Cyclic Vomiting Syndrome
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Childhood Functional Gastrointestinal Disorders: Child/Adolescent
Gastroenterology 2016;150:1456–1468 Childhood Functional Gastrointestinal Disorders: Child/ Adolescent Jeffrey S. Hyams,1,* Carlo Di Lorenzo,2,* Miguel Saps,2 Robert J. Shulman,3 Annamaria Staiano,4 and Miranda van Tilburg5 1Division of Digestive Diseases, Hepatology, and Nutrition, Connecticut Children’sMedicalCenter,Hartford, Connecticut; 2Division of Digestive Diseases, Hepatology, and Nutrition, Nationwide Children’s Hospital, Columbus, Ohio; 3Baylor College of Medicine, Children’s Nutrition Research Center, Texas Children’s Hospital, Houston, Texas; 4Department of Translational Science, Section of Pediatrics, University of Naples, Federico II, Naples, Italy; and 5Department of Gastroenterology and Hepatology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina Characterization of childhood and adolescent functional Rome III criteria emphasized that there should be “no evi- gastrointestinal disorders (FGIDs) has evolved during the 2- dence” for organic disease, which may have prompted a decade long Rome process now culminating in Rome IV. The focus on testing.1 In Rome IV, the phrase “no evidence of an era of diagnosing an FGID only when organic disease has inflammatory, anatomic, metabolic, or neoplastic process been excluded is waning, as we now have evidence to sup- that explain the subject’s symptoms” has been removed port symptom-based diagnosis. In child/adolescent Rome from diagnostic criteria. Instead, we include “after appro- IV, we extend this concept by removing the dictum that priate medical evaluation, the symptoms cannot be attrib- “ ” fi there was no evidence for organic disease in all de ni- uted to another medical condition.” This change permits “ tions and replacing it with after appropriate medical selective or no testing to support a positive diagnosis of an evaluation the symptoms cannot be attributed to another FGID. -
Cannabinoid Hyperemesis Syndrome: Diagnosis, Pathophysiology, and Treatment—A Systematic Review
J. Med. Toxicol. (2017) 13:71–87 DOI 10.1007/s13181-016-0595-z REVIEW Cannabinoid Hyperemesis Syndrome: Diagnosis, Pathophysiology, and Treatment—a Systematic Review Cecilia J. Sorensen1 & Kristen DeSanto2 & Laura Borgelt3 & Kristina T. Phillips4 & Andrew A. Monte1,5,6 Received: 26 September 2016 /Revised: 25 November 2016 /Accepted: 1 December 2016 /Published online: 20 December 2016 # American College of Medical Toxicology 2016 Abstract Cannabinoid hyperemesis syndrome (CHS) is a removed, 1253 abstracts were reviewed and 183 were in- syndrome of cyclic vomiting associated with cannabis cluded. Fourteen diagnostic characteristics were identi- use. Our objective is to summarize the available evidence fied, and the frequency of major characteristics was as on CHS diagnosis, pathophysiology, and treatment. We follows: history of regular cannabis for any duration of performed a systematic review using MEDLINE, Ovid time (100%), cyclic nausea and vomiting (100%), resolu- MEDLINE, Embase, Web of Science, and the Cochrane tion of symptoms after stopping cannabis (96.8%), com- Library from January 2000 through September 24, 2015. pulsive hot baths with symptom relief (92.3%), male pre- Articles eligible for inclusion were evaluated using the dominance (72.9%), abdominal pain (85.1%), and at least Grading and Recommendations Assessment, weekly cannabis use (97.4%). The pathophysiology of Development, and Evaluation (GRADE) criteria. Data CHS remains unclear with a dearth of research dedicated were abstracted from the articles and case reports and to investigating its underlying mechanism. Supportive were combined in a cumulative synthesis. The frequency care with intravenous fluids, dopamine antagonists, topi- of identified diagnostic characteristics was calculated cal capsaicin cream, and avoidance of narcotic medica- from the cumulative synthesis and evidence for patho- tions has shown some benefit in the acute setting. -
Acute Abdomen
