Portal Hypertension: Introduction
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General Signs and Symptoms of Abdominal Diseases
General signs and symptoms of abdominal diseases Dr. Förhécz Zsolt Semmelweis University 3rd Department of Internal Medicine Faculty of Medicine, 3rd Year 2018/2019 1st Semester • For descriptive purposes, the abdomen is divided by imaginary lines crossing at the umbilicus, forming the right upper, right lower, left upper, and left lower quadrants. • Another system divides the abdomen into nine sections. Terms for three of them are commonly used: epigastric, umbilical, and hypogastric, or suprapubic Common or Concerning Symptoms • Indigestion or anorexia • Nausea, vomiting, or hematemesis • Abdominal pain • Dysphagia and/or odynophagia • Change in bowel function • Constipation or diarrhea • Jaundice “How is your appetite?” • Anorexia, nausea, vomiting in many gastrointestinal disorders; and – also in pregnancy, – diabetic ketoacidosis, – adrenal insufficiency, – hypercalcemia, – uremia, – liver disease, – emotional states, – adverse drug reactions – Induced but without nausea in anorexia/ bulimia. • Anorexia is a loss or lack of appetite. • Some patients may not actually vomit but raise esophageal or gastric contents in the absence of nausea or retching, called regurgitation. – in esophageal narrowing from stricture or cancer; also with incompetent gastroesophageal sphincter • Ask about any vomitus or regurgitated material and inspect it yourself if possible!!!! – What color is it? – What does the vomitus smell like? – How much has there been? – Ask specifically if it contains any blood and try to determine how much? • Fecal odor – in small bowel obstruction – or gastrocolic fistula • Gastric juice is clear or mucoid. Small amounts of yellowish or greenish bile are common and have no special significance. • Brownish or blackish vomitus with a “coffee- grounds” appearance suggests blood altered by gastric acid. -
Developmental Venous Anomaly: MR and Angiographic Features
JBR–BTR, 2014, 97: 17-20. DEVELOPMENTAL VENOUS ANOMALY: MR AND ANGIOGRAPHIC FEATURES M. Faure1, M. Voormolen1, T. Van der Zijden1, P.M. Parizel1 Developmental venous anomaly (DVA) is probably the most common anomaly of the intracranial vasculature. DVAs consist of multiple, radially oriented dilated medullary veins that converge into a transcerebral vein. We describe the imaging findings of this vascular anomaly in different patients and the role of different imaging modalities. Key-words: Cerebral blood vessels, abnormalities – Cerebral blood vessels, MR – Cerebral angiography. Developmental venous anomaly (DVA) was first considered a rare vascular malformation (1, 2). Nowa- days, with the advent of Computed Tomography (CT) and especially Magnetic Resonance Imaging (MRI), DVAs are seen every week to month by radiologists (3, 4). Most DVAs are solitary, asymptomatic lesions and are discovered incidentally. They have a relatively benign nature with a low incidence of hemorrhage. When they do bleed, this is thought to be due to associated vascular mal- formations, like cavernous angiomas. The typical angiographic appearance of a DVA is a caput medusae appear- ance in the venous phase. MRI com- bined with MR angiography (MRA) replaces angiography in most un- A B complicated cases as a non-invasive alternative (3, 5). Case reports Case 1 A 32-year-old woman presented with headache, with no particular location and no neurological deficit. MRI of the brain was made in another hospital that showed a flow void running transcerebral, suggestive for a vascular malformation (Fig. 1A,B). Initially, there was no gadolinium contrast given and an arterial feeder could thus not be excluded with MRI. -
Congestive Cholecystopathy; a Frequent Sonographic Sign of Evolving Esophageal Varices in Cirrhotics
