Dosing Dilemmas in Sustained Low Efficiency Dialysis

Dosing Dilemmas in
Sustained Low Efficiency
Dialysis
Kellie L. Fortier, PharmD
Banner Baywood
Medical Center
Mesa, AZ
Objectives
• Differentiate SLED from other
CRRT modalities
• List the benefits to SLED
• Make antibiotic recommendations
for patients receiving SLED
SLED
• Many names
–
–
–
–
Sustained Low Efficiency Dialysis
Slow Extended Daily Dialysis
Extended Daily Dialysis
Slow Low Efficiency Dialysis
• Hybrid modality
• Uses diffusion and ultrafiltration
Types of CRRT
Heintz BH, et al. Antimicrobial dosing concepts and recommendations for critically ill adult patients receiving continuous renal replacement therapy or intermittent hemodialysis.
Pharmacotherapy 2009; 29(5):562-77.
Advantages to SLED
•
•
•
•
•
•
Hemodynamic stability
Uses same equipment as IHD
No need for customized solutions
Avoids interruption of therapy
Good solute removal
Generally no need for anticoagulation
Vancomycin
• 11 ICU pts received 15 mg/kg
• Vd 0.84 L/kg, t1/2 43.1 hrs, Cl 24.3
ml/min
• 10 ICU pts 1 gm infused
• Cl 35 ml/min, t1/2 = 11.2 while on
SLED and Cl 26 ml/min, t1/2 =37hrs
off.
• Load with 15-25 mg/kg and check
24 hr level post infusion.
Ahern, JW, et al. Experience with vancomycin in patients receiving slow low-efficiency dialysis. Hosp Pharm 2004; 39:138-43.
Kielstein JT, et al. Pharmacokinetics and total elimination of meropenem and vancomycin in ICU patients undergoing extended daily dialysis. Crit Care Med 2006; 34:51-6.
Linezolid
• Compared IHD, SLED, CVVH
• Single dose 600 mg given to 5 ICU
pts receiving SLED (8hr run)
• 34 % of dose removed
• Recommendation to give at the end
of SLED
Fiaccadori E, et al. Removal of linezolid by conventional intermittent hemodialysis, sustained low-efficiency dialysis, or continuous venovenous hemofiltration in patients with acute renal
failure. Cri Care Med 2004; 32:2437-42.
Daptomycin
• 1 ICU pt received 6 mg/kg of
daptomycin, run time 12 hrs
• t1/2 = 9 hrs comparable to nl fxn
• 52% of dose was removed
• Administer q24hr
Burkhardt O, et al. Elimination of daptomycin in a patient with acute renal failure undergoing extended daily dialysis. J Antimicrob Chemother 2008; 61:224-5.
Gentamicin
• Single dose of 0.6 mg/kg base on
ABW (home CKD pts), 8 hr run
• Vd = 0.28 L/kg, Cl = 76 ml/min,
t1/2 = 3.7 hrs while on SLED
• 70% of drug removed
• Authors recommend 2-2.5 mg/kg
post SLED
• Not at steady state and single dose
Manley HJ, et al. Gentamicin pharmacokinetics during slow daily home hemodialysis. Kidney Int 2003; 63:1072-8.
Carbapenems
• Meropenem – 10 ICU pts received 1
gm, 8 hr run
• t1/2 = 3.7 hr, 51% of drug removed
• Recommend 0.5 – 1 gm q8hr
• Ertapenem- 6 ICU pts received 1 gm,
8 hr run time
• Cl = 49.5 ml/min, t1/2 6.7 hrs
• Recommend 1 gm q24
Kielstein JT, et al. Pharmacokinetics and total elimination of meropenem and vancomycin in ICU patients undergoing extended daily dialysis. Crit Care Med 2006; 34:51-6.
Burkhardt O, et al. Pharmacokinetics of ertapenem in critically ill patients with acute renal failure undergoing extended daily dialysis. Nephrol Dial Transplant 2009; 24:267-71.
Fluoroquinolones
• Levo – 5 ICU pts 500 mg dose with 8
hr run time
• Fraction removed 17-27%, t1/2 = 10.3
on and 34.5 off.
• Dose adjustment recommended
• Moxi – 10 ICU pts 400 mg dose, 8 hr
run time
• Kinetics similar to pt nl renal fxn
• Give Moxifloxacin 400 q24 after
SLED
Czock D, et al. Pharmacokinetics of moxifloxacin and levofloxacin in intensive care unit patients who have acute renal failure and undergo extended daily dialysis. Clin J Am Soc
Nephrol 2006; 1:1263-8.
Application to Practice
• Assess risk vs. benefits (ADR’s,
severity of infection, etc.)
• Most of these studies advocate for
more aggressive dosing compared
to HD
• Consider aggressive tx for
– residual renal fxn
– longer run times
• TDM if able (Vanco, AG)
Recommendations
• Work closely with nephrologist, ID,
dialysis staff
• Educate RN’s to distinguish the
difference between SLEDD and HD
• Q24 hr dosing administer after SLED
• Consider dosing for CrCl 15-30
ml/min for run times 6-8 hours and
30-50 ml/min for longer run times.
– Review article recommends CrCl 10-50
• Consistent timing for SLED
Mushatt D, et al. Antibiotic dosing in slow extended daily dialysis. CID 2009; 49:433-7.
Self Assessment
• 1. A 78 y/o WM admitted with respiratory
failure and acute AKI. Pt is started on daily
SLED therapy, run time 6 hours daily.
Pharmacy consult for dosing of antibiotics is
ordered. Pt is on Vancomycin 1 gm IV after
each HD and Zosyn 3.375 gm IV q6 hr for
empiric treatment of pneumonia . How would
you adjust your antibiotics?
• a. Adjust for CrCl >50
• b. Adjust for CrCl 30-50
• c. Adjust for CrCl 15-29
• d. Adjust for CrCl <15
Clinical Pearls:
Propylene glycol toxicity associated
with lorazepam continuous infusion
Lindsay Davis, Pharm.D.
Introduction to propylene glycol

