Gastrointestinal Emergencies E-Book

• Herausgeber: John Wiley & Sons
• Kategorie: Fachliteratur
• Sprache: Englisch

Seitenzahl: 799

Veröffentlichungsjahr: 2016

Beschreibung

Gastrointestinal Emergencies 3E provides practical, up-to-date guidance for gastroenterologists, endoscopists, surgeons, emergency and acute physicians, medical students and trainees managing patients presenting with GI complications and/or emergencies.

Combining a symptom section, a specific conditions section and a section that examines complications (and solutions) of GI procedures, focus throughout is on clear, specific how-to guidance, for use before a procedure or immediately after emergency stabilization.  An evidence-based approach to presentation, diagnosis and investigation is utilized throughout.

New to this third edition are several brand new chapters covering various complications of procedures and specific conditions not previously featured, as well as a thorough look at the many diagnostic and therapeutic advances in recent years.  In addition, every chapter from the current edition has undergone wholesale revision to ensure it is updated with the very latest in management guidelines and clinical practice.  Once again, full range of emergencies encountered in daily clinical practice will be examined, such as acute pancreatitis, esophageal perforation, capsule endoscopy complications, acute appendicitis, and the difficulties after gastrointestinal procedures. International guidelines from the world’s key gastroenterology societies will be included in relevant chapters.

Gastrointestinal Emergencies 3E is the definitive reference guide for the management of gastrointestinal emergencies and endoscopic complications, and the perfect accompaniment for the modern-day gastroenterologist, surgeon, emergency and acute physicians.

Every Emergency Department, GI/endoscopy unit, medical/surgical admission unit should keep a copy close at hand for quick reference. 

Leseprobe

Gastrointestinal Emergencies

EDITED BY

Tony C. K. Tham

Consultant Gastroenterologist,Ulster Hospital,Dundonald, Belfast,Northern Ireland, UK

John S. A. Collins

Associate Postgraduate Dean,Northern Ireland Medical and Dental Training AgencyFormerly Consultant Gastroenterologist,Royal Victoria Hospital,Belfast, Northern Ireland, UK

Roy Soetikno

Chief, GI Section,Veterans Affairs Palo Alto Health Care System,Palo Alto;Associate Professor,Stanford University,Stanford, CA, USA

THIRD EDITION

This edition first published 2016 © 2016 by John Wiley & Sons, LtdSecond edition published 2009First edition published 2000© 2000, 2009 by Blackwell Publishing Ltd

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Library of Congress Cataloging-in-Publication Data

Gastrointestinal emergencies (Tham) Gastrointestinal emergencies / edited by Tony C.K. Tham, John S.A. Collins, Roy Soetikno. – Third edition.  p. ; cm. Includes bibliographical references and index.

 ISBN 978-1-118-63842-2 (pbk.)I. Tham, Tony C. K., editor. II. Collins, John S. A., editor. III. Soetikno, Roy, editor. IV. Title.[DNLM: 1. Gastrointestinal Diseases–therapy. 2. Emergency Treatment. 3. Endoscopy, Gastrointestinal. WI 140] RC801 616.3′3–dc   232015024791

A catalogue record for this book is available from the British Library.

Wiley also publishes its books in a variety of electronic formats. Some content that appears in print may not be available in electronic books.

Cover image: © Paul Bradbury/GettyImages

Notes on contributors

Seiichiro AbeNational Cancer Center Hospital, Tokyo, Japan

Aijaz Ahmed MDDivision of Gastroenterology and Hepatology, Stanford University School of Medicine, Stanford, CA, USA

Patrick B. Allen MB, FRCP, BScConsultant Gastroenterologist, Ulster Hospital, Belfast, Northern Ireland, UK

Constantinos P. Anastassiades MBBS (Lond), FACPConsultant, Division of Gastroenterology & Hepatology, Khoo Teck Puat Hospital, SingaporeAdj. Assistant Professor of Medicine, Case Western Reserve University School of Medicine, Cleveland, OH, USA

Stephen Attwood MCh, FRCS, FRCSIConsultant Upper GI and Laparoscopic Surgeon, Honorary Professor, Durham University, Durham, UK

Andrés Cárdenas MD, MMSc, PhD, AGAFFaculty Member/Senior Specialist, GI Unit, Institute of Digestive Diseases, Hospital Clinic, IDIBAPS, University of Barcelona, Barcelona, Spain

David L. Carr-Locke MB, Bchir, FRCP, FASGEChief, Division of Digestive Diseases, Associate Chair of Medicine, Mount Sinai Beth Israel Medical Center, New York, USAProfessor, Icahn School of Medicine, New York, USA

W. Johnny Cash MD, FRCPConsultant Hepatologist, Royal Victoria Hospital, Belfast, Northern Ireland, UK

John S. A. Collins MDAssociate Postgraduate Dean, Northern Ireland Medical and Dental Training AgencyFormerly Consultant Gastroenterologist, Royal Victoria Hospital, Belfast, Northern Ireland, UK

Wallace Dinsmore MD, FRCP, FRCPI, FRCPEdProfessor of Medicine, Department of GU Medicine, Royal Victoria Hospital, Belfast, UK

Shai Friedland MDAssistant Professor, Stanford University School of Medicine and VA Palo Alto, Stanford, CA, USA

