Download Palliative Care in Winnipeg

“I am Sick of
Feeling Sick”
Managing Nausea
and Vomiting in the
Palliative Patient
Paul Daeninck
WRHA Palliative Care Program
Greg Harochaw
Taché Pharmacy
Declaration
Advisor or Paid Speaker for the following:
Valeant Pharmaceuticals
Bayer
Wyeth Pharmaceuticals
Objectives
At the end of this session, the attendee will be able to:
Identify the numerous GI issues causing
nausea and vomiting in the palliative
patient
Discuss the principles in determining the
therapies for specific situations of
nausea and vomiting
Recognize the complex physiology and
potential for use of alternative routes in
treating nausea and vomiting
GI Issues Causing
Nausea/Vomiting
Medications
Radiation
Constipation
Bowel obstruction
Diarrhea
Ascites
Hemorrhage
Viscus perforation
Esophageal/gastric/
biliary duct obstruction
Liver failure
Pancreatic failure
Absorption syndromes
Infections
Electrolytes
Approach To Symptom Control
Thorough assessment
history; physical examination
Discussion
goals of care, hopes, expectations, anticipated course of illness
(impact on investigations & interventions)
Investigations
blood tests, X-Ray, CT, MRI, etc
Treatments
pharmacological and non-pharmacological; interventions
Ongoing reassessment/review
Options, goals, expectations, etc.
Symptom Prevalence
Pain
Fatigue/Asthenia
Constipation
Dyspnea
Nausea
Vomiting
Delirium
Depression/suffering
80 - 90+%
75 - 90%
70%
60+%
50 - 60%
30%
30 - 90%
40 - 60%
Mechanisms of
Nausea & Vomiting
vomiting centre: medulla
activated by stimuli from:
Chemoreceptor Trigger Zone (CTZ)
area postrema, floor of 4th ventricle
outside BBB (fenestrated venules)
Upper GI tract & pharynx
Vestibular apparatus/Cerebellum
Higher cortical centres
Chemoreceptor
Trigger Zone
Vo m
Vestibular
Cerebellar
Opioids
Cerebellar Tumor
Increased
Intracranial Press
Primary or
Metastatic Tumor
G. Michael Downing
Integrative
Vomiting
Centre (IVC)
iti
ng
au
sea
Sights, Smells
Memories
N
Cerebral
High CNS
Toxic
Cancer
Infection
Radiation
Drugs
Chemotherapy
Opioids
Digoxin, etc
Biochemical
Uremia
Hypercalcemia
GI Tract
Vagal
Distension
Over-eating
Gastric Stasis
Ext. Pressure
Obstruction
High, mid, low
Constipation
Chemical Irritants
Blood, drugs
Pathogenesis
of chemo- &
RT-induced
emesis
(CIE, RIE)
Area postrema
3rd
vent
N/V Related Problems
Medical
dehydration / electrolyte abnormalities
esophageal tears / GI bleed
aspiration pneumonia
Decreased QoL
weight loss / anorexia
weakness / lethargy
Psychological distress
Refusal of beneficial therapy
Principles of Therapy
Treat the underlying cause
Environmental measures
Antiemetic use:
anticipate need
use adequate, regular doses
aim at receptor involved
combinations if necessary
anticipate need for alternate routes
Environmental Measures
Limit exposure to food smells
open food trays prior to presentation
Bland foods (BRAT)
Small, frequent snacks/meals
Good oral hygene
Fresh air, calming environment
Sitting upright post meal
Avoid alcohol
Acupuncture/pressure
Not as well studied
Safe in trained hands
Often used in conjunction with meds
Some evidence in CINV, delayed NV
Theory behind wrist/pressure bands
Dibble et al. Oncol Nurs Forum 2007 34:813-20
Weightman et al. BMJ 1987 295:1379
Anti-Emetic Agents
Transdermal scopolamine
Benzodiazepines
Antihistamines
Cannabinoids
Metoclopramide, Domperidone
Neuroleptics / Anti-psychotics
Corticosteroids
5-HT3 Antagonists
NK1 Antagonists (aprepitant)
Chemoreceptor
Trigger Zone
Vo m
iti
Vestibular
Cerebellar
H1 Antagonist
Dimenhydrinate
Methotrimeprazine
Anticholinergic
Scopolamine
Atropine
Cannabinoids
Increased
Intracranial Press
Dexamethasone
? VP Shunt
G. Michael Downing
Integrative
Vomiting
Centre (IVC)
Anticholinergic
Scopolamine
Atropine
H1 Antagonist
Dimenhydrinate
Cyclizine
Methotrimeprazine
5HT2 Antagonist
Methotrimeprazine
5HT3 Antagonist
Ondansetron
ng
au
sea
Benzodiazepines
Cannabinoids
Relaxation
N
Cerebral
High CNS
D2 Antagonist
Prochlorperazine
Haloperidol
Methotrimeprazine
Gastrokinetics
Metoclopromide
5HT3 Antagonist
Ondansetron
Granisetron
Olanzepine?
