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. Some causes are treatable and so potentially reversible 2. 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 Bowel obstruction opioids, chemotherapy, Upper/lower digoxin, etc etc etc Constipation Radiotherapy Raised intracranial Especially gut area pressure Biochemical Cerebellar Hypercalcaemia, metastases uraemia Liver failure Anxiety, fear, Gastric stasis conditioned response Substance P 5HT3 Antagonists: antagonist:
Drugs: Drug: Ondansetron/Granisitron Aprepitant Phosaprepitant
chemotherapy/radioth prevent acute and delayed sickness that erapy can be caused by chemotherapy given to patients whose Side effects: nausea and vomiting Constipation, was severe and was not controlled by the usual headache 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 drinks/ice Reassurance lollies Fresh air Complimentary therapies: Remove predisposing stimuli - acupressure - behavioural Oral hygiene strategies Small appetising snacks 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 be partial or complete
Can 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?