Nausea and Vomiting Presentation · PDF filetreatment of nausea and vomiting in Palliative Care patients ... Plan? + Case study (2) Your ... Nausea and Vomiting Presentation 2016

+Nausea and

Vomiting

Dr Alistair McKeown

Consultant in Palliative Medicine

Prince and Princess of Wales Hospice

+Overview

� Aims and Objectives

� Background

� Definitions

� Pathways� Pathways

� Patterns, interventions and medications

� Case Study

� Summary

+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� 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 antiemetics and their specific receptor activity

� Select the appropriate first (and second) line antiemetic regime

+Why is it important?

� A common and debilitating symptom

� Affects up to 70% patients with advanced cancer

� Many mechanisms, patterns and treatmentsMany mechanisms, patterns and treatments

� Usually a single cause

� Ranked a highly distressing symptom, often more so than

pain or breathlessness

� A good understanding is important to guide best effective

treatment

+What is nausea?

+What is vomiting?

+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 & abdo 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

+What is it?

� Primitive defense mechanism against ingested toxins

� Mediated via

� Higher centres - sight, smell, taste (learned response)

� Receptors in upper gut� Receptors in upper gut

� Chemoreceptor trigger zone (floor of 4th ventricle)

� Vestibular system

+What is it (2)

� Controlled by integrated vomiting centre in medulla

� Stimulated by input from various pathways

� Specific neurotransmitters are involvedSpecific neurotransmitters are involved

� Specific drugs act on specific receptors

� (More of which later)

+Mechanics

� Autonomic

� Lack of interest in surroundings, excess salivation, sweating, hyperventilation, tachycardia

� Somatic

� Retching � Retching

� Diaphragm contracts against closed glottis sucking gastric contents into lower oesophagus

� Vomiting

� Glottis opens, retrograde peristalsis in oesophagus, abdominal muscles contract and contents of stomach expelled

+What are the causes on N+V?

+Causes

� Drugs

� opioids, chemotherapy,

� digoxin, etc etc etc

� Radiotherapy

Especially gut area

� Bowel obstruction

� Upper/lower

� Constipation

� Raised intracranial pressure � Especially gut area

� Biochemical

� Hypercalcaemia, uraemia

� Liver failure

� Gastric stasis

� Raised intracranial pressure

� Cerebellar metastases

� Anxiety, fear, conditioned

+Pathways

+

+Drugs

Drug Receptor Site of action Route

Cyclizine H1 VC PO,PR,IM,CSCI

Domperidone D CTZ/Stomach PO/PR

Metoclopramide D, 5HT4 CTZ, Stomach,

Gut

PO, PR, IM,CSCI

Haloperidol D2 CTZ PO, IM,CSCI

Procloperazine D2, Ach/H1 CTZ/VC PO, Buccal, PR, Procloperazine D2, Ach/H1 CTZ/VC PO, Buccal, PR,

IM

Levomepromazine 5HT2, D,

Ach/H1

VC/CTZ PO/CSCI

Hyoscine

Hydrobromide

Ach/H1 VC/Gut PO, patch, IM,

CSCI

Hyoscine Butyl Ach/H1 Gut PO, IM,CSCI

Ondansetron 5HT3 Gut, CTZ PO, IM, CSCI

Aprepitant NK1 CTZ PO

+Other helpful options:

� Dexamethasone

� Octreotide

� Erythromycin

� Other options

AntacidsAntacids

Laxatives

Relaxation

Sedation

Acupuncture

+Treating

� Relies on:

� Being able to recognise patterns of N&V

� Identifying likely cause in individual patients

� Understanding mode of action of commonly used anti-emetics� Understanding mode of action of commonly used anti-emetics

� Prescribing most appropriate antiemetic

� Choosing most appropriate route

� Negotiating with patient to ensure compliance

+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

+Asking the right questions

� Nausea? Retching? Vomiting?

� When: did it start? Time(s) of day? Constant/not?

� What: does vomit look like? Amount? Blood?What: does vomit look like? Amount? Blood?

� How: did it start? How has it been treated so far?

� Why: Exacerbating (& relieving) factors

+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.� 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…..

+Patterns of N+V

� Gastric Stasis

� Chemical or Metabolic

� Motion SicknessMotion Sickness

� Raised Intra-Cranial Pressure

� Bowel Obstruction

� Unknown or Multiple causes

+Gastric Stasis

� Characteristics

� Epigastric fullness

� Early satiety

� Large volume vomits (?projectile)

� Hiccups

� Regurgitation

� (?Minimal) Nausea quickly relieved by vomiting

+Gastric Stasis 2

� Contributing factors:

� Stomach emptying problems

� (eg Autonomic: eg Diabetes, Gastritis, Peptic Ulcer)

� Compression of gastric outflow

� (eg Tumour, Hepatomegaly, Ascites)

� Drug Side-Effects

� (eg Anti-Cholinergics, Opioids)

+Treating Gastric Stasis

� Reduce volume of oral intake: Little & often

� Reduce Gastric secretions: PPI (eg Omeprazole, H2 blockers)

� Can try octreotide – often minimal effect with high

obstruction

� Pro-kinetic agents: Dopamine D2-Antagonists

� Metoclopramide

� 10mg QDS

� Can use higher doses – up to 120mg via CSCI

� Domperidone (doesn’t cross blood:brain barrier)

+Other options

� NG Tube

� Venting Gastrostomy

+Chemical or metabolic N+V

� Characteristics:

� Constant nausea

� Less or variable vomitingLess or variable vomiting

� Worsened by sights/smells

+Chemical N+V cont

� Stimulation of CTZ: D2 and 5HT3 receptors

� Contributing factors:

� Chemical: Drugs Chemical: Drugs

� (many: esp Opioids, Antibiotics, Digoxin, NSAIDs, SSRIs,

Chemotherapy)

� Metabolic

� (eg Renal / Liver failure, Hypercalcaemia of Malignancy,

Hyponatraemia, sepsis)

+Treating chemical N+V

� Reverse the reversible

� Treat hypercalcaemia (if approrpiate)

� Treat renal failure (if appropriate)

� Correct biochemical abnormalities (if appropriate)

� Stop chemotherapy?

