DOCSLIB.ORG

Palliation of Nausea and Vomiting in Malignancy

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Palliation of Nausea and Vomiting in Malignancy CME Palliative care Palliation of nausea Nausea and vomiting are common Mechanisms of nausea and symptoms that can cause enormous vomiting misery for cancer patients, undermining and vomiting in quality of life and contributing to weak- Emesis is a protective reflex triggered by ness, anorexia and nutritional problems.1 physical stimuli that include poisoning malignancy Evidence-based recommendations for and overdistension of hollow viscera, the management of treatment-induced psychological stimuli or vestibular emesis are available, but the manage- stimulation (including motion sickness). Kathryn Mannix MB BS FRCP, Consultant in ment of nausea arising as a consequence The various nerve pathways activated by Palliative Medicine, Royal Victoria Infirmary of the disease itself is less well researched. 4 and Marie Curie Hospice, Newcastle upon these stimuli are summarised in Fig 1. Tyne This article summarises palliative care Chemical triggers to nausea are guidelines derived from animal models detected at the chemoreceptor trigger and validated in a range of human Clin Med 2006;6:144–7 zone (CTZ) in the floor of the 4th studies.2,3 ventricle. Here, there is effectively no Higher centres: D receptors • pain 2 • haloperidol Chemicals in • fear 5HT receptors blood: • memory 3 • ‘–setrons’ • drugs • metabolites • toxins D2 5HT3 CTZ H receptors 1 Ach • cyclizine m Achm receptors • hyoscine hydrobromide Achm 5HT2 receptors VIII • levomepromazine nucleus VC H1 H1 5HT2 Autonomic afferents Stretch receptors in serosae and viscera: • head and neck • thorax Emesis: • abdomen and pelvis • nausea • retching • vomiting © Kathryn Mannix 2005 Fig 1. Pathways and neurotransmitters involved in nausea and vomiting. Achm = muscarinic acetylcholine receptors; CTZ = chemoreceptor trigger zone; D2 = dopamine type 2; H1 = histamine type 1; 5HT2 and 3 = serotonin receptor subtypes 2 and 3; po = oral; pr = per rectum; sc = subcutaneous; sl = sublingual; TD = transdermal; VC = vomiting centre. Copyright retained by K Mannix. 144 Clinical Medicine Vol 6 No 2 March/April 2006 CME Palliative care blood-brain barrier so water-soluble more selective the binding of a drug, the 6 Give the drug regularly and titrate the chemicals in blood can diffuse into the fewer its side effects. Relative binding dose carefully, with frequent review cerebrospinal fluid and stimulate the affinities are summarised in Table 1. of the patient. chemoreceptors there. 7If symptoms persist, review all the The vomiting centre (VC) in the brain- steps: The eight key steps to stem integrates all the components of the Is another cause also present, reflex, resulting in nausea, salivation, successful management of • nausea requiring an additional pallor, sweating, retching, protective anti-emetic? closure of the glottis and vomiting. The 1 Identify the likely cause(s) of nausea Is a different cause more likely VC receives sensory input from auto- • and/or vomiting: to make an accurate now that there has been more nomic nerves; stretch receptors on these diagnosis of cause(s) requires a time to assess the patient? nerve terminals detect distortion such as thorough assessment including 8Consider whether the trigger can be liver capsule stretch by metastatic disease, history, examination and diagnostic removed: for example, treat peritoneal distortion by para-aortic tests, including biochemistry, hypercalcaemia, reverse intestinal lymphadenopathy or bowel dilatation due infection screen, imaging etc. to obstruction or constipation. Afferents obstruction and reduce raised 2 Identify the pathway by which each include the vagus, sympathetic trunk and intracranial pressure. Maintain cause triggers the vomiting reflex glossopharyngeal nerve. The VC also anti-emetics until the trigger is (Fig 1). receives input from higher centres, for reversed: if reversal is not possible, 3 Identify the neurotransmitter receptor example, fear, pain and memory. long-term anti-emetic therapy may involved in each pathway identified. be necessary to maintain palliation. 