1, 2-propanediol

Vehicle used as a drug solubilizer in
hydrophobic topical, oral, & IV compounds

Common IV drugs containing PG:
Drug & Concentrations
Amount of PG/ml
(volume/volume)
Etomidate 2 mg/ml
362.6 mg (35%)
Diazepam 5 mg/ml
413 mg (40%)
Esmolol 250 mg/ml
258 mg (25%)
Lorazepam 2mg/ml, 4mg/ml
830 mg (80%)
Nitroglycerin 5mg/ml
518 mg (30%)
Phenytoin 50 mg/ml
414.4 mg (40%)
Phenobarbital 65 mg/ml, 130mg/ml
702.4 mg (67.8%)
Why worry about propylene glycol?

Propylene glycol toxicity has been linked with:
◦
◦
◦
◦
◦
◦
◦
◦

Metabolic acidosis
Lactic acidosis
Nephrotoxicity (Acute tubular necrosis)
Hemolysis
Hypotension
Central nervous system depression
Seizures
Arrhythmias
FDA considers PG safe for use in drugs & cosmetics
◦ As a food additive, the maximum daily permissible intake
of PG is 25 mg/kg of body weight
◦ For a 70 kg patient, this limit would be met with only
4.2 mg IV lorazepam / day
Case Study


48 year old male with h/o alcohol abuse
Admitted for respiratory failure 2/2 aspiration PNA

VDRF  continuous infusion lorazepam for sedation & alcohol
withdrawal

1st 7 days of hospitalization  received 1,070 mg lorazepam (444 g PG)
Hospital days 6 & 7 AG:19, HCO3- :13, pH:7.16, Cr:2.2
Sepsis considered as cause  abx started
Despite abx  AG:22, HCO3- : 10, pH:7.11
All cultures negative
Serum osmolality: 405 mOsm/kg (n: 285-295)








Lorazepam d/c’d  midazolam started
Within 24 h, all metabolic abnormalities resolved
Serum PG level = 144 mg/dL (levels >18 associated with toxicity)
Wilson KC, Reardon C, Theodore AC, et al. Propylene glycol toxicity: A severe iatrogenic illness in ICU
patients receiving IV benzodiazepines. CHEST. 2005;128:1674-1681.
What did we learn?