Acute abdomen: Shaking down the Acute abdominal pain can be difficult to diagnose, requiring astute assessment skills and knowledge of abdominal anatomy 2.3 ANCC to discover its cause. We show you how to quickly and accurately CONTACT HOURS uncover the clues so your patient can get the help he needs. By Amy Wisniewski, BSN, RN, CCM Lehigh Valley Home Care • Allentown, Pa. The author has disclosed that she has no significant relationships with or financial interest in any commercial companies that pertain to this educational activity. NIE0110_124_CEAbdomen.qxd:Deepak 26/11/09 9:38 AM Page 43 suspects Determining the cause of acute abdominal rapidly, indicating a life-threatening process, pain is often complex due to the many or- so fast and accurate assessment is essential. gans in the abdomen and the fact that pain In this article, I’ll describe how to assess a may be nonspecific. Acute abdomen is a patient with acute abdominal pain and inter- general diagnosis, typically referring to se- vene appropriately. vere abdominal pain that occurs suddenly over a short period (usually no longer than What a pain! 7 days) and often requires surgical interven- Acute abdominal pain is one of the top tion. Symptoms may be severe and progress three symptoms of patients presenting in www.NursingMadeIncrediblyEasy.com January/February 2010 Nursing made Incredibly Easy! 43 NIE0110_124_CEAbdomen.qxd:Deepak 26/11/09 9:38 AM Page 44 the ED. Reasons for acute abdominal pain Visceral pain can be divided into three Your patient’s fall into six broad categories: subtypes: age may give • inflammatory—may be a bacterial cause, • tension pain. -
Nutritional Approaches to Chronic Nausea and Vomiting
NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #168 NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #168 Carol Rees Parrish, M.S., R.D., Series Editor Nutritional Approaches to Chronic Nausea and Vomiting Nitin K. Ahuja In addition to a relative lack of definitive diagnostics and effective therapies, maintenance of adequate nutritional intake can represent a significant challenge for patients with chronic nausea and vomiting. The strength and specificity of available dietary recommendations vary by underlying diagnosis, each of which has a tendency to overlap with others. The relevance of particular clinical distinctions (e.g. gastric emptying delay) is not yet certain, in light of which it may be the case that dietary recommendations for one patient category can be selectively applied to others with similar benefits. This brief review will consider the existing evidence basis for nutritional approaches to a variety of non-structural causes of chronic nausea and/or vomiting, including gastroparesis, chronic nausea and vomiting syndrome, functional dyspepsia, cyclic vomiting syndrome, and rumination syndrome. INTRODUCTION or a variety of reasons, chronic nausea and there is keen interest in potentially mitigating dietary vomiting can be difficult complaints to manage strategies. Chronic nausea and vomiting also may Fclinically. In cases of severe or refractory limit the adequacy of nutritional intake, which can symptoms, quality of life can be markedly diminished, necessitate consideration of enteral or parenteral which often corresponds with significant healthcare feeding alternatives. While several options exist for resource utilization.1 Objective testing modalities pharmacologic and mechanical intervention among beyond endoscopy and scintigraphy are also limited, patients with chronic nausea and vomiting, this review leading to a sometimes frustrating lack of etiologic will focus on nutrition-based approaches to their specificity and often empiric patterns of therapeutic longitudinal support. -
Travelers' Diarrhea
Travelers’ Diarrhea What is it and who gets it? Travelers’ diarrhea (TD) is the most common illness affecting travelers. Each year between 20%-50% of international travelers, an estimated 10 million persons, develop diarrhea. The onset of TD usually occurs within the first week of travel but may occur at any time while traveling and even after returning home. The primary source of infection is ingestion of fecally contaminated food or water. You can get TD whenever you travel from countries with a high level of hygiene to countries that have a low level of hygiene. Poor sanitation, the presence of stool in the environment, and the absence of safe restaurant practices lead to widespread risk of diarrhea from eating a wide variety of foods in restaurants, and elsewhere. Your destination is the most important determinant of risk. Developing countries in Latin America, Africa, the Middle East, and Asia are considered high risk. Most countries in Southern Europe and a few Caribbean islands are deemed intermediate risk. Low risk areas include the United States, Canada, Northern Europe, Australia, New Zealand, and several of the Caribbean islands. Anyone can get TD, but persons at particular high-risk include young adults , immunosuppressed persons, persons with inflammatory-bowel disease or diabetes, and persons taking H-2 blockers or antacids. Attack rates are similar for men and women. TD is caused by bacteria, protozoa or viruses that are ingested by eating contaminated food or beverages. For short-term travelers in most areas, bacteria are the cause of the majority of diarrhea episodes. What are common symptoms of travelers’ diarrhea? Most TD cases begin abruptly. -
