Download key concepts in acute pain management

KEY CONCEPTS IN ACUTE PAIN
MANAGEMENT SURGERY RESIDENTS
Feb. 7, 2006
John Penning MD FRCPC
Director Acute Pain Service
Objectives

General Key Concepts
– The “real cost” of acute pain
– Multi-modal analgesia

Discuss key concepts of each modality
– Always a COX-inhibitor before opioid
– Tylenol # 3 has it’s limitations

Review principles discussed by case
presentation
– Opioid tolerance, conversion from IV to PO
– When, how to use naloxone
– Assessing the hypotensive epidural patient
Consequences of poorly managed
acute post-operative pain

The Patient suffers
–
–
–
–
–
–
CVS: MI, dysrhythmias
Resp: atelectasis, pneumonia
GI: ileus, anastamosis failure
Endocrine: “stress hormones”
Hypercoagulable state: DVT, PE
Impaired immunological state
• Infection, cancer, wound healing
– Psychological:
• Anxiety, Depression, Fatigue
– Chronic Post-surgery/trauma Pain
Consequences of poorly managed
acute post-operative pain

The Hospital
–
–
–
–
–

Increased costs $$$
Poor staff morale
Reputation/Standing in the Community, Nationally
Accreditation
Litigation
The Healthcare professional
– Morale
– Complaints to College
– Litigation
Benefits of Optimal Acute PostOperative Pain Management

The Hospital
– Increased patient satisfaction
– Increased staff morale
– Compliance with national guidelines, accreditation
criteria
– Cost Savings
• Earlier ambulation and enteral feeding
• Decreased complications/ICU expenditures
• Decreased Length of Stay
The New Challenges in Managing Acute
Pain after Surgery and Trauma

Patients/Society more “aware” of their
rights to have good pain control
– We are being held accountable

Pressure from hospital to minimize
length of stay
– Control pain, limit S/E and complications
The New Challenges in Managing Acute
Pain after Surgery and Trauma

The Opioid Tolerant Patient
– The greatest change in practice/attitudes in
the last 10 years is the now wide spread
acceptance of the use of opioids for
CHRONIC NON-MALIGNANT PAIN
– Renders the “usual” standard “box” orders
totally inadequate in these patients

Get an accurate Drug History
What is the “Best Way” to manage
acute post-operative pain?

FIRST, DO NO HARM
Therefore, the “best way” is a BALANCE
Patient
Safety
Effective
Analgesic
Modalities
KEY POINTS


“Emphasis is placed on the utilization of a
multimodal analgesic approach to maximize
analgesia while minimizing side-effects.”
– Transduction
– Transmission
– Modulation
– Perception
There is as of yet no single silver bullet!!
Pain Pathways
Acute Pain Management Modalities

Cyclo-oxygenase inhibitors
– Non-specific COX inhibitors(classical NSAIDs)
– Selective COX-2 inhibitors, the “coxibs”
– Acetaminophen is probably COX-3


Opioids
NMDA antagonists
– Ketamine, dextromethorphan

Anti-convulsants
– Gabapentin, Pregabalin

Local anesthetics
Tissue Trauma
Cell Membrane Phospholipids
Phospholipase
Arachidonic Acid
C
O
X
Cyclo-oxygenase
Endoperoxides
Thromboxane
Prostaglandins
Toxic Oxygen Radicals
Prostacyclin
Case Problem: Inadequate Analgesia with IV
PCA after Open Cholecystectomy

45 yr. female c/o severe pain at rest and difficulty
breathing due to incisional pain- 4 hrs. post-op
– IV PCA morphine: 1mg bolus, 5 min. lock-out, no
continuous infusion
– 150 demands : 28 good
– has stopped using PCA because, “it is making me
sick(N/V) and it’s not working”
– received 25 mg gravol X 2 one hour ago which
helped just a little with the N/V, but did make her
quite groggy

Solution!
– Continuous infusion? Increase bolus dose?
Case Problem: Inadequate Analgesia with IV
PCA after Open Cholecystectomy

Problem: Patient unable to attain required
morphine blood level due to intolerable side-effects
(N/V, sedation)