Congestive Cholecystopathy; A Frequent Sonographic Sign of Evolving Esophageal Varices in Cirrhotics KHALID REHMAN YOUSAF, MIAN SAJID NISAR*, SALMAN ATIQ, AZHAR HUSSAIN*, AMNA RIZVI*, M. ISMAIL KHALID YOUSAF, ZAHID MANSOOR. Departments of Radiology and * Medicine, Omer Hospital, Lahore, Pakistan. Correspondence to Dr. Khalid Rehman Yousaf, Radiologist, New Radiology Department, SIMS/ S.H.L. Cell 923009458404 Email: [email protected] ABSTRACT Background: Gallbladder wall congestion (congestive cholecystopathy) is frequent sonographic feature demonstrated in patients with chronic liver disease. Hypoalbuminemia is still considered as a most probable cause of gallbladder wall thickness in cirrhotics. Objective: To demonstrate and establish congestive cholecystopathy as a consistent sonographic sign of developing portal hypertension and its association with evolving esophageal varices in Child’s class B (compensated) and C (decompensated) cirrhotic patients. Methodology: This cross-sectional study was conducted in Department of Radiology in collaboration with Department of Medicine, Omer Hospital, Lahore, between September 2009 and January 2011. We included 103 randomly sampled cirrhotic patients (67 men, 36 women; age range 38-79 years) who were clinically categorized into Class B and Class C liver disease through modified Child Pugh Classification. Upper gastrointestinal video endoscopy was performed for assessment of esophageal varices in all patients according to Japanese Research Society. Gall bladder targeted transabdominal ultrasound was performed on gray scale as well as color Doppler. Gallbladder wall thickness (4mm as a reference upper normal limit), pattern of wall thickening (striated or non-striated) and flow in wall were evaluated. Results: Out of 103 patients, 57 (55.3%) cases were of Child’s B and 46 (44.7%) of Child’s C class. -
Editorial Has the Time Come for Cyanoacrylate Injection to Become the Standard-Of-Care for Gastric Varices?
Tropical Gastroenterology 2010;31(3):141–144 Editorial Has the time come for cyanoacrylate injection to become the standard-of-care for gastric varices? Radha K. Dhiman, Narendra Chowdhry, Yogesh K Chawla The prevalence of gastric varices varies between 5% and 33% among patients with portal Department of Hepatology, hypertension with a reported incidence of bleeding of about 25% in 2 years and with a higher Postgraduate Institute of Medical bleeding incidence for fundal varices.1 Risk factors for gastric variceal hemorrhage include the education Research (PGIMER), size of fundal varices [more with large varices (as >10 mm)], Child class (C>B>A), and endoscopic Chandigarh, India presence of variceal red spots (defined as localized reddish mucosal area or spots on the mucosal surface of a varix).2 Gastric varices bleed less commonly as compared to esophageal Correspondence: Dr. Radha K. Dhiman, varices (25% versus 64%, respectively) but they bleed more severely, require more blood E-mail: [email protected] transfusions and are associated with increased mortality.3,4 The approach to optimal treatment for gastric varices remains controversial due to a lack of large, randomized, controlled trials and no clear clinical consensus. The endoscopic treatment modalities depend to a large extent on an accurate categorization of gastric varices. This classification categorizes gastric varices on the basis of their location in the stomach and their relationship with esophageal varices.1,5 Gastroesophageal varices are associated with varices along -
Management of Liver Complications in Sickle Cell Disease
| MANAGEMENT OF SICKLE CELL DISEASE COMPLICATIONS BEYOND ACUTE CHEST | Management of liver complications in sickle cell disease Abid R. Suddle Institute of Liver Studies, King’s College Hospital, London, United Kingdom Downloaded from https://ashpublications.org/hematology/article-pdf/2019/1/345/1546038/hem2019000037c.pdf by DEUSCHE ZENTRALBIBLIOTHEK FUER MEDIZIN user on 24 December 2019 Liver disease is an important cause of morbidity and mortality in patients with sickle cell disease (SCD). Despite this, the natural history of liver disease is not well characterized and the evidence basis for specific therapeutic intervention is not robust. The spectrum of clinical liver disease encountered includes asymptomatic abnormalities of liver function; acute deteriorations in liver function, sometimes with a dramatic clinical phenotype; and decompensated chronic liver disease. In this paper, the pathophysiology and clinical presentation of patients with acute and chronic liver disease will be outlined. Advice will be given regarding initial assessment and investigation. The evidence for specific medical and surgical interventions will be reviewed, and management recommendations made for each specific clinical presen- tation. The potential role for liver transplantation will be considered in detail. S (HbS) fraction was 80%. The patient was managed as having an Learning Objectives acute sickle liver in the context of an acute vaso-occlusive crisis. • Gain an understanding of the wide variety of liver pathology Treatment included IV fluids, antibiotics, analgesia, and exchange and disease encountered in patients with SCD blood transfusion (EBT) with the aim of reducing the HbS fraction • Develop a logical approach to evaluate liver dysfunction and to ,30% to 40%. With this regimen, symptoms and acute liver dys- disease in patients with SCD function resolved, but bilirubin did not return to the preepisode baseline. -
