflam- he had intact arterial pulses in all four extremities. matory state that can involve the joints, eyes, liver, skin and haematological system. Generally, the INVESTIGATIONS systemic inflammatory response consists of fevers, Laboratory studies determined that he had iron chills, night sweats, myalgias and chronic fatigue. deficiency anaemia (haemoglobin 5.7 g/dL, mean Elevation of acute phase reactants like the eryth- corpuscular volume 57 fL, undetectable serum iron rocyte sedimentation rate and C reactive protein and ferritin of 9 mg/dL) from chronic gastrointes- can also be observed. Common complications are tinal blood loss, normal bilirubin (total: 0.8 mg/ on 2 October 2021 by guest. Protected copyright. gastrointestinal (GI) stricture and fistula forma- dL and unconjugated: 0.4 mg/dL) and creatinine tion, perforation, haemorrhage, malabsorption (0.6 mg/dL) levels, increased prothrombin time and hypercoagulability. The disease may induce a (16.6 s), hypoalbuminaemia (2.2 g/dL) and elevated prothrombotic state leading to occlusion in both liver enzymes (alkaline phosphatase: 138 U/L; arteries and veins. Thrombosis have been reported alanine transaminase: 83 U/L; aspartate transam- to occur in hepatic veins, portal veins and in the inase: 81 U/L). Stool examination revealed posi- inferior vena cava (IVC).1 Hepatic venous outflow tive faecal leucocytes but was otherwise negative obstruction is the underlying cause of Budd-Chiari for faecal culture for enteric pathogens including syndrome (BCS), classically presenting with a clinical Clostridium difficile toxin, Giardia antigen, Cryp- triad of abdominal pain, ascites and hepatomegaly. tosporidium antigen and other ova and parasites. CD as a precipitant of BCS, although recognised, The elevation of his liver enzymes remained unex- To cite: Simoes CC, is extremely rare and there have been few reported plained, as he had no history of alcohol abuse and Ghouri YA, Merwat SN, et al. cases.2–7 Here, we are presenting a unique case of serological studies for hepatotropic viruses were BMJ Case Rep Published Online First: [please BCS in a patient with CD who concomitantly devel- negative. Laboratory studies performed to evaluate include Day Month Year]. oped hepatic vein and IVC thrombosis leading to for Wilson’s disease, alpha-1 antitrypsin deficiency, doi:10.1136/bcr-2017- the development of cirrhosis and showed substan- autoimmune hepatitis, non-alcoholic steatohepatitis 222946 tial improvement with treatment. and primary biliary cholangitis were also negative. Simoes CC, et al. BMJ Case Rep 2018. doi:10.1136/bcr-2017-222946 1 Unusual association of diseases/symptoms BMJ Case Reports: first published as 10.1136/bcr-2017-222946 on 17 January 2018. Downloaded from with hepatic cirrhosis due to BCS. Except for the liver fibrosis, no other extraintestinal manifestations of CD were present. TREATMENT The patient was transfused with packed red blood cells for his symptomatic anaemia and started on oral prednisone and a low dose of 20 mg intravenous furosemide every 12 hours for 2 days followed by oral spironolactone and furosemide for his CD and anasarca, respectively. To prevent detrimental changes in osmo- lality, no albumin infusion was given to the patient, since he had already received multiple packed red blood cell transfusions which raises serum osmolality. He was also started on heparin intravenous infusion and then transitioned to oral apixaban for long-term anticoagulation therapy. He was not evaluated for an underlying hypercoagu- Figure 1 Endoscopic image of second portion of duodenum showing lable state during his illness due to financial constraints and his multiple superficial ulcers with mucosal erythema. uninsured status. OUTCOME AND FOLLOW-UP Abdominal ultrasound showed hepatomegaly with moderate Eventually the patient’s clinical status improved and he was ascites. Ascitic fluid was sampled which showed <250 neutro- discharged. He was followed up in clinic and was started on phils and serum ascites albumin gradient of >1.1 consistent with azathioprine