Australia Elsevier proofs...

Activate your eBook at evolve.elsevier.com

Pharmacology Handbook for Physiotherapists is an essential quick-reference guide to common medications, designed specifically for student and professional physiotherapists to assist in their everyday practice.Providing practical and accessible evidence-based information, the handbook will equip physiotherapists with the right knowledge to maximise the benefit of pharmacology and physiotherapy treatments. Written by a multidisciplinary team of specialists, the text is designed to be comprehensive and easy-to-read and is set out by body system to allow quick retrieval of useful information related to the particular condition and medications involved.

Key featuresn Written specifically for physiotherapists to assist their understanding of

pharmacology principles in conjunction with physiotherapy treatmentn Each chapter is written by three experts in their respective fields: a

physiotherapist, a physician and a pharmacist n ‘Physiotherapy practice points’ explain the effects that drugs may have on

treatment and provide valuable information on the actions of medications and how these interact with physiotherapy treatment

n 11 chapters cover basic pharmacology principles, legal and ethical issues, the body systems, women’s and men’s health, as well as a final chapter on medication issues in the young and elderly

THE EDITORSJacqueline Reznik BAppSci, MAPA, MCSP, GradDip(Teaching), GradDip(Neurology), PhDInternational Physiotherapy Consultant, Kfar Yona, Israel; Townsville, Queensland, AustraliaOfer Keren MDDirector of Acquired Brain Injury Rehabilitation Department, Sheba Medical Center, Tel Hashomer; Clinical Senior Lecturer, Sackler School of Medicine, Tel Aviv University, Tel Aviv, IsraelJoanne Morris BSc (Hons) Physiotherapy, MSc (Hons) Clinical Biomechanics, Grad Dip Extended Scope Physiotherapy, Doctoral CandidateExtended Scope Physiotherapist, Canberra Hospital and Health Services, Canberra, Australian Capital Territory, AustraliaIftah Biran MD Neurologist and Psychiatrist, Psychotherapist and Behavioural Neurologist; Working as a Psychiatrist Consult (Liaison Psychiatry) to the Department of Neurology, Tel Aviv Medical Center , Tel Aviv; Psychoanalytic candidate, Max Eitingon Institute of Psychoanalysis, Jerusalem, Israel

ISBN 978-0-7295-4214-2

9

>780729 542142

PH

AR

MA

CO

LOG

Y H

AN

DB

OO

K FO

R P

HY

SIOT

HER

AP

ISTS

REZ

NIK

KER

ENM

OR

RIS

BIR

AN Sam

ple pro

ofs @

Elsevie

r Austr

alia

Reznik_2142_Title page_main.indd 1 8/16/2016 3:25:28 PM

�� !� �� "�#�� "�� $��"

Sample

proofs

@ Else

vier A

ustrali

a

Reznik_2142_Title page_main.indd 3 8/16/2016 3:25:29 PM

�� !� �� "�#�� "�� $��"

Sample

proofs

@ Else

vier A

ustrali

a

Elsevier Australia. ACN 001 002 357(a division of Reed International Books Australia Pty Ltd)Tower 1, 475 Victoria Avenue, Chatswood, NSW 2067

Copyright 2017 Elsevier Australia

All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from the publisher. Details on how to seek permission, further information about the Publisher’s permissions policies and our arrangements with organisations such as the Copyright Clearance Center and the Copyright Licensing Agency, can be found at our website: www.elsevier.com/permissions.

This book and the individual contributions contained in it are protected under copyright by the Publisher (other than as may be noted herein).

NoticeThis publication has been carefully reviewed and checked to ensure that the content is as accurate and current as possible at time of publication. We would recommend, however, that the reader verify any procedures, treatments, drug dosages or legal content described in this book. Neither the author, the contributors, nor the publisher assume any liability for injury and/or damage to persons or property arising from any error in or omission from this publication.

National Library of Australia Cataloguing-in-Publication entry Reznik, Jacqueline, author.Pharmacology handbook for physiotherapists / Jacqueline Reznik, Ofer Keren, Joanne Morris, Iftah Biran.

9780729542142 (paperback)Pharmacology–Australia–Handbooks, manuals, etc. Physical therapy–Practice. Physical therapy–Handbooks, manuals, etc.

Keren, Ofer, author. Morris, Joanne, author. Biran, Iftah, author.