Correlation of Portal Vein Size with Esophageal Varices Severity in Patients with Cirrhosis of Liver with Portal Hypertension
International Journal of Scientific and Research Publications, Volume 5, Issue 1, January 2015 1 ISSN 2250-3153 Correlation of Portal Vein Size with Esophageal Varices Severity in Patients with Cirrhosis of Liver with Portal Hypertension. Dr. K.V.L. Sudha Rani*, Dr. B. Sudarsi**, Dr. R. Siddeswari***, Dr. S. Manohar, **** * M.D., Asst. Prof. of Medicine ** M.D., Asst Prof. of Medicine *** M.D., Prof. of Medicine ****M.D., Prof. & HOD of Medicine. Abstract- This study was conducted to correlate the portal vein Complications of cirrhosis include portal hypertension, diameter measured by ultrasound to development of oesophageal spontaneous bacterial peritonitis, hepato renal syndrome, hepatic varices in patients with cirrhosis of liver with portal encephalopathy and hematological abnormalities. hypertension. Portal vein is formed by confluence of superior mesenteric 92 patients with cirrhosis admitted in OGH were selected for vein and splenic vein. Portal hypertension is defined as elevation the study USG was conducted in all patients to note portal vein of hepatic venous pressure gradient more than 5 mmHg. Portal size and splenic size. Upper GI endoscopy was done to detect hypertension is caused by. 1) Increased intra hepatic resistance to presence of varices with different grades. passage of blood flow through the liver due to cirrhosis and 2) In this study 65 patients had varices. Out of 65 patients 30 increased splanchnic blood flow secondary to vasodilation with had large varices (Grade III & IV) of 65 patients, 53 patients in splanchnic vascular bed. with varices have portal vein diameter > 13 mm patients, with Congestive splenomegaly is common in patients with portal small varices and those without varices portal vein diameter is < hypertension. -
Atypical Abdominal Pain in a Patient with Liver Cirrhosis
IMAGE IN HEPATOLOGY January-February, Vol. 17 No. 1, 2018: 162-164 The Official Journal of the Mexican Association of Hepatology, the Latin-American Association for Study of the Liver and the Canadian Association for the Study of the Liver Atypical Abdominal Pain in a Patient With Liver Cirrhosis Liz Toapanta-Yanchapaxi,* Eid-Lidt Guering,** Ignacio García-Juárez* * Gastroenterology Department. National Institute of Medical Science and Nutrition “Salvador Zubirán”. Mexico City. Mexico. ** Interventional Cardiology. National Institute of Cardiology “Ignacio Chávez”. Mexico City. Mexico. ABSTRACTABSTABSTABSTRACT The causes of abdominal pain in patients with liver cirrhosis and ascites are well-known but occasionally, atypical causes arise. We report the case of a patient with a ruptured, confined abdominal aortic aneurysm. KeyK words.o d .K .Key Liver cirrhosis. Abdominal aortic aneurysm. INTRODUCTION CASE REPORT Abdominal pain in cirrhotic patients is a challenge. A 47-year-old male with the established diagnosis of Clinical presentation can be non-specific and the need for alcohol-related liver cirrhosis, presented to the emer- early surgical exploration may be difficult to assess. Coag- gency department for abdominal pain. He was classified ulopathy, thrombocytopenia, varices, and ascites need to as Child Pugh (CP) C stage (10 points) and had a model be taken into account, since they can increase the surgical for end stage liver disease (MELD) - sodium (Na) of 21 risk. Possible differential diagnoses include: Complicated points. The pain was referred to the left iliac fossa, with umbilical, inguinal or postoperative incisional hernias, an intensity of 10/10. It was associated to low back pain acute cholecystitis, spontaneous bacterial peritonitis, pep- with radicular stigmata (primarily S1). -
High Risk Percutaneous Endoscopic Gastrostomy Tubes: Issues to Consider