Solution:
– Administer NSAID
• Toradol IV/IM, Naprosyn 500 mg PR Q12H and
this may be changed to 250 mg PO TID with
meals once eating
– Control N/V
• Maxeran/Stemetil, Ondansetron, Decadron
• May need to consider changing opioid i.e.
Demerol
# of Deaths in thousands
Mortality From NSAID-Induced GI
Complications vs Other Diseases in US
25
20
15
10
5
0
Leukemia
HIV
NSAIDs- Multiple Asthma
Myeloma
GI
Cause of Deaths
Wolfe MM: NEJM 1999; 340: 1888-99
Cervial
Cancer
Penning’s Pessimistic Policy on
Pain Pills

Pick your “Poison” Pursuant to Patient
Profile

COX-inhibitors are potential killers
“in the long run”

Opioids are potential killers
“in the short run”
Analgesia with Opioids alone

The harder we “push” with single mode analgesia,
the greater the degree of side-effects
Side-effects
Analgesia
Multi-modal Analgesia

“With the multimodal analgesic approach there is
additive or even synergistic analgesia, while the sideeffects profiles are different and of small degree.”
Side-effects
Analgesia
Case Problem:
Severe Respiratory
Depression after Toradol?

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Healthy 34 yr. patient c/o severe incisional pain in
PACU after ovarian cystecomy
Received 200 g fentanyl with induction and 10 mg
morphine during case
PCA morphine started in PACU, plus nurse
supplements totaled 26 mg in 90 minutes
Still c/o pain, 30 mg Toradol IM given with some relief
after 15 minutes, so patient sent to ward
60 minutes later found unresponsive, cyanotic, RR
4/min.
Case Problem:
Severe Respiratory
Depression after Toradol?




Pharmacodynamic drug interaction between
morphine and NSAID
– morphine’s respiratory depressant effect opposed
by the stimulatory effects of pain, busy PACU
environment
– NSAID decreases pain, morphine’s effect
unappossed
Gain control of acute pain with fast onset, short acting
opioid(fentanyl)
Add NSAID adjunct early
Monitor closely for sedation and respiratory
depression after pain is alleviated by any means
The problem with the “Little Pain – Little Gun”,
“Big Pain – Big Gun” Approach


With opioids analgesic efficacy is limited by
side-effects
“Optimal” analgesia is often difficult to titrate
– 10 – fold variability in opioid dose:response for
analgesia
– A dose of opioid that is inadequate for patient A
can lead to significant S/E or even death in patient
B.
• Many patient factors add to the difficulty
– Opioid tolerance, anxiety, obstructive sleep
apnea, sleep deprivation, concomitantly
administered sedative drugs
The rationale for COX-Inhibitors in
acute pain management

The problem with the “Little Pain – Little
Big Pain – Big Gun Approach”
Gun,
– Patient Safety!! If the “Big Gun” is failing due to
dose limiting sedation/respiratory depression, the
addition at that time of the “Little Gun” may kill the
patient.
NSAID and Acetaminophen
CONCEPT # 1
The foundation of all acute pain Rx protocols.
”First on last off”





sole agent in mild /moderate pain
Analgesic efficacy is limited inherently
In contrast, with opioids efficacy is limited by S/E
adjunctive analgesic for patients requiring opioids
opioid sparing effect 30-60 %
The rationale for pre-operative
administration

The benefits of “Pre-emptive Analgesia”
– Goal: prevent the establishment of peripheral and
central sensitization (“wind-up”), conditions that
lead to an augmented response to pain stimuli
• i.e. prevention of “hyper-algesic” state
– Requirements: the analgesic must be
pharmacologically active at the time of surgical
incision and it’s activity must be maintained perioperatively. ( > 1 hr. pre-op for PO/PR NSAIDs)
The rationale for pre-operative
administration

Pre-emptive Analgesic effect of Rofecoxib
after Ambulatory Arthroscopic Knee Surgery.
Scott S. Reuben et al. Anesth Analg 2002;94:
55-9.
– Showed that 50 mg of rofecoxib PO one hour
before surgery is better than 50 mg PO upon
completion of surgery. VAS at 24 hours
• Control
• Post-incision
• Pre-incision
Rest 3.5
Rest 2.3
Rest 1.8
Movement 4.0
Movement 3.1
Movement 2.4
Cyclo-oxygenase inhibitors
Acetaminophen
Naproxen
Celecoxib
Ketorolac
Rofecoxib
Cell Membrane Phospholipids
Phospholipase
Arachidonic Acid
COX-1
COX-2
Prostaglandins
Prostaglandins
Gastric Protection
Platelet Hemostasis
Renal Function
Acute Pain
Inflammation
Fever
Why a COX-2 inhibitor?