Subrata Ghosh MD, FRCP, FRCPE, FRCPC, FCAHSProfessor of Medicine, Microbiology & Immunology, University of Calgary, Alberta, Canada

Pere Ginès MD, PhDChief of Hepatology, Liver Unit, Institute of Digestive Diseases Hospital Clinic, IDIBAPS, Professor of Medicine, University of Barcelona, Spain

Isabel GrauperaInstitut de Malalties Digestives i Metabolisme, Hospital Clinic, IDIBAPS, University of Barcelona, Barcelona, Spain

Philip S. J. Hall MRCP, MB, BChSpecialty registrar in Gastroenterology, Gastroenterology training program, Altnagelvin Hospital, Londonderry, Northern Ireland, UK

Paul Kevin Hamilton BSc (Hons), MD, FRCPESpecialty Registrar, Department of Clinical Biochemistry; Formerly Consultant Physician and Clinical Pharmacologist; Belfast Health and Social Care Trust, Belfast, Northern Ireland, UK

Brian J. HoganSpecialty Registrar, Sheila Sherlock Liver Centre, Royal Free London NHS Foundation Trust, Royal Free Hospital, London, UK

Marietta Iacucci MD, PhDClinical Associate Professor of Medicine Division of Gastroenterology, University of Calgary, Alberta, Canada

Tonya Kaltenbach MD, MSVeterans Affairs Palo Alto Health Care System, Clinical Assistant Professor of Medicine (Affiliated), Stanford University, Palo Alto, CA, USA

Joseph K. N. KimIcahn School of Medicine, New York, USA

Jennifer M. Kolb MDIcahn School of Medicine at Mount Sinai, Internal Medicine, New York, NY, USA

Bee Chan Lee MB, MRCPConsultant Gastroenterologist, Warwick Hospital, Warwicks, England, UK

David R. Lichtenstein MDDirector of Endsocopy & Associate Professor of Medicine, Boston Medical Center, Boston University School of Medicine, Boston, MA, USA

Ian McAllister MDConsultant Surgeon, Ulster Hospital, Dundonald, Belfast, Northern Ireland, UK

Daniel F. McAuleyProfessor and Consultant in Intensive Care Medicine, Royal Victoria Hospital and Queen’s University of Belfast, Belfast, Northern Ireland, UK

Kevin McCallionConsultant Surgeon, Ulster Hospital, Dundonald, Belfast, Northern Ireland, UK

Emma McCartyConsultant in Genitourinary Medicine, Royal Victoria Hospital, Belfast, Northern Ireland, UK

James J. McNamee FCARCSI, FRCA, FCICM, FFICMConsultant in Intensive Care Medicine, Royal Victoria Hospital, Belfast, Northern Ireland, UK

Graham Morrison MB, MRCPConsultant Gastroenterologist, Altnagelvin Hospital, Londonderry, Northern Ireland, UK

Ichiro Oda MDNational Cancer Center Hospital, Tokyo, Japan

Khalid Osman FRCSNorth Tyneside General Hospital, Tyne & Wear, UK

Kelvin Palmer FRCP(Edin)Formerly Consultant Gastroenterologist, Western General Hospital, Edinburgh, UK

Ioannis S. PapanikolaouDepartment of Internal Medicine and Research Unit, “Attikon” University General Hospital, University of Athens, Greece

David W.M. Patch MBBS, FRCPConsultant Hepatologist, Department of Hepatology, Royal Free Hospital, London, UK

Ryan B. Perumpail MDStanford Hospital and Clinics, Stanford, CA, USA

Aarti K. Rao MDResident Physician, Department of Internal Medicine, Stanford University; Department of Gastroenterology, Veterans Affairs Palo Alto Health Care System, CA, USA

Michele B. RyanBrigham and Women’s Hospital, Harvard Medical School, Boston, MA, USA

Andres Sanchez-Yague MD, PhDChief, Gastroenterology Unit, Vithas Xanit International Hospital, Benalmadena, SpainConsultant, Gastroenterology Unit, Hospital Costa del Sol, Marbella, Spain

Allison R. SchulmanBrigham and Women’s Hospital, Harvard Medical School, Boston, MA, USA

Reza Shaker MD, FACPProfessor and Chief, Division of Gastroenterology and Hepatology; Director, Digestive Disease Center, Medical College of Wisconsin, Milwaukee, WI, USA

Peter D. Siersema MD, PhDProfessor of Gastroenterology and Chief, Department of Gastroenterology and Hepatology, University Medical Center, Utrecht, The Netherlands

Maria Cecilia M. Sison-OhMedical Center Manila, Manila, Philippines

Roy Soetikno MD, MS (Health Service Research)Chief, GI Section, Veterans Affairs Palo Alto Health Care System, Palo AltoAssociate Professor, Stanford University, Stanford, CA, USA

Daniel J. Stein MDAssistant Professor of Medicine, Division of Gastroenterology and Hepatology, Medical College of Wisconsin, Milwaukee, WI, USA

Matthias SteverlynckCentre Hospitalier de Mouscron, Belgium

Haruhisa SuzukiNational Cancer Center Hospital, Tokyo, Japan

Tony C. K. Tham MD, FRCP, FRCPIConsultant Gastroenterologist, Dundonald, Ulster Hospital, Belfast, Northern Ireland, UK