615.82 Senior Content Strategist: Melinda McEvoySenior Content Development Specialist: Natalie HuntSenior Project Manager: Anitha RajarathnamCover and Internals Design by Natalie BowraEdited by Linda LittlemoreProofread by Forsyth Publishing ServicesIndex by Robert SwansonTypeset by Toppan Best-set Premedia LimitedPrinted by 1010 Printing International Ltd

Reznik_2142_Copyright page_main.indd 4 8/16/2016 3:25:22 PM

�� !� �� "�#�� "�� $��"

Sample

proofs

@ Else

vier A

ustrali

a

Contents

Foreword ix

Preface/How to use this book x

About the editors xi

Contributors xii

Reviewers xv

Acknowledgements xvi

1 Introduction and background concepts 1

Introduction 1Gregory Kyle, Jacqueline Reznik, Joanne Morris, Ofer Keren

Legal and ethical issues 3Joanne Morris

Basic pharmacology and pharmacokinetic concepts 7Gregory Kyle

Administration and monitoring of medications 13Gregory Kyle, Jacqueline Reznik, Ofer Keren

Physiology of the autonomic nervous system 19Pam Megaw

2 Cardiovascular system 27Bernie Bissett, Imogen Mitchell, Karlee Johnston, Gregory Kyle

3 Respiratory system 46Bernie Bissett, Imogen Mitchell, Karlee Johnston, Richard Talbot

4 Women’s and men’s health 72Kathryn Vine, Miriam Lawrence, Roberto Orefice

5 Orthopaedic and musculoskeletal systems 106Joanne Morris, Miriam Lawrence, Bryan Ashman

6 Neurological system 167Jacqueline Reznik, Ofer Keren, Iftah Biran, Ilana Schumacher

7 Pain and analgesia 199Anthony Wright, Heather AE Benson, Robert Will

Reznik_2142_Table of contents_main.indd 7 8/16/2016 3:25:27 PM

�� !� �� "�#�� "�� $��"

Sample

proofs

@ Else

vier A

ustrali

a

viii PHARMACOLOGY HANDBOOK FOR PHYSIOTHERAPISTS

8 Endocrine system 226Joanne Morris, Chandima Perera, Jacqueline Reznik, Ofer Keren, Iftah Biran

9 Haematological system 251Anthony Hall, Jacqueline Reznik, Ofer Keren, Iftah Biran

10 Mental health 276Iftah Biran, Jacqueline Reznik

11 Medication issues in the young and the elderly 315Ian Heslop, Jacqueline Reznik, Ofer Keren

Index 326

Reznik_2142_Table of contents_main.indd 8 8/16/2016 3:25:27 PM

�� !� �� "�#�� "�� $��"

Sample

proofs

@ Else

vier A

ustrali

a

This book is not designed to be read ‘cover to cover’ but rather as a handbook that allows easy access to information on disease processes, their signs and symptoms and the medications that are being prescribed for your patients to alleviate those signs and symptoms. The text incorporates many tables that are designed to allow the reader to quickly retrieve useful information regarding a patient’s drug regimen including possible side effects and duration of action, which may be particularly relevant to physiotherapists, both undergraduate and postgraduate. The book is divided into 11 chapters based on body systems, with a background chapter that includes basic pharmacology and legal implications at the beginning and a chapter for age-related implications of medications at the end. Chapters 2 through 10 deal with medications prescribed for various conditions by body system: cardiovascular, respiratory, women’s and men’s health, orthopaedic and musculoskeletal, neurological, pain and analgesia, endocrinological, haematological and mental health. This allows the reader to quickly access the information they require by searching via body system for the desired condition or medication.

This handbook is also not intended to compete with the larger and more concise pharmacotherapeutic textbooks or physiotherapeutic textbooks and, for that reason, more detail regarding the medications and physiotherapeutic interventions has not been included. The physiotherapy practice points outlined in each chapter are designed to explain to the reader the effects that the drugs may have on their treatment and provide valuable information on the actions of medications and when and how this interacts with physiotherapy treatment.

The book is not intended to be a ‘do as I say book’. It tries, albeit on a limited scale, to describe the ‘bigger picture’. Each chapter has been coauthored by a pharmacist, doctor and physiotherapist specialising in that particular area and, where possible, medications used to alleviate signs and symptoms have been described rather than those used for specific conditions. In those cases where exclusive drugs are designed for particular conditions, they have been referred to specifically. All drugs have been referred to by their generic (not brand) names.