4 Prescribe the most potent antagonist Choosing an anti-emetic to each receptor identified (Table 1). Other anti-emetic drugs With knowledge both of the central path- It is usually sufficient to block one ways that mediate nausea and vomiting receptor at the VC. • Corticosteroids are known to have and of the neuroreceptors involved, it is 5Choose a route of administration that intrinsic anti-emetic action which is possible to select specific receptor antago- ensures the drug will reach its not well understood. In addition, nist drugs as anti-emetics.5 The efficacy of receptors: gastric stasis is usually their mass-reducing effects may a drug as an anti-emetic is proportional to present in nausea, often precluding reduce stimulus to nausea in its binding affinity for its receptor.6 The the oral route. advanced cancer. Table 1. Receptor binding affinities of commonly used receptor-specific anti-emetic drugs. Receptor binding Achm H1 5HT3 αAd (antagonists Drug Recommended D2 5HT2 (VC and VIII (VC and VIII (vagal afferent cause dose (CTZ) (VC) nucleus) nucleus) endings) hypotension) Haloperidol 1.5–3 mg daily po or sc +++ – – – – – Metoclopramide 10–20 mg tds po or sc ++ – – – (+) – Cyclizine 50 mg tds po or sc – – (+) +++ – – Levomepromazine 6.25–12.5 mg daily po or sc + +++ + + – – Domperidone (does 10–20 mg tds po + – – – – – not cross blood- 30–60 mg tds pr brain barrier) Prochlorperazine + – + + – + (not recommended) Hyoscine 400 µg qds sl or sc – – +++ – – – hydrobromide 500–1,500 µg/72 h TD patch Granisetron, – – – – +++ – ondansetron, etc (not recommended) αAd = α-adrenergic; Achm = muscarinic acetylcholine receptors; CTZ = chemoreceptor trigger zone; D2 = dopamine type 2; H1 = histamine type 1; 5HT2 and 5HT3 = serotonin receptor subtypes 2 and 3; po = oral; pr = per rectum; sc = subcutaneous; sl = sublingual; TD = transdermal; VC = vomiting centre. Clinical Medicine Vol 6 No 2 March/April 2006 145 CME Palliative care Serotonin-3 (5HT ) receptor Clinical examples • 3 antagonists are widely overprescribed. 1 Bowel obstruction below jejunum They are effective for early emesis Triggers to nausea: stretch behind obstruction stimulates VC induced by chemotherapy or during pain (bowel inflammation and colic) stimulates VC radiotherapy across the absorption of bacterial toxins stimulates CTZ gastrointestinal tract (eg low thoracic Management: Establish whether or not surgery or stenting is appropriate: many spine, total body irradiation) but patients with advanced disease or peritoneal metastases are not candidates for surgery7 and require medical palliation. probably have no role in other types of nausea caused by cancer. Cyclizine 50 mg tds sc or per rectum to block VC activity. Constipation is a major side effect of Haloperidol 1.5–3 mg sc daily in addition, if nausea persists. Once nausea is controlled, oral dosing is effective. this class of drugs. Consider: Anticholinergic agents (hyoscine butylbromide 40–120 mg/day or • Neurokinin-1 (NK1) receptor glycopyrrolate 0.1–0.2 mg tds sc) or octreotide 200–1,000 µg/day8 blockers are effective anti-emetics. can be used as antisecretory agents and will also relax smooth NK1 receptors are widely distributed muscle, thus reducing colic. in the brain. An oral NK1-receptor High-dose corticosteroids may help to reduce pressure and restore patency in malignant bowel obstruction, at least temporarily antagonist is licensed for use in (eg dexamethasone 12–16 mg daily).9 chemotherapy-induced nausea; its Correction of dehydration may reduce symptoms.8 role in palliative care has yet to be The use of nasogastric tubes and prolonged intravenous fluids is unnecessary; nasogastric explored. tubes may aggravate nausea by glossopharyngeal stimulation and vigorous rehydration will enhance intraluminal secretion of fluid, increasing pressure, colic and nausea. Non-pharmacological measures Patients can eat and drink for pleasure; they should be warned to expect intermittent mechanical vomits, although it should be possible to control nausea. Attention should be paid to mood and 2 Ureteric obstruction morale, reducing exposure to strong Triggers to nausea: ureteric stretch stimulates VC cooking smells and providing small, uraemia stimulates CTZ palatable meals. Carbohydrate meals are toxic drug accumulation due stimulates CTZ often better tolerated; sour flavours may to reduced renal clearance be preferred by some patients (eg citrus Management: Ureteric stenting will palliate both stretch and chemical stimulation of sorbets, lemon drinks). nausea, but is not always possible. Psychological techniques to palliate Cyclizine 50 mg tds sc or per rectum to block VC activity. Haloperidol 1.5–3 mg sc daily in addition, if there is renal insufficiency. nausea due to advanced disease have not Doses of renally-excreted drugs will