Christopher C. ThompsonBrigham and Women’s Hospital, Harvard Medical School, Boston, MA, USA

Philip Toner MRCPSpecialty Registrar, Department of General Medicine, Belfast Health and Social Care Trust, Belfast City Hospital, Belfast, UK

George Triadafilopoulos MD, DScClinical Professor of Medicine, Division of Gastroenterology and Hepatology, Stanford University School of Medicine, Stanford, CA, USA

Jo Vandervoort MDDepartment of Gastroenterology, Onze-Lieve-Vrouw Ziekenhuis, Aalst, Belgium

Barbara WillandtKU Leuven, Netherlands

Richard C. K. Wong BSc, MBBS(Lond), FASGE, FACG, AGAF, FACPProfessor of Medicine, Case Western Reserve University School of Medicine, Cleveland, OH, USAMedical Director, DHI Endoscopy Unit, University Hospitals Case Medical Center, Cleveland, OH, USA

Robert J. Wong MD, MSStanford University School of Medicine, Stanford, CA, USA

SECTION 1Approach to specific presentations

CHAPTER 1Approach to dysphagia

John S. A. Collins

Northern Ireland Medical and Dental Training Agency, Royal Victoria Hospital, Belfast, UK

Definitions

Dysphagia refers to a subjective sensation of the obstruction of swallowed solids or liquids from mouth to stomach. Patients most frequently complain that food “sticks” in the retrosternal area or simply will “not go down.” Patients may complain of a feeling of choking and chest discomfort. In some cases food material is rapidly regurgitated to relieve symptoms.

Dysphagia can be divided into two types:

oropharyngeal dysphagia,

where there is an inability to

initiate

the swallowing process and may involve disorders of striated muscle. There may be a sensation of solids or liquids left in the pharynx.

esophageal dysphagia,

which involves disorders of the smooth muscle of the esophagus and results in symptoms within seconds of the Initiation of swallowing.

Odynophagia is the sensation of pain on swallowing which is usually felt in the chest or throat. Globus is the sensation of a lump, fullness or tightness in the throat.

Differential diagnosis

The causes of the above types of dysphagia are shown in Tables 1.1 and 1.2.

Table 1.1 Etiology of oropharyngeal dysphagia.

Neurological disorders

Cerebrovascular disease

Amyotrophic lateral sclerosis

Parkinson’s disease

Multiple sclerosis

Bulbar poliomyelitis

Wilson’s disease

Cranial nerve injury

Brainstem tumors

Striated muscle disorders

Polymyositis

Dermatomyositis

Muscular dystrophies

Myasthenia gravis

Structural lesions

Inflammatory – pharyngitis, tonsillar abscess

Head and neck tumors

Congenital webs

Plummer–Vinson syndrome

Cervical osteophytes

Surgical procedures to the oropharynx

Pharyngeal pouch (Zenker diverticulum)

Cricopharyngeal bar

Metabolic disorders

Hypothyroidism

Hyperthyroidism

Steroid myopathy

Table 1.2 Etiology of esophageal dyphagia.

Neuromuscular/dysmotility disorders

Achalasia

CRST syndrome

Diffuse esophageal spasm

Nutcracker esophagus

Hypertensive lower esophageal shincter

Nonspecific esophageal dysmotility

Chaga disease

Mixed connective tissue disease

Mechanical strictures – intrinsic

Peptic related to GERD

Carcinoma

Esophageal webs

Esophageal diverticula

Lower esophageal ring (Schatzki)

Benign tumors

Foreign bodies

Acute esophageal mucosal infections

Pemphigus/pemphigoid

Crohn’s disease

Mechanical lesions – extrinsic

Bronchial carcinoma

Mediastinal nodes

Vascular compression

Mediastinal tumors

Cervical osteoarthritis/spondylosis

History and examination

Acute dysphagia is a relatively uncommon, but dramatic, presenting symptom and constitutes a gastrointestinal emergency. The patient will complain of difficulty initiating swallowing or state that food is readily swallowed but results in the rapid onset of chest discomfort or pain, which is only relieved by passage or regurgitation of the swallowed food bolus. The latter sensation can result after swallowing a mouthful of liquid. In the acute case it is important to ask the patient about the presence of other neurological symptoms.

If oropharyngeal dysphagia is suspected, the following points are important:

The patient may complain of nasal regurgitation of liquid, coughing or choking during swallowing or a change in voice character which may indicate nasal speech due to palatal weakness.

Patients may describe repeated attempts at the initiation of swallowing.

Symptoms are noticed within a second of swallowing.

Patients with cerebrovascular disease may give a history of symptoms of transient ischemic attacks (TIA) – these would include visual disturbance, dysphasia, or transient facial or limb weakness.

There may be progressive muscular weakness and dysphagia is only part of the symptom complex, in contrast to esophageal dysphagia where swallowing disorder is the most prominent symptom.

Patients should have a careful neurological examination and evaluation of the pharynx and larynx including direct laryngoscopy.