GI Tract
Vagal
D2 Antagonist
Gastrokinetics
Metoclopromide
Domeperidone
Phenothiazines
Methotrimeprazine
5HT4 Agonist
Metoclopromide
5HT3 Antagonist
Ondansetron
Octreotide
Dexamethasone
Cannabinoids
Antiemetics and Dosing
Haloperidol 0.5 - 1 mg po/sq/iv q4-12h
DOPAMINE
ANTAGONISTS
MTMZ 5 - 10 mg po/sl/sq q4-8h
ANTIMUSCARINIC
Scopolamine patch (Transderm-V)
PROKINETIC
Prochlorperazine 5 - 20 mg po/pr/iv
CPZ 25 - 50 mg po/pr/iv
Metoclopramide 10 - 20 mg po/sq/pr q4-8h
Domperidone 10 mg po q4-8h
Antiemetics and Dosing
H1
ANTAGONISTS
Dimenhydrinate 25 - 100 mg po/pr q4-8h
SEROTONIN
ANTAGONISTS
Ondansetron 8 -16 mg q 12 h po/sq/iv
Granisetron 1- 2 mg q 12 h po/sq
MISCELLANEOUS
Promethazine 25 mg po/iv q4-6h (Not sq)
Meclizine 25 mg po q6-12h
Dexamethasone 4-16 mg po/sq/iv daily
Lorazepam 0.5 - 1 mg po/sl q4-12h
Nabilone 0.5-1 mg po/sl q8-12h
Olanzepine 2.5-10 mg OD
Olanzepine
Atypical antipsychotic agent
Used in schizophrenia, delirium
Blocks multiple receptors
D1-4, 5-HT2/3/6, α1adrenergic, H1, M1-4
High affinity for serotonin vs dopaminergic
Well tolerated
Few drug interactions
Olanzepine
Has been used in several case studies
Recently used in CINV and delayed NV
Good results with few problems
May also have some appetite benefits
Less expensive than 5-HT3 antagonists
Navari et al. Support Care Cancer 2007 Mar 21
Navari et al. Support Care Cancer 2005 13:529-34
Passik et al. Cancer Invest 2004 22:383-8
Passik et al. JPSM 2003 25:485-89
Srivastava et al. JPSM 2003 25:578-82
Jackson et al. J Pall Med 2003 6:251-55
Cannabinoids & Nausea
• The Nucleus of the Solitary
Tract (NTS) receives
information about:
Blood-borne emetics via
the brainstem (BS) CTZ
Abdominal irritants via
vagal afferents
• NTS neurons, in turn, project to
a BS central pattern generator,
which coordinates emesis
behavior
Cortex
Limbic
System
• Higher cortical and limbic
Brainstem
Emetic
Circuitry
Dorsal Vagal
Complex—NTS
Stomach Wall
regions (governing taste,
smell, sight, pain, memory
and emotion) can suppress
or stimulate nausea and
vomiting through descending
connections to the BS emetic
circuitry
• Cannabinoids are thought to
exert their antiemetic effects
primarily via action on CB1
receptors in the NTS and higher
cortical and limbic regions
Indirect, partial actions on
5-HT and DA signaling via
5-HT3 and D2 receptors are
implicated
Cannabinoids in CINV
20 pts, RCT, P vs THC, X-over
10 or 15 mg/m2 po q4h x 3, various
tumours
Chemotherapy not specified
Anti-emetic effect seen in 14/20 THC vs
0/22 P (p<0.001)
No patients vomited while “high”
Sallan et al, NEJM 1975 293: 795-797
Cannabinoids in CINV
30 RCTs systematically reviewed
N=1366 pts; 25 trials X-over design
Nabilone, dronabinol, levonantradol (IM)
Stemitil, domperidone, metoclopramide
Variety of tumours
Low to highly emetogenic chemotherapies
Studied first 24 h (acute efficacy)
Tramer et al, BMJ 2001 323:16-23
Cannabinoids in CINV
Oral nabilone (16)
Prochlorperazine (7)
metoclopramide, alizapride
domperidone (2)
chlorpromazine, placebo (4)
Oral dronabinol (13) prochlorperazine (6)
metoclopramide (2)
haloperidol, placebo (6)
IM levonantradol (1) chlorpromazine
Tramer et al, BMJ 2001 323:16-23
Control of N/V with Cannabinoids:
Systematic Review
Cannabinoid
Control (Placebo or Active)
Event rate (%)
70%
66%
59%
57%
57%
45%
43%
34%
vs. Placebo
Nausea
vs. Active
vs. Placebo
vs. Active
Vomiting
active control= prochlorperazine, metoclopramide, chlorpromazine, thiethylperazine, haloperidol,
domperidone, alzapride
Tramèr MR, et al. BMJ. 2001;323:1-8.