also need to be modified. been systematically studied, but studies of relaxation using progressive muscle 3 Gastric stasis relaxation and guided mental imagery in Gastric emptying may be delayed by anticholinergic drugs, increased intra-abdominal pressure or compression of the gastric outlet. chemotherapy patients have shown that the stress of treatment-related nausea Symptoms: Stretching of the stomach by ingested food, drink and air, and by gastric secretions causes distortion of the oesophageal sphincter. This can be reduced by these methods. permits acid reflux causing heartburn, whilst the distending stomach Acupuncture and acupressure have irritates the diaphragm causing hiccups. demonstrated useful
Load more

Recommended publications
  • The American Society of Colon and Rectal Surgeons Clinical Practice Guidelines for the Management of Inherited Polyposis Syndromes Daniel Herzig, M.D
    CLINICAL PRACTICE GUIDELINES The American Society of Colon and Rectal Surgeons Clinical Practice Guidelines for the Management of Inherited Polyposis Syndromes Daniel Herzig, M.D. • Karin Hardimann, M.D. • Martin Weiser, M.D. • Nancy Yu, M.D. Ian Paquette, M.D. • Daniel L. Feingold, M.D. • Scott R. Steele, M.D. Prepared by the Clinical Practice Guidelines Committee of The American Society of Colon and Rectal Surgeons he American Society of Colon and Rectal Surgeons METHODOLOGY (ASCRS) is dedicated to ensuring high-quality pa- tient care by advancing the science, prevention, and These guidelines are built on the last set of the ASCRS T Practice Parameters for the Identification and Testing of management of disorders and diseases of the colon, rectum, Patients at Risk for Dominantly Inherited Colorectal Can- and anus. The Clinical Practice Guidelines Committee is 1 composed of society members who are chosen because they cer published in 2003. An organized search of MEDLINE have demonstrated expertise in the specialty of colon and (1946 to December week 1, 2016) was performed from rectal surgery. This committee was created to lead interna- 1946 through week 4 of September 2016 (Fig. 1). Subject tional efforts in defining quality care for conditions related headings for “adenomatous polyposis coli” (4203 results) to the colon, rectum, and anus, in addition to the devel- and “intestinal polyposis” (445 results) were included, us- opment of Clinical Practice Guidelines based on the best ing focused search. The results were combined (4629 re- available evidence. These guidelines are inclusive and not sults) and limited to English language (3981 results), then prescriptive.
    [Show full text]
  • Hepatoblastoma and APC Gene Mutation in Familial Adenomatous Polyposis Gut: First Published As 10.1136/Gut.39.6.867 on 1 December 1996
    Gut 1996; 39: 867-869 867 Hepatoblastoma and APC gene mutation in familial adenomatous polyposis Gut: first published as 10.1136/gut.39.6.867 on 1 December 1996. Downloaded from F M Giardiello, G M Petersen, J D Brensinger, M C Luce, M C Cayouette, J Bacon, S V Booker, S R Hamilton Abstract tumours; and extracolonic cancers of the Background-Hepatoblastoma is a rare, thyroid, duodenum, pancreas, liver, and rapidly progressive, usually fatal child- brain.1-4 hood malignancy, which if confined to the Hepatoblastoma is a rare malignant liver can be cured by radical surgical embryonal tumour of the liver, which occurs in resection. An association between hepato- infancy and childhood. An association between blastoma and familial adenomatous hepatoblastoma and familial adenomatous polyposis (FAP), which is due to germline polyposis was first described by Kingston et al mutation of the APC (adenomatous in 1982,6 and since then over 30 additional polyposis coli) gene, has been confirmed, cases have been reported.7-15 Moreover, a but correlation with site of APC mutation pronounced increased relative risk of hepato- has not been studied. blastoma in patients affected with FAP and Aim-To analyse the APC mutational their first degree relatives has been found spectrum in FAP families with hepato- (relative risk 847, 95% confidence limits 230 blastoma as a possible basis to select and 2168).16 kindreds for surveillance. FAP is caused by germline mutations of the Patients-Eight patients with hepato- APC (adenomatous polyposis coli) gene blastoma in seven FAP kindreds were located on the long arm of chromosome 5 in compared with 97 families with identified band q2 1.17-'20The APC gene has 15 exons and APC gene mutation in a large Registry.