In cases of esophageal dysphagia, the following points are important:

Is the sensation of dysphagia worse with liquids or solids? If a progressive obstructive lesion is the cause of symptoms, the patient will notice difficulty swallowing solids initially and liquids later. Difficulty with both solids and liquids suggests dysmotility.

Is the dysphagia intermittent or progressive? Intermittent dysphagia may indicate a motility disorder such as diffuse esophageal spasm whereas a progressive course is more characteristic of an esophageal tumor.

How long have symptoms been present? A long history usually greater than 12 months suggests a benign cause, whereas a short history less than 4 weeks suggests a malignant etiology.

Has the patient a history of heartburn suggesting gastroesophageal reflux disease (GERD)? While a history of heartburn does not rule out gastroesophageal cancer as a cause of dysphagia, a long history in the presence of slow onset, non-progressive symptoms may point to a benign peptic stricture as the cause.

A diagnostic algorithm for the symptomatic assessment of the patient with dysphagia is shown in Fig. 1.1.

Fig. 1.1 Diagnostic algorithm for the symptomatic assessment of the patient with dysphagia.

Source: Yamada 1995. Reproduced with permission of Wiley.

The etiology of esophageal dysphagia is summarized in Table 1.2.

While acute dysphagia may be painful, especially in relation to foreign body or food bolus impaction above an existing stricture, a history of odynophagia usually suggests an inflammatory condition or disruption of the esophageal mucosa leading to the irritation of pain receptors. The causes of odynophagia are:

Candida

herpes simplex

cytomegalovirus

pill-induced ulceration

reflux disease/stricture

radiation esophagitis

caustic injury

motility disorders stimulated by swallowing

cancer

graft-versus-host disease

foreign body.

Clinical signs in patients who present with dysphagia are uncommon. On examination, the following signs should be noted:

loss of weight

signs of anemia

cervical lymphadenopathy

hoarseness

concomitant neurological especially bulbar signs

respiratory signs if history of cough/choking

hepatomegaly

oral ulcers or signs of

Candida

goiter.

Investigation

Dysphagia is considered to be an “alarm symptom” and should be investigated as a matter of urgency in all cases. Upper gastrointestinal endoscopy is a safe investigation in experienced hands provided the intubation is carried out under direct visualization of the oropharynx and upper esophageal sphincter. The endoscopist should be alert to the possibility of a high obstruction and the likelihood of retained food debris or saliva if dysphagia has been present for some time. If there is a history of choking, the patient should have a liquid-only diet for 24 hours followed by a 12-hour fast prior to the procedure. In some cases, the careful passage of a nasoesophageal tube to aspirate retained luminal contents may be necessary. At endoscopy, obstructing lesions can be biopsied and peptic strictures can be dilated with a balloon or bougie.

The presence of a dilated food and saliva-filled esophagus in the absence of a stricture raises the possibility of achalasia.

Barium studies are not a prerequisite for endoscopy but should be considered complementary in dysphagia. Barium swallow may give additional information in the following situations:

in cases of suspected oropharyngeal dysphagia, especially if videofluoroscopy is employed;

where a high esophageal obstruction is suspected prior to endoscopy;

where a motility disorder is suspected as a method to assess lower esophageal relaxation.

In some cases, a barium swallow may be a useful investigation in certain circumstances:

Where there is suspected proximal obstruction, e.g. laryngeal cancer, Zenker's diverticulum;

Following a negative endoscopy or obstructive symptoms as lower esophageal rings may be more easily detected at fluoroscopy.

Esophageal manometry is indicated if both endoscopy and barium studies are inconclusive in the presence of persistent symptoms. Manometry requires intubation of the esophagus with a multilumen recording catheter attached to a polygraph. Pressure changes are recorded during water bolus swallows along the esophageal body and at the upper and lower esophageal sphincters.

Management of dysphagia

The management of dysphagia depends on the underlying cause. In a patient presenting with total dysphagia who is unable to swallow even small amounts of liquid or saliva, urgent treatment is indicated (Fig. 1.2).

Fig. 1.2 Approach to management of total dysphagia.

The management of oropharyngeal dysphagia can be treated by control of the underlying neurological or metabolic disorder. Dietary modification under the supervision of a speech and language therapist may maintain oral swallowing and avoid gastrostomy tube placement in patients with stroke and pseudobulbar or bulbar palsy. Gastrostomy tube placement may be the only management option in patients with inoperable mouth or throat tumors, or in cases where recurrent pulmonary aspiration is life threatening.

Peptic stricture

When the endoscopic appearances are characteristic of a benign peptic stricture, dilatation can usually be carried out at the time of the procedure using either wire-guided bougies or a balloon. If the stricture is complex, very tight or associated with esophageal scarring, it may be safer to carry out wire-guided dilatation using graded bougies. The majority of patients will gain symptomatic relief and the risk of complications is low (see Chapter 21, Esophageal Perforation).

It is essential that all patients are treated with an adequate dose of a proton pump inhibitor to prevent recurrence. Repeat dilatations are necessary in some cases and repeat inspection and biopsy is advised if there is any concern about mucosal dysplasia or malignancy.

Esophageal carcinoma

Suspected carcinoma, which is detected at endoscopy, requires biopsy confirmation and subsequent staging so that a management plan can be formulated. The most accurate modality for staging is endoscopic ultrasound which can assess depth of local invasion and regional lymph node status. Chest and abdominal computerized tomography (CT) is a less accurate technique but CT/positron emission tomography (PET) scanning enhances staging accuracy, especially in adenocarcinomas.