and sulfasalazine with a plan to slowly taper his portal hypertension. Oesophagogastroduodenoscopy and colo- steroids. This was followed by initiation of adalimumab therapy. noscopy to further evaluate his bleeding and history of IBD were During his sequential follow-up visits, his abdominal pain performed. Oesophagogastroduodenoscopy revealed erythema improved, GI bleeding was absent, bowel movements were in the antrum of stomach and multiple superficial duodenal reduced to about two per day, he gained 10 kg of weight, lower ulcers (figure 1). Biopsies from the upper and lower GI tract showed gastroduodenitis, a granuloma in the stomach (figure 2) extremity swelling resolved and abdominal distension nearly and terminal ileitis. Colonoscopy revealed prominent ulceration normalised. in terminal ileum and caecum with few areas of erythema in the rest of colon. Based on these features, including the endoscopic DISCUSSION appearance and histology findings, a diagnosis of CD was made. The incidence of IBD has increased dramatically during the last He underwent abdominal CT scan, which showed evidence of four decades, with approximately 5 million individuals affected 8 thrombi in the hepatic vein, IVC and portal vein; hepatomegaly in North America and Europe. Although IBD primarily affects with areas of liver injury and relative sparing of caudate lobe and the bowel, there are many known secondary effects on patients large volume ascites (figure 3). A transcutaneous liver biopsy was with IBD that are now widely accepted, including an increased http://casereports.bmj.com/ obtained which showed stage 4, primarily centrizonal fibrosis, risk of venous thromboembolic events, liver disease, cancer with partially obliterated central veins, areas of hepatocyte and bone disease.8–10 Thrombosis in IBD is characterised by dropout and clusters of perivenular haemosiderin-laden macro- both systemic venous thromboembolic events and focal micro- phages (figure 4). The histopathological features were consistent thrombi in the vasculature of the inflamed intestine.11 There are on 2 October 2021 by guest. Protected copyright. Figure 2 (A) Gastric mucosal biopsy showing non-necrotising granulomatous lymphocytic inflammation in a background of chronic active gastritis, consistent with the patient’s diagnosis of Crohn’s disease (CD) (H&E
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]
  • What Is Dvt? Deep Vein Thrombosis (DVT) Occurs When an Abnormal Blood Clot Forms in a Large Vein
    What is DVt? Deep vein thrombosis (DVT) occurs when an abnormal blood clot forms in a large vein. These clots usually develop in the lower leg, thigh, or pelvis, but can also occur in other large veins in the body. If you develop DVT and it is diagnosed correctly and quickly, it can be treated. However, many people do not know if they are at risk, don’t know the symptoms, and delay seeing a healthcare professional if they do have symptoms. CAn DVt hAppen to me? Anyone may be at risk for DVT but the more risk factors you have, the greater your chances are of developing DVT. Knowing your risk factors can help you prevent DVt: n Hospitalization for a medical illness n Recent major surgery or injury n Personal history of a clotting disorder or previous DVT n Increasing age this is serious n Cancer and cancer treatments n Pregnancy and the first 6 weeks after delivery n Hormone replacement therapy or birth control products n Family history of DVT n Extended bed rest n Obesity n Smoking n Prolonged sitting when traveling (longer than 6 to 8 hours) DVt symptoms AnD signs: the following are the most common and usually occur in the affected limb: n Recent swelling of the limb n Unexplained pain or tenderness n Skin that may be warm to the touch n Redness of the skin Since the symptoms of DVT can be similar to other conditions, like a pulled muscle, this often leads to a delay in diagnosis. Some people with DVT may have no symptoms at all.
    [Show full text]
  • A 12-Years Rectal Bleeding Complicated with Deep Vein Thrombosis, Is Hemorrhoid the Real Cause?