Equivalent analgesic efficacy with nonselective COX-inhibitors

No effects on platelets!

Better GI tolerability
– Less dyspepsia, less N/V
Cyclo-oxygenase inhibitors
The
CAMPAIGN
COX-2 for U?

COX-2 blockers, like Celebrex may not be
suitable for patients at risk for thrombotic
complications peri-operatively

We need an other campaign slogan?
Cyclo-oxygenase inhibitors
The
CAMPAIGN
Two hours before surgery associated
with post-op pain
1.
Celecoxib 400 mg PO
Healthy patients
2.
Naproxen 500 mg PO
Patients at risk for thrombotic complications
3.
Acetaminophen 1000 mg PO
Contra-indications to NSAID
36 yr. Open Cholecystectomy patient
experiencing difficulty weaning from IV PCA

Endometriosis, fibromyalgia and chronic low
back pain- has been on Tylenol #3 for several
years- functions well and stable usage of 810/day

Day 3 post-op Tylenol #3, 2 tabs Q4h started
and IV PCA D/C

Patient c/o severe pain, not able to go home
36 yr. Open Cholecystectomy patient
experiencing difficulty weaning from IV PCA

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
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A better way?
Celecoxib 400 mg PO > 2 hours pre-op, after
Naproxen 500 mg PR Q12H to 250 mg PO TID
On day 2, when patient is tolerating diet, review the
24 hour consumption of IV PCA morphine
Multiply the total by 2(for conservative IV to PO
conversion) and divide by 6 to derive the Q4H PO
morphine dose
90 mg IV X 2 = 180 mg, 180 mg/6 = 30 mg PO Q4H
Order the PO morphine straight, plus an additional
half dose for breakthrough pain, prn
Permit 6 hours overlap between IV PCA and PO
The Opioids

We have to stop trying to put every
patient in the “analgesic dose box”
Meperidine
75 mg
IM Q4H
prn
Tylenol #3
1 – 2 PO
Q4H
prn
Opioids

Concept # 2
The dose of opioid administered is
dependant upon multiple factors
• Pharmacological tolerance to opioids?
• Route of administration
– PO, IM/SC, IV bolus, intrathecal
• Age
• Weight
• Severity of pain
Opioids
CONCEPT # 3
Pharmacokinetic + Pharmacodynamic
patient to patient variability results in1000 %
variability in opioid dose requirements
(standardized procedure, opioid naïve patient)
– opioid dosage must be individualized
– therefore, if parenteral therapy indicated, IV
PCA much better suited to individual patient
needs than IM/SC
Opioids
*Cancer Pain Monograph (H&W, 1984)
CONCEPT # 4
Under utilization of high efficacy PO opioids

PO opioid equivalence of 10 mg morphine IM/SC *
Morphine 20 mg
Hydromorphone 4 mg
oxycodone 10 mg
meperidine 200 mg
codeine 200 mg
True or False?



One opioid is just like any other, in
terms of analgesic efficacy and sideeffects.
The is considerable variability between
patients in response to different opioids
Meperidine should be eliminated from
the hospital formulary
Opioids – Do they all act the same?


Opioids work as analgesics by
activating endogenous pain modulating
systems
Opioid receptors
– Mu, Delta and Kappa
– Large genetic variability in expression

Good choice in one patient may be poor
choice in another
– Analgesic efficacy
– Side-effect profile
Opioids – Are they all the same?

Morphine
Hydromorphone (dilaudid)
Oxycodone

Meperidine (demerol)


Meperidine
Morphine
Atropine
Fentanyl
Bupivacaine
Meperidine Pharmacology

Opioid agonist – Mu and some kappa

NMDA antagonist (weak)
Local anesthetic action – equipotent to
lidocaine
SSRI (weak)
Muscaric blockade – “atropine-like”



– Central anti-cholinergic effects often causes
confusion in the elderly
Meperidine’s major problem

Normeperidine
– The “ugly” metabolite
• Neuroexcitatory: twitches, dilated pupils,
hallucinations, hyperactive DTR, seizures
• Non-opioid receptor mediated, no tolerance
• Half-life is 15 – 20 hours
N-demethylation
Meperidine and MAO Inhibitors

Meperidine blocks the neuronal re-uptake of
serotonin, may result in serotonergic crisis in
patients being treated with MAO inhibitors
– Excitatory reaction with delirium, hyper or hypo
tension, hyperthermia, rigidity, seizures, coma,
death
– Supportive management, ? Benzos,
dopaminergics?
When to use Meperidine?