This patient had PG toxicity, definitively diagnosed by
serum PG level, but clinically manifested as AG
metabolic acidosis & elevated SCr

Sepsis initially considered as cause for metabolic
abnormalities

Elevated osmolality  suspicion of PG in lorazepam

Rapid resolution of metabolic abnormalities with
discontinuation of lorazepam

Assays to monitor PG concentrations are unavailable at
most hospitals & results are often delayed

Use of osmol gap as surrogate marker of PG toxicity
Osmolality & Osmolarity

Terminology expressing calculated & measured
osmotic activity

Used to describe fluid movement between body
compartments

Can be used to detect foreign substances in the blood

Osmotically active compounds include ethanol,
methanol, isopropyl alcohol, & propylene glycol
Osmolality & Osmolarity

Osmolality (mOsm/kg of solvent)
◦ Value derived by an osmometer in clinical laboratories
Normal osmolality: 285 – 295 mOsm/kg

Osmolarity (mOsm/L of solution)
◦ Bedside calculation of osmotic activity by clinicians using
patient’s laboratory data
Serum osmolarity = (2 x serum Na+) + (BUN / 2.8) + (glucose / 18)
Normal osmolarity: 285 – 295 mOsm/L

Osmol gap
◦ Mathematical difference between the osmolality & osmolarity
Osmol gap = osmolality (measured) – osmolarity (calculated)
Normal osmol gap is defined as < 10
Propylene Glycol Metabolism

Renal elimination (12-50%)

Hepatic metabolism (50+%)
◦ via alcohol dehydrogenase  oxidized to lactic
or pyruvic acid

t ½ = 2 – 4 hours (adults)
Propylene glycol toxicity

Serum PG concentrations > 18 mg/dL are
associated with ADE/toxicity
◦ Predominant manifestation of PG accumulation is an AG
metabolic acidosis with corresponding elevated osmol gap

The portion of the serum osmolality contributed
by presence of PG can be calculated
◦ osmolality due to PG = [PG] / 7.6
◦ If this component explains an osmolar gap > 10, then no
other osmotically active particles are contributing to the gap
Lorazepam dose > 1 mg/kg/day
Yahwak JA, Riker RR, Fraser GL, et al. Determination of a lorazepam dose threshold for using the osmol
gap to monitor for propylene glycol toxicity. Pharmacotherapy. 2008; 28(8):984-991.
Lorazepam dose > 1 mg/kg/day
Results:

9/14 (64%) had PG concentrations > 18 mg/dL

6/9 (67%) developed transient AKI and/or metabolic acidosis
Conclusions:

Osmol gap > 10 was predictive of elevated PG concentrations

Osmol gap > 12 was predictive of clinical changes suggestive of PG toxicity

Consider screening for PG toxicity when doses > 1 mg/kg/day are required
Yahwak JA, Riker RR, Fraser GL, et al. Determination of a lorazepam dose threshold for using the osmol
gap to monitor for propylene glycol toxicity. Pharmacotherapy. 2008; 28(8):984-991.
Summary: Propylene glycol toxicity

Large volume of drug  large volume of diluent

PG toxicity is potentially life-threatening

PG toxicity is likely common & is preventable

Consider PG toxicity when a patient has:
- unexplained anion gap
- hyperosmolality
- metabolic acidosis
- clinical deterioration

A threshold dose of lorazepam that does NOT result in
PG accumulation has yet to be defined

