Palliative Care in Advanced Liver Disease (Marsano 2018)
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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. -
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 -
Chapter 156: Upper Gastrointestinal Bleeding
8/23/2018 Principles and Practice of Hospital Medicine, 2e > Chapter 156: Upper Gastrointestinal Bleeding Stephen R. Rotman; John R. Saltzman INTRODUCTION Key Clinical Questions What is the timing and treatment of peptic ulcer disease? What are the factors in diagnosis and treatment of aortoenteric fistula? What treatments are available for each etiology of upper GI bleeding? What is the appropriate management and follow-up of variceal bleeding? How do you estimate the severity of bleeding so that you can triage appropriate patients to the ICU, medical floor, or observation unit? Which patients are more likely to rebleed and hence require continued observation in the hospital aer their bleeding has apparently stopped, and for how long? Upper gastrointestinal (GI) bleeding is responsible for over 300,000 hospitalizations per year in the United States. An additional 100,000 to 150,000 patients develop upper GI bleeding during hospitalizations. The annual cost of treating nonvariceal acute upper GI bleeding in the United States exceeds $7 billion. Upper GI bleeding is defined as a bleeding source in the GI tract proximal to the ligament of Treitz. The presentation varies depending on the nature and severity of bleeding and includes hematemesis, melena, hematochezia (in rapid upper GI bleeding), and anemia with heme-positive stools. Bleeding can be associated with changes in vital signs, including tachycardia and hypotension including orthostatic hypotension. Given the range of presentations, pinpointing the nature and severity of GI bleeding may be a challenging task. The natural history of nonvariceal upper GI bleeding is that 80% of patients will stop bleeding spontaneously and no further urgent intervention will be needed. -
1 Fluid and Elect. Disorders of Serum Sodium Concentration
DISORDERS OF SERUM SODIUM CONCENTRATION Bruce M. Tune, M.D. Stanford, California Regulation of Sodium and Water Excretion Sodium: glomerular filtration, aldosterone, atrial natriuretic factors, in response to the following stimuli. 1. Reabsorption: hypovolemia, decreased cardiac output, decreased renal blood flow. 2. Excretion: hypervolemia (Also caused by adrenal insufficiency, renal tubular disease, and diuretic drugs.) Water: antidiuretic honnone (serum osmolality, effective vascular volume), renal solute excretion. 1. Antidiuresis: hyperosmolality, hypovolemia, decreased cardiac output. 2. Diuresis: hypoosmolality, hypervolemia ~ natriuresis. Physiologic changes in renal salt and water excretion are more likely to favor conservation of normal vascular volume than nonnal osmolality, and may therefore lead to abnormalities of serum sodium concentration. Most commonly, 1. Hypovolemia -7 salt and water retention. 2. Hypervolemia -7 salt and water excretion. • HYFERNATREMIA Clinical Senini:: Sodium excess: salt-poisoning, hypertonic saline enemas Primary water deficit: chronic dehydration (as in diabetes insipidus) Mechanism: Dehydration ~ renal sodium retention, even during hypernatremia Rapid correction of hypernatremia can cause brain swelling - Management: Slow correction -- without rapid administration of free water (except in nephrogenic or untreated central diabetes insipidus) HYPONA1REMIAS Isosmolar A. Factitious: hyperlipidemia (lriglyceride-plus-plasma water volume). B. Other solutes: hyperglycemia, radiocontrast agents,. mannitol. -
Evaluation and Treatment of Alkalosis in Children
Review Article 51 Evaluation and Treatment of Alkalosis in Children Matjaž Kopač1 1 Division of Pediatrics, Department of Nephrology, University Address for correspondence Matjaž Kopač, MD, DSc, Division of Medical Centre Ljubljana, Ljubljana, Slovenia Pediatrics, Department of Nephrology, University Medical Centre Ljubljana, Bohoričeva 20, 1000 Ljubljana, Slovenia J Pediatr Intensive Care 2019;8:51–56. (e-mail: [email protected]). Abstract Alkalosisisadisorderofacid–base balance defined by elevated pH of the arterial blood. Metabolic alkalosis is characterized by primary elevation of the serum bicarbonate. Due to several mechanisms, it is often associated with hypochloremia and hypokalemia and can only persist in the presence of factors causing and maintaining alkalosis. Keywords Respiratory