Cyclical Vomiting Syndrome (CVS) Is a Rare Condition Affecting ~3 in 100,000 Children, with Caucasian but No Sex Predominance
orphananesthesia Anaesthesia recommendations for patients suffering from Cyclical (or cyclic) vomiting syndrome Disease name: Cyclical (or cyclic) vomiting syndrome ICD 10: G43.A0 Synonyms: Cyclical vomiting, not intractable; persistent vomiting, cyclical; cyclic vomiting, psychogenic Cyclical vomiting syndrome (CVS) is a rare condition affecting ~3 in 100,000 children, with Caucasian but no sex predominance. It is generally a disorder of childhood with symptom onset in pre or early school age. Adult cases (onset in 3rd to 4th decade) are also reported. As patients are well in between episodes, there is usually a delay in diagnosis (2-3 years in children, longer in adults), with frequent emergency department presentations. It is a diagnosis of exclusion. Diagnostic criteria have been published by various bodies including the North American Society for Pediatric Gastroenterology, Hepatology and Nutrition, the Rome Foundation (Rome IV 2016 under functional gastrointestinal disorders) and also the International Classification of Headache Disorders (3rd edition beta version). This reflects the uncertainty about the pathophysiology of the syndrome, described variously as functional, psychiatric, neurological either epileptogenic or autonomic dysfunction, association with or triggered by cannabis use versus a migraine variant or as episodic symptoms associated with migraine. Medicine in progress Perhaps new knowledge Every patient is unique Perhaps the diagnostic is wrong Find more information on the disease, its centres of reference and patient organisations on Orphanet: www.orpha.net 1 Disease summary The pattern experienced by an individual is stereotypical: a prodrome including nausea, a hyperemesis/vomiting phase (typically 6-8 episodes per hour for a few days; associated with continuing nausea, headache and abdominal pain), recovery phase and an asymptomatic phase of a few to several weeks. -
GASTROINTESTINAL COMPLAINT Nausea, Vomiting, Or Diarrhea (For Abdominal Pain – Refer to SO-501) I
DESCHUTES COUNTY ADULT JAIL SO-559 L. Shane Nelson, Sheriff Standing Order Facility Provider: October 17, 2018 STANDING ORDER GASTROINTESTINAL COMPLAINT Nausea, Vomiting, or Diarrhea (for Abdominal Pain – refer to SO-501) I. ASSESSMENT a. History i. Onset and duration ii. Frequency of vomiting, nausea, or diarrhea iii. Blood in stool or black stools? Blood in emesis or coffee-ground appearance? If yes, refer to SO-510 iv. Medications taken – do they help? v. Do they have abdominal pain? If yes, refer to SO-501 Abdominal Pain. vi. Do they have other symptoms – dysuria, urinary frequency, urinary urgency, urinary incontinence, vaginal/penile discharge, hematuria, fever, chills, flank pain, abdominal/pelvic pain in females or testicular pain in males, vaginal or penile lesions/sores? (if yes to any of the above – refer to Dysuria SO-522) vii. LMP in female inmates – if unknown, obtain HCG viii. History of substance abuse? Are they withdrawing? Refer to appropriate SO based on substance history and withdrawal concerns. ix. History of IBS or other known medical causes of chronic diarrhea, nausea, or vomiting? Have prescriptions been used for this in the past? x. History of abdominal surgeries? xi. Recent exposure to others with same symptoms? b. Exam i. Obtain Vital signs, including temperature ii. If complaints of dizziness or lightheadedness with standing, obtain orthostatic VS. iii. Is there jaundice present? iv. Are there signs of dehydration – tachycardia, tachypnea, lethargy, changes in mental status, dry mucous membranes, pale skin color, decreased skin turgor? v. Are you concerned for an Acute Gastroenteritis? Supersedes: March 20, 2018 Review Date: October 2020 Total Pages: 3 1 SO-559 October 17, 2018 Symptoms Exam Viruses cause 75-90% of acute gastroenteritis here in the US. -
Recurrent Abdominal Pain and Vomiting