    Case Report Clinical Case Reports Volume 10:11, 2020 DOI: 10.37421/jccr.2020.10.1395 ISSN: 2165-7920 Open Access A 12-Years Rectal Bleeding Complicated with Deep Vein Thrombosis, Is Hemorrhoid the Real Cause? Yi-Qun Zhang, Meng Niu and Chun-Xiao Chen* Department of Gastroenterology, First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, P. R. China Abstract Colorectal venous malformation is a rare condition that can cause massive rectal bleeding. This is the first report of colorectal venous malformation complicated with massive bleeding and lowers limb deep vein thrombosis, and the two life-threatening conditions were both treated successfully. Keywords: Colorectal venous malformation • Rectal bleeding • Sclerotherapy • Deep vein thrombosis Introduction A 16-year-old man presented to the clinic with long-standing recurrent hematochezia and profound anemia. Per the mother, his rectal bleeding was first noticed around the age of 4 with one episode per 2-3 months that was diagnosed as hemorrhoids without specific treatment. It had worsened for 2 months with progression to 1 bloody bowel movement daily. He had no family history of hematologic disorders or vascular anomalies. The patient had accepted 600 ml red-blood cell perfusion and intravenous sucrose-iron transfusions for severe anemia with hemoglobin 5.8 g/dL, hematocrit 25.9% and MCV 69.7 fL at local hospital. Case Report Upon admission, the patient’s vital signs were within normal limits. His abdomen was supple and without tenderness. Digital rectal examination confirmed partially thrombosed, circumferential mixed hemorrhoids. Laboratory tests revealed a hemoglobin 8.0 g/L and D-dimer 15760 g/L.
    [Show full text]
  • Treatment Strategies for Patients with Lower Extremity Chronic Venous Disease (LECVD)
    Evidence-based Practice Center Systematic Review Protocol Project Title: Treatment Strategies for Patients with Lower Extremity Chronic Venous Disease (LECVD) Project ID: DVTT0515 Initial publication date if applicable: March 7, 2016 Amendment Date(s) if applicable: May 6th, 2016 (Amendments Details–see Section VII) I. Background for the Systematic Review Lower extremity chronic venous disease (LECVD) is a heterogeneous term that encompasses a variety of conditions that are typically classified based on the CEAP classification, which defines LECVD based on Clinical, Etiologic, Anatomic, and Pathophysiologic parameters. This review will focus on treatment strategies for patients with LECVD, which will be defined as patients who have had signs or symptoms of LE venous disease for at least 3 months. Patients with LECVD can be asymptomatic or symptomatic, and they can exhibit a myriad of signs including varicose veins, telangiectasias, LE edema, skin changes, and/or ulceration. The etiology of chronic venous disease includes venous dilation, venous reflux, (venous) valvular incompetence, mechanical compression (e.g., May-Thurner syndrome), and post-thrombotic syndrome. Because severity of disease and treatment are influenced by anatomic segment, LECVD is also categorized by anatomy (iliofemoral vs. infrainguinal veins) and type of veins (superficial veins, perforating veins, and deep veins). Finally, the pathophysiology of LECVD is designated typically as due to the presence of venous reflux, thrombosis, and/or obstruction. LECVD is common
    [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]
  • Venous Ulcers: Diagnosis and Treatment
    Venous Ulcers: Diagnosis and Treatment Susan Bonkemeyer Millan, MD; Run Gan, MD; and Petra E. Townsend, MD University of Florida Health Wound Care and Hyperbaric Center and the University of Florida College of Medicine, Gainesville, Florida Venous ulcers are the most common type of chronic lower extremity ulcers, affecting 1% to 3% of the U.S. population. Venous hypertension as a result of venous reflux (incompetence) or obstruction is thought to be the primary underlying mechanism for venous ulcer formation. Risk factors for the development of venous ulcers include age 55 years or older, family history of chronic venous insufficiency, higher body mass index, history of pulmonary embolism or superficial/deep venous throm- bosis, lower extremity skeletal or joint disease, higher number of pregnancies, parental history of ankle ulcers, physical inactivity, history of ulcers, severe lipodermatosclerosis, and venous reflux in deep veins. Poor prognostic signs for heal- ing include ulcer duration longer than three months, initial ulcer length of 10 cm or more, presence of lower limb arterial disease, advanced age, and elevated body mass index. On physical examination, venous ulcers are generally irregular and shallow with well-defined borders and are often located over bony prominences. Signs of venous disease, such as varicose veins, edema, or venous dermatitis, may be present. Other associated findings include telangiectasias, corona phlebectatica, atrophie blanche, lipodermatosclerosis, and inverted champagne-bottle deformity of the lower leg. Chronic venous ulcers significantly impact quality of life. Severe complications include infection and malignant change. Current evidence supports treatment of venous ulcers with compression therapy, exercise, dressings, pentoxifylline, and tissue products.