NUTRITIONINFLAMMATORY ISSUES BOWEL IN GASTROENTEROLOGY, DISEASE: A PRACTICAL SERIES APPROACH, #105 SERIES #73 Carol Rees Parrish, M.S., R.D., Series Editor High Risk Percutaneous Endoscopic Gastrostomy Tubes: Issues to Consider Iris Vance Neeral Shah Percutaneous endoscopy gastrostomy (PEG) tubes are a valuable tool for providing long- term enteral nutrition or gastric decompression; certain circumstances that complicate PEG placement warrant novel approaches and merit review and discussion. Ascites and portal hypertension with varices have been associated with poorer outcomes. Bleeding is one of the most common serious complications affecting approximately 2.5% of all procedures. This article will review what evidence exists in these high risk scenarios and attempt to provide more clarity when considering these challenging clinical circumstances. INTRODUCTION ince the first Percutaneous Endoscopic has been found by multiple authors to portend a poor Gastrostomy tube was placed in 1979 (1), they prognosis in PEG placement (3,4, 5,6,7,8). This review Shave become an invaluable tool for providing will endeavor to provide more clarity when considering long-term enteral nutrition (EN) and are commonly used these challenging clinical circumstances. in patients with dysphagia following stroke, disabling motor neuron diseases such as multiple sclerosis and Ascites & Gastric Varices amyotrophic lateral sclerosis, and in those with head The presence of ascites is frequently viewed as a and neck cancer.They are also used for patients with relative, if not absolute, contraindication to PEG prolonged mechanical intubation, as well as gastric placement. Ascites adds technical difficulties and the decompression in those with severe gastroparesis, risk for potential complications (see Table 1). -
Portal Vein: a Review of Pathology and Normal Variants on MDCT E-Poster: EE-005
Portal vein: a review of pathology and normal variants on MDCT e-Poster: EE-005 Congress: ESGAR2016 Type: Educational Exhibit Topic: Diagnostic / Abdominal vascular imaging Authors: C. Carneiro, C. Bilreiro, C. Bahia, J. Brito; Portimao/PT MeSH: Abdomen [A01.047] Portal System [A07.231.908.670] Portal Vein [A07.231.908.670.567] Hypertension, Portal [C06.552.494] Any information contained in this pdf file is automatically generated from digital material submitted to e-Poster by third parties in the form of scientific presentations. References to any names, marks, products, or services of third parties or hypertext links to third-party sites or information are provided solely as a convenience to you and do not in any way constitute or imply ESGAR’s endorsement, sponsorship or recommendation of the third party, information, product, or service. ESGAR is not responsible for the content of these pages and does not make any representations regarding the content or accuracy of material in this file. As per copyright regulations, any unauthorised use of the material or parts thereof as well as commercial reproduction or multiple distribution by any traditional or electronically based reproduction/publication method is strictly prohibited. You agree to defend, indemnify, and hold ESGAR harmless from and against any and all claims, damages, costs, and expenses, including attorneys’ fees, arising from or related to your use of these pages. Please note: Links to movies, ppt slideshows and any other multimedia files are not available in the pdf version of presentations. www.esgar.org 1. Learning Objectives To review the embryology and anatomy of the portal venous system. -
Vessels and Circulation
CARDIOVASCULAR SYSTEM OUTLINE 23.1 Anatomy of Blood Vessels 684 23.1a Blood Vessel Tunics 684 23.1b Arteries 685 23.1c Capillaries 688 23 23.1d Veins 689 23.2 Blood Pressure 691 23.3 Systemic Circulation 692 Vessels and 23.3a General Arterial Flow Out of the Heart 693 23.3b General Venous Return to the Heart 693 23.3c Blood Flow Through the Head and Neck 693 23.3d Blood Flow Through the Thoracic and Abdominal Walls 697 23.3e Blood Flow Through the Thoracic Organs 700 Circulation 23.3f Blood Flow Through the Gastrointestinal Tract 701 23.3g Blood Flow Through the Posterior Abdominal Organs, Pelvis, and Perineum 705 23.3h Blood Flow Through the Upper Limb 705 23.3i Blood Flow Through the Lower Limb 709 23.4 Pulmonary Circulation 712 23.5 Review of Heart, Systemic, and Pulmonary Circulation 