Complete Control of N/V with
Cannabinoids
Nausea
NNT (95% CI)
Versus placebo (4 studies)
8.0 (4.0-775)
Versus active control (7 studies)
6.4 (4.0-16)
Vomiting
Versus placebo (4 studies)
3.3 (2.4-5.7)
Versus active control (6 studies)
8.0 (4.5-38)
0.5
1.0
1.5
2.0
Relative risk (95% CI)
Favors cannabinoids
2.5
NNT= number needed to treat; active control= prochlorperazine, metoclopramide, chlorpromazine,
thiethylperazine, haloperidol, domperidone, alzapride.
Tramèr MR, et al. BMJ. 2001;323:1-8
Patients’ Preference
for Cannabinoids
Preference for cannabinoids
NNT (95% CI)
Versus placebo (4 studies)
1.6 (1.4-1.8)
Versus active control (14 studies)
2.8 (2.4-3.3)
0.5 1.0 2.0 4.0 6.0 8.0
Relative risk (95% CI)
Favors cannabinoids
10.0
NNT = number needed to treat; active control= prochlorperazine, metoclopramide, chlorpromazine, thiethylperazine,
haloperidol, domperidone, alzapride
Tramèr MR, et al. BMJ. 2001;323:1-8.
Cannabinoids in CINV
Cannabinoids may be superior to conventional
therapies in low-moderate emetogenic setting
Patient preference for cannabinoids ranged from
38-90% (placebo 4-20%)
Cannabinoids produced significantly more side
effects (good & bad), more pt withdrawals
“In selected patients, cannabinoids may be
useful as mood enhancing adjuvants for the
control of chemotherapy related sickness”
Tramer et al, BMJ 2001 323:16-23
Cannabinoids in CINV
8-THC less psychotropic, less $, stable
Less psychomimetic effects in children
Phase II trial, 8 pts (3-13 yrs)
Variety of cancers, chemotherapy
Starting dose of 5 mg/m2
Nausea and vomiting eliminated
No psychotropic effects seen
Abrahamov et al, Life Sci 1995 56:2097
Experimental Emesis
Linda Parker et al, Wilfred Laurier U.