The osmol gap may represent a surrogate marker for
PG toxicity  especially if lorazepam dose exceeds
1mg/kg/day
References
1.
Arroliga AC, Shehab N, McCarthy K, et al. Relationship of continuous infusion
lorazepam to serum propylene glycol concentration in critically ill adults. Crit Care
Med. 2004; 32(8):1709-1714.
2.
Erstad BL. Osmolality and osmolarity: Narrowing the terminology gap.
Pharmacotherapy. 2003; 23(9):1085-1086.
3.
Glover ML, Reed MD. Propylene glycol: The safe diluents that continues to harm.
Pharmacotherapy. 1996; 16(4):690-693.
4.
Reynolds HN, Teiken P, Regan ME, et al. Hyperlactatemia, increased osmolar gap, and
renal dysfunction during continuous lorazepam infusion. Crit Care Med. 2000;
28(5):1631-1634.
5.
Wilson KC, Reardon C, Theodore AC, et al. Propylene glycol toxicity: A severe
iatrogenic illness in ICU patients receiving IV benzodiazepines. A case series and
prospective, observational pilot study. CHEST. 2005; 128:1674-1681.
6.
Yahwak JA, Riker RR, Fraser GL, et al. Determination of a lorazepam dose threshold
for using the osmol gap to monitor for propylene glycol toxicity. Pharmacotherapy.
2008; 288(8):984-991.
7.
Yaucher NE, Fish JT, Smith HW, et al. Propylene glycol-associated renal toxicity from
lorazepam infusion. Pharmacotherapy. 2003; 23(9):1094-1099.
Does Your Patient Have
Unexplained Abdominal Pain?
A Review of Porphyria
Mindy Throm Burnworth, PharmD, BCPS
Midwestern University College of Pharmacy – Glendale
Associate Professor – Pharmacy Practice
[email protected]
6th Annual AzPA Annual Meeting
Biltmore Resort & Spa, Phoenix, Arizona
Sunday, July 18, 2010
Objectives/Disclosure
| To
review the pathophysiology,
clinical signs and symptoms,
diagnosis, treatment, and
management of porphyria
| No disclosures
1
|
|
|
|
|
|
28 yo F with severe abdominal pain
HPI: 3 days ago pt developed severe N/V
(~ 5/day), diffuse abdominal pain, constipation,
& fatigue. States urine is dark tinged (no
burning on urination). Reports hearing voices.
PMH: dysmenorrhea (estrogen)
SH: smoking (+), alcohol (social), no IVDA
VS: AF, BP 150/90, HR 88
Labs: Amylase/lipase, LFTs, CBC WNL;
UA unremarkable/urine cx NGTD;
CDT (-), O/P (-); impaction ruled out;
BMP WNL except Na 131, K 3.2
What is porphyria?
“well-defined genetic disorders of heme biosynthesis”
Disease
Acute intermittent
porphyria (AIP)
Hereditary coproporphyria
(HCP)
Variegate porphyria
(VP)
5-aminolevulinic acid [ALA]
dehydratase
deficient porphyria (ADP)
Deficient
% Normal
Enzyme
Activity
Porphobilinogen
~50
deaminase
Coproporphyrinogen
~50
oxidase
Protoporphyrinogen
~50
oxidase
ALA dehydratase
~5
Anderson KE et al. Ann Intern Med 2005;142:439-50
2
www.porphyria-europe.com
Heme Biosynthetic Pathway
What causes acute attacks
of porphyria?
|
|
Fasting, dieting, smoking/alcohol, stress from illness
Medications
z Barbituates, carbamazepine, ethosuximide, phenytoin,
primidone, valproic acid
z Carisoprodol
z Clonazepam (high doses)
www.porphyriafoundation.com
z Danazol
www.porphyria-europe.com
z Diclofenac/NSAIDs
www.drugs-porphyria.com
z Ergots
www.cpf-inc.ca
z Estrogen, progesterone
www.porphyria.uct.ac.za
z Metoclopramide
z Pyrazinamide, rifampin
z Sulfonamide antibiotics
Anderson KE et al. Ann Intern Med 2005;142:439-50
3
What are signs and
symptoms of porphyria?
Women of reproductive age
; Abdominal pain
; Muscle weakness
; Hyponatremia
; Dark or reddish urine
;
Anderson KE et al. Ann Intern Med 2005;142:439-50
Anderson KE et al. Ann Intern Med 2005;142:439-50
What are signs and
symptoms of porphyria?
Signs & Symptoms
GASTROINTESTINAL
Abdominal pain
Vomiting
Constipation
Diarrhea
NEUROLOGIC
Pain in extremities, back, chest, neck, or head
Paresis
Respiratory paralysis
Mental symptoms
Convulsions
CARDIOVASCULAR
Tachycardia
Systemic arterial HTN
Incidence (%)
85-95
43-88
48-84
5-12
50-70
42-68
9-20
40-58
10-20
28, 64-85
36-55
4
How is porphyria diagnosed?