As a third line opioid when other choices
have failed
– Especially if patient has Hx of such

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
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Less than 600 mg per day
Short duration of 2 days or less
Avoid in elderly or renal failure patients
May be useful in small IV doses to
supplement other opioids
– 25 mg IV Q1H prn
True or False?
Codeine is a “weak” opioid?
 Codeine is inherently safer than the
more potent opioids?

CODEINE – A drug whose time
has come and gone?
N Engl J Med 351; 27 Dec. 30, 2004
Problems with Codeine


62 yr. male with CLL, presents with
bilateral pneumonia.
Broncho-lavage revealed yeast
– Anti-biotics: Ceftriaxone, clarithromycin,
voriconazole
– Codeine 25 mg PO TID for cough
Problems with Codeine

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Day 4 became markedly sedated, pinpoint pupils and ABG reveals PaCO2 of
80 mmHg. Marked improvement with
Naloxone.
What’s the expected morphine blood
level?
Answer: 1 to 4 mcg/L
This patient’s morphine blood level?
– 80 mcg/L
Codeine Metabolism in Normal
Circumstances

The major pathways convert codeine to
inactive metabolites
– CYP3A4 pathway yields norcodeine
– Glucuronidation

The minor pathway, about 10%, yields
morphine
– CYP2D6, essential for analgesic effect
60 mg Codeine PO – approx. 4 mg morphine SC

Variability! 60 mg PO Codeine yields
potentially 0 to 60 mg parenteral morphine
Potential Codeine Drug Interactions

Major pathway – CYP3A4
– Inducers decrease codeine effect
– Inhibitors increase codeine effect

Minor pathway - CYP2D6
– Inducers increase codeine effect
– Inhibitors decrease codeine effect
Inhibitors of CYP2D6
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SSRIs (potent) especially PAXIL
Cimetidine, Ranitidine
Desipramine
Propranolol
Quinidine (potent)
Viagra
Many anti-biotics and chemo
Instead of Tylenol # 3 ?

Acetaminophen 650 mg PO Q4H

Morphine 10 – 20 mg PO Q4H prn
– OR
Dilaudid 2 – 4 mg PO Q4H prn

Why combination analgesics are not
a great idea




Acetaminophen-Induced Acute Liver Failure:
Results of a USA Multicenter, Prospective
Study. Hepatology, Vol. 42, No. 6, 2005.
Larson et al.
22 centers, 662 cases ’98 – ’03.
50% cases due to acetaminophen
50% of acetaminophen cases inadvertent
The Limitations of Tylenol # 3

The problem with combination drugs
– The codeine dose is limited by the maximum
allowed dose for acetaminophen
•
•
•
•
•
4 grams/day = 12 tabs/day
12 X 30 mg = 360 mg codeine = 60 mg morphine
60 mg PO = 15 – 30 parenteral morphine
Equals about 1 mg/hr IV/s.c.
Adequate for moderate pain in average patient?
– Net result is limited efficacy
The Limitations of Tylenol # 3

The problem with combination drugs
– Acetaminophen therapy may be limited by
intolerance to codeine
• Patient sensitive to codeine may only want to
take 1 T#3 or even 1/2. If all they can tolerate
is 15 mg of codeine Q4H, the patient is not
receiving the benefit of optimum dose of
acetaminophen
The Limitations of Tylenol # 3

The constipation problem
– Codeine may be more constipating than other
opioids

The codeine “allergy” problem
– True immunological allergy is extremely rare
– 99.9% of “allergy” are sensitivities
• N/V, excessive sedation, confusion
• Need to perform adequate drug history,
otherwise problems may arise when an even
more potent opioid, such as Percocet is
substituted for T#3.
The Limitations of Tylenol # 3
1/ Codeine is a “pro-drug”
2/ The problem with combination drugs
a. The codeine dose is limited by the maximum allowed
dose for acetaminophen
b. Acetaminophen therapy may be limited by intolerance to
codeine
c. Acetaminophen toxicity
3/ The constipation problem
4/ The codeine “allergy” problem
Solution to the T #3 limitations
Provided codeine works in your Patient
The oral analgesic ladder
T#3
T#3
T#3
T
T
T
T#3
T#3
Oxy
5 mg
Solution to the T #3 limitations
Every 12 hours
Cox-inh
Long Acting
Long Acting
Opioid
For breakthough pain
Regular opioid PO Q4h prn
Acetaminophen 650 mg PO Q4h prn
Opioids
STOP
Hydromorphine 1 – 4 mg PO/IM/IV Q4H prn
NOT!
This represents up to 30 fold range in peak
effect in any given patient
1 mg PO ---- 4 mg IV bolus
homeopathic dose ---- potentially lethal
Opioids: Rational multi-route
orders?