714 23.6 Aging and the Cardiovascular System 715 23.7 Blood Vessel Development 716 23.7a Artery Development 716 23.7b Vein Development 717 23.7c Comparison of Fetal and Postnatal Circulation 718 MODULE 9: CARDIOVASCULAR SYSTEM mck78097_ch23_683-723.indd 683 2/14/11 4:31 PM 684 Chapter Twenty-Three Vessels and Circulation lood vessels are analogous to highways—they are an efficient larger as they merge and come closer to the heart. The site where B mode of transport for oxygen, carbon dioxide, nutrients, hor- two or more arteries (or two or more veins) converge to supply the mones, and waste products to and from body tissues. The heart is same body region is called an anastomosis (ă-nas ′tō -mō′ sis; pl., the mechanical pump that propels the blood through the vessels. -
Venous Angiomas of the Brain A
- REVIEW ARTICLE systems," Venous angiomas may be Venous angiomas of quite small, draining a limited region of the brain, or may be very large, the brain a sometimes draining an entire hemi- • sphere. They can be single or multi- ple, and even bilateral.P" The com- review monest sites of occurrence are in the frontal and parietal lobes of the cere- venous anomaly' or DVA, pointing bral hemispheres and in the cerebel- Ian C Duncan out that these abnormalities actual- Ium.':" They can also be found in the ly represented an extreme anatomi- FFRad(D)SA occipital and temporal lobes, basal cal variant of the normal venous ganglia and pons." Unitas Interventional Unit POBox 14031 drainage of the brain. Lytlelton Imaging 0140 Pathology The classical radiographic appear- The theory of the development of ance of these abnormalities accurately venous angiomas is that there is fail- reflects the anatomical picture with Introduction ure of regression of normal embryon- multiple enlarged transmedullary Venous angiomas of the brain, also ic transmedullary venous channels. veins radiating in a wedge or radial termed venous malformations or These persistent transmedullary veins pattern toward the larger collecting developmental venous anomalies run axially through the white matter vein producing the pathognomic (DVA) are commonest of the to drain into a single larger calibre col- 'caput medusae' or 'spoke wheel' intracranial vascular malformations lecting venous trunk. The dilated ter- appearance during the venous phase comprising between 50% and 63% of minal collecting vein then penetrates of a cerebral angiogram (Figs 1,2).14,15 all intracranial vascular malforma- the cortex to drain either superficially A similar appearance is often seen on tions. -
Skin Manifestations of Liver Diseases
medigraphic Artemisaen línea AnnalsA Koulaouzidis of Hepatology et al. 2007; Skin manifestations6(3): July-September: of liver 181-184diseases 181 Editorial Annals of Hepatology Skin manifestations of liver diseases A. Koulaouzidis;1 S. Bhat;2 J. Moschos3 Introduction velop both xanthelasmas and cutaneous xanthomas (5%) (Figure 7).1 Other disease-associated skin manifestations, Both acute and chronic liver disease can manifest on but not as frequent, include the sicca syndrome and viti- the skin. The appearances can range from the very subtle, ligo.2 Melanosis and xerodermia have been reported. such as early finger clubbing, to the more obvious such PBC may also rarely present with a cutaneous vasculitis as jaundice. Identifying these changes early on can lead (Figures 8 and 9).3-5 to prompt diagnosis and management of the underlying condition. In this pictorial review we will describe the Alcohol related liver disease skin manifestations of specific liver conditions illustrat- ed with appropriate figures. Dupuytren’s contracture was described initially by the French surgeon Guillaume Dupuytren in the 1830s. General skin findings in liver disease Although it has other causes, it is considered a strong clinical pointer of alcohol misuse and its related liver Chronic liver disease of any origin can cause typical damage (Figure 10).6 Therapy options other than sur- skin findings. Jaundice, spider nevi, leuconychia and fin- gery include simvastatin, radiation, N-acetyl-L-cys- ger clubbing are well known features (Figures 1 a, b and teine.7,8 Facial lipodystrophy is commonly seen as alco- 2). Palmar erythema, “paper-money” skin (Figure 3), ro- hol replaces most of the caloric intake in advanced al- sacea and rhinophyma are common but often overlooked coholism (Figure 11).