Porphobilinogen/Porphyrin Levels
Disease
Erythrocyte Urine
Fecal
Plasma
Acute intermittent
▼
▲
►◄,▲ ►◄,▲
porphyria
(AIP)
Hereditary
►◄
▲
▲
►◄
coproporphyria
(HCP)
Variegate porphyria ►◄
▲
▲
▲
(VP)
Anderson KE et al. Ann Intern Med 2005;142:439-50
How is porphyria treated?
|
|
Withdraw unsafe medications
Nutritional support & symptomatic treatment
z
z
z
z
z
|
|
Seizure (gabapentin, vigabatrin, BZD)
IVF/electrolytes
Narcotic analgesics
Phenothiazines
β-blockers
IV glucose (10%, 300 g/day)
Hemin 3-4 mg/kg IV daily x 4 days ($8K)
Anderson KE et al. Ann Intern Med 2005;142:439-50
5
What should the
pharmacist know?
9
9
9
|
|
|
|
|
|
Screen the patient’s medication profile for
drugs that may precipitate and/or
exacerbate porphyria
Be familiar with porphyria references
(electronic)
Add porphyria to “allergy” or “drug-disease”
database
28 yo F with severe abdominal pain, N/V,
weakness, dark tinged urine, hearing voices,
HTN/tachycardia
Dysmenorrhea (estrogen), smoking/alcohol (+)
Tests/Labs: All negative except Na 131 (no
seizures), urine porphobilinogen level 100 mg/d
(0-4 mg/d) [Trace PBG Kit],
erythrocyte/fecal/plasma pending
PharmD consult (stop estrogen, smoke/EtOH)
Carbohydrate load, IVF with K
PRN IV morphine, promethazine,
metoprolol, lorazepam
6
Does Your Patient Have
Unexplained Abdominal Pain?
A Review of Porphyria
Mindy Throm Burnworth, PharmD, BCPS
Midwestern University College of Pharmacy – Glendale
Associate Professor – Pharmacy Practice
[email protected]
6th Annual AzPA Annual Meeting
Biltmore Resort & Spa, Phoenix, Arizona
Sunday, July 18, 2010
7
USP <797>: Improving Patient
Outcomes Through
Compliance
Christi Larson, Pharm. D.
Infusion Pharmacist
Chief Consultant, I.V. Insights
www.IVinsights.com
MAIN OBJECTIVE
At the end of this presentation you will be able to:
• Identify the most
common cause of
contamination when
preparing sterile
products for patient
use.
OBJECTIVES
You will also learn:
• What is USP 797?
• Who does USP 797
really apply to?
• Why should you be
familiar with USP 797?
What is USP 797?
•
The 797th chapter of US
Pharmacopeia
• Chapter became
effective January 1,
2004
• Revisions June 2008
• USP 797 is a set of
enforceable sterile
compounding
standards
What Does USP 797 Entail:
•
•
•
•
•
Clean room operation and construction
Aseptic technique and compounding procedures
Facility cleaning and maintenance procedures
Staff training and demonstration of ongoing competency
Policies, procedures, documentation and action plans
*Being compliant with USP 797 means being able to demonstrate
through policies, procedures, documentation and actions plans that
all aspects of USP 797 are being met and the highest standards of
sterile compounding practices are being upheld*
Who Does USP 797 Apply ?
•
“ALL persons who prepare
CSPs (compounded sterile
products and all places
where CSPs are prepared
(e.g. hospitals and other
healthcare institutions,
patient treatment clinics,
pharmacies, physician’s
practice facilities, and other
locations and facilities in
which CSPs are prepared,
stored and transported).”
Who Does USP 797 Apply (cont.)?
• “ Compounded biologics, diagnostics, drugs, nutrients, and
radiopharmaceuticals, including…dosage forms that must
be sterile when they are administered to patients: aqueous
bronchial and nasal inhalations, baths and soaks for live
organs and tissues, injections, irrigations for wounds and
body cavities, ophthalmic drops and ointments, and tissue
implants.”
Who Does USP 797 NOT apply to?
• USP 797 only pertains to the “preparation, storage and
handling of (CSPs) up to the point before administration to
patients.”
• “Compounding does not include mixing, reconstituting, or
similar acts that are performed in accordance with the
directions consistent with that labeling.”
Q&A
Q: Why Should I be Familiar with USP
797?
A: Because Patient Outcomes are at
Stake!