alkalosis is a consequence of dysfunction of respiratory system’s control ► alkalosis center. There are no pathognomonic symptoms. History is important in the evaluation ► children of alkalosis and usually reveals the cause. It is important to evaluate volemia during ► chloride physical examination. Treatment must be causal and prognosis depends on a cause. Introduction hydrogen ion concentration and an alkalosis is a pathologic Alkalosis is a disorder of acid–base balance defined by process that causes a decrease in the hydrogen ion concentra- elevated pH of the arterial blood. According to the origin, it tion. Therefore, acidemia and alkalemia indicate the pH can be metabolic or respiratory. Metabolic alkalosis is char- abnormality while acidosis and alkalosis indicate the patho- acterized by primary elevation of the serum bicarbonate that logic process that is taking place.3 can result from several mechanisms. It is the most common Regulation of hydrogen ion balance is basically similar to form of acid–base balance disorders. -
Overview of Esophageal and Gastric Varices
pISSN 2287-2728 eISSN 2287-285X https://doi.org/10.3350/cmh.2020.0022 Review Clinical and Molecular Hepatology 2020;26:444-460 Managing liver cirrhotic complications: Overview of esophageal and gastric varices Cosmas Rinaldi Adithya Lesmana1,2, Monica Raharjo1, and Rino A. Gani1 1Division of Hepatobiliary, Department of Internal Medicine, Dr. Cipto Mangunkusumo National General Hospital, Medical Faculty Universitas Indonesia, Jakarta; 2Digestive Disease & GI Oncology Centre, Medistra Hospital, Jakarta, Indonesia Managing liver cirrhosis in clinical practice is still a challenging problem as its progression is associated with serious complications, such as variceal bleeding that may increase mortality. Portal hypertension (PH) is the main key for the development of liver cirrhosis complications. Portal pressure above 10 mmHg, termed as clinically significant portal hypertension, is associated with formation of varices; meanwhile, portal pressure above 12 mmHg is associated with variceal bleeding. Hepatic vein pressure gradient measurement and esophagogastroduodenoscopy remain the gold standard for assessing portal pressure and detecting varices. Recently, non-invasive methods have been studied for evaluation of portal pressure and varices detection in liver cirrhotic patients. Various guidelines have been published for clinicians’ guidance in the management of esophagogastric varices which aims to prevent development of varices, acute variceal bleeding, and variceal rebleeding. This writing provides a comprehensive review on development of PH and varices in liver cirrhosis patients and its management based on current international guidelines and real experience in Indonesia. (Clin Mol Hepatol 2020;26:444-460) Keywords: Liver cirrhosis; Hypertension, Portal; Esophageal and gastric varices INTRODUCTION tes, hepatic encephalopathy, coagulation dysfunction, hepatorenal syndrome, and even cardiac and pulmonary complications. -
Managing Hyponatremia in Patients with Syndrome of Inappropriate Antidiuretic Hormone Secretion
REVIEW Managing Hyponatremia in Patients With Syndrome of Inappropriate Antidiuretic Hormone Secretion Joseph G. Verbalis, MD Division of Endocrinology and Metabolism, Department of Medicine, Georgetown University Medical Center, Washington DC. J.G. Verbalis received an honorarium funded by an unrestricted educational grant from Otsuka America Pharmaceuticals, Inc., for time and expertise spent in the composition of this article. No editorial assistance was provided. No other conflicts exist. This review will address the management of hyponatremia caused by the syndrome of inappropriate antidiuretic hormone secretion (SIADH) in hospitalized patients. To do so requires an understanding of the pathogenesis and diagnosis of SIADH, as well as currently available treatment options. The review will be structured as responses to a series of questions, followed by a presentation of an algorithm for determining the most appropriate treatments for individual patients with SIADH based on their presenting symptoms. Journal of Hospital Medicine 2010;5:S18–S26. VC 2010 Society of Hospital Medicine. Why is SIADH Important to Hospitalists? What Causes Hyponatremia in Patients with SIADH? Disorders of body fluids, and particularly hyponatremia, are Hyponatremia can be caused by 1 of 2 potential disruptions among the most commonly encountered problems in clinical in fluid balance: dilution from retained water, or depletion medicine, affecting up to 30% of hospitalized patients. In a from electrolyte losses in excess of water. Dilutional hypo- study of 303,577 laboratory samples collected from 120,137 natremias are associated with either a normal (euvolemic) patients, the prevalence of hyponatremia (serum [Naþ] <135 or an increased (hypervolemic) extracellular fluid (ECF) vol- mmol/L) on initial presentation to a healthcare provider was ume, whereas depletional hyponatremias generally are asso- 28.2% among those treated in an acute hospital care setting, ciated with a decreased ECF volume (hypovolemic). -
