19 sept dolor (pp tshare)
TRANSCRIPT
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DOLOR
2008
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Dolor: Definición
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Prevalencia Dolor Neuropático.
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Dolor Crónico: Prevalencia
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Dolor y Sexo.
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Dolor y Edad.
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Dolor e Intensidad.
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Dolor y Vida Diaria.
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Dolor Crónico
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Dolorímetro.
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Dolor. Discriminación y Cuantificación
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Dolor. Escalas de Evaluación.
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Mixed Type
Nociceptive vs Neuropathic Pain
NociceptivePain
Neuropathic Pain
Postoperativepain
Mechanicallow back pain
Arthritis
Sports/exerciseinjuries
Postherpeticneuralgia
Neuropathic low back pain
Trigeminalneuralgia
Polyneuropathy (diabetic, HIV)
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Mixed TypeCaused by a
combination of both primary injury and secondary effects
Nociceptive vs Neuropathic LBP
NociceptivePain
Caused by activity in neural pathways in
response to potentially tissue-damaging stimuli
Neuropathic Pain
Initiated or caused by primary lesion or dysfunction in the nervous system
Postoperativepain
HNP* withoutnerve root
compression
Facet jointarthropathy
Sciatica
Sports/exerciseinjuries
*Herniated nucleus pulposus.
Medial branchneuropathyHNP* with
nerve rootcompression
Internal discdisruption
Degenerative
disc disease
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Dolor Neuropático.
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Dolor Neuropático.
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Dolor Neuropático.
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Generador de Dolor.
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Percepción de Dolor.Fisiología.
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Patología
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Mecanismos PeriféricosHiperexitabilidad.
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Nervo Nervorum
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Dolor NeuropáticoMecanismos.
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Control de Dolor Neuropático.Objetivos.
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Where Can We Intervene?
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Topical Agents Act Locally
• Aspirin Preparations– eg, aspirin in chloroform or ethyl ether
• Capsaicin– extracted from chili peppers
• EMLA (eutectic mixture of local anesthetics)
• Lidocaine patch 5%
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Agentes Tópicos.
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Tratamiento Tópico
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Dolor Neuropático Tratamiento Tópico.
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Tratamiento Neuropático
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Dolor Neuropático.Tratamiento Farmacológico.
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Polineuropatía Diabética y Neuralgia Postherpética.
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Polineuropatía Diabética.Tratamiento.
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Neuralgia Postherpética.Tratamiento.
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Opioides
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Antidepresivos.
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Dolor e Inhibidores de Recaptura de Serotonina.
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Antidepresivos Tricíclicos.
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Efectos Adversos.Antidepresivos.
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Dolor Neuropático. Anticonvulsivos.
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Tratamiento de Dolor con Anticonvulsivos.
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Dolor y Corticoesteroides.
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Resumen de Tratamiento Dolor Neuropático
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Dolor.Guias de Tratamiento OMS
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Dolor Neuropático que no emplear.
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Dolor Crónico.Patologías Asociadas.
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Dolor Neuropático .Patologías Asociadas.
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Dolor Crónico.Enfermedades Psiquiatricas.
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Dolor y Ansiedad.
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Dolor y Depresión
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Dolor y Sueño.
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Dolor y Adicciones.
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Evolución Disturbios Asociados.
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Dolor y Patologías Asociadas.
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Dolor y Educación.
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Dolor y Comorbilidad Tratamiento.
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Dolor y Biofeedback
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Dolor: Importancia.
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Dolor Persistente.
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Dolor :Tratamiento Oportuno.
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Dolor: Transmisión Neural.
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Anatomía del Dolor.
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Dolor y sus Vías
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Dolor. Sinapsis.
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Dolor Neuropático Tratamiento Intervencionista.
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Bloqueo Nervioso.
• Diagnóstico
• Terapéutico.
• Pronóstico.
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Estimulación Corteza Cerebral.
• La estimulación de la corteza cerebral motora alivia dolor neuropático.
• Dolor central secundario a Stroke.
• Neurálgia Trigeminal atípica.
• Craniotomía y electrodo epidural/corteza motora
• Neuronavegación, RM funcional, Potenciales evocados.
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Estimulación Cerebral Profunda.
• Talámica.
• Sustancia Gris Periacueductal.
• Implantes x Estereotaxia y Generador Permanente.
• Principalmente en Dolor Nociceptivo. (ej.
• Failed Back Sx.
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Estimulación de Médula Espinal.
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Estimulación Eléctrica.
• Bloquea vías dolorosas.
• Electrodos en espacio epidural percutáneos o por laminectomía.
• Paciente despierto durante implante.
• Útil en zonas con parestesias.
• Transitorio o Definitivo.
• Programable el voltaje, la frecuencia y amplitud del pulso.
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Dolor y Estimulación Eléctrica.
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Dolor y Estimulación Eléctrica.
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Estimulación Eléctrica.Indicaciones.
• Failed Back Sindrome.• Dolor isquémico.• Dolor Vascular. (ej Raynaud)• Neuralgia postherpética.• Dolor Regional Complejo.• Lesión Médula espinal.• Lesión nerviosa.• Neuropatía periférica.
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Medicamentos Intraespinales.
• Permite mayor concentración del mismo en el neuroeje.
• Evita aumento de dosis sistémicas.
• Indicado en cáncer.
• Cateter percutáneo subdural.
• Reservorio externo/interno.
• Recarga percutánea.
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Medicamentos Intraespinales.
• Morfina.
• Morfina + Bupivacaina.
• Morfina + Lidocaina.
• Morfina + Clonidina. (dolor Neuropático.)
• Complicaciónes: Depresión Respiratoria, Supresión de eje hipotálamo/hipofisario.
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Cingulotomía.
• Sufrimiento intolerable asociado a dolor por cáncer..
• No se modula dolor sino el impacto emocional.
• Alivio en 50% de los casos.
• Útil bilateral.
• Estereotaxia y Radiofrecuencia.
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Mesencefalotomía.
• Proximidad de Tracto espinotálmico, sustancia gris periacueductal y tracto trigémino-talámico.