Need More Reasons to be Familiar
with USP 797…?
• Opportunity for
pharmacy to contribute
to infection control
efforts.
• Reimbursement for
services may be
affected.
Why Does Compliance Matter?
2 Simple Reasons:
1. Clinical patient outcomes (i.e. decreased infection,
decreased length of stay…etc)
2. The bottom line (i.e. $$$$$)
Improved Patient Outcomes
• There is currently no single study that concludes that,
“Following USP 797 will undoubtedly decrease
contamination and reduce infection rates in patients.”
• There are studies that have demonstrated that NOT
following certain aspects of USP 797 (hand hygiene,
aseptic technique) can lead to negative patient
outcomes.
• USP 797 is an important tool, perhaps the most important
and comprehensive resource we have available that we
can look to to provide a model of how we should be
compounding sterile products to reduce the risk of
infection.
What We Do Know…
• Touch contamination presents the most common cause of
product contamination when preparing sterile
compounded products.
• Therefore ensuring proper aseptic technique through the
recommendations set forth in USP<797> is critical.
• Ensuring ongoing compliance with aseptic practices
through proper training, competency testing and
documentation is key.
• Proper cleanroom layout, cleaning and disinfecting
procedures, and proper product storage only further
contribute to decreasing the risk of product
contamination.
Improved Patient Outcomes:
1.
2.
3.
4.
5.
6.
7.
8.
Archibald LK, Ramos M, Arduino MJ et al, Enterobacter cloacae and Pseudomonas aeruginosa
polymicrobial bloodstream infections traced to extrinsic contamination of a dextrose multidose vial. J
Pediatr 1998: 133(5): 640-644.
Anon. US Department of Health and Human Services. Centers for Disease Control and Prevention.
Exophiala infection from contaminated steroids prepared by a compounding pharmacy—United States,
July-November 2002. Morbidity and Mortality Weekly Report (MMWR) (serial online) 2002; 51(49): 1109-1112.
Available at: www.cdc.gov/mmw.
Anon. US Department of Health and Human Services. Centers for Disease Control and Prevention.
Pseudomonas bloodstream infections associated with a heparin/saline flush—Missouri, New York, Texas
and Michigan, 2004-2005. Morbidity and Mortality Weekly Report (MMWR) (serial online) 2005; 54(11): 269272. Available at: www.cdc.gov/mmw.
Hallisy E, Russell S. Who’s mixing your drugs? Bad medicine: Pharmacy mix-ups a recipe for misery, some
drugstores operate with very little oversight. San Francisco Chronicle. June 23, 2002: A-1.
Selenic D, Dodson DR, Jensen B et al. Enterobacter cloacae bloodstream infections in pediatric patients
traced to a hospital pharmacy. Am J Health Syst Pharm 2003; 60(14):1440-1446.
Thomas M, Sanborn MD, Couldry R I.V. admixture contamination rates. Traditional practice site versus a
class 1000 cleanroom Am J Health Syst Pharm 2005; 62(22): 2386-2392.
Vos MC, de Haas PE, Verbrugh HA et al. Nosocomial Mycobacterium bovisbacille Calmette-Guerin
infections due to contamination of chemotherapeutics: Case findings and route of transmission. J Infect
Dis 2003; 188(9): 1332-1335.
And the list goes on and on…etc
$$$$: The Universal Language
•
Not complying with USP 797 can indirectly affect your
bottom line in several different ways
1. Mandatory infection rate reporting
2. Increased length of stay
3. Added cost of treating preventable infections
4. Non-compliance with USP 797 can affect a
facility’s ability to become accredited
Tips
•
Steps to compliance:
•
Define compounding risk level
•
Perform gap analysis
•
Come up with an action plan
•
Implement/monitor action plan
•
Adjust action plan and monitor criteria as
needed.
Tips (cont.)
•
Reach for ‘low hanging fruit’ first (i.e. documentation,
training, cleaning procedures) then tackle reconstruction if
you like.
•
If one does not want to spend money on clean room