Surgery offers the only chance of cure but only 30% of tumors are resectable and 5-year survival is 10% in European studies. Contraindications to surgery include invasion of vascular structures, metastatic disease and patients with comorbidity and high operative risk.

Palliative management will be indicated in 70% of patients following staging. Esophageal dilatation, followed by the endoscopic placement of a metal stent, gives adequate swallowing relief in the majority of cases. In situations where there is complete obstruction of the esophageal lumen by tumor, endoscopic laser therapy can provide adequate palliation of dysphagia. The prognosis is poor with a mean survival of 10 months after diagnosis with a 5-year survival of 5%. Where surgical resection is completed after staging and selection, 5-year survival can be up to 25%.

Radiation injury

Following radiotherapy to the thorax or head and neck, some patients develop esophagitis, which may progress to stricturing and fibrosis. The diagnosis is confirmed by endoscopy and biopsy. Treatment consists of balloon or bougie dilatation and may have to be repeated in severe cases.

Esophageal webs and rings

Both of these esophageal lesions can result in dysphagia or lead to food bolus impaction. Webs are typically composed of thin mucosal tissue covered with squamous epithelium. They tend to occur proximally in the upper cervical esophagus and may be missed or ruptured at endoscopy, which is both diagnostic and therapeutic in these cases. They have been associated with chronic iron deficiency anemia. Rings are mucosal circular structures associated with dysmotility and seen at the esophagogastric junction. A Schatzki ring is a solitary thin rim of mucosa usually seen in the distended lower oesophagus. They are usually treated by dilatation and may be recurrent.

Food bolus impaction

See Chapter 20, Foreign Body Impaction in the Esophagus.

Eosinophilic esophagitis

This is an increasingly recognized cause of dysphagia and is diagnosed by characteristic endoscopic appearances and the finding of a dense eosinophilic infiltrate in esophageal mucosal biopsies (>15 per high power field). Dilatation is rarely required and the condition responds to low-dose swallowed topical steroids, administered by a metered inhaler.

Further reading

American Gastroenterology Association medical position statement on management of oropharyngeal dysphagia.

Gastroenterology

1999;

116

:452.

Castell DO. Approach to the patient with dysphagia. In

Textbook of Gastroenterology

, Yamada T, Alpers DH, Owyang C, Powell DW, Silverstein FE (eds). Lippincott, Philadelphia, 1995.

Falk GW, Richter JE. Approach to the patient with acute dysphagia, odynophagia, and non-cardiac chest pain. In

Gastrointestinal Emergencies 2nd edition

, Taylor MB (ed.). Williams & Wilkins, Baltimore, 1997:65–84.

Kahrilas PJ, Smout AJ. Esophageal disorders.

Am. J. Gastroenterol.

2010;

105

:747.

Prasad GA,Talley NJ, Romero Y, et al. Prevalence and predictive factors of eosinophilic esophagitis in patients presenting with dysphagia: a prospective study.

Am. J. Gastroenterol.

2007;102:2627.

Yamada T, Alpers DH, Owyang C, Powell DW, Silverstein FE (eds).

Textbook of Gastroenterology

. Lippincott, Philadelphia, 1995.

CHAPTER 2Approach to vomiting

Bee Chan Lee1 and John S. A. Collins2

1 Warwick Hospital, Warwick, UK

2 Northern Ireland Medical and Dental Training Agency, Royal Victoria Hospital, Belfast, UK

Definition

Acute nausea with or without vomiting is a common symptom. Nausea is described as an unpleasant sensation of imminent vomiting. Vomiting is defined as the forceful expulsion of gastric contents through the mouth and it should be differentiated from retching and regurgitation. Retching is the term that describes the labored, rhythmic respiratory activity and abdominal muscular contractions, which usually precede vomiting. Regurgitation is the effortless propulsion of gastric contents into the mouth without abdominal diaphragmatic muscular contractions.

The act of vomiting is initiated by the vomiting center in the medulla or the chemoreceptor trigger zone (CTZ) in the floor of the fourth ventricle, via a combination of motor and autonomic responses. Vomiting starts with salivation and then reverse peristalsis in the small intestines and a relaxed pyloric sphincter. Subsequent glottis closure (to prevent aspiration), abdominal and gastric muscular contractions and relaxation of the lower esophageal sphincter result in the final act of vomiting.

Etiology

The causes of acute nausea and vomiting are extensive and are summarized in Table 2.1.

Visceral (gut and peritoneum)

– visceral pain from a variety of intra-abdominal causes is often associated with an acute abdomen, including sepsis and mechanical obstruction. Gastric outlet obstruction leads to prolonged vomiting of the projectile nature.

CNS causes

– these include head injuries, intracranial infections/inflammation and raised intracranial pressure. Stimulation or disorders of the vestibular system such as motion sickness should not be overlooked.

Drugs

– nausea and vomiting are common side effects of chemotherapeutic agents, antibiotics, analgesics, and narcotics but the list of other offending drugs is endless. It is also important to enquire about recreational druguse, of which the commonest is alcohol abuse. Acetominophen/paracetamol and salicylate toxicity also result in nausea or vomiting, and this needs to be excluded.