    [Show full text]
  • Hypertension and the Prothrombotic State
    Journal of Human Hypertension (2000) 14, 687–690 2000 Macmillan Publishers Ltd All rights reserved 0950-9240/00 $15.00 www.nature.com/jhh REVIEW ARTICLE Hypertension and the prothrombotic state GYH Lip Haemostasis Thrombosis and Vascular Biology Unit, University Department of Medicine, City Hospital, Birmingham, UK The basic underlying pathophysiological processes related to conventional risk factors, target organ dam- underlying the major complications of hypertension age, complications and long-term prognosis, as well as (that is, heart attacks and strokes) are thrombogenesis different antihypertensive treatments. Further work is and atherogenesis. Indeed, despite the blood vessels needed to examine the mechanisms leading to this being exposed to high pressures in hypertension, the phenomenon, the potential prognostic and treatment complications of hypertension are paradoxically throm- implications, and the possible value of measuring these botic in nature rather than haemorrhagic. The evidence parameters in routine clinical practice. suggests that hypertension appears to confer a Journal of Human Hypertension (2000) 14, 687–690 prothrombotic or hypercoagulable state, which can be Keywords: hypercoagulable; prothrombotic; coagulation; haemorheology; prognosis Introduction Indeed, patients with hypertension are well-recog- nised to demonstrate abnormalities of each of these Hypertension is well-recognised to be an important 1 components of Virchow’s triad, leading to a contributor to heart attacks and stroke. Further- prothrombotic or hypercoagulable state.4 Further- more, effective antihypertensive therapy reduces more, the processes of thrombogenesis and athero- strokes by 30–40%, and coronary artery disease by 2 genesis are intimately related, and many of the basic approximately 25%. Nevertheless the basic under- concepts thrombogenesis can be applied to athero- lying pathophysiological processes underlying both genesis.
    [Show full text]
  • Thrombosis and Embolism After Injury J Clin Pathol: First Published As 10.1136/Jcp.S3-4.1.86 on 1 January 1970
    J. clin. Path., 23, Suppl. (Roy. Coll. Path.), 4, 86-101 Thrombosis and embolism after injury J Clin Pathol: first published as 10.1136/jcp.s3-4.1.86 on 1 January 1970. Downloaded from S. SEVITT From the Birmingham Accident Hospital Thrombosis is frequent in injured patients. It classified as follows, namely, local thrombosis, takes different forms, and at least one of them, deep vein thrombosis, pulmonary microem- deep vein thrombosis in the lower limbs, is a bolism, glomerular microthrombosis, allied to common cause of morbidity and death through the Schwartzman reaction, occasional cases of embolic detachment. The different kinds may be arterial thrombosis, and rarely, abacterial vege- tative endocarditis. Thrombi form in flowing blood and are layered structures, unlike blood clots which form copyright. in static blood. They contain platelets, fibrin, red cells, and leucocytes, or a variable mixture, the differences depending on size, genesis, age, and venous or arterial location; but whatever the origin, the building blocks of enlarging thrombi are closely packed clumps of platelets with narrow fibrin borders (Fig. 1). Two main pro- http://jcp.bmj.com/ cesses are involved, namely, coagulation and platelet aggregation. These are interlinked and local release of thrombin is probably the key factor; thrombin promotes platelet clumping at a low concentration and fibrin formation at a higher concentration. Further, the release of substances from platelets can set in motion the coagulation on September 30, 2021 by guest. Protected process. Local Thrombosis and Haemostasis Thrombosis is frequent as a direct response to injury. In burned skin, for example, small venous thrombi may become prominent in the subdermis and subcutaneous tissue.