    [Show full text]
  • Familial Adenomatous Polyposis Polymnia Galiatsatos, M.D., F.R.C.P.(C),1 and William D
    American Journal of Gastroenterology ISSN 0002-9270 C 2006 by Am. Coll. of Gastroenterology doi: 10.1111/j.1572-0241.2006.00375.x Published by Blackwell Publishing CME Familial Adenomatous Polyposis Polymnia Galiatsatos, M.D., F.R.C.P.(C),1 and William D. Foulkes, M.B., Ph.D.2 1Division of Gastroenterology, Department of Medicine, The Sir Mortimer B. Davis Jewish General Hospital, McGill University, Montreal, Quebec, Canada, and 2Program in Cancer Genetics, Departments of Oncology and Human Genetics, McGill University, Montreal, Quebec, Canada Familial adenomatous polyposis (FAP) is an autosomal-dominant colorectal cancer syndrome, caused by a germline mutation in the adenomatous polyposis coli (APC) gene, on chromosome 5q21. It is characterized by hundreds of adenomatous colorectal polyps, with an almost inevitable progression to colorectal cancer at an average age of 35 to 40 yr. Associated features include upper gastrointestinal tract polyps, congenital hypertrophy of the retinal pigment epithelium, desmoid tumors, and other extracolonic malignancies. Gardner syndrome is more of a historical subdivision of FAP, characterized by osteomas, dental anomalies, epidermal cysts, and soft tissue tumors. Other specified variants include Turcot syndrome (associated with central nervous system malignancies) and hereditary desmoid disease. Several genotype–phenotype correlations have been observed. Attenuated FAP is a phenotypically distinct entity, presenting with fewer than 100 adenomas. Multiple colorectal adenomas can also be caused by mutations in the human MutY homologue (MYH) gene, in an autosomal recessive condition referred to as MYH associated polyposis (MAP). Endoscopic screening of FAP probands and relatives is advocated as early as the ages of 10–12 yr, with the objective of reducing the occurrence of colorectal cancer.
    [Show full text]
  • Cancer Treatment and Survivorship Facts & Figures 2019-2021
    Cancer Treatment & Survivorship Facts & Figures 2019-2021 Estimated Numbers of Cancer Survivors by State as of January 1, 2019 WA 386,540 NH MT VT 84,080 ME ND 95,540 59,970 38,430 34,360 OR MN 213,620 300,980 MA ID 434,230 77,860 SD WI NY 42,810 313,370 1,105,550 WY MI 33,310 RI 570,760 67,900 IA PA NE CT 243,410 NV 185,720 771,120 108,500 OH 132,950 NJ 543,190 UT IL IN 581,350 115,840 651,810 296,940 DE 55,460 CA CO WV 225,470 1,888,480 KS 117,070 VA MO MD 275,420 151,950 408,060 300,200 KY 254,780 DC 18,750 NC TN 470,120 AZ OK 326,530 NM 207,260 AR 392,530 111,620 SC 143,320 280,890 GA AL MS 446,900 135,260 244,320 TX 1,140,170 LA 232,100 AK 36,550 FL 1,482,090 US 16,920,370 HI 84,960 States estimates do not sum to US total due to rounding. Source: Surveillance Research Program, Division of Cancer Control and Population Sciences, National Cancer Institute. Contents Introduction 1 Long-term Survivorship 24 Who Are Cancer Survivors? 1 Quality of Life 24 How Many People Have a History of Cancer? 2 Financial Hardship among Cancer Survivors 26 Cancer Treatment and Common Side Effects 4 Regaining and Improving Health through Healthy Behaviors 26 Cancer Survival and Access to Care 5 Concerns of Caregivers and Families 28 Selected Cancers 6 The Future of Cancer Survivorship in Breast (Female) 6 the United States 28 Cancers in Children and Adolescents 9 The American Cancer Society 30 Colon and Rectum 10 How the American Cancer Society Saves Lives 30 Leukemia and Lymphoma 12 Research 34 Lung and Bronchus 15 Advocacy 34 Melanoma of the Skin 16 Prostate 16 Sources of Statistics 36 Testis 17 References 37 Thyroid 19 Acknowledgments 45 Urinary Bladder 19 Uterine Corpus 21 Navigating the Cancer Experience: Treatment and Supportive Care 22 Making Decisions about Cancer Care 22 Cancer Rehabilitation 22 Psychosocial Care 23 Palliative Care 23 Transitioning to Long-term Survivorship 23 This publication attempts to summarize current scientific information about Global Headquarters: American Cancer Society Inc.
