+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?