    [Show 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.
    [Show full text]
  • Budd-Chiari Syndrome Secondary to Catheter-Associated Inferior Vena
    CASE REPORT | RELATO DE CASO Budd-Chiari syndrome secondary to catheter-associated inferior vena cava thrombosis Síndrome de Budd-Chiari secundária a trombose de veia cava inferior associada a cateter Authors ABSTRACT RESUMO Gustavo N. Araujo 1 Luciane M. Restelatto 1 Introduction: Patients with chronic Introdução: Pacientes com doença renal crô- Carlos A. Prompt 1,2 kidney disease (CKD) are at increased nica (DRC) apresentam risco aumentado de Cristina Karohl 1,2 risk for thrombotic complications. The complicações trombóticas e o uso de cateter use of central venous catheters as dialysis venoso central para realização de hemodiáli- vascular access additionally increases se aumenta este risco. Nós descrevemos um 1 Hospital de Clínicas de this risk. We describe the first case of caso de síndrome de Budd-Chiari (SBC) cau- Porto Alegre. Budd-Chiari syndrome (BCS) secondary sado pelo mal posicionamento de um cateter 2 Universidade Federal do to central venous catheter misplacement de diálise em um paciente com DRC e, para Rio Grande do Sul. in a patient with CKD. Case report: A nosso conhecimento, este é o primeiro caso 30-year-old female patient with HIV/AIDS relatado na literatura. Caso clínico: Paciente and CKD on hemodialysis was admitted feminina, 30 anos, com diagnóstico de HIV/ to the emergency room for complaints of SIDA e DRC em hemodiálise foi admitida fever, prostration, and headache in the na emergência com queixas de febre, pros- last six days. She had a tunneled dialysis tração e cefaleia há 6 dias. Ela apresentava catheter placed at the left jugular vein. um cateter de diálise tunelizado implantado The diagnosis of BCS was established 7 dias antes na veia jugular esquerda.
    [Show full text]
  • Diagnosis of Deep Venous Thrombosis and Pulmonary Embolism JASON WILBUR, MD, and BRIAN SHIAN, MD, Carver College of Medicine, University of Iowa, Iowa City, Iowa
    Diagnosis of Deep Venous Thrombosis and Pulmonary Embolism JASON WILBUR, MD, and BRIAN SHIAN, MD, Carver College of Medicine, University of Iowa, Iowa City, Iowa Venous thromboembolism manifests as deep venous thrombosis (DVT) or pulmonary embolism, and has a mortal- ity rate of 6 to 12 percent. Well-validated clinical prediction rules are available to determine the pretest probability of DVT and pulmonary embolism. When the likelihood of DVT is low, a negative D-dimer assay result excludes DVT. Likewise, a low pretest probability with a negative D-dimer assay result excludes the diagnosis of pulmonary embo- lism. If the likelihood of DVT is intermediate to high, compression ultrasonography should be performed. Imped- ance plethysmography, contrast venography, and magnetic resonance venography are available to assess for DVT, but are not widely used. Pulmonary embolism is usually a consequence of DVT and is associated with greater mortality. Multidetector computed tomography angiography is the diagnostic test of choice when the technology is available and appropriate for the patient. It is warranted in patients who may have a pulmonary embolism and a positive D-dimer assay result, or in patients who have a high pre- test probability of pulmonary embolism, regardless of D-dimer assay result. Ventilation-perfusion scanning is an acceptable alternative to computed tomography angiography in select settings. Pulmonary angiography is needed only when the clinical suspicion for pulmo- nary embolism remains high, even when less invasive study results are negative. In unstable emergent cases highly suspicious for pulmo- nary embolism, echocardiography may be used to evaluate for right ventricular dysfunction, which is indicative of but not diagnostic for pulmonary embolism.
    [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]