� Dopamine D2-Antagonist:

� Haloperidol

� Metoclopramide

� 5HT3-Antagonist

� Ondansetron

� Granisetron

+Motion sickness

� Characteristics:

� Vomiting on movement

� DizzinessDizziness

� ?Nystagmus

+Motion sickness cont

� Stimulation of Vestibular System:

� H1 & ACh receptors

� Contributing factors:

� Stimulation of vestibular system� Stimulation of vestibular system

� Opioids can increase vestibular sensitivity

� ?Intracerebral cause

� Brain mets

� CVA

+Motion sickness cont

� Anti-Histamine and Anti-Cholinergic Agents:

� Cyclizine

� Steroids

+Raised ICP

� Characteristics:

� Symptoms worse in the morning

� Headache Headache

� Nausea

� Vomiting (?projectile)

+Raised ICP Cont

� Anti-Histamine and Anti-Cholinergic Agents:

� Cyclizine

� Depends on cause: eg ?SOL:

� Steroids� Steroids

� Radiotherapy

� Neurosurgery

+Bowel Obstruction

� Symptoms may depend of level of obstruction

� Partial or complete?

� Stomach

� similar to gastric stasis� similar to gastric stasis

� Small bowel

� partially/undigested foodstuffs

� Large volume, feels well inbetween

� Large bowel

� faeculent vomiting

� Less frequent?

+Bowel obstruction cont

� Reverse the reversible

� Constipation

� Surgery

� Medications� Medications

� Steroids – reduce oedema, may allow passage

� If partial – prokinetics (metoclopramide)

� If complete – levomepromazine or cyclizine/haloperidol

� Somatostatin analogues – octreotide

� Hyoscine butylbromide – reduce spasms and secretions

May not stop vomiting completely

+Bowel obstruction cont

� NG

� Venting gastrostomy

+Unknown or multiple

� Levomepromazine – useful and broad spectrum

� Non-Drug Measures:

� Address anxiety as a trigger

� Minimise smells � Minimise smells

� (eg perfume, cooking, fungating tumour)

� Try cool fizzy drinks

� (more palatable than hot still drinks)

� Acupuncture / Acupressure

� Ginger

� Hypnotherapy

+Other causes

� Hiatus hernia

� Gastritis

� GastroenteritisGastroenteritis

� Vestibular disturbance

� Cough

� Pharyngeal irritation

� Conditioning/association

+Extra-Pyramidal Side Effects

� Akathisia

� Dystonia

� Tardive Dyskinesia

� Haloperidol, metoclopramide

(especially high dose) and

levomepromazine can all cause

these.

� Parkinsonism

� Tremor

� Rigidity

� Bradykinesia

+MHRA warnings

+MHRA warnings

+MHRA Cont…

+MHRA cont

+

Cautions

� IV Metoclopramide + IV Ondansetron:

� may cause serious cardiac arrhythmias

� Metoclopramide/Domperidone + Cyclizine

� Metoclopramide/Domperidone are motility agents while � Metoclopramide/Domperidone are motility agents while

Cyclizine slows down GI transit – makes no sense!

� Metoclopramide (and others)

� Oculogyric crisis

� Especially in young women SC route

+Syringe Drivers

� NOT JUST FOR TERMINAL CARE

� CSCI of SC meds over 24hrs

� If vomiting - very usefulIf vomiting - very useful

� Home/ NH/ Hospital/ Hospice

+Case Study (1)

� 46 year old woman

� Localised ovarian malignancy

� Previously fit and well

� Some abdominal pain, seeing oncologists, not yet on CTX� Some abdominal pain, seeing oncologists, not yet on CTX

� Complains of nausea and comes to see you

� Questions?

� Investigations?

� Plan?

+Case study (2)

� Your treatment works!

� Several weeks later, nausea returns

� Worse

� Still constant� Still constant

� Comes to see you

� Questions?

� Investigations?

� Plan?

+Case study (3)

� Hospital admission reveals bilateral hydronephrosis

� Extensive intra abdominal disease

� Ureteric stents and U+Es normal

� Ongoing CTX� Ongoing CTX

� Several weeks pass

� Nausea returns and back to you again:

� Questions?

� Investigations?

� Plan?

+Case study (4)

� Responds to metoclopramide and steroids

� Deteriorating condition

� Call from husbandCall from husband

� Progressive worsening, nausea and vomiting main symptom

� Colic

� House call

� Questions?

� Investigations?

� Plan?

+Case study (5)

� Rotation to levomepromazine (or cyclizine/haloperidol)

� Buscopan/octreotide

� Declined NG

� Symptoms improved – still vomiting every 3/7� Symptoms improved – still vomiting every 3/7

� Ongoing deterioration accepted, nil reversible

� Died at home

+Summary

� There is a single cause in 66% cases.

� Optimise non-pharmacological measures.

� Reverse the reversible.

� Diagnose a cause before initiating drug treatment.� Diagnose a cause before initiating drug treatment.

� Give the most suitable drug by the most suitable route.

� When multiple drugs are required, they should have different

modes of action.

� Review at least every 24 hours.

+Any Questions?