Massive Gastric Variceal Hemorrhage Due to Splenic Vein Thrombosis
Journal of Liver Research, Disorders & Therapy Case Report Open Access Massive gastric variceal hemorrhage due to splenic vein thrombosis; a rare initial presentation of asymptomatic metastatic pancreatic adenocarcinoma Introduction Volume 4 Issue 3 - 2018 Isolated sinistral portal hypertension (SPH) is extremely rare, 1,2 representing less than 5% of all portal hypertension cases. Splenic Kelley Nguyen,1 Daniel S Zhang,2 Mark A vein thrombosis is typically discovered incidentally on imaging and Sultenfuss,3 David W Victor III2 is often asymptomatic. Variceal bleeding can ensue in SPH, which 1Texas A&M University College of Medicine, USA develops due to increased pressure on the left side of the portal system.3 2Department of Medicine, Section of Gastroenterology and While most gastric varices are caused by cirrhotic portal hypertension, Hepatology, Methodist Hospital, USA rare cases occur due to non-cirrhotic splenic venous thrombosis. Here, 3Department of Radiology, Methodist Hospital, USA we present massive gastric variceal bleeding splenic vein thrombosis as the initial presentation of pancreatic adenocarcinoma. Correspondence: David Victor III, Associate Professor of Clinical Medicine, Weill-Cornell Medical College, Section of Case report Hepatology & Transplant Medicine, Sherrie and Alan Conover Center for Liver Disease and Transplantation, Houston A 71-year old man presented to the emergency department with Methodist J.C. Walter , Transplant Center, Houston Methodist acute onset massive hematemesis and epigastric pain. He denied Hospital, 6550, annin St., Ste 1201 Houston, TX 77030, USA, Tel jaundice, NSAID use or prior hematemesis. Relevant medical 7134-4133-72, Email [email protected] history included heavy tobacco use in the past but denied alcohol Received: June 18, 2018 | Published: June 25, 2018 use. -
Real Facts About Fluid Overload
Real Facts About Fluid Overload Venkat K. Iyer, MD, MBA Assistant Professor, Mayo School of Medicine Medical Director, Quality and Process Improvement, Mayo Clinic Dialysis System ©2017 MFMER | slide-1 Disclosure • None Objectives Discuss the meaning of fluid overload and its negative physiological effects on the body of a person who has kidney failure. Two major functions of dialysis Uremic solute removal Excess ECF volume removal Main Process Diffusion Ultrafiltration How is adequacy Clearance of surrogate BP control, Dry weight measured? solute - urea Quantification of spKt/V, Std Kt/V, URR No objective measure to quantify adequacy adequacy of fluid removal. Trial & Error method to achieve DW Debate Small versus middle What is the best method to molecular clearance quantify ECF volume removal. (diffusive versus Clinical versus Non-clinical Convective clearance) methods What is dry weight? • Lowest tolerated post-dialysis weight achieved via a gradual reduction in post dialysis weight at which there are minimal signs or symptoms of hypovolemia or hypervolemia Dry Weight ECF volume LBM Initiation of HD High Low Adequate Maintenance HD Euvolemic Improves Acute illness Increases Decreases Negative Effects of Fluid Overload (“Volutrauma”) Acute Fluid Overload Chronic Fluid Overload • Dyspnea • Hypertension • CHF • LVH • Hospitalization • CHF • Decreased vascular compliance • Increased cardiovascular mortality • Organ dysfunction • Gut edema: malabsorption • Tissue edema: poor wound healing • Renal edema: renal BF, reduced GFR • Pulmonary edema Cost of Hospitalization for Volume Overload % of Fluid Overload admission % of 41,699 episodes 25,291 pts of 176,790 100 86 14.3 80 60 40 85.7 20 9 5 0 Inpatient ED Observation FO admission Others care Average cost per episode $6,372 Total cost $266 million • Arneson et al. -
Outcome of Acute Kidney Injury: How to Make a Difference?