Infections

– food poisoning (bacterial and viral) is the commonest. Others include epidemic viral infections, e.g. Norwalk agent and non-gastrointestinal infections such as otitis media and urinary tract infection.

Endocrine and metabolic

– commoner ones are hypercalcemia and uremia; less common cause includes acute intermittent porphyria.

Miscellaneous

– pregnancy (hyperemesis gravidarum), postoperation, cardiac causes (myocardial infarction, and congestive cardiac failure), psychogenic vomiting, and cyclical vomiting syndrome.

Functional nausea and vomiting.

This is a diagnosis of exclusion in some patients who present with chronic or episodic symptoms in the absence of a positive physical cause and despite full investigation.

Table 2.1 Causes of acute vomiting.

Visceral stimuli

Peritonitis

Small bowel obstruction

Pseudo-obstruction

Acute pancreatitis

Acute cholecystitis

Acute appendicitis

Gastric outlet obstruction

Mesenteric ischemia

CNS

Vestibular disorders

CNS tumors

Meningitis

Cerebral abscess

Subarachnoid hemorrhage

Head injury

Migraine

Reye’s syndrome

Drugs

Chemotherapeutic agents

Antibiotics/antivirals

Narcotics

Analgesics

Digoxin

Infections

Sporadic viral infections

Gastroenteritis (bacterial/viral)

Hepatitis viruses

Non-gastrointestinal infections

Endocrine/metabolic

Diabetic ketoacidosis

Adrenal insufficiency

Hypercalcemia

Uremia

Acute intermittent porphyria

Miscellaneous

Psychogenic

Ethanol abuse

Radiotherapy

Pregnancy

Carcinomatosis

Postoperation

Cyclical (functional) vomiting

History

A detailed history is crucial in elucidating the cause of vomiting. The above causes should be considered. Constitutional symptoms of fever, myalgia, headache, or possible infectious contacts in the family, school, workplace, or institutions should alert the clinicians to an infectious etiology. Foreign travel and ingestion of inadequately cooked meat raise the suspicion of gastroenteritis. In these situations, a stool sample may reveal Norwalk agent, Salmonella, Campylobacter, Staphylococcus aureus, or Bacillus cereus.

Any associated abdominal pain with guarding points to an acute abdomen. Bilious vomiting suggests a proximal intestinal obstruction, while feculant vomiting is due to a more distal obstruction. Gastric outlet obstruction usually leads to postprandial projectile vomiting. When vomiting is associated with jaundice, anorexia and nausea, a hepatic etiology should be considered.

If there are no obvious symptoms of infection or acute abdomen, pregnancy should be excluded in female patients who are in their reproductive years. A thorough drug history, including over-the-counter medication and herbal remedies, may reveal the cause. Patients should also be asked about recent relevant CNS symptoms of vertigo, headache, blurred vision, or head injury. If no organic causes are obvious, then consider psychogenic or functional vomiting.

Examination

Signs of dehydration – dry tongue, decreased skin turgor, postural hypotension.

Smell of alcohol or ketones on the breath.

Abdominal examination for signs of peritonism, gastric stasis, or acute intestinal obstruction. A succussion “splash” is suggestive of gastric outlet obstruction.

CNS signs of meningism, nystagmus or papilledema.

Other important clinical features to look out for include:

Signs of uremia – sallow appearance, pericardial rub.

Signs of hypoadrenalism – pigmentation, postural hypotension.

Characteristic skin blisters of acute intermittent porphyria.

Investigations

In all cases, basic laboratory tests such as full blood count, urea, electrolytes, and inflammatory markers are essential. A pregnancy test should be performed in any female of reproductive age, preferably before any radiographic studies are performed. Subsequent investigations will be directed towards the suspected cause elicited from the history.

If infection is suspected:

Liver function tests.

Viral hepatitis serology.

Stool culture.

Urinalysis and urine culture (particularly in elderly patients).

If a visceral cause is suspected:

Serum pancreatic enzymes (amylase and lipase) – if acute epigastric tenderness suggests acute pancreatitis.

Plain abdominal radiographs (erect and supine) – in the presence of peritonism, they may show an ileus, small bowel obstruction or free gas due to perforation.

Abdominal ultrasound – may show gallstones and a thickened gallbladder wall if biliary signs are present.

Upper endoscopy or barium meal – to confirm gastric outlet obstruction, preferably

after

the residual gastric contents have been emptied using a nasogastric tube.

If a central nervous system cause is suspected:

Computerized tomography or magnetic resonance imaging of brain;

Lumbar puncture – should be avoided until the presence of raised intracranial pressure has definitely been excluded.

Vestibular testing.

Other tests to consider are synacthen test and urinary porphyrins.

Management of acute nausea and vomiting

A three-step approach is advocated:

Correction of any complications of vomiting such as dehydration and acid/electrolyte abnormalities.

Targeted therapy of identified cause of vomiting.

Symptomatic treatment if necessary.

Fluid replacement

If the patient is dehydrated and cannot tolerate oral fluids, intravenous fluid replacement using normal saline should be started. Potassium supplements may be required in patients with gastric outlet obstruction or if the vomiting has been associated with prolonged diarrhea. Management of diabetic ketoacidosis should be tailored according to local hospital guidelines.