A SELF-TEST IM BOARD REVIEW ON A CME EDUCATIONAL OBJECTIVE: Readers will be aware of narcotic bowel syndrome as a consequence CLINICAL CREDIT of prolonged narcotic use. CASE MARKUS AGITO, MD MAGED RIZK, MD Department of Internal Medicine, Quality Improvement Officer, Digestive Akron General Medical Center, Disease Institute, Cleveland Clinic; Assistant Akron, OH Professor, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH Recurrent abdominal pain and vomiting 32-year-old man presents to the emer- Based on the information available, which A gency department with excruciating is the least likely cause of his symptoms? abdominal pain associated with multiple epi- 1 sodes of vomiting for the past 2 days. He re- □ Acute pancreatitis ports no fevers, headaches, diarrhea, constipa- □ Cyclic vomiting syndrome tion, hematochezia, melena, musculoskeletal □ Acute intermittent porphyria symptoms, or weight loss. His abdominal pain □ Gastroparesis is generalized and crampy. It does not radiate Acute pancreatitis and has no precipitating factors. The pain is Acute pancreatitis is the least likely cause of relieved only with intravenous narcotics. his symptoms. It is commonly caused by gall- stones, alcohol, hypertriglyceridemia, and cer- See related editorial, page 441 tain drugs.1 The associated abdominal pain is usually epigastric, radiates to the back, and is He does not smoke, drink alcohol, or use accompanied by nausea or vomiting, or both. illicit drugs. He has no known drug or food The onset of pain is sudden and rapidly increas- allergies. He says that his current condition es in severity within 30 minutes. CT shows en- causes him emotional stress that affects his largement of the pancreas with diffuse edema, A year ago, performance at work. -
Status of Brain Imaging in Gastroparesis
Review Status of Brain Imaging in Gastroparesis Zorisadday Gonzalez * and Richard W. McCallum Division of Gastroenterology, Center for Neurogastroenterology and GI Motility, Department of Internal Medicine, Texas Tech University Health Sciences Center, 4800 Alberta Ave., El Paso, TX 79905, USA; [email protected] * Correspondence: [email protected] Received: 6 March 2020; Accepted: 7 April 2020; Published: 9 April 2020 Abstract: The pathophysiology of nausea and vomiting in gastroparesis is complicated and multifaceted involving the collaboration of both the peripheral and central nervous systems. Most treatment strategies and studies performed in gastroparesis have focused largely on the peripheral effects of this disease, while our understanding of the central nervous system mechanisms of nausea in this entity is still evolving. The ability to view the brain with different neuroimaging techniques has enabled significant advances in our understanding of the central emetic reflex response. However, not enough studies have been performed to further explore the brain–gut mechanisms involved in nausea and vomiting in patients with gastroparesis. The purpose of this review article is to assess the current status of brain imaging and summarize the theories about our present understanding on the central mechanisms involved in nausea and vomiting (N/V) in patients with gastroparesis. Gaining a better understanding of the complex brain circuits involved in the pathogenesis of gastroparesis will allow for the development of better antiemetic prophylactic and treatment strategies. Keywords: gastroparesis; brain imaging; functional magnetic resonance imaging (fMRI); positron emission tomography (PET) scan; central nervous system (CNS) 1. Introduction Gastroparesis is a chronic heterogeneous motor disorder with variable clinical manifestations including episodic nausea, vomiting, retching, post-prandial fullness, early satiety, and/or upper abdominal pain in the absence of mechanical obstruction [1]. -
Management of Gastrointestinal Disorders in Rett Syndrome
Management of gastrointestinal disorders in Rett syndrome Jenny Downs & Helen Leonard Telethon Kids Institute, Perth, Western Australia What is meant by gastrointestinal disorders? The three most common gastro-intestinal problems affecting girls and women with Rett syndrome are: constipation, Gastro-Oesophageal Reflux Disease or Gastro-Esophageal Reflux Disease (GORD/GERD or reflux) and abdominal bloating. Constipation occurs where stools are dry, hard and difficult to pass. Constipation can cause considerable discomfort and pain. Reflux occurs when the muscle at the lower end of the oesophagus does not close properly after food has passed through to the stomach. As a result, stomach contents can pass back up the oesophagus which can be painful, and in extreme cases, damage to the oesophagus lining. Acid may also flow back