    [Show full text]
  • Sporadic (Nonhereditary) Colorectal Cancer: Introduction
    Sporadic (Nonhereditary) Colorectal Cancer: Introduction Colorectal cancer affects about 5% of the population, with up to 150,000 new cases per year in the United States alone. Cancer of the large intestine accounts for 21% of all cancers in the US, ranking second only to lung cancer in mortality in both males and females. It is, however, one of the most potentially curable of gastrointestinal cancers. Colorectal cancer is detected through screening procedures or when the patient presents with symptoms. Screening is vital to prevention and should be a part of routine care for adults over the age of 50 who are at average risk. High-risk individuals (those with previous colon cancer , family history of colon cancer , inflammatory bowel disease, or history of colorectal polyps) require careful follow-up. There is great variability in the worldwide incidence and mortality rates. Industrialized nations appear to have the greatest risk while most developing nations have lower rates. Unfortunately, this incidence is on the increase. North America, Western Europe, Australia and New Zealand have high rates for colorectal neoplasms (Figure 2). Figure 1. Location of the colon in the body. Figure 2. Geographic distribution of sporadic colon cancer . Symptoms Colorectal cancer does not usually produce symptoms early in the disease process. Symptoms are dependent upon the site of the primary tumor. Cancers of the proximal colon tend to grow larger than those of the left colon and rectum before they produce symptoms. Abnormal vasculature and trauma from the fecal stream may result in bleeding as the tumor expands in the intestinal lumen.
    [Show full text]
  • VARYING DEGREES of MALIGNANCY in CANCER of the BREAST Differences in the Degree of Malignancy of Malignant Tumors Have Been Reco
    VARYING DEGREES OF MALIGNANCY IN CANCER OF THE BREAST ROBERT 13. GREENOUGH BOSTON Differences in the degree of malignancy of malignant tumors have been recognized by pathologists for many years. Indeed, Virchow’s original conception of a malignant tumor was one composed of cells, derived from the tissue cells of the individual, but differing from the normal cells in the rapidity and independ- ence of their growth. Hansemann (1) carried this idea somewhat further and intro- duced the word “anaplasia” to indicate the process by which cancer cells came to differ from the normal type cell of the body tissue concerned. Anaplasia involves a loss of differentiation and an increase of reproductive power, so that the anaplastic cell fulfils only in abortive fashion, if at all, its normal function, such as secretion or keratinization; while it shows by increased number of mitotic figures, and especially by the irregularity and abnormality of its nuclear chromatic elements and figures, the increase in rapidity of cell division and of cell growth which is characteristic of malignancy. X number of attempts have been made to grade the malig- nancy of different breast tumors by distinguishing their histo- logical characteristics, such as adenocarcinoma, medullary, scirrhus, colloid, etc. ; but with the exception of adenocarcinoma and colloid, these divisions have proved of little value in prognosis. There the matter rested till 1921, when, under the influence of MacCarty (2) of the Mayo Clinic, Broders published a paper suggesting the classification of cancer tissue according to the degree of malignancy, as estimated by loss of differentiation and increase of reproductive characteristics.