construction, you can focus on ‘immediate use’ meds in
the facility when they you able and outsource the rest.
•
When compounding chemotherapy, one may consider
using Closed System Transfer Devices (CSTD) if you are
not able to provide a properly constructed chemo
compounding area.
USP 797 Resources
•
www.USP.org
•
www.USP797.org
•
www.ashp.org
•
www.nhia.org
•
www.ascp.org
•
www.IVInsights.com
The Bottom Line
•Not complying with USP 797 can compromise patient
health
•Not complying with USP 797 can impact the bottom line
•You have the power to impact patient outcomes and
improve the bottom line.
You're Getting Very Sleepy:
Assessment and prevention of
opioid-induced sedation.
Rachel S Smallwood, PharmD, BCPS
Banner Baywood Medical Center
Objective
„
Upon completion of this activity, the
participant should be able to identify
risk factors for opioid-induced sedation
1
Opioid-Induced Sedation
„
Definition “sedation”: depression of
brain functioning by a medication,
manifested by sleepiness, drowsiness,
fatigue, slowed brain activity, reduced
wakefulness, and
impaired performance.
Opioid-Induced Sedation
„
„
„
„
„
„
20-60% patient taking opioids
Opioid naïve vs opioid tolerant
Acute pain vs chronic pain
Tolerance within a few days
Dose- dependent effects
Precursor to respiratory depression
2
Assessment of sedation
Pasero Opioid-Induced Sedation
Scale (POSS)
– Appropriate vs inappropriate levels of
sedation
„
„
When is it safe to give doses
When is it safe to increase doses
– Documentation
„
Consistency among caregivers
Nisbet and Mooney-Cotter. Pain Management Nursing 2009;10(3):154-164
Pasero Opioid-Induced
Sedation Scale (POSS)
S = Sleep, easy to arouse
„ Acceptable,
no action necessary, may
increase dose
„
1. Awake and alert
„ Acceptable,
no action necessary, may
increase dose
„
2. Slightly drowsy, easily aroused
„ Acceptable,
no action necessary, may
increase dose
Pasero. Journal of PeriAnesthesia Nursing 2009;24:186-90
3
Pasero Opioid-Induced Sedation
Scale (POSS)
„
3. Frequently drowsy, arousable, drifts to
sleep during conversation
„ Unacceptable,
monitor respiratory status until
sedation level<3, decrease dose 2525-50% or notify
prescriber
„
4. Somnolent, minimal or no response to
verbal or physical stimulation
„ Unacceptable,
stop opioid, consider administering
naloxone if respiratory status is compromised,
notify prescriber, monitor until sedation level<3
Prevention of sedation
„
„
Identify patients at risk
Complete/accurate patient history
– Disease that affect drug metabolism
„ Renal/hepatic/respiratory
failure
– Look for signs of undiagnosed conditions
„ Snoring=
OSA
– History of complications with anesthesia
or narcotics
„
Medication Review
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Risk Factors
„
„
„
„
„
„
„
Opioid naïve
Rapid dose escalation
Drug accumulation/additive effect
Dose conversions
OSA or undiagnosed sleep disorders
Polypharmacy/Drug interactions
Obesity
Nisbet and Mooney-Cotter. Pain Management Nursing 2009;10(3):154-164
Drug Interactions
„
Sedatives
– BZD, hypnotics, diphenhydramine
„
Anticholinergics
– Dicyclomine, TCA, hyoscamine,
phenothiazines
„
Others
– Antiparkinson’s agents, antipsychotics,
muscle relaxants.
Pattinson KTS. Br J Anaesthia 2008;100(6):747-758
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Summary
„
„
Assessment of sedation using POSS
can increase patient safety
Prevention is key to minimizing opioidinduced sedation
– Identify risk factors
– Complete patient history
– Minimize drug interactions
„ Advocate
nonnon-narcotic medications
Assessment Question
„
Which of the following is NOT a risk
factor for opioid-induced sedation?
– A) Obstructive Sleep Apnea
– B) Rapid dose escalation
– C) Concurrent use of promethazine and
dicyclomine
– D) No previous history of narcotic use
– E) None of the above
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