into the oesophagus when the stomach doesn’t empty properly. This is known as delayed gastric emptying. Abdominal bloating describes the swelling of the abdomen, accompanied by feelings of tightness, fullness, discomfort and pain. Why do gastrointestinal disorders occur in Rett syndrome? As the digestive system operates alongside other systems in the body (the nervous, circulatory, muscular -skeletal, respiratory and endocrine systems), disruptions to any of these systems can affect the healthy operation of the digestive system. • Reduced intestinal motility, physical activity and some side effects from various medications may cause individuals with Rett syndrome to suffer constipation. • Reflux is likely to occur in individuals with restricted mobility and/or scoliosis. • The tendency to hyperventilate, breath hold and swallow air can cause abdominal bloating. Pain, anxiety and excitement may exacerbate these issues and increase discomfort. -
ORIGINAL ARTICLE Non-Caucasian Race, Chronic Opioid Use and Lack
AJHM Volume 5 Issue 1 (Jan-March 2021) ORIGINAL ARTICLE ORIGINAL ARTICLE Non-Caucasian Race, Chronic Opioid Use and Lack of Insurance or Public Insurance were Predictors of Hospitalizations in Cyclic Vomiting Syndrome Vikram Kanagala, MD1; Sanjay Bhandari, MD2; Tatyana Taranukha, MD1; Lisa Rein, PhD3; Ruta Brazauskas, PhD3; Thangam Venkatesan, MD1 1Division of Gastroenterology and Hepatology, Department of Internal Medicine, Medical College of Wisconsin, Milwaukee, WI 2Division of General Internal Medicine, Department of Internal Medicine, Medical College of Wisconsin, Milwaukee, WI 3Department of Biostatistics, Medical College of Wisconsin, Milwaukee, WI. Corresponding author: Thangam Venkatesan, MD. 8701 Watertown Plank Rd. Medical Education Building. ([email protected]) Received: April 24, 2020. Revised: January 2, 2021. Accepted: March 3, 2021. Published: March 31, 2021. Am j Hosp Med 2021 Jan;5(1):2021. DOI: https://doi.org/10.24150/ajhm/2021.001 Introduction: Cyclic vomiting syndrome (CVS) is associated with frequent hospitalizations; risk factors for this are unknown. We sought to determine predictors of increased hospitalizations and length of hospital stay (LOS). Methods: We performed a retrospective review of patients with CVS at a tertiary referral center. Clinical characteristics and details about yearly hospitalizations and LOS were assessed; follow- up was divided into two one-year periods before and after the initial clinic visit. Negative binomial regression was used to assess predictors of hospital admission and total length of stay for each time period; the regression results are presented as ratio ratios (RRs). Results: Of 118 patients (70% female, 73% Caucasian), mean follow up was 3.4 2 years. During the first year of follow up, chronic opioid use (Rate Ratio [RR] 2.22) and being uninsured or having public health insurance (RR, 2.39) were associated with higher rates of hospitalization. -
TUMOUR and TREATMENT SIDE-EFFECTS
TUMOUR and TREATMENT SIDE-EFFECTS TUMOUR TUMOUR TREATMENT EFFECTS RADIATION SITE EFFECTS CHEMOTHERAPY SURGERY THERAPY Head & Neck Difficulty Nausea Mucositis Impaired chewing & chewing or Vomiting Stomatitis swallowing swallowing Diarrhea Dysgeusia, Xerostomia Stomatitis hypogeusia Xerostomia, dysphagia Difficulty chewing secondary to dental decay or infection Viscous saliva Oropharyngeal ulceration Osteoradionecrosis Fistula Trismus Esophagus Dysphagia Nausea Dysphagia Decreased gastric secondary to Esophagitis motility esophageal Esophageal fibrosis or Decreased gastric obstruction stricture acid production Regurgitation Fistula Fistula of meals Nausea Esophageal stenosis Edema Regurgitation Steatorrhea Stomach Early satiety Nausea Nausea Fat malabsorption & Vomiting after Vomiting Vomiting diarrhea meals Stomatitis Decreased gastric Diarrhea motility "Dumping" syndrome Hypoglycemia Protein malabsorption Deficiences in iron, calcium, fat-soluble vitamins & vitamin B12 Esophagitis Pancreas & Malabsorption Nausea Nausea Diabetes mellitus biliary tree &/or diabetes Vomiting Vomiting Malabsorption of fat, secondary to Stomatitis protein, & fat-soluble pancreatic Diarrhea vitamins & insufficiency Minerals Dysgeusia Nausea Small Bowel Nausea Gastrointestinal Loss of bile salts, intestine obstruction Stomatitis ulceration calcium, magnesium, Malabsorption Diarrhea Villous hypoplasia zinc Malabsorption Metabloic acidosis secondary to Increased risk of decreased enzyme renal stones production Postoperative gastric Intestinal fistula hypersecretion