Series of studies with rats/shrews
Model for anticipatory nausea
THC or CBD >> ondansetron
THC/CBD maybe most effective
Limebeer and Parker Neuroreport 1999
Parker et al Neuroreport 2002
Parker et al Psychopharm 2004
Limebeer et al Physiol Behav 2006
Cannabinoids in CINV
Several RCTs in chemotherapy-induced
emesis (CINV)
Pre 5-HT3 antagonist era (ondansetron)
Oral or IM meds vs best treatment
No comparison with 5-HT3 antagonist
No controlled trials of inhaled marijuana
Inhaled Marijuana
Cross-over CINV study, placebo control,
marijuana vs dronabinol
n= 20 (15 men), 14 NSCLC
25% no vomiting, 15% no nausea
35% hallucinations or time perception changes
Preference:
20% marijuana, 35% dronabinol, 45% no pref
THC > marijuana therapeutic potency
Levitt et al, JCO 1984 abstract C-354
Inhaled Marijuana
CINV, open trial, no control
n=74, chronic users, 25% dropped out
Preference:
18 (34%) v effective, 26 (44%) mod effective
12 (22%) no benefit
Side Effects:
sedation 88%, dry mouth 77%, dizziness 39%
13% no A/E
Vinciguerra et al, N Y State J Med 1988, 88:525
Special Situations
Constipation
Obstruction
Symptom Prevalence
Pain
Fatigue/Asthenia
Constipation
Dyspnea
Nausea
Vomiting
Delirium
Depression/suffering
80 – 90+%
75 - 90%
70%
60+%
50 - 60%
30%
30 - 90%
40 - 60%
Malignancy
Direct effects
obstruction by tumor in wall
external compression by tumor
neural damage
L/S spinal cord
cauda equina/pelvic plexus
hypercalcemia
Malignancy
Secondary effects
poor po intake
dehydration
weakness/inactivity
confusion
depression
unfamiliar toilet arrangements
Medications
Opioids
 Ileocecal & anal sphincter tone
 Peristaltic activity (SI & C)
Impaired defecation reflex
 sensitivity to distension
 internal anal sphincter tone
 Water, electrolyte absorption (SI & C)
Concurrent Disease
Diabetes
Hypothyroidism
Hypokalemia
Hernia
Anal fissure/stenosis
Hemorrhoids
Autonomic neuropathy
diabetes
spinal cord disease
chemotherapy
Parkinson’s disease
ALS/MS
Dementia
Treatment
Prophylaxis
good symptom control
activity
adequate hydration
recognize drug effect
create a favorable environment
Treatment: Laxatives
>80% pts on opioids need laxatives
Little research to guide choice
Softener and stimulant best first choice
May require oral/rectal routes
Enemas useful in impaction
Bulk forming agents worsen situation
Treatment: Laxatives
Surfactants: docusate
Contact cathartics: senna, bisacodyl
Osmotic laxatives: lactulose
Saline osmotics: MgOH, Phosphasoda
Enemas: oil, saline, soap suds, Fleet
Other Approaches
Prokinetic agents: domperidone,
metoclopramide
Antibiotics: erythromycin
Herbal preparations: mulberry, rhubarb,
licorice, prune juice
New Agents
Selective opioid antagonists
Active in periphery, esp. gut
Methylnaltrexone, Alvimopan
Studies used IV and oral application
S/E
abd cramping, flatulence, nausea, dizziness
Bowel Obstruction
Common problem
Associated with advanced cancers
GI, ovarian, lymphoma
Relapse / local spread of intrabdominal tumour
Diffuse peritoneal carcinomatosis, encasement by
tumour
Multiple partial bowel occlusions
(delaying or preventing propulsion of intestinal contents)
Symptoms of nausea/vomiting
abdominal pain, distention
Pandha et al. Anti-Cancer Drugs, 1996; 7:5-10
Bowel Obstruction: Etiology
Mechanical obstruction causes:
 secretions, gas proximal to the obstruction
distention from gas, ingested fluids, digestive
secretions in turn causes  secretions
secretion
distention
Mercadante et al. JPSM 1997
Bowel Obstruction
Standard Therapy
NG tube/IV fluids (“drip & suck”)
Bowel rest
Pain control (opioids)
Radiological assessment
Surgical intervention
Bowel Obstruction
Palliative Therapy
Opioid analgesics, dexamethasone
Promotility agents
metoclopramide/domperidone
Octreotide (Sandostatin)
Hyoscine butylbromide (Buscopan)
Somatostatin Analogues
Octreotide, vapreotide, lanreotide
Receptor activity
brain, pituitary, pancreas, GI tract, immune cells
Used in many conditions
Prolongs GI transit time
 fluid secretion in jejunum
 water/electrolyte absorption
decreases peristasis
reduces GI blood flow
Inhibits exocrine pancreatic secretion
Bowel Obstruction in
Ovarian Cancer
13 pts, advanced ovarian cancer, inoperable
GI obstruction
Octreotide dose of 300 - 600 µg/day
Octreotide controlled vomiting in all cases
Vomiting stopped in 2-3 days of starting tx
Mangili et al., Gynecologic Oncology 1996
Bowel Obstruction in
Ovarian Cancer
NG drainage  from 2000 to <100 ml/day
Complete relief of symptoms within 3 days
(range 1-6 days)
8/13 pts D/C from hospital, continued
treatment at home
Mangili et al., Gynecologic Oncology 1996
Delivery Routes for
Medications
Standard
Oral
Intravenous
Inhalation (nebulized)
Subcutaneous
GH
Alternative
Sublingual
transmucosal
mouthwashes
Intranasal
Transdermal (topical)
Rectal
Vaginal
Intraosseus
Think “Outside the Box”
Alternative Routes of Drug
Administration
Alternative delivery routes
transmucosal
transdermal (topical)
rectal
Review of the science
Oral Mucosal Delivery
Advantages:
High vascular permeability
Avoids “first pass” hepatic elimination
High potency of drug (small volumes)
Less intimidating/ “low-tech” administration
easier in home, PCH, LTC
Alternate administration route
pt NPO, difficulty swallowing, SBO, etc.