Foundation of Acetaminophen/NSAID

Morphine 5 - 10 mg PO Q4h prn
Morphine 2.5 - 5 mg s.c. Q4h prn
Morphine 1-2 mg IV bolus Q1h prn
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Hydromorphone 1 - 2 mg PO Q4h prn
Hydromorphone 0.5 – 1 mg s.c Q4h prn
Hydromorphone 0.25 – 0.5 mg IV Q1h prn
When a fast onset/short duration
opioid is required!

Fentanyl 25 - 50 ug IV bolus Q 2 - 3 minutes
– onset in 30 seconds
– peak effect in 5 min. (30 min. with morphine)
– “short duration of action due to lipid solubility,
redistribution half-life is 15 minutes
– very potent respiratory depressant, give
supplemental Oxygen, monitor SaO2
– be very careful when benzodiazepines are also
administered ie. Versed
– Airway management skills/equipment available
– Naloxone
Case Problem:
32 yr. Male with multiple ribs #
Patient previously healthy, MVA with no other
injuries.
In Trauma Unit, c/o 9/10 pain. Difficultly
breathing due to severe splinting.
Analgesic orders are:
Morphine 2 – 10 mg PO, SC, IV Q4H prn
Nurse just gave 5 mg PO one hour ago and
now won’t give anything for 3 hours!
What do you do?
Case Problem:
32 yr. Male with multiple ribs #
Review of PHx reveals no drug use.
Patient has received total of 24 mg
morphine in the 6 hours since
admission.
Case Problem:
32 yr. Male with multiple ribs #
Ketorolac 30 mg IV stat followed by 10
mg IV Q4H.
Morphine 10 – 15 mg s.c. Q4H
Morphine 2 - 3 mg IV Q1H prn
Ketamine 2.5 – 5 mg IV Q30 min. prn
NMDA Antagonists as “analgesics”


Really anti-hyperalgesics, anti-pronociceptive
Central system of facilitatory pain pathways
that employ excitatory neurotransmitters
– Aspartate, glutamate


Involved with central sensitization, Opioid
tolerance and Opioid Induced Hyper-algesia
NMDA antagonists block the facilitatory pain
pathways that induce “pathological” acute
pain
– Hyperalgesia, allodynia
Hyperalgesia
Excitatory Mechanisms
NMDA Agonists
PAIN
Inhibitory Mechanisms
OPIOIDS
Analgesia
NMDA Receptor Antagonists To prevent or reverse “pathological” acute pain

Ketamine, Dextromethorphan
– Ketamine is widely known as a dissociative
“general anesthetic” - 3 mg/Kg IV bolus
– Ketamine 2.5 - 5.0 mg IV bolus for
analgesia in post-op patient – Ketamine as co-analgesic - combined 1:1
with morphine IV PCA. Better analgesia,
less S/E
– Dextromethorphan 30 mg PO Q8H
available OTC as Benylin DM, 3 mg/ml.
Case Problem:
32 yr. Male with multiple ribs #
IV PCA with morphine / ?ketamine
Ketorolac changed to naproxen when
eating. 250 mg TID
Or
Celecoxib 200 mg Q12H for 5 days then
100 mg daily until no longer needed.
Case Problem:
32 yr. Male with multiple ribs #
On day three patient is doing well and
planning for D/C tomorrow.
Convert to PO morphine.
Daily IV PCA use is 100 mg per day.
Equals about 200 mg per day orally.
Order about 50% as long acting.
60 mg MS Contin Q12H and 10 – 20 mg
PO Q4H prn.
Case Problem:
32 yr. Male with multiple ribs #
Weaning instructions:
As daily “breakthough” morphine requirements
decrease, reduce the MS Contin dose by
25% increments.
The COX-inhibitor is the last to be D/C
Acetaminophen may be used in addition to
NSAIDs and Coxibs
Opioids
Issue
With parenteral opioids the patient may experience intolerable side
effects before adequate analgesia is attained
Opioids
CONCEPT # 3
Targeted regional
administration of opioid
results in enhancement of
the therapeutic index (ratio
of analgesia/side effects)
Acute Pain Management Modalities:
Who Gets What and Why??