    [Show full text]
  • Early Pancreatic Cancers: Pearls, Pitfalls and Mimics
    Early Pancreatic Cancers: Pearls, Pitfalls and Mimics H A Siddiki, MD, J G Fletcher, MD, N Takahashi, MD, J L Fidler, MD, N Dajani, MD, J E Huprich, MD, D M Hough, MD Department of Radiology, Mayo Clinic, Rochester, MN PURPOSE Overview and Test Cases Discussion Atypical Findings of Pancreatic Cancer Pitfalls in Tumor Detection Pancreatic Cancer Mimics •Autoimmune pancreatitis To display a spectrum of early • Isoattenuating mass • Sub-optimal scanning • Chronic pancreatitis and atypical presentations of • Exophytic tumors • Pancreatitis (acute or chronic) Atypical Findings Mimics • Perineural and perivascular infiltration • Metastases Isoattenuating Mass . Despite multiphasic, thin section CT, adenocarcinoma of the • Occult neoplasms Autoimmune Pancreatitis (AIP). A1 A2 approximately 10-15% of pancreatic adenocarcinomas are A3 Characteristic imaging findings of AIP • Neoplasms that mimic pancreatic cancer isoattenuating. In such instances secondary signs such as pancreatic without mass • Presence of a stent include diffuse pancreatic enlargement pancreas, in addition to imaging ductal dilation and cutoff, loss of fatty marbling, contour abnormality, or and/or capsule-like rim. Focal mass-like • Intrapancreatic splenule atrophic distal pancreatic parenchyma must be relied upon to visualize • Diffusely infiltrating tumors enlargement of the pancreas is not the mass. Similarly, some pancreatic cancers may demonstrate pitfalls and mimics, in a case- uncommon and may be indistinguishable isointense signal at MR. Case on the right with a 2 cm pancreatic head • Cystic change • Focal fat from pancreatic cancer. Extrapancreatic carcinoma. CT portovenous phase (right images) and MR post contrast based presentation and review. involvement of bile ducts (thickening or LAVA ( left images) show an isointense and isoattenuating mass.
    [Show full text]
  • The Pathology of Cancer
    University of Massachusetts Medical School eScholarship@UMMS Cancer Concepts: A Guidebook for the Non- Oncologist Radiation Oncology 2018-08-03 The Pathology of Cancer Chi Young Ok The University of Texas MD Anderson Cancer Center Et al. Let us know how access to this document benefits ou.y Follow this and additional works at: https://escholarship.umassmed.edu/cancer_concepts Part of the Cancer Biology Commons, Medical Education Commons, Neoplasms Commons, Oncology Commons, Pathological Conditions, Signs and Symptoms Commons, and the Pathology Commons Repository Citation Ok CY, Woda BA, Kurian E. (2018). The Pathology of Cancer. Cancer Concepts: A Guidebook for the Non- Oncologist. https://doi.org/10.7191/cancer_concepts.1023. Retrieved from https://escholarship.umassmed.edu/cancer_concepts/26 Creative Commons License This work is licensed under a Creative Commons Attribution-Noncommercial-Share Alike 4.0 License. This material is brought to you by eScholarship@UMMS. It has been accepted for inclusion in Cancer Concepts: A Guidebook for the Non-Oncologist by an authorized administrator of eScholarship@UMMS. For more information, please contact [email protected]. The Pathology of Cancer Citation: Ok CY, Woda B, Kurian E. The Pathology of Cancer. In: Pieters RS, Liebmann J, eds. Chi Young Ok, MD Cancer Concepts: A Guidebook for the Non-Oncologist. Worcester, MA: University of Massachusetts Bruce Woda, MD Medical School; 2017. doi: 10.7191/cancer_concepts.1023. Elizabeth Kurian, MD This project has been funded in whole or in part with federal funds from the National Library of Medicine, National Institutes of Health, under Contract No. HHSN276201100010C with the University of Massachusetts, Worcester.