Oral Mucosal Delivery
Barriers:
Lipophilic Rx: needs intact mucosal cell
membrane
Hydrophilic Rx: poor absorption
Volume of dose
Ideally  0.5 ml; > 1-2 ml  swallowed
Excessive salvation  swallowing of dose
Acceptable delivery vehicle/taste
Oral Mucosal Delivery
Oral transmucosal drugs
Lorazepam
Olanzapine wafers
(Zyprexa Zydis®)
Proclorperazine buccal tabs
(Stemetil®)
Mirtazapine (Remeron® RD)
Highly lipophilic  better than oral
absorption??
Oral Mucosal Delivery
Haloperidol (Haldol®)
Protect from light & freezing
Store below 40ºC  discoloration & grayishred precipitate
Methotrimeprazine (Nozinan®)
25 mg/ml injectable
(store room temp, protect from light)
Topical Route
Oral route not desirable
Mucositis
Inability to swallow
Nausea/vomiting
Obstruction
Poor taste of product
Dry mouth
More localized action
Topical Route: Advantages
Avoids the GI tract and hepatic first-pass
metabolism
Delivers to a specific site
Controls absorption rate
Provides constant dosing  depot effect
with anhydrous gels
Reduces systemic side effects
Heir, Gary DMD, et al. IJPC 2004; 8:337-343
Topical Route: Advantages
Improves compliance
Allows ↑ concentration of Rx at site of
application
Plasma concentrations of <10%
compared to oral route
Heir, Gary DMD, et al. IJPC 2004; 8:337-343
Topical Route: Drawbacks
Variations in the stratum corneum barrier
Delivery dosing may require adjustment
Rate of absorption may vary
Rash most common SE
Heir, Gary DMD, et al. IJPC 2004; 8:337-343
Topical Route
Mouthwash/rinses
Misoprostol, Diphenhydramine, Lidocaine, Triamcinolone,
Sucralfate, Dry Mouth Formulations
Transdermal Route
Fentanyl, Oxybutinin, Estrogen, Nitrate patches
Transdermal gels
Buccal spray
Morphine, Fentanyl, Triamcinolone, Lidocaine
Medicated lollipops
Fentanyl, Nicotine, Tetracaine, Dextromethorphan,
Diphenyhydramine, Nystatin
Topical Anti-Nauseant Gels
Scopolamine 0.25mg/0.1ml
Transderm V patch releases ~1mg over 72
hr
~0.1mg Q8H vs 0.25mg
Apply 0.1 – 0.2ml Q8H
Expiry date about 6 months
Topical Anti-Nauseant Gels
ABHR
Ativan/Benadryl/Haldol/Reglan
Lorazepam 2- 4 mg higher brain (cortex)
Diphenhydramine 50-100 mg  vestibular
Haloperidol 2-4 mg  CTZ
Metoclopramide 40-80 mg/ml  afferent impulses
from periphery
Dose 0.25ml inner wrist QID
Moon RB Intl J Pharm Compound 2006 10:95-8
Subcut Antiemetics
Haloperidol 0.5 - 1 mg po/sq/iv q4-12h
MTMZ 5 - 10 mg po/sl/sq q4-8h
Metoclopramide 10 - 20 mg po/sq/pr q4-8h
Ondansetron 8 -16 mg q 12 h po/sq/iv
Granisetron 1- 2 mg q 12 h po/sq
Dexamethasone 4-16 mg po/sq/iv daily
Dimenhydrinate 25 - 100 mg po/pr/sq q4-8h
Scopolamine 0.3-0.6 mg sq
Promethazine (Not sq)
Case: Maria de J.
35 y o, mother of 3, works in textiles
Lower abdominal pain, nausea
Investigations reveal ovarian mass,
resection: adenocarcinoma
Chemo with platinum/paclitaxel, nausea
with first 2 cycles, N/V subsequently
Admitted for IV hydration, pt wants to stop
tx
gh
Case: Maria de J.