Intrathecal morphine
– simple technique
– potent analgesia for 12 -16 hrs.
– highly effective for pain in lower abdomen
and lower limbs
– risk of delayed onset of respiratory
depresson
– C/S, Vag. Hyst., Rad. Prostatectomy,
Arthroplasty
Neuraxial Morphine Side-effects
Intrathecal 300µg Epidural 3 mg

Pruritus
– >60% of post-partum patients
– easily treated with nalbuphine
– increased risk reactivation of oral herpes simplex

Urinary Retention
– suggest leave foley in for 12 hours

Delayed Respiratory depression
– Peaks at 4-6 hours after administration
– Incidence depends on patient population
– Rare in properly selected patients
What is an “EPIDURAL”?

Anatomical
– Location of the catheter, C7 – L5
• Cervical, thoracic and lumbar epidurals
• Segmental Blockade

Drugs
– Opioids (hydrophillic vs. lipophillic)
• morphine, hydromorphone, demerol, fentanyl
• Hydrophillic drugs migrate rostrally and also
yield greater spinal selectivity
What is an “EPIDURAL”?

Drugs
– Local Anesthetics :
• Lidocaine, bupivacaine, ropivacaine
Varying concentrations/drug mass produces
“Differential Blockade”
sympathetics > somatosensory > motor
– Adjuncts: epinephrine, ketamine

Mode of Drug Delivery
– Intermittent bolus vs. continuous infusions
True or False?

Epidural analgesia impairs the
resolution of post-operative ileus i.e. it
“slows down the gut” delaying return of
normal bowel function.

Epidural analgesia necessitates a foley
catheter until the epidural is removed
Acute Pain Management Modalities:
Who Gets What and Why??

Why bother with epidural local anesthetics?
– In major bowel surgery the period of postoperative ileus is markedly decreased with the use
of epidural infusions of local anesthetics and by
the avoidance of high doses of opioids
– promotes vascular graft patency in the early postoperative period
– superior analgesia with fewer side-effects
– improved outcome and decreased health-care
costs in high risk patients having major surgery
Case Presentation:
Somnolence and
hypoxemia while on epidural infusion of
hydromorphone/bupivacaine

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65 yr. Female with Ca pancreas had partial
“Whipple’s”. Epidural at T8/9, standard dilaudid/bup
PMHx: Angioplasty 9 yr. ago, MI, CHF in past
– Moderate COPD, NIDDM
– Dilaudid 4 mg PO Q4H for the last month
Early Post-op: Required double strength but did well
Day 4 became increasingly lethargic, somnolent and
not able to maintain SaO2 > 90% despite
supplemental O2.
Is Narcan Indicated? Urgently?
Case Presentation:
Somnolence and
hypoxemia while on epidural infusion of
hydromorphone/bupivacaine
 Further patient evaluation

– Patient arousable, RR 8-16, pupils slightly
constricted, BP 130/70, pulse 90 and reg.
– Chest: A/E fair bil. And some mild basilar creps
– ABG: pH 7.46 pCO2 50 pO2 55 BiCarb 36 FiO2 > .50
– Chest X-ray: Extensive bilateral, diffuse,
interstitial infiltrate consistent with ARDS
Naloxone would probably have had a serious
adverse effect on this patient. Hypoxemia despite
supplemental O2 in a breathing patient. Look
beyond the Opioids!
Case Presentation:
Somnolence and
hypoxemia while on epidural infusion of
hydromorphone/bupivacaine

Management of suspected opioid induced
respiratory depression
–
–
–
–
–
Support A/W
Simulate breathing
Supply supplemental oxygen
Assess SaO2, BP, Pulse
Naloxone titration, IF INDICATED
• 0.04 mg Q5 min. X 3 as needed


Hypoxemia is a medical emergency
Hypercarbia is NOT
Epidural Pit-falls for the Surgeon


