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Nausea and Vomiting Julia Newell Jan Siddall 2016 Aims and Objectives AIM To increase your knowledge and confidence in the causes and treatment of nausea and vomiting in palliative care patients OBJECTIVES By the end of the session you will be able to Describe the various patterns of N+V Describe the biochemical and physical pathways involved Consider appropriate investigations/interventions Be aware of anti-emetics and their receptor activity Select the appropriate first line antiemetic regime Background - Why is it important? It’s a common and debilitating symptom Affects up to 70% patients with advanced cancer There are many mechanisms, patterns and treatments It usually a has a single cause Ranked as a highly distressing symptom, often more so than pain or breathlessness An accurate assessment and a good understanding of the mechanics of nausea and vomiting is important to guide best effective treatment Definitions Nausea: Unpleasant feeling of need to vomit accompanied by autonomic symptoms (pallor, cold sweat, salivation, tachycardia, diarrhoea) Retching: Rhythmic laboured spasmodic movements of the diaphragm & abdominal muscles (usually occurs with nausea and results in vomiting – but not always) Vomiting: The forceful propulsion of gastric contents through the mouth Regurgitation: Effortless expulsion of foodstuffs – e.g. oesophageal obstruction Ask the right questions Is it Nausea? Retching? Vomiting? When: did it start? Time(s) of day? Constant/not? What: does vomit look like? Amount? Blood? How: did it start? How has it been treated so far? Why: Exacerbating (& relieving) factors Why identify cause/s…? 1. 2. Some causes are treatable and so potentially reversible Each antiemetic targets a specific pathway / ‘cause’ Assessment Distinguish between vomiting, expectoration and regurgitation Note contents and volume Assess relationship between nausea and vomiting Record severity Review drug regime (opioids, digoxin etc) Examine mouth, pharynx and abdomen Check plasma urea, creatinine, calcium, albumin, digoxin as appropriate Examine fundi if raised intracranial pressure possible Reason for accurate assessment Being able to recognise patterns of N&V Identifying likely cause in individual patients Once this is understood we can plan treatment by: Understanding mode of action of commonly used anti-emetics Prescribing most appropriate antiemetic Choosing most appropriate route Negotiating with patient to ensure compliance Potential Causes of nausea and vomiting Drugs opioids, chemotherapy, digoxin, etc etc etc Radiotherapy Especially gut area Biochemical Hypercalcaemia, uraemia Liver failure Gastric stasis Bowel obstruction Upper/lower Constipation Raised intracranial pressure Cerebellar metastases Anxiety, fear, conditioned response 5HT3 Antagonists: Substance P antagonist: Drugs: Ondansetron/Granisitron Drug: Aprepitant Phosaprepitant chemotherapy/radioth erapy Side effects: Constipation, headache prevent acute and delayed sickness that can be caused by chemotherapy given to patients whose nausea and vomiting was severe and was not controlled by the usual anti-emetic regimen Management Correct the reversible Pain, infection, cough, hypercalcaemia, raised ICP, constipation, address fears/anxieties Non drug treatment Control malodour e.g from colostomy or fungating wound Fresh air. Good oropharyngeal hygiene. Suitable distractions. Nurse in the upright position. Avoidance of emetogenic smells and foods. Avoidance of situations in which N&V is a conditioned response. Drug treatment – depends on pattern and cause….. Metoclopramide Pathways: Peripheral : Prokinetic - gastric stasis, functional bowel obstruction Central : Chemoreceptor Trigger Zone (CTZ) - metabolic induced: ie opioids, hypercalcaemia Dose :10mg pre-meal tds PO or 30-120mg Continuous Subcutaneous Infusion (CSCI) Side Effects: extrapyramidal, colic, diarrhoea In renal impairment need dose reduction NB Domperidone: has same action as metoclopramide Haloperidol Pathway: Central: Chemoreceptor Trigger Zone (CTZ) - most metabolic causes of vomiting (e.g. hypercalcaemia, renal failure). Dose: 0.5 - 10mg PO/CSCI Long half life Can be given as a once daily dose at night Side effects: sedation, extrapyramidal Cyclizine Pathway: Central: vomiting centre - antihistamine and anti muscarinic Has peripheral antimuscarinic effect which blocks action of prokinetic drugs ie metoclopramide/domperidone NB: Drugs with antimuscarinic effects should not be used concurrently with prokinetic drugs. Dose: 50mg tds PO/ 150mg CSCI Side effects: sedation, urine retention, dry mouth, constipation NB: Can be skin irritant as S/C injection and not compatible with all drugs in CSCI Levomepromazine (Nozinan) Pathway: Central: acts at many receptor sites, therefore a broad spectrum antiemetic 2nd line: only used if 1st line antiemetics do not work Dose: 6 – 25mg OD PO, 6.25-25mg CSCI Side effects: reflect broad spectrum activity – sedation, constipation, hypotension NB: has sedative properties, so can be used for agitation in higher doses Other Side effects IV Metoclopramide + IV Ondansetron: may cause serious cardiac arrhythmias Metoclopramide/Domperidone + Cyclizine Metoclopramide/Domperidone are motility agents while Metoclopramide (and others) Oculogyric crisis Especially in young women Remember… Different antiemetics act at different points in the vomiting mechanism – the drug must be appropriate to the cause of the nausea and vomiting. Always: identify cause treat reversible cause identify emetic pathway which is triggering vomiting If using > 1 antiemetic: - combine drugs with different actions - do not combine drugs which are antagonistic (blocking) select antiemetic for identified pathway Extra-pyramidal side effects Akathisia Dystonia Tardive Dyskinesia Parkinsonism Tremor Rigidity Bradykinesia Haloperidol, metoclopramide (especially high dose) and levomepromazine can all cause these. Non pharmacological measures Rest Cold Reassurance Fresh air Remove predisposing stimuli Oral hygiene Small appetising snacks lollies drinks/ice Complimentary therapies: - acupressure - behavioural strategies Aims and Objectives Aims Defining Bowel Obstruction Examine the symptoms Management Options Complications Objectives An understanding of bowel obstruction Other options Venting Gastrostomy NG free drainage Definition of Bowel Obstruction A blockage to a section of the bowel, reducing the motility of the contents of the gut. Can Can be partial or complete fluctuate between partial and complete making diagnosis difficult Cause of Bowel Obstruction Anything which causes an obstruction Hard faeces Foreign body Tumour (internal) Tumour (pressure on bowel) Symptoms Nausea: persistent, fullness Vomiting: large volume? faeculant? Abdominal pain Colic pain: wave like, spasm Constipation: - can mimic bowel obstruction - impaction/overflow Medical management Nausea and vomiting If no colic = metoclopramide in syringe driver If colic = haloperidol + hyoscine butylbromide (buscopan) in syringe driver Large volume vomits hyoscine butylbromide (buscopan) octreotide Reduction of colic: hyoscine butylbromide (buscopan) Any questions?