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+Nausea and
Vomiting
Dr Alistair McKeown
Consultant in Palliative Medicine
Prince and Princess of Wales Hospice
and South Glasgow Acute
+
Overview
Aims and Objectives
Background
Definitions
Pathways
Patterns, interventions and medications
Case Study
Summary
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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 antiemetics and their specific receptor activity
Select the appropriate first (and second) line antiemetic regime
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Why is it important?
A common and debilitating symptom
Affects up to 70% patients with advanced cancer
Many 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
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What is nausea?
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What is vomiting?
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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
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What is it?
Primitive defense mechanism against ingested toxins
Mediated via
Higher centres - sight, smell, taste (learned response)
Receptors in upper gut
Chemoreceptor trigger zone (floor of 4th ventricle)
Vestibular system
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What is it (2)
Controlled by integrated vomiting centre in medulla
Stimulated by input from various pathways
Specific neurotransmitters are involved
Specific drugs act on specific receptors
(More of which later)
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Mechanics
Autonomic
Lack of interest in surroundings, excess salivation, sweating,
hyperventilation, tachycardia
Somatic
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
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What are the causes on N+V?
+
Causes
Drugs
opioids, chemotherapy,
digoxin, etc etc etc
Especially gut area
Biochemical
Hypercalcaemia, uraemia
Liver failure
Gastric stasis
Bowel obstruction
Upper/lower
Constipation
Raised intracranial pressure
Cerebellar metastases
Anxiety, fear, conditioned
Radiotherapy
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Pathways
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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
Prescribing most appropriate antiemetic
Choosing most appropriate route
Negotiating with patient to ensure compliance
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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?
How: did it start? How has it been treated so far?
Why: Exacerbating (& relieving) factors
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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,
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
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Other helpful options:
Dexamethasone
Octreotide
Erythromycin
Other options
Antacids
Laxatives
Relaxation
Sedation
Acupuncture
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Extra-Pyramidal Side Effects
Akathisia
Dystonia
Tardive Dyskinesia
Parkinsonism
Tremor
Rigidity
Bradykinesia
Haloperidol, metoclopramide
(especially high dose) and
levomepromazine can all cause
these.
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Cautions
IV Metoclopramide + IV Ondansetron:
Metoclopramide/Domperidone + Cyclizine
may cause serious cardiac arrhythmias
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
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MHRA warnings
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MHRA warnings
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MHRA Cont…
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MHRA cont
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Management
Correct the reversible
Non-drug treatment
Pain, infection, cough, hypercalcaemia, raised ICP, constipation,
address fears/anxieties
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…..
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Patterns of N+V
Gastric Stasis
Chemical or Metabolic
Motion Sickness
Raised Intra-Cranial Pressure
Bowel Obstruction
Unknown or Multiple causes
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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
Compression of gastric outflow
(eg Autonomic: eg Diabetes, Gastritis, Peptic Ulcer)
(eg Tumour, Hepatomegaly, Ascites)
Drug Side-Effects
(eg Anti-Cholinergics, Opioids)
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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)
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Other options
NG Tube
Venting Gastrostomy
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Chemical or metabolic N+V
Characteristics:
Constant nausea
Less or variable vomiting
Worsened by sights/smells
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Chemical N+V cont
Stimulation of CTZ: D2 and 5HT3 receptors
Contributing factors:
Chemical: Drugs
(many: esp Opioids, Antibiotics, Digoxin, NSAIDs, SSRIs,
Chemotherapy)
Metabolic
(eg Renal / Liver failure, Hypercalcaemia of Malignancy,
Hyponatraemia, sepsis)
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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
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Motion sickness
Characteristics:
Vomiting on movement
Dizziness
?Nystagmus
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Motion sickness cont
Stimulation of Vestibular System:
H1 & ACh receptors
Contributing factors:
Stimulation of vestibular system
Opioids can increase vestibular sensitivity
?Intracerebral cause
Brain mets
CVA
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Motion sickness cont
Anti-Histamine and Anti-Cholinergic Agents:
Cyclizine
Steroids
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Raised ICP
Characteristics:
Symptoms worse in the morning
Headache
Nausea
Vomiting (?projectile)
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Raised ICP Cont
Anti-Histamine and Anti-Cholinergic Agents:
Cyclizine
Depends on cause: eg ?SOL:
Steroids
Radiotherapy
Neurosurgery
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Bowel Obstruction
Symptoms may depend of level of obstruction
Partial or complete?
Stomach
Small bowel
similar to gastric stasis
partially/undigested foodstuffs
Large volume, feels well inbetween
Large bowel
faeculent vomiting
Less frequent?
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Bowel obstruction cont
Reverse the reversible
Constipation
Surgery
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
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Bowel obstruction cont
NG
Venting gastrostomy
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Unknown or multiple
Levomepromazine – useful and broad spectrum
Non-Drug Measures:
Address anxiety as a trigger
Minimise smells
(eg perfume, cooking, fungating tumour)
Try cool fizzy drinks
(more palatable than hot still drinks)
Acupuncture / Acupressure
Ginger
Hypnotherapy
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Other causes
Hiatus hernia
Gastritis
Gastroenteritis
Vestibular disturbance
Cough
Pharyngeal irritation
Conditioning/association
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Syringe Drivers
NOT JUST FOR TERMINAL CARE
CSCI of SC meds over 24hrs
If vomiting - very useful
Home/ NH/ Hospital/ Hospice
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Case Study (1)
46 year old woman
Localised ovarian malignancy
Previously fit and well
Some abdominal pain, seeing oncologists, not yet on CTX
Complains of nausea and comes to see you
Questions?
Investigations?
Plan?
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Case study (2)
Your treatment works!
Several weeks later, nausea returns
Worse
Still constant
Comes to see you
Questions?
Investigations?
Plan?
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Case study (3)
Hospital admission reveals bilateral hydronephrosis
Extensive intra abdominal disease
Ureteric stents and U+Es normal
Ongoing CTX
Several weeks pass
Nausea returns and back to you again:
Questions?
Investigations?
Plan?
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Case study (4)
Responds to metoclopramide and steroids
Deteriorating condition
Call from husband
Progressive worsening, nausea and vomiting main symptom
Colic
House call
Questions?
Investigations?
Plan?
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Case study (5)
Rotation to levomepromazine (or cyclizine/haloperidol)
Buscopan/octreotide
Declined NG
Symptoms improved – still vomiting every 3/7
Ongoing deterioration accepted, nil reversible
Died at home
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Summary
There is a single cause in 66% cases.
Optimise non-pharmacological measures.
Reverse the reversible.
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.
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Any Questions?