Epidural hematoma
– > 50 reported cases in USA in patients treated
with LMWH
– Epidural insertion and removal of the catheter
– Risk factors: Elderly, low body weight, twice daily
dosing, anti-coagulation vs. prophylactic dose
range
The decision to fully anti-coagulate a patient with an
epidural in-situ should be made in consultation with
anesthesia and thrombosis medicine
Epidural Pit-falls for the Surgeon

“Masked-Mischief”
– The potential high efficacy of the modality
could block pain related to complications
• Peritonitis; anastomosis dehiscence
• Wound infection, wound hematoma
• Limb ischemia, compartment syndrome
– Delay in appropriate therapy, diagnosis
• Neurological problems inappropriately
attributed to the epidural i.e. anterior spinal
artery syndrome
• Hypovolemia
The “Hypotensive” Patient with
an Epidural
64 yr. female, 48 kg, with no Hx of CVS problems, had
an esophagectomy for cancer with combined
GA/epidural anesthesia.
Later that evening you are called because the patient’s
BP is 85/50.
Epidural at T5/6 and running hydromorphone 10 µg/ml
in 0.01% bupivacaine at 8 ml/hr
The “Hypotensive” Patient with an
Epidural
Possibilities?
 “Normal” for this patient



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– all is well and confirmed by Hx and absence of
postural changes in BP or HR
– vascular patients may have marked discrepancy
between arms – establish baseline pre-op
Surgical complications
Medical complications
Side-effect of Epidural induced sympathetic block
– decreased venous return and decreased SVR
Combination of any 4 above
Is the Epidural causing the hypotension?
What drugs have been administered epidurally?

Pure opioids: morphine, hydromorphone,
fentanyl
– sympathetics not blocked directly so look for
another cause

Demerol
– mild direct sympatholytic effect and some systemic
effects in large doses. Rarely cause of significant
Hypotension. Be careful to R/O other causes.

Local Anesthetics +/- opioids
– In a euvolemic patient with normal CVS function
hypotension is unlikely if < 8 sensory dermatomes
blocked
Is the Epidural Local Anesthetic
causing the hypotension?

Intrathecal catheter migration

Inadvertent overdose

“Un-masking” of problem with the patient.

“Sensitive” patient
Is the Epidural Local Anesthetic causing the
hypotension?
Management
 ABCs
– supplemental O2, fluid bolus, elevate legs
– ephedrine 5 mg or phenylephrine 50 µg IV bolus
– Hold the epidural infusion

Quantify the extent of block
– motor block? Thoracic epidural?, that’s a problem!
– Sensory block (cold, sharp)
• In a euvolemic patient with normal CVS
function hypotension is unlikely if < 8 sensory
dermatomes blocked
Management of Hypotension
Cont’d

High thoracic epidural blockade may block
the compensatory tachycardia response to
hypovolemia.
– Cardio-accelerator sympathetic nerve fibres arise
from T1 - T4
– sympathetic block may extend several
dermatomes above the sensory blockade


Correct the underlying cause
Remove bupicacaine and change to epidural
hydromorphone if patient remains
hemodynamically unstable
ACUTE PAIN MANAGEMENT:
SCIENTIFIC EVIDENCE 2nd Edition June ‘05
Australian and New Zealand College of Anaesthetists
And Faculty of Pain Medicine.
http://www.anzca.edu.au/publications/acutepain.pdf
The above web site has the entire document and is freely
Available to download.
Conclusion: Key Concepts






The foundation of all acute pain Rx protocols is
NSAIDS and acetaminophen.
Codeine is a “pro-drug”. Problems may occur with
under or over conversion to morphine
Under utilization of high efficacy PO opioids
Pharmacokinetic + Pharmacodynamic variability
Order opioid dosages rationally, especially with
patient Hx and route of administration in mind
Naloxone can be a dangerous drug, careful titration
is almost always possible
Opioid Conversions – Parenteral to Oral
and Equivalents (approx.)
Morphine 10 mg
Morphine 20 mg
Hydromorphone 2 mg Hydro…. 4 mg
Meperidine 75 mg
Meperidine 200 mg
Codeine 120 mg
Codeine 200 mg
Oxycodone (n/a)
Oxycodone 10 mg
Opioid Conversions – Oral to Parenteral
and Equivalents (approx.)
Morphine 40 mg
Hydromorphone 8 mg
Meperidine 300 mg
Codeine 300 mg
Oxycodone 15 mg
Morphine 10 mg
Hydro…. 2 mg
Meperid.. 75 mg
Codeine 120 mg
Oxycodone (n/a)