4th cycle delayed x 1 week, P & S clinic
Full assessment reveals anticipatory
nausea, constipation on AXR
Oral and PR laxatives given, BZD
prechemo
No vomiting, still nauseated, avoids po
route
Refuses hospital stay
gh
Case: Maria de J.
Use of triple suppository advised (tid –
qid) dexamethasone 2 mg
metoclopramide 10 mg
diphenhydramine 25 mg
Nausea controlled for final 2 cycles, no
hydration necessary
Rectal Route
Drug absorption
Limiting factors
Conditions/methods of administration
Care Beyond Cure: A Pharmacotherapeutic Guide to
Palliative Care; Andree Neron Editor, 2000
Rectal Drug Absorption
First 6-8cm of rectum drain directly into
systemic circulation
Drugs admin by this route: no hepatic
first-pass effect
Rx high hepatic extraction may  in
bioavailability; variable due to:
Patient
Absorption site
Drug formulation, penetration of mucosa
Care Beyond Cure, 2000
Rectal Drug Absorption
Rectum vs upper GI tract:
Absorption area
rectal mucosa: 200-400 cm² (no villi in rectum)
small intestine: 2,000,000 cm²
pH
Fluid content
Absorption mechanisms same (passive
diffusion)
Formulation of drug is critical factor
May have to increase dosage interval i.e. Q8H vs Q12H
Care Beyond Cure, 2000
Rectal Limiting Factors
Drug insertion level
6-8cm (lower rectum)  systemic circulation
15-20cm (upper rectum)
 portal vein  hepatic first-pass effect
Solutions:
Aqueous & alcohol solutions are the best
and most rapidly absorbed
Fecal matter in rectum
Defecation reflex, involuntary expulsion
Care Beyond Cure, 2000
Rectal Administration
Use liquid formulations whenever possible
Use volumes <10-25 ml
>80 ml ↑ risk of spontaneous expulsion
Administer liquids with a small lubricated
syringe
Rectal canula or catheter tip syringes beneficial
Cut a NG tube (#14) to 5 cm; attach to prefilled
syringe
reduces chance of portal vein absorption
Care Beyond Cure, 2000
Rectal Administration
Administer capsules and tablets directly
into the rectum
Compounding pharmacy: “designer” rectal
suppositories
Administration a lot easier
Hepatic absorption usually not a problem
with the use of suppositories
Care Beyond Cure, 2000
Rectal Administration
Lorazepam
Use parenteral preps or tablets
Bioavailability of injection > 80%
Serum concentrations < ½ of IV route
Metoclopramide
Tablets or suspensions
Phenobarbital
Excellent bioavailability  90-100%
Peaks at ~ 4 hours
Baines, MJ BMJ 1997;315:1148-1150
Rectal Administration
For refractory cases, use combinations
that act at different receptor sites
Cerebral cortex
CTZ
GI tract
Severe or refractory nausea may benefit
from corticosteroid
Care Beyond Cure, 2000
Triple Suppository
Metoclopramide 10 - 20mg
Dimenhydrinate 25 - 75mg
Prochloperazine 10 - 25mg
Use a formulation with a single
medication or combinations of up to 3
medications
Other Antinauseant
Suppositories
Dimenhydrinate 75mg/Metoclopramide
15mg/Prochloperazine 10mg
Dimenhydrinate 25mg/Metoclopramide 10mg/
Prochloperazine 15mg
Metoclopramide 10mg/Haloperidol 1mg
Dimenhydrinate 25mg/ Metoclopramide 20mg/
Prochloperazine 10mg/ Dexamethasone 2mg
Summary
GI symptoms in palliative care varied
Assessment important
Tailor therapy to meet pt needs
Research in area lacking
Help is available
WRHA Pall Care pgm: 237-2400
Physician on call: 237-2053 (24 hrs)
Case example
Young woman, chronic pain
Compression of C6 root, migraine,
constant, rated 8/10
Attempted pain control using methadone,
not tolerated
Lost to F/U until Jan 07, returned on
meperidine (Demerol®)
Case example
GP requested IV anti-nauseants
Good effect but cumbersome
Topical compound (/ml, in PLO):
metoclopramide 20 mg
dimenhydrinate 25 mg
Benefit, but required adjustment to (/ml):
dimenhydrinate 100 mg
haloperidol 4 mg
metoclopramide 80 mg