Jamme et al. Ann. Intensive Care (2021) 11:60 https://doi.org/10.1186/s13613-021-00849-x REVIEW Open Access Outcome of acute kidney injury: how to make a diference? Matthieu Jamme1,2,3* , Matthieu Legrand4 and Guillaume Geri2,3,5 Abstract Background: Acute kidney injury (AKI) is one of the most frequent organ failure encountered among intensive care unit patients. In addition to the well-known immediate complications (hydroelectrolytic disorders, hypervolemia, drug overdose), the occurrence of long-term complications and/or chronic comorbidities related to AKI has long been underestimated. The aim of this manuscript is to briefy review the short- and long-term consequences of AKI and discuss strategies likely to improve outcome of AKI. Main body: We reviewed the literature, focusing on the consequences of AKI in all its aspects and the management of AKI. We addressed the importance of clinical management for improving outcomes AKI. Finally, we have also pro- posed candidate future strategies and management perspectives. Conclusion: AKI must be considered as a systemic disease. Due to its short- and long-term impact, measures to prevent AKI and limit the consequences of AKI are expected to improve global outcomes of patients sufering from critical illnesses. Keywords: Acute kidney injury, Long-term outcome, Chronic kidney disease, Intensive care Introduction Why physicians should worry about AKI? Acute kidney injury (AKI) is one of the most frequent Occurrence of AKI represents a sharp prognostic turn organ failure encountered in intensive care units (ICU). for patients by afecting both short- and long-term Since his frst defnition by Homer W. -
Esophageal Varices
World Gastroenterology Organisation Global Guidelines Esophageal varices JANUARY 2014 Revision authors Prof. D. LaBrecque (USA) Prof. A.G. Khan (Pakistan) Prof. S.K. Sarin (India) Drs. A.W. Le Mair (Netherlands) Original Review team Prof. D. LaBrecque (Chair, USA) Prof. P. Dite (Co-Chair, Czech Republic) Prof. Michael Fried (Switzerland) Prof. A. Gangl (Austria) Prof. A.G. Khan (Pakistan) Prof. D. Bjorkman (USA) Prof. R. Eliakim (Israel) Prof. R. Bektaeva (Kazakhstan) Prof. S.K. Sarin (India) Prof. S. Fedail (Sudan) Drs. J.H. Krabshuis (France) Drs. A.W. Le Mair (Netherlands) © World Gastroenterology Organisation, 2013 WGO Practice Guideline Esophageal Varices 2 Contents 1 INTRODUCTION ESOPHAGEAL VARICES............................................................. 2 1.1 WGO CASCADES – A RESOURCE -SENSITIVE APPROACH ............................................. 2 1.2 EPIDEMIOLOGY ............................................................................................................ 2 1.3 NATURAL HISTORY ...................................................................................................... 3 1.4 RISK FACTORS .............................................................................................................. 4 2 DIAGNOSIS AND DIFFERENTIAL DIAGNOSIS...................................................... 5 2.1 DIFFERENTIAL DIAGNOSIS OF ESOPHAGEAL VARICES /HEMORRHAGE ......................... 5 2.2 EXAMPLE FROM AFRICA — ESOPHAGEAL VARICES CAUSED BY SCHISTOSOMIASIS .. 6 2.3 OTHER CONSIDERATIONS ............................................................................................ -
Luis S. Marsano, MD, FACG, FASGE, AGAF, FAASLD
Luis S. Marsano, MD, FACG, FASGE, AGAF, FAASLD Professor of Medicine Division of Gastroenterology, Hepatology & Nutrition University of Louisville and Louisville VAMC 2018 Magnitude of the Problem Incidence: 36-100 per 170,000 persons 40% > 60 years old Self limited in 80% EGD in < 24 hours done in 90% Endoscopic hemostasis done in 25% Mortality: 10,000 to 20,000 per year Overall: 14 % (10-36%) Admission for GI bleed: 11 % mortality GI bleed in the hospitalized: 33 % mortality Timing of EGD (“< 6 h”, VS. “within 48 h”) (Gastrointestinal Endoscopy 2004; 60:1-8) : No effect in transfusion needs nor LOS No effect on need for surgery No effect on mortality More “high risk” lesions found on early EGD good for training & may decrease re-bleeding rate. Hematemesis: bleed above ligament of Treitz. Red blood emesis, or Coffee ground emesis Melena: may be upper or lower source > 200 mL blood in stomach, or Up to 150 mL blood in cecum) Hematochezia: - usually lower source; 11% from upper source. Needs > 1000 mL blood from upper source Upper orthostatic @ 3 min: BPs drop =/> 10 mmHg and/or HR increase > 20 bpm. > 150 mL blood in Right colon, or > 100 mL blood in Left colon. 50% of bleedings from duodenal lesion have (-) NGT aspirate (Gastrointest Endosc 1981;27:94-103) Compared with endoscopy, NGT aspirate detects UGI bleeding with (Arch Intern Med 1990;150:1381-4) : 79% Sensitivity & 55% Specificity. Clear or bilious aspirate: 14% have high-risk lesions (Gastrointest Endosc 2004;59:172-8). Aspirate of blood: 42% have “clean base” or “pigmented spot”.