    [Show full text]
  • The 2016 Revision to the World Health Organization Classification of Myeloid Neoplasms and Acute Leukemia
    From www.bloodjournal.org by guest on January 9, 2019. For personal use only. Review Series THE UPDATED WHO CLASSIFICATION OF HEMATOLOGICAL MALIGNANCIES The 2016 revision to the World Health Organization classification of myeloid neoplasms and acute leukemia Daniel A. Arber,1 Attilio Orazi,2 Robert Hasserjian,3 J¨urgen Thiele,4 Michael J. Borowitz,5 Michelle M. Le Beau,6 Clara D. Bloomfield,7 Mario Cazzola,8 and James W. Vardiman9 1Department of Pathology, Stanford University, Stanford, CA; 2Department of Pathology, Weill Cornell Medical College, New York, NY; 3Department of Pathology, Massachusetts General Hospital, Boston, MA; 4Institute of Pathology, University of Cologne, Cologne, Germany; 5Department of Pathology, Johns Hopkins Medical Institutions, Baltimore, MD; 6Section of Hematology/Oncology, University of Chicago, Chicago, IL; 7Comprehensive Cancer Center, James Cancer Hospital and Solove Research Institute, The Ohio State University, Columbus, OH; 8Department of Molecular Medicine, University of Pavia, and Department of Hematology Oncology, Fondazione IRCCS Policlinico San Matteo, Pavia, Italy; and 9Department of Pathology, University of Chicago, Chicago, IL The World Health Organization (WHO) the prognostic relevance of entities cur- The 2016 edition represents a revision classification of tumors of the hemato- rently included in the WHO classification of the prior classification rather than poietic and lymphoid tissues was last and that also suggest new entities that an entirely new classification and at- updated in 2008. Since then, there have should be added. Therefore, there is a tempts to incorporate new clinical, prog- been numerous advances in the identifi- clear need for a revision to the current nostic, morphologic, immunophenotypic, cation of unique biomarkers associated classification.
    [Show full text]
  • The Natural History of Familial Adenomatous Polyposis Syndrome: a 24 Year Review of a Single Center Experience in Screening, Diagnosis, and Outcomes
    Journal of Pediatric Surgery 49 (2014) 82–86 Contents lists available at ScienceDirect Journal of Pediatric Surgery journal homepage: www.elsevier.com/locate/jpedsurg The natural history of familial adenomatous polyposis syndrome: A 24 year review of a single center experience in screening, diagnosis, and outcomes Raelene D. Kennedy a,⁎, D. Dean Potter a, Christopher R. Moir a, Mounif El-Youssef b a Division of Pediatric Surgery, Department of Surgery, Mayo Clinic, Rochester, MN 55905 b Division of Gastroenterology and Hepatology, Department of Pediatrics, Mayo Clinic, Rochester, MN 55905 article info abstract Article history: Purpose: Understanding the natural history of Familial Adenomatous Polyposis (FAP) will guide screening and Received 17 September 2013 aid clinical management. Accepted 30 September 2013 Methods: Patients with FAP, age ≤20 years presenting between 1987 and 2011, were reviewed for presentation, diagnosis, extraintestinal manifestations, polyp burden, family history, histology, gene Key words: mutation, surgical intervention, and outcome. Familial adenomatous polyposis Results: One hundred sixty-three FAP patients were identified. Diagnosis was made by colonoscopy (69%) or Pediatric genetic screening (25%) at mean age of 12.5 years. Most children (58%) were asymptomatic and diagnosed via Screening screening due to family history. Rectal bleeding was the most common (37%) symptom prompting evaluation. Colon polyps appeared by mean age of 13.4 years with N50 polyps at the time of diagnosis in 60%. Cancer was found in 1 colonoscopy biopsy and 5 colectomy specimens. Family history of FAP was known in 85%. 53% had genetic testing, which confirmed APC mutation in 88%. Extraintestinal manifestations included congenital hypertrophy of the retinal pigment epithelium (11.3%), desmoids (10.6%), osteomas (6.7%), epidermal cysts (5.5%), extranumerary teeth (3.7%), papillary thyroid cancer (3.1%), and hepatoblastoma (2.5%).