At the time of going to print all of the information provided in this book is up to date.

Preface/How to use this book

Reznik_2142_Preface_main.indd 10 8/16/2016 3:25:25 PM

�� !� �� "�#�� "�� $��"

Sample

proofs

@ Else

vier A

ustrali

a

CHAPTER

5

Orthopaedic and

musculoskeletal systems

Joanne Morris, Miriam Lawrence, Bryan Ashman

O B J E C T I V E S This chapter will discuss the role that medications have in the supplementary management of the most common musculoskeletal conditions treated by physiotherapists. By the end of this chapter (including cross-referencing with other relevant chapters) the reader should have an understanding of:◆ the major classification of musculoskeletal disorders according to

structure, location, signs and symptoms◆ pharmacotherapy options for the major musculoskeletal disorders◆ usual dosages, routes of administration and major contraindications and

precautions of these medications◆ any potential impact of these medications on physiotherapeutic

management.

O V E R V I E W Arthritis

OsteoarthritisSeptic arthritisRheumatoid arthritis and other synovial joint disordersPsoriatic arthritisCrystal arthropathies

Joint conditions

Adhesive capsulitisAvascular necrosisOsteomyelitisTumours

Maxillofacial disorders

Trigeminal neuralgiaTemporomandibular joint disordersBell’s palsy

Soft tissue conditions

Soft tissue injuries – sprains, strains and contusionsAcute tendon painSubacute/chronic tendon pain

Nerve compression syndromes

BursitisConnective tissue disorders

Spinal conditions

Ankylosing spondylitisSpondylosis/spondyloarthropathy

Trauma

Fractures/acute traumaDislocation

Miscellaneous

%�&��'()*+)(,��-(��"��*./ 0121).*/��34+/4-0��5

�� !� �� "�#�� "�� $��"

Sample

proofs

@ Else

vier A

ustrali

a

107CHAPTER 5 ORTHOPAEDIC AND MUSCULOSKELETAL SYSTEMS

Introduction

Musculoskeletal conditions are conditions of the bones, muscles and their attachments (e.g. joints and ligaments) (Australian Institute of Health and Welfare [AIHW] 2015).

According to the Australian Institute of Health and Welfare (AIHW) 28% of Australians, approximately 6.1 million people, have arthritis and other musculoskeletal conditions (AIHW 2015) (see Figure 5.1).

Fourteen percent of Australians (3.0 million) are affected by back conditions, 8% with osteoarthritis (1.8 million), 3% with osteoporosis (728,000) and 2% with rheumatoid arthritis (445,000) according to 2011–12 self-reported figures (AIHW 2015).

Physiotherapists are key members of the primary and secondary care treating teams for patients with musculoskeletal disorders (MSD) and often are the primary treating clinician. Physiotherapy is a clinically- and cost-effective management strategy for patients with a musculoskeletal disorder. The most common complaints of patients with an MSD are pain, swelling and altered function. Therefore, the predominant reason a patient with an MSD takes medication is to manage pain and inflammation.

In this chapter the classification of musculoskeletal disorders proposed by the National Institute for Health and Care Excellence (NICE) will be followed (NICE 2015):1 arthritis2 congenital conditions (not included)3 joint conditions4 maxillofacial conditions5 soft tissue conditions6 spinal conditions7 trauma8 vasculitis.Overview of general factors affecting choice of medication

This chapter follows the Australian approved indications as specified in the Therapeutic Goods Administration approved product information. Emphasis

Figure 5.1 Percentage of Australians with musculoskeletal conditions. Adapted with permission from: Australian Institute of Health and Welfare (AIHW), 2015. Arthritis, Osteoporosis and Other Musculoskeletal Conditions. <http://www.aihw.gov.au/arthritis-and-musculoskeletal-conditions/>.

Back problems

Osteoarthritis

Osteoporosis

Rheumatoid arthritis

14%

8%

3%

2%

%�&��'()*+)(,��-(��"��*.6 0121).*/��34+/4-2��5

�� !� �� "�#�� "�� $��"

Sample

proofs

@ Else

vier A

ustrali

a

108 PHARMACOLOGY HANDBOOK FOR PHYSIOTHERAPISTS

will be placed on those signs and symptoms