• Útil en dolor de cabeza y cuello.
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Mielotomía.Lesión Columnas Dorsales.
• Indicaciónes: Dolor Visceral.
• Espasticidad Dolorosa.
• Lesión Medular.
• Éxito en 60-70%.
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Mielotomía Cervical Percutánea
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Cordotomía.Sección T. Espino-Talámico.
• Indicación: Dolor Nociceptivo y Neuropático.
• Bilateral : Dolor Abdominal, Pélvico o ambas extremidades inferiores.
• Laminectomía o Percutánea.
• Restringido a dolor por Cancer.
• Efecto por 2 años.
• No útil en Cervical.
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Simpatectomía.Ablación de Cadena Simpática.
• Indicaciones:
• Sx de Dolor Regional Complejo.
• Toracotomía.
• Toracoscopía Endoscópica.
• Bloqueo de prueba.
• 30% Recidiva a 5 años
• Hiperhidrosis compensatoria.
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Lesión Médula Espinal.
• Tratamiento Difícil.
• Mielotomía: en Espasticidad Dolorosa.
• DREZ: en Dolor intermitente.
• Estimulación Medular: en lesión incompleta.
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DREZ (Dorsal Root Entry Zone)
• Indicaciones :Avulsión Cervical / Lumbar.
• Lesión Medular Espinal con dolor restringido al nivel de la lesión.
• Requiere Laminectomía amplia.
• Requiere apoyo Neurofisiológico.
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Problemas Específicos.Cáncer:
• Bomba Infusión.
• Cordotomía.Dolor Extremidades.
• Mielotomía: Dolor Visceral.
• Mesencefalotomía: Dolor cabeza y cuello.
• Cingulotomía
• Estimulación médula espinal.
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Neurálgia Trigeminal:1
• Craniectomía: Descompresión Microvascular.
• Percutánea: 1) Lesión con glicerol, Alcohol absoluto.
• 2) Termocoagulación por radiofrecuencia.
• 3) Compresión con balón.
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Neurálgia Trigeminal : 2
• Radiocirugía (gama knife) 8000 Rads 80Gy.
• Repetible.
• Alivio diferido. 2-6/12.
• 70% alivio completo al año.
• 56% alivio a los 5 años.
• Anestesia dolorosa.
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Neuralgia Trigeminal Tratamiento:
• Compresión por Balón.
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Failed Back Síndrome.
• Dolor Neuropático y Nociceptivo.
• Estimulación.
• Estimulación Cerebral Profunda.
• Bomba de Infusión
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Chronic Pain Affects All Aspects of Patient’s Life
Social Consequences• Marital/family
relations• Intimacy/sexual activity• Social isolation
Socioeconomic
Consequences
• Healthcare costs
• Disability
• Lost workdays
Quality of Life• Physical functioning• Ability to perform
activities of daily living• Work• Recreation
Psychological Morbidity• Depression• Anxiety, anger• Sleep disturbances• Loss of self-esteem
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Opioides.
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Dolor y Comorbilidad.
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Problem Solving in Persistent Pain Syndromes:
a case-based approach
Copyright © 2005 Thomson Professional Postgraduate Services®. All rights reserved.
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Pain, Neural Excitation (“Wind-up”), and the HPA Axis
• Neuropathic pain induces changes in peripheral and central nervous system
• In the dorsal horn this results in dramatic increase in firing of neurons– from 1 every 3 seconds – to up to 30/second
• In the brain, hypothalamic activation by increased nociceptive input causes activation of the hypothalamic-pituitary-adrenal (HPA) axis, resulting in discharge of peripheral cortisol and activation of vasoactive immune system compounds
Blackburn-Munro G, et al. J Neuroendocrinology. 2001;13:1009-1023.17
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Wind-up Pain: Mood Effects
• Activation of serotonergic and noradrenergic centers in brain stem
• Stimulation and dysfunction of limbic system, prefrontal cortex, hypothalamus, dorsal horn of spinal cord
• Depression, anxiety, panic, vegetative signs of depression, suicidal thoughts, and chronic pain
Blackburn-Munro G, et al. J Neuroendocrinology. 2001;13:1009-1023.
Stahl SM. J Clin Psychiatry. 2002;63:382-383.18
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DorsalHorn
BRAIN
Pharmacologic Agents Affect Pain Differently
Descending Modulation
PeripheralSensitization
Central Sensitization
PNS
Local Anesthetics
Topical Analgesics
Anticonvulsants
Tricyclic Antidepressants
Opioids
Anticonvulsants
Opioids
NMDA-Receptor Antagonists
Tricyclic/SNRI Antidepressants
Anticonvulsants
Opioids
Tricyclic/SNRI Antidepressants
20
SPINALCORDCNS
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Mechanisms of Action: Analgesic Agents
• Anticonvulsants– sodium-channel blockade (oxcarbazepine)– calcium-channel blockade (gabapentin)
• Antidepressants– inhibit reuptake of norepinephrine and serotonin into
presynaptic neurons (duloxetine)• Opioids
– block neurotransmitter-release by nociceptive fibers, thus decreasing transmission of pain-producing signals (oxycodone)
• Topical Analgesics– sodium-channel blockade (lidocaine patch 5%)– vanilloid receptor (capsaicin)
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FDA-Approved Treatments for Neuropathic Pain
• Carbamazepine– trigeminal neuralgia
• Duloxetine– peripheral diabetic neuropathy
• Gabapentin– postherpetic neuralgia
• Lidocaine Patch 5%– postherpetic neuralgia
• Pregabalin– peripheral diabetic neuropathy– postherpetic neuralgia
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Antidepressants in Neuropathic Pain Disorders*
• Multiple proposed sites and mechanisms of action – central and peripheral nervous system– anticholinergic, serotonergic, noradrenergic
• RCTs show benefit (especially amitriptyline, nortriptyline, desipramine)
• Improvements in insomnia, anxiety, depression
*Not approved by FDA for this use.
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Amitryptyline – Sites of Action
Descending Modulation
PeripheralSensitization
Amitriptyline(anticholinergic,
Inhibits 5-HT and NE
reuptake)
Tricyclic antidepressants are thought to affect pain transmission primarily in the CNS by inhibiting the reuptake of norepinephrine and serotonin, both of which influence descending pain pathways.
Maizels M, McCarberg B. Am Fam Phys. 2005;71:483-490.
Na channel
blocker
DorsalHorn
BRAIN
PNS
SPINALCORD
CNS
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Tricyclic Antidepressants: Adverse Effects
• Commonly reported AEs (generally anticholinergic):– blurred vision– cognitive changes– constipation– dry mouth– orthostatic hypotension– sedation– sexual dysfunction– tachycardia– urinary retention
• Desipramine
• Nortriptyline
• Imipramine
• Doxepin
• Amitriptyline
FewestAEs
Most AEsAEs = adverse effects.
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Tricyclic Antidepressantsfor Neuropathic Pain Disorders*
• Consider preprescription cardiac evaluation• Intolerable side effects more frequent with amitriptyline
– not recommended in patients 601
• Use drug with fewer side effects • Can split dose to reduce side effects• Start at 10 to 25 mg at bedtime
– increase every week as tolerated to a target dose of 25 to 150 mg– expect individual variability in treatment response
• Expect partial effect– use multiple agents (other classes and mechanism)
• Not being used simultaneously to treat depression
*Not approved by FDA for this use.1. AGS Panel on Persistent Pain in Older Persons. JAGS. 2002;50:S205-S224.31
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Lidocaine Patch 5% Works Locally Through Sodium Channels
36
Descending Modulation
DorsalHorn
BRAIN
PNS
SPINALCORD
CNS
CentralSensitization
PeripheralSensitization
Lidocaine Patch 5%
Na channel
blocker
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Lidocaine Patch 5% for Diabetic Neuropathy*
Barbano RL et al. Arch Neurol. 2004;61:914-918.
BPI=Brief Pain Inventory.
*Not approved by FDA for this use.†P0.001 at Week 3 versus baseline.
BPI: Daily Pain Diary Ratings and Pain Relief Scores
6.3
3.6
0123456789
10
Baseline Week 3
Mea
n d
aily
pai
n r
atin
g
Mea
n p
ain
rel
ief
sco
re (
%)
28.6
63.4
0102030405060708090
100
Baseline Week 3
N=53
†
†
37
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Gabapentin Works Centrally Through Calcium Channels
Anticonvulsants act at several sites that may be relevant to pain, but the precise mechanism of analgesic effect remains unclear. They are thought to limit neuronal excitation and enhance inhibition at various ion channels, especially the calcium channels.
Maizels M, McCarberg B. Am Fam Phys. 2005;71:483-490.40
DorsalHorn
BRAIN
PNS
SPINALCORD
CNS
PeripheralSensitization
Gabapentin
Descending Modulation
Gabapentin
Central Sensitization
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Lidocaine Patch 5% With Gabapentin
41
DorsalHorn
BRAIN
PNS
SPINALCORD
CNSDescending Modulation
Central Sensitization
PeripheralSensitization
Lidocaine Patch 5%
Gabapentin
Gabapentin
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Gabapentin in Neuropathic Pain Disorders*
• FDA approved for PHN
• Anticonvulsant: alpha2delta calcium channel antagonist
• Limited intestinal absorption• Usually well tolerated; serious adverse effects rare
– dizziness and sedation can occur• No significant drug interactions• Peak time: 2 to 3 h; elimination half-life: 5 to 7 h• Usual dosage range for neuropathic pain up to
3,600 mg/d (tid–qid)*
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0
2
4
6
8
10
Screening 1 2 3 4 5 6 7 8
Week
Mea
n p
ain
sco
re
*Not approved by FDA for this use.† P<0.01. ‡ P<0.05.
Gabapentin in the Treatment of Painful Diabetic Neuropathy*
PlaceboGabapentin
Adapted from Backonja M et al. JAMA. 1998;280:1831-1836.
N=165
†
†
‡†
‡ ‡ ‡
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Anticonvulsant Drugs for Neuropathic Pain Disorders
• Postherpetic neuralgia– gabapentin*– pregabalin*
• Diabetic neuropathy– carbamazepine– gabapentin– lamotrigine– phenytoin– pregabalin*
• HIV-associated neuropathy – lamotrigine
• Trigeminal neuralgia– carbamazepine*– lamotrigine– oxcarbazepine
• Central poststroke pain– lamotrigine
*Approved by FDA for this use.HIV = human immunodeficiency virus.
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Serotonin and Norepinephrine Reuptake Inhibitors
Randomized clinical trials show benefit from dual
action neurotransmitter reuptake inhibitors
• Duloxetine – FDA approved for peripheral diabetic
neuropathy
• Venlafaxine
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DorsalHorn
BRAIN
PNS
SPINALCORD
CNS
Duloxetine Works Centrally in Descending Pathways and Spinal
CordDescending Modulation
PeripheralSensitization
Central Sensitization
Duloxetine is a dual reuptake inhibitor that enhances the levels of the neurotransmitters serotonin and norepinephrine.
Duloxetine
Duloxetine
50
NE, 5-HT
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Duloxetine Is Effective for Diabetic
Neuropathic Pain
-3.5
-3
-2.5
-2
-1.5
-1
-0.5
0
1 2 3 4 5 6 7 8 9 10 11 120
Week
Mea
n c
han
ge
in 2
4-h
ou
r av
erag
e p
ain
sev
erit
y sc
ore
Placebo (n=108)Duloxetine 60 mg qd (n=114)Duloxetine 60 mg bid (n=112)
** *
* * * * * * * *
** * * * * * * * * *
*
*P<0.001 vs placebo.
Wernicke J et al. J Pain. 2004;5(suppl 1):S48.
*
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Duloxetine
• Approved 9-7-2004 for management of pain association with diabetic neuropathy
• Once-daily dosing available in 20, 30, and 60 mg strengths
• Contraindicated in patients with uncontrolled narrow-angle glaucoma and patients taking monoamine oxidase inhibitors (MAOIs)
• Common sides effects include nausea, diarrhea, constipation, dizziness, drowsiness, anxiety, nervousness, insomnia
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Short- and Long-acting Opioids
• Morphine sulfate• Codeine• Hydrocodone • Oxycodone• Hydromorphone • Oxymorphone• Fentanyl
• Methadone • Sustained-release
morphine • Sustained-release
oxycodone• Transdermal fentanyl• Levorphanol
Short-acting Opioids Long-acting Opioids
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Opioid Efficacy Studies in Neuropathic Pain
Disorders• Diabetic neuropathy
– tramadol– oxycodone
• Nonmalignant neuropathic pain disorders– IV fentanyl
• Postherpetic neuralgia– IV morphine– controlled-release oxycodone
• Phantom limb pain– oral morphine
IV = intravenous.55
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0
10
20
30
40
50
60
70
80
90
Mean daily pain Steady pain Brief pain Skin pain
Placebo (benztropine 0.25 mg)
CR oxycodone (10 mg)
CR Oxycodonefor Diabetic Neuropathy*
†† †
†
*Not approved by FDA for this use.†P=0.0001.
VA
S (
mm
)
Adapted from Watson CP et al. Pain. 2003;105:71-78.
N=36
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Efficacy of Tramadol in Painful Polyneuropathy
Adapted from Sindrup SH et al. Pain. 1999;83:85-90.
Placebo
Med
ian
rat
ing
(0–1
0 p
oin
t sc
ale)
0
2
4
6
8
10
Pain Paresthesia Touch-evoked pain
6
4
6
4
5
3
Tramadol
P=0.001 P=0.001
P<0.001
N=45
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Summary
• Customize therapy due to variance in response, individual clinical/social circumstances, and toxicity
• Rational polypharmacy – mechanisms, drug synergy, additive effects, or complementary effects
• Consider consultation for complex cases or patients who are refractory to first- or second-line therapies
• Never lose focus on managing the whole patient
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Algorithm for Opioid Treatment of Chronic Pain
Patient Selection
Initial Patient Assessment
Trial of Opioid Therapy
Alternatives
to Opioid Therapy
Patient Reassessment
Implement Exit Strategy Continue Opioid Therapy
Comprehensive Pain Management Plan
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Patient Selection
• Persistent pain despite reasonable trials of non-opioid analgesics and adjuvants
or
• Severe pain requiring rapid relief
or
• Patient characteristics contraindicate use of other analgesics
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Pain Assessment: Making the Diagnosis
• Defining medical diagnosis and potential primary treatments
• Pain diagnosis is not always readily defined and may change with time
• More common pain diagnoses include: back pain, fibromyalgia, neuropathic pain, cancer-related pain
• Chronic pain itself may be considered a diagnosis that merits consideration of all available treatment options
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Why Assess Pain?
• Inadequate assessment a major barrier to treatment
• Appropriate decisions regarding opioid therapy require comprehensive assessment
• Comprehensive assessment required by JCAHO
• Assessment required by opioid treatment guidelines
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Pain Assessment: When to Refer?
• Previous failure with opioids or other analgesics
• Significant psychosocial issues
• Conviction of a drug-related crime
• Current use of illicit drugs
• Regular contact with drug high-risk groups
• History of substance abuse
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Algorithm for Opioid Treatment of Chronic Pain
Patient Selection
Initial Patient Assessment
Trial of Opioid Therapy
Alternatives
to Opioid Therapy
Patient Reassessment
Implement Exit Strategy Continue Opioid Therapy
Comprehensive Pain Management Plan
8
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Comprehensive Pain Management Plan Components
• Bio/Physical Approaches – pharmacologic and/or
nonpharmacologic therapies
– physical rehabilitation• physical/
occupational therapy• home exercise
program
• Psychological Intervention– mood disturbances– coping skills– sleep disturbance
• Social Issues– family/social
relations– work issues
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Algorithm for Opioid Treatment of Chronic Pain
Patient Selection
Initial Patient Assessment
Trial of Opioid Therapy
Alternatives
to Opioid Therapy
Patient Reassessment
Implement Exit Strategy Continue Opioid Therapy
Comprehensive Pain Management Plan
10
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Alternatives to Opioid Therapy
• Alternative pain management strategies– adjuvant analgesics– nonpharmacologic modalities– complementary medicine
• Refer complex or high-risk patients for– multidisciplinary pain management
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Questions to Consider Before Initiating
a Trial of Opioid Therapy• What pain syndromes are appropriate for
opioid analgesia?• What patients are appropriate candidates
for opioid analgesia?• Should opioids be the first analgesic class
prescribed?• What patients are at high risk for abuse and
diversion of opioids?
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Initiating Opioid Therapy
You’ve made the decision to prescribe opioid analgesics
for your patient. Now you must:
• Consider cost, tolerability, ease of administration, compliance
• Decide whether to start a short-acting opioid analgesic or a low dose of a long-acting opioid analgesic, with or without short-acting “rescue” doses if breakthrough pain occurs
• Develop and document an Exit Strategy
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Create an Exit Strategy
• Upon initiating opioid therapy, agree with patient on criteria for failure of the trial
• Common failure criteria include:– lack of significant pain reduction– lack of improvement in function– persistent side effects– persistent noncompliance
• Document method for tapering off opioids if trial is not successful
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Algorithm for Opioid Treatment of Chronic Pain
Patient Selection
Initial Patient Assessment
Trial of Opioid Therapy
Alternatives
to Opioid Therapy
Patient Reassessment
Implement Exit Strategy Continue Opioid Therapy
Comprehensive Pain Management Plan
16
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Patient Reassessment ModelThe "Four A's of Pain"
Analgesia
Activities of daily living
Adverse effects
Aberrant drug-taking behaviors
Important to remember two other “A’s”
Assessment
Action (treatment plan)
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Questions to Consider In Modifying a
Trial of Opioid Therapy• When should opioid dose be raised?
• When should a different opioid be tried?
• What factors guide the choice of a second opioid?
• How reliable are urine screenings?
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Deciding to Convert From a Short-acting to a Long-acting
OpioidShort-acting Opioids
Long-acting Opioids
Advantages
Fast-acting; appropriate for acute pain, breakthrough pain
May be more appropriate for patients with a constant pain component; analgesic stability
Disadvantages
Need for repetitive dosing
Initial delayed onset of action
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Rationale for Opioid Rotation
• Ineffectiveness of initial opioid
• Adverse effects/toxicity of initial opioid
• Inter-patient variability of response
• Incomplete cross-tolerance
Note: Conservative dose-conversion ratios are advised
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Side Effects Amelioration
Management of Opioid Side Effects
Nausea and vomiting Switch opioids;anti-emetics
Sedation Lower dose (if possible); add co-analgesics; add stimulants
Constipation Treat prophylactically with stool softeners, bowel stimulants; non-pharmacological measures; switch opioids
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Side Effects Amelioration
Management of Opioid Side Effects (cont’d)
Itching Switch opioids; antihistamines
Endocrine dysfunction/ reduced libido
Endocrine monitoring; testosterone replacement; endocrine consultation
Edema and sweating Switch opioids
Dizziness Antivertiginous agents(eg, scopolamine)
Confusion Titrate dose; switch opioids
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Trial of Opioid Therapy
ApparentTolerance
Opioid Dose Escalation
Worsening Pain State
Worsening Pain State
CellularMechanisms
CellularMechanisms
PharmacologicalTolerance
PharmacologicalTolerance
Opioid-Induced Pain Sensitivity
Opioid-Induced Pain Sensitivity
Development of Tolerance
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Algorithm for Opioid Treatment of Chronic Pain
Patient Selection
Initial Patient Assessment
Trial of Opioid Therapy
Alternatives
to Opioid Therapy
Patient Reassessment
Implement Exit Strategy Continue Opioid Therapy
Comprehensive Pain Management Plan
24
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Continue Opioid Therapy
• An option if there is – effective pain relief– improvement in ADLs and psychosocial functioning– management of side effects
• Reassessment using the "Four A's of pain" model should be ongoing to – guide optimal pain management– decide if continuation, modification, or
discontinuation is needed
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Regulatory Issues
• Risk of regulatory censure low if procedures are followed and documented
• Relevant regulations include:– federal (DEA)– state policies
• Useful model guideline from Federation of State Medical Boards. Available at: www.fsmb.org
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Opioid Release/Delivery Systems and Formulations in Development
• Extended-release formulations – eg, oxymorphone (FDA approved June 24, 2006 for relief
of moderate-to-severe pain) • New methods of drug delivery
– implantable device (eg, Chronogesic™ [sufentanil]) – disposable ambulatory PCA opioid device– Iontophoresis-based patch (eg, E-TRANS® fentanyl)
• Methods of controlling administration rate– new implantable pump or continuous release technology
with computer-assisted rate settings• Methods to reduce abuse liability/tampering
– addition of high-viscosity release component (eg, Remoxy™)
– new formulations (eg, inseparable matrices)
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Algorithm for Opioid Treatment of Chronic Pain
Patient Selection
Initial Patient Assessment
Trial of Opioid Therapy
Alternatives
to Opioid Therapy
Patient Reassessment
Implement Exit Strategy Continue Opioid Therapy
Comprehensive Pain Management Plan
28
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Exit Strategy
• Documentation of lack of pain reduction and/or lack of functional improvement– criteria for tapering emphasized in the initial
patient agreement
• Distinguish between abandoning opioid therapy, abandoning pain management, and abandoning patient
• Taper off opioid therapy, with or without specialty assistance
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Summary: Ground Rules for Prescribing
Opioid AnalgesicsREMEMBER!
• Proper patient selection is THE key
• Proper patient assessment is mandatory
• Opioid analgesics are but one component of a comprehensive treatment plan
• Prescribing opioids on a trial basis MUST be monitored
• Patient reassessment is KEY to ongoing monitoring of opioid therapy
• Any medical treatment can be continued, discontinued, or modified
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Algorithm for Opioid Treatment of Chronic Pain
Patient Selection
Initial Patient Assessment
Trial of Opioid Therapy
Alternatives
to Opioid Therapy
Patient Reassessment
Implement Exit Strategy Continue Opioid Therapy
Comprehensive Pain Management Plan
2
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Patient Selection
• Persistent pain despite reasonable trials of non-opioid analgesics and adjuvants
or
• Severe pain requiring rapid relief
or
• Patient characteristics contraindicate use of other analgesics
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Algorithm for Opioid Treatment of Chronic Pain
Patient Selection
Initial Patient Assessment
Trial of Opioid Therapy
Alternatives
to Opioid Therapy
Patient Reassessment
Implement Exit Strategy Continue Opioid Therapy
Comprehensive Pain Management Plan
4
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Pain Assessment: Making the Diagnosis
• Defining medical diagnosis and potential primary treatments
• Pain diagnosis is not always readily defined and may change with time
• More common pain diagnoses include: back pain, fibromyalgia, neuropathic pain, cancer-related pain
• Chronic pain itself may be considered a diagnosis that merits consideration of all available treatment options
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Why Assess Pain?
• Inadequate assessment a major barrier to treatment
• Appropriate decisions regarding opioid therapy require comprehensive assessment
• Comprehensive assessment required by JCAHO
• Assessment required by opioid treatment guidelines
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Pain Assessment: When to Refer?
• Previous failure with opioids or other analgesics
• Significant psychosocial issues
• Conviction of a drug-related crime
• Current use of illicit drugs
• Regular contact with drug high-risk groups
• History of substance abuse
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Algorithm for Opioid Treatment of Chronic Pain
Patient Selection
Initial Patient Assessment
Trial of Opioid Therapy
Alternatives
to Opioid Therapy
Patient Reassessment
Implement Exit Strategy Continue Opioid Therapy
Comprehensive Pain Management Plan
8
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Comprehensive Pain Management Plan Components
• Bio/Physical Approaches – pharmacologic and/or
nonpharmacologic therapies
– physical rehabilitation• physical/
occupational therapy• home exercise
program
• Psychological Intervention– mood disturbances– coping skills– sleep disturbance
• Social Issues– family/social
relations– work issues
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Algorithm for Opioid Treatment of Chronic Pain
Patient Selection
Initial Patient Assessment
Trial of Opioid Therapy
Alternatives
to Opioid Therapy
Patient Reassessment
Implement Exit Strategy Continue Opioid Therapy
Comprehensive Pain Management Plan
10
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Alternatives to Opioid Therapy
• Alternative pain management strategies– adjuvant analgesics– nonpharmacologic modalities– complementary medicine
• Refer complex or high-risk patients for– multidisciplinary pain management
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Algorithm for Opioid Treatment of Chronic Pain
Patient Selection
Initial Patient Assessment
Trial of Opioid Therapy
Alternatives
to Opioid Therapy
Patient Reassessment
Implement Exit Strategy Continue Opioid Therapy
Comprehensive Pain Management Plan
12
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Questions to Consider Before Initiating
a Trial of Opioid Therapy
• What pain syndromes are appropriate for opioid analgesia?
• What patients are appropriate candidates for opioid analgesia?
• Should opioids be the first analgesic class prescribed?
• What patients are at high risk for abuse and diversion of opioids?
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Initiating Opioid Therapy
You’ve made the decision to prescribe opioid analgesics
for your patient. Now you must:
• Consider cost, tolerability, ease of administration, compliance
• Decide whether to start a short-acting opioid analgesic or a low dose of a long-acting opioid analgesic, with or without short-acting “rescue” doses if breakthrough pain occurs
• Develop and document an Exit Strategy
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Create an Exit Strategy
• Upon initiating opioid therapy, agree with patient on criteria for failure of the trial
• Common failure criteria include:– lack of significant pain reduction– lack of improvement in function– persistent side effects– persistent noncompliance
• Document method for tapering off opioids if trial is not successful
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Algorithm for Opioid Treatment of Chronic Pain
Patient Selection
Initial Patient Assessment
Trial of Opioid Therapy
Alternatives
to Opioid Therapy
Patient Reassessment
Implement Exit Strategy Continue Opioid Therapy
Comprehensive Pain Management Plan
16
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Patient Reassessment Model
The "Four A's of Pain"
Analgesia
Activities of daily living
Adverse effects
Aberrant drug-taking behaviors
Important to remember two other “A’s”
Assessment
Action (treatment plan)
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Questions to Consider In Modifying a Trial of Opioid Therapy
• When should opioid dose be raised?
• When should a different opioid be tried?
• What factors guide the choice of a second opioid?
• How reliable are urine screenings?
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Deciding to Convert From a Short-acting to a Long-acting Opioid
Short-acting OpioidsLong-acting Opioids
Advantages
Fast-acting; appropriate for acute pain, breakthrough pain
May be more appropriate for patients with a constant pain component; analgesic stability
Disadvantages
Need for repetitive dosing
Initial delayed onset of action
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Rationale for Opioid Rotation
• Ineffectiveness of initial opioid
• Adverse effects/toxicity of initial opioid
• Inter-patient variability of response
• Incomplete cross-tolerance
Note: Conservative dose-conversion ratios are advised
20
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Side Effects Amelioration
Management of Opioid Side Effects
Nausea and vomiting Switch opioids;anti-emetics
Sedation Lower dose (if possible); add co-analgesics; add stimulants
Constipation Treat prophylactically with stool softeners, bowel stimulants; non-pharmacological measures; switch opioids
21
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Side Effects Amelioration
Management of Opioid Side Effects (cont’d)
Itching Switch opioids; antihistamines
Endocrine dysfunction/ reduced libido
Endocrine monitoring; testosterone replacement; endocrine consultation
Edema and sweating Switch opioids
Dizziness Antivertiginous agents(eg, scopolamine)
Confusion Titrate dose; switch opioids
22
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Trial of Opioid Therapy
ApparentTolerance
Opioid Dose Escalation
Worsening Pain State
Worsening Pain State
CellularMechanisms
CellularMechanisms
PharmacologicalTolerance
PharmacologicalTolerance
Opioid-Induced Pain Sensitivity
Opioid-Induced Pain Sensitivity
Development of Tolerance
23
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Algorithm for Opioid Treatment of Chronic Pain
Patient Selection
Initial Patient Assessment
Trial of Opioid Therapy
Alternatives
to Opioid Therapy
Patient Reassessment
Implement Exit Strategy Continue Opioid Therapy
Comprehensive Pain Management Plan
24
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Continue Opioid Therapy
• An option if there is – effective pain relief– improvement in ADLs and psychosocial functioning– management of side effects
• Reassessment using the "Four A's of pain" model should be ongoing to – guide optimal pain management– decide if continuation, modification, or
discontinuation is needed
25
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Regulatory Issues
• Risk of regulatory censure low if procedures are followed and documented
• Relevant regulations include:– federal (DEA)– state policies
• Useful model guideline from Federation of State Medical Boards. Available at: www.fsmb.org
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Opioid Release/Delivery Systems and Formulations in Development
• Extended-release formulations – eg, oxymorphone (FDA approved June 24, 2006 for relief
of moderate-to-severe pain) • New methods of drug delivery
– implantable device (eg, Chronogesic™ [sufentanil]) – disposable ambulatory PCA opioid device– Iontophoresis-based patch (eg, E-TRANS® fentanyl)
• Methods of controlling administration rate– new implantable pump or continuous release technology
with computer-assisted rate settings• Methods to reduce abuse liability/tampering
– addition of high-viscosity release component (eg, Remoxy™)
– new formulations (eg, inseparable matrices)27
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Algorithm for Opioid Treatment of Chronic Pain
Patient Selection
Initial Patient Assessment
Trial of Opioid Therapy
Alternatives
to Opioid Therapy
Patient Reassessment
Implement Exit Strategy Continue Opioid Therapy
Comprehensive Pain Management Plan
28
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Exit Strategy
• Documentation of lack of pain reduction and/or lack of functional improvement– criteria for tapering emphasized in the initial
patient agreement
• Distinguish between abandoning opioid therapy, abandoning pain management, and abandoning patient
• Taper off opioid therapy, with or without specialty assistance
29
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Summary: Ground Rules for Prescribing
Opioid AnalgesicsREMEMBER!• Proper patient selection is THE key
• Proper patient assessment is mandatory
• Opioid analgesics are but one component of a comprehensive treatment plan
• Prescribing opioids on a trial basis MUST be monitored
• Patient reassessment is KEY to ongoing monitoring of opioid therapy
• Any medical treatment can be continued, discontinued, or modified
30
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Key Learning Points From: Clinically Managing Chronic
Low Back Pain
Copyright © 2006 Thomson Professional Postgraduate Services®. All rights reserved.
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Natural History of LBP• Acute LBP
– inflammatory or neuropathic injury
– resolves spontaneously with minimal treatment
• Intermittent, relapsing LBP – more challenging diagnostic and treatment dilemma
– precipitates symptomatic care and more aggressive interventions aimed at specific underlying pathology
• Unremitting, recurring chronic LBP– structural, neurophysiological, and biopsychosocial
pathology
– requires management at all these levels
– major public health problem
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Referred LBP Is Remote From Source of Pain
• LBP may radiate into – groin – buttocks– upper thigh
areas that share an interconnecting nerve supply• Source of somatic referred pain is a skeletal or myofascial
structure of the lumbar spine• Source of visceral referred pain is within a body organ
– ovarian cysts may refer pain to low back– cancer of head of pancreas can present as low back
pain becoming excruciating at night
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Radicular LBP Results From Irritation of Spinal Nerve or Its
Roots• Damage to specific nerve root
– pain may radiate along the nerve down the lower extremity
• Lumbosacral radiculopathy often manifests as sciatica
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LBP Patient Treatment Prototypes
• Chronic axial LBP– pain does not extend beyond mid-buttock– absence of radicular pain or sensory symptoms below
the knee• Chronic axial LBP with radiation
– pain with radiation beyond mid-buttock– absence of radicular pain or sensory symptoms below
the knee• Chronic axial LBP with radicular component
– radicular pain or sensory symptoms below the knee
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Structure of Lumbar Spine Basic functional units of spine—motion
segments—consist of two posterior zygapophyseal (facet) joints and an intervertebral disc, forming a tri-joint complex
Zygapophyseal joint
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Lumbar Structural Pathology and Degenerative Cascade
• In all individuals, there is natural, progressive degeneration of the motion segments over time
• This results in anatomic, biochemical, and clinical sequelae
• Although lumbar motion segment degeneration is not a normal process, it may not be painful
Three phases of degenerationDysfunction
Instability
Stabilization
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Sources of LBP• Damage to several
structures in the low back can result in severe pain– vertebrae– thoracolumbar fascia– ligaments– joints
• specifically sacroiliac joint
– discs– muscle
Deyo RA, Weinstein JN. N Engl J Med. 2001;344:363-370.
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LBP Psychological Factors• Prolonged back pain may be associated with
a psychological disturbance, manifesting as– behavioral– cognitive– affective– somatoform (psychophysiological)
• Psychological factors that may contribute to or be caused by chronic LBP include– depression– anxiety – somatization– post-traumatic stress disorder– pre-existing bipolar or other disorders
Andersson GBJ. Lancet. 1999;354:581-585.
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Social Issues May Contribute to Chronic LBP
• Job dissatisfaction/loss of ability to work
• Pursuit of disability compensation
• Substance abuse
• Family dynamics
• Financial issues
• Loss of social identity or context
• Loss of ability to participate in recreational activities
Wheeler AH, Stubbart JR. Pathophysiology of chronic back pain. Available at: www.emedicine.com/neuro/topic516.htm.
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Goals of Clinical Assessment
Medical History
General
Neurologic
Psychosocial
Pain Scales/Questionnaires
Factors in the Elderly
Making the Diagnosis
Physical Examination
Neurologic
Diagnostic Studies
Evaluation of the Elderly
Considerations in the Clinical Assessment and Diagnosis of
Chronic LBP
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Medical History
• Symptom onset/cause of LBP
• Duration, location, and character of LBP (pain scales/questionnaires)
• Physical/functional impairment
• Factors that exacerbate or relieve LBP
• Associated features or secondary signs/symptoms
• Neurologic history
• Psychosocial history
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Red Flags• Diagnostic tests indicated early on for
– current medical history: significant trauma, recent intervention, pain unrelieved or worse with lying down, pain worse at night, progressive neurological deficit
– past medical history: cancer, recent rapid weight loss, immunosuppression or systemic steroids, IV drug use, recent bacterial infection, chills or fever, first incident of back pain in older patient
• Patient offered appointment within 24 hours for– fever lasting >48 h, new below-the-knee pain or numbness, new leg
weakness, loss of bladder or bowel control (retention or incontinence), progressive neurologic deficit
• Psychosocial red flags
– suicidal ideation, social withdrawal, panic attacks, serious financial reversal, homelessness: refer for psychiatric consultation or send to psychiatric crisis center
Deyo RA, Weinstein JN. N Engl J Med. 2001;344:363-370.Institute for Clinical Systems Improvement (ICSI). Adult low back pain. Bloomington, Minn: ICS;
September 2003:63.
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Neurologic History• Symptoms• Onset• Common etiologic factors
– leg pain (HNP with nerve root compression L4, L5, S1 )
– leg weakness (HNP, extrusion, fragment)– groin pain (HNP with nerve root compression L2, L3)– back pain with allodynia of skin (inflammatory
recruitment of non-nociceptors)
– non-dermatomal leg pain with weakness, mottling of skin, temperature change, asymmetric hair growth, sweating, allodynia, hyperalgesia (CRPS 1 or 2)
HNP=herniated nucleus pulposus; CRPS=complex regional pain syndrome
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Musculoskeletal Examination
• Observation– pain behaviors–groaning, position changes, grimacing, etc– atrophy, swelling, asymmetry, color changes
• Palpation– palpate area of pain for temperature, spasm, and pain
provocation– point palpation for trigger points/tender points
• Range of motion– active and passive– flexion, extension, rotational, lateral bending– leg raising
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Neurologic Exam Determines Presence/Absence and Level of Radiculopathy and Myelopathy
• Motor elements– muscle bulk/tone
• atrophy/flaccidity
– muscle strength– coordination– gait
• Sensory elements– sensory deficits, eg, touch,
position sense, temperature, vibration
– allodynia: light touch– hyperalgesia: single or multiple
pinpricks
• Autonomic elements– limb temperature– sweating– hair/nail growth– skin color changes
• Deep tendon reflexes
The exam should include
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Medical Red Flags = Early Warning
• Cauda equina syndrome– LBP; sciatica
– saddle anesthesia
– urinary incontinence/hesitancy
– fecal incontinence
– unilateral or bilateral lower extremity motor and sensory loss
• Spinal epidural hematoma/abscess– severe pain– urinary/fecal
incontinence– focal neurologic findings
Boukobza M, et al. Neuroradiology. 1994;36:456-459.Gleave JR, Macfarlane R. Br J Neurosurg. 2002;16:325-328.
Thongtrangan I, et al. Neurosurg Focus. 2004;16(6):e6.
Surgical emergency procedures scheduled
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When to Refer for Surgical Consultation
• Motor weakness of one or both legs
• New bowel and urinary incontinence
• MRI HNP compressing nerve root
• MRI of grade 3 spondylolisthesis
• MRI/CT evidence of severe spinal stenosis with correlative leg weakness and pain
• Standing flexion/extension films showing significant movement
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Surgery Options• Primarily involve correction or stabilization of the underlying
pathological condition• Principal reasons are to relieve pressure and nerve irritation
caused by a prolapsed lumbar disc or to stabilize spinal structures
• Techniques include:– spinal fusion
• one or more vertebrae are fused to prevent motion– decompression
• removal of bone or disc material to prevent pinching of the nerve (neural impingement)
• Surgery may improve pain and lead to more effective nonsurgical pain interventions
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Pharmacotherapy Options*
• Antidepressants
• Anticonvulsants
• Muscle relaxants
• Opioid analgesics
• Corticosteroids
• NSAIDs
• Topical analgesics
* Except for certain opioids, none of these agents are indicated for chronic LBP.
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Constant burning, stabbing, or deep aching groin or leg pain
Treatment Strategies for LBP
Moskowitz MH. Curr Pain Headache Rep. 2003;7:178-187.
Clinical Presentation
Possible Cause of LBP Treatment Strategies
Intermittent unilateral leg pain, numbness, weakness radiating to foot
Intermittent nerve entrapment with nerve root inflammation
• Short-acting opioids
• NSAIDs
• Topical analgesics
Permanent nerve damage
• Opioids
• Tricyclic antidepressants
• Anticonvulsants
• Topical analgesics
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Treatment Strategies for LBP (cont’d)
Moskowitz MH. Curr Pain Headache Rep. 2003;7:178-187.
Clinical Presentation
Possible Cause of LBP Treatment Strategies
Axial, aching, throbbing and/or stabbing LBP with trigger points radiating to buttocks and anterior thigh
Inflammation of surrounding tissue or joint, myofascial
• NSAIDs
• Opioids
• Topical analgesics
Pain > expected from injury, burning, electrical, to one or both limbs, edema, mottling, nail, skin, and hair changes, temperature change, allodynia, hyperalgesia
Sympathetically maintained pain
• Opioids
• Tricyclic antidepressants
• Anticonvulsants
• Topical analgesics
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Interventional Treatment Options
• Neural blockade– selective nerve root blocks– facet joint blocks, medial branch blocks
• Neurolytic techniques– radiofrequency neurotomies– pulse radio frequency
• Stimulatory techniques– spinal cord stimulation– peripheral nerve stimulation
• Intrathecal medication pumps– delivery into spinal cord and brain via CSF
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Physical Treatment Options• Exercise (stabilization training)• Neutral position• Soft tissue mobilization• Transcutaneous electrical nerve stimulation
(TENS)• Electrothermal therapy• Complementary measures (acupuncture;
relaxation/hypnotic/biofeedback therapy)• Spinal manipulative therapy• Multidisciplinary treatment programs (back
schools/education/counseling/pain clinic)
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Summary• Chronic LBP is a disease, not a symptom
• Progress is focused on targeting treatment at the mechanisms that produce pain rather than ameliorating the symptoms
• Biopsychosocial approach is critical for the successful management of chronic LBP
• Promising treatments for chronic LBP include– new agents– new uses of agents– new combinations of agents
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• Wong-Baker FACES Pain Rating Scale • No Hurt Hurts Little Bit Hurts Little More Hurts Even
More Hurts Whole Lot Hurts Worst
• Explain to the person that each face is for a person who feels happy because he has no pain (hurt) or sad because he has some or a lot of pain. Face 0 is very happy because he doesn’t hurt at all. Face 1 hurts just a little bit. Face 2 hurts a little more. Face 3 hurts even more. Face 4 hurts a whole lot. Face 5 hurts as much as you can image, although you don’t have to be crying to feel this bad. Ask the person to choose the face that best describes how he is feeling.
• Rating scale is recommended for persons age 3 years and older. • Brief word instructions: Point to each face using the words to
describe the pain intensity. Ask the child to choose face that best describes own pain and record the appropriate number.
• From Wong DL, Hockenberry-Eaton M, Wilson D, Winkelstein ML, Schwartz P: Wong’s Essentials of Pediatric Nursing, 6/e, St. Louis, 2001, P. 1301. Copyrighted by Mosby, Inc. Reprinted by permission.
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Key Learning Points From:
Advances in Opioid Analgesia: Maximizing Benefit While Minimizing Risk
Copyright © 2006 Thomson Professional Postgraduate Services ®. All rights reserved.
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