    [Show full text]
  • ACR Appropriateness Criteria® Radiologic Management of Hepatic Malignancy
    Date of origin: 2007 Last review date: 2015 American College of Radiology ® ACR Appropriateness Criteria Clinical Condition: Radiologic Management of Hepatic Malignancy Variant 1: Hepatocellular carcinoma: Solitary tumor <3 cm. Treatment/Procedure Rating Comments Systemic chemotherapy 3 Resection 8 Transplantation 9 Chemical ablation 5 Thermal ablation 8 Stereotactic body radiotherapy (SBRT) 5 Transarterial embolization (TAE) 5 Transarterial chemoembolization (TACE) 5 Selective internal radiation therapy (SIRT) 5 Rating Scale: 1,2,3 Usually not appropriate; 4,5,6 May be appropriate; 7,8,9 Usually appropriate Variant 2: Hepatocellular carcinoma: Solitary tumor 5 cm. Treatment/Procedure Rating Comments Systemic chemotherapy 3 Resection 8 Transplantation 9 The tumor is too large for chemical ablation. Chemical ablation 3 This procedure can be used instead of or in addition to thermal ablation, depending on the tumor location. Thermal ablation 5 Stereotactic body radiotherapy (SBRT) 4 Transarterial embolization (TAE) 6 This procedure refers to either conventional Transarterial chemoembolization (TACE) 7 TACE or DEB-TACE. This procedure is especially applicable in portal Selective internal radiation therapy (SIRT) 7 vein thrombosis or extensive bilobar disease. Transarterial chemoembolization (TACE) 7 combined with thermal ablation Rating Scale: 1,2,3 Usually not appropriate; 4,5,6 May be appropriate; 7,8,9 Usually appropriate ACR Appropriateness Criteria® 1 Radiologic Management of Hepatic Malignancy Clinical Condition: Radiologic Management of Hepatic Malignancy Variant 3: Hepatocellular carcinoma: More than 1 tumor, at least 1 of them >5 cm. Treatment/Procedure Rating Comments Consider this procedure for patients not amenable Systemic chemotherapy 6 to other localized therapies. Consider resection following neoadjuvant TAE or Resection 5 TACE in the noncirrhotic patient.
    [Show full text]
  • Criteria of Malignancy Evaluation Score
    30 5 Diagnostic Criteria Criteria of Malignancy Table 5.2 lists criteria in contrast-enhancing MR mam- crease 90 % in the first minute after CM administra- mography that strongly indicate the presence of malig- tion, or increase in normalized units 500) have a sig- nancy or are unspecific. nificantly lower specificity at an equivalent sensitivity Unifactorial evaluation protocols that take only one than do multifactorial evaluation protocols (Table 5.3). threshold parameter into consideration (e.g., signal in- Table 5.2 Morphological and Dynamic Criteria for Differentia- Table 5.3 Comparison of Unifactorial and Multifactorial Eval- tion between Malignant and Benign Lesions in Contrast-en- uation Protocols (author’s studies) hanced MR Mammography Protocol Sensi- Speci- Ac- Criterion Suspicious for Unspecific tivity ficity curacy Malignancy Unifactorial Form Branching, spiculated Round Threshold 90 % 96 % 31 % 78 % Margins Indistinct Well-defined Threshold 500 NU 98 % 27 % 86 % Pattern Ring-enhancement Inhomogenous Multifactorial Kinetics Centripetal Unchanging Initial signal increase Dynamics (initial) Strong increase Moderate + postinitial signal increase + CM distribution Dynamics Wash-out Plateau + margin definition 98 % 59 % 87 % (postinitial) NU, normalized unit Evaluation Score Table 5.4 Multifactorial Evaluation Protocol Criterion Points It is very helpful for the evaluation of lesions to use a 1 Form: Round 0 multifactorial protocol in which each evaluation crite- Oval 0 rion receives a point value. Using the system presented Polygonal 0 in Table 5.4, findings with a total score of less than 3 Linear 0 points generally correspond to benign lesions, whereas Branching 1 Spiculated 1 a total score greater than 3 points indicates malignancy (Fig.
    [Show full text]