Antiemetic drugs

These agents are useful in the acute phase in the majority of cases of acute vomiting where the underlying etiology is not clear but urgent symptomatic relief is necessary. In some cases, more than one agent may be required. The main types of antiemetic drugs are summarized in Table 2.2 and their clinical uses in Table 2.3.

Prochlorperazine (Stemetil®):

Particularly effective in vestibular vomiting. Its main side effects are extrapyramidal symptoms. It must be cautiously used in patients with Parkinson disease, narrow angle glaucoma and a history of phenothiazine sensitivity.

Oral prochlorperazine – 20 mg initially followed by 10 mg after 2 hours. For prevention, give 5–10 mg 2–3 times daily.

Sublingual (Buccastem®) – a 3 mg tablet can be placed high up between the upper lip and gums and left to dissolve. Recommended dosage is 1–2 tablets twice daily.

Suppository – a 25 mg suppository can be placed rectally stat, followed by oral dose after 6 hours if necessary.

Injection – give 12.5 mg stat by deep intramuscular injection, followed by oral dose after 6 hours if necessary.

Cyclizine (Valoid®):

This is a histamine H1 receptor antagonist and is effective in patients where there is a contraindication to the above. It can cause drowsiness and should be used with caution in the elderly. For severe vomiting or in patients who cannot tolerate oral medication, give 50 mg stat either by intramuscular or intravenous injection and this can be repeated 8-hourly. For less severe vomiting, oral dose 50 mg 8-hourly can be given.

Domperidone (Motilium®)

and metoclopramide (Maxolon

®

): These drugs are dopamine receptor antagonists and also function as prokinetic agents. Domperidone has not been approved for use in the USA. Metoclopramide is contraindicated in gastrointestinal obstruction and perforation. Domperidone can be given orally (10–20 mg) or rectally (30–60 mg) every 4–8 hours. Alternatively, give metoclopramide 10 mg, either oral or injections (intramuscular/intravenous) every 8 hours.

Ondansetron (Zofran®):

If all above fail, this serotonin 5-HT3 receptor antagonist can be given as a 4 mg dose either by intramuscular or intravascular injection. It can also be given as 16 mg suppositories. If vomiting is controlled after the initial dose, the oral form can be given up to a daily maximum dose of 32 mg in the 4 or 8 mg tablet form. 5-HT3 receptor antagonists are regarded as first line antiemetics for chemotherapy-induced vomiting and they are generally well tolerated.

Erythromicin

: This antibiotic can enhance gastric emptying but may not improve nausea. It has been used as a prokinetic agent in cases of gastroparesis, but there is not a clear evidence base for prolonged benefit.

Antidepressants

: These drugs have been used in cases of functional nausea and vomiting where conventional antiemetics have been unsuccessful. They should be used in conjunction with psychological supportive therapy. There are few data or strong evidence base from trial to support their efficacy.

Table 2.2 Classes of antiemetic drug.

Antimuscarinic

Scopalamine (hyoscine)

Antihistamine

Cyclizine

Promethazine

Meclozine

Cinnarazine

Antidopaminergic

Prochlorperazine

Domperidone

Metoclopramide

Antiserotoninergic

Ondansetron

Granisetron

Tropisetron

Table 2.3 Clinical uses of different antiemetics.

Antimuscarinic

Motion sickness

Antihistamine

Motion sickness, vestibular causes

AntidopaminergicExtensive indications including gastroenteritis, postoperative, chemo/radiotherapy-induced vomiting, medication

Antiserotoninergic

As above indications

Further reading

American Gastroenterology Association medical position statement: nausea and vomiting. Gastroenterology 2001;120:261.

Tack J, Talley NJ, Camilleri M, et al. Functional gastrointestinal disorders. In Rome III, The Functional Gastrointestinal Disorders, 3rd ed, Drossman DA, et al (eds), Degnon Associates, McLean, VA, 2006.

Flake ZA, Scalley RD, Bailey AG. Practical selection of anti-emetics. Am. Fam. Physician 2004;69:1169.

Management of specific causes of acute vomiting is described in detail in relevant chapters in this book.

CHAPTER 3Approach to upper gastrointestinal bleeding

Patrick B. Allen and Tony C. K. Tham

Ulster Hospital, Dundonald, Belfast, UK

Introduction

Upper gastrointestinal bleeding (UGIB) is a common presentation to emergency departments and associated with higher mortality with in-patients who experience UGIB. It commonly present with hematemesis (vomiting of blood) and/or melena (passage of black and tarry stools). The initial management of patients with UGIB involves an initial assessment, resuscitation if required, and then endoscopy to achieve hemostasis. A small number of patients may be discharged from the emergency department (ED) if they are deemed “low-risk” and an urgent endoscopy can be subsequently arranged; however, this practice varies throughout countries and institutions.

At endoscopy the major aim is to stratify the patients into low, medium, and high risk, depending on their initial findings and to perform therapeutic intervention if required to stop the bleeding and reduce the risk of recurrent bleeding post-endoscopy (rebleeding).

This chapter will summarize the approach and up-to-date management in patients with UGIB. (See also Chapter 22 on Acute Upper Non-variceal Gastrointestinal Hemorrhage and Chapter 25 on Variceal Hemorrhage.)

History

The symptoms and signs of patients presenting with upper gastrointestinal bleeding may include:

dyspepsia

epigastric pain

heartburn

weakness

syncope

hematemesis (e.g. coffee-ground vomitus, bright red vomitus, etc.)

melena (black stools)

hematochezia (bright red rectal bleeding)

weight loss

dysphagia.

Hematemesis suggests bleeding proximal to the ligament of Treitz. The character of vomitus can assist with the severity of bleeding – frank blood suggests active and more severe bleeding, whereas dark and coffee-ground vomitus suggests less active bleeding. The majority of patients with melena can have bleeding from the upper gastrointestinal tract; however, a small proportion may have bleeding from the small bowel or proximal right colon.

Causes of upper gastrointestinal bleeding

The causes of UGIB are summarized in Table 3.1 [1].

Table 3.1 Causes of upper gastrointestinal bleeding.

Source: Laine 2001 (1). Reproduced with permission of McGraw-Hill Education.

Source of bleeding

Frequency (%)

Peptic ulcer

35–62%

Gastroesophageal varices

4–31%

Mallory–Weiss tear

4–13%

Gastroduodenal erosions

3–11%

Erosive esophagitis

2–8%

Malignancy

1–4%

Unidentified source

7–25%

Past medical history

It is necessary to document the recent use of antiplatelet therapies and non-steroidal anti-inflammatory drugs (NSAIDs). Warfarin/low-molecular-weight heparins, and patients receiving newer anticoagulants such as Dabigatrin (Pradaxa®) and Rivaroxaban (Xarelto®), should be documented.

As peptic ulcers can recur, it is important to elicit a past medical history of peptic ulcer disease. A history of chronic alcohol abuse or likelihood of chronic viral hepatitis (B or C) increases the likelihood of variceal hemorrhage or portal gastropathy.

Examination and assessment

The initial evaluation of a patient with UGIB includes: a full history, physical examination, laboratory tests, and in some centers, nasogastric tube insertion (to estimate the volume and activity of the blood loss).

The benefit of a full initial evaluation is to assess the quantity of the bleed, the severity of the bleed, possible causes of the bleed, and any associated conditions that may be associated with a higher mortality (e.g. chronic liver disease).

In a recent meta-analysis on the indicators for UGIB, the specific indicators include: melena (likelihood ratio LR 5.1–5,9), melena identified on per-rectal exam (LR 25), blood or coffee ground-like vomitus detected during nasogastric lavage (LR 9.6), and a ratio of blood urea nitrogen to serum creatinine greater than 30 (LR 7.5) [2].

Specific factors associated with “severe bleeding” included red blood detected during nasogastric lavage (LR 3.1), tachycardia (LR 4.9), and or hemoglobin less than 8 g/dL (LR 4.5–6.2).

The majority of patients with melena can have bleeding from the upper gastrointestinal tract; however, a small proportion may have bleeding from the small bowel or proximal colon.

Initial assessment: risk stratification

See Chapter 22, Acute Upper Non-variceal Hemorrhage, for more details.

An urgent assessment of patients who present with UGIB should allow triage into low, medium-, and high-risk, and patients can be stratified according to risk with various risk calculators. The widely used calculators are the Glasgow Blatchford Score (GBS) (Table 3.2) and the Rockall Score (pre- and postendoscopy) (Table 3.3), and the AIMS-65 scoring systems (Table 3.4) (3,4).

Table 3.2 Glasgow-Blatchford Score for upper gastrointestinal bleeding.

Source: Blatchford 2013 (3) and Rockall 1996 (4). Reproduced with permission of Elsevier and the BMJ.

Admission risk marker

Score component value

Blood urea

≥6·5 <8·0

2

≥8·0 <10·0

3

≥10·0 <25·0

4

≥25

6

Hemoglobin (g/L) for men

12.0 <13.0

1

≥10.0 <12.0

3

<10.0

6

Hemoglobin for women

≥10.0 <12.0

1

<10.0

6

Systolic blood pressure (mmHg)

100–109

1

90–99

2

<90

3

Other markers

Pulse ≥100 (per min)

1

Presentation with melena

1

Presentation with syncope

2

Hepatic disease

2

Cardiac failure

2

Scores of 6 or greater were associated with a greater than 50% risk of requiring an intervention (3,4).

Table 3.3 Rockall Score for upper gastrointestinal bleeding.

Source: Rockall 1996 (4). Reproduced with permission of Elsevier and the BMJ.

Variable

Score 0

Score 1

Score 2

Score 3

Age

<60

60–79

>80

Shock

No shock

Pulse > 100 BP > 100 systolic

Systolic < 100

Co-morbidity

Nil

CCF, IHD, major morbidity

Renal failure, liver failure, metastatic cancer

Diagnosis

Mallory–Weiss tear

All other diagnoses

GI malignancy

Evidence of bleeding

None

Blood, adherent clot, spurting vessel

Table 3.4 Components of the pre-endoscopy AIMS 65 Score.

Source: Saltzman 2011 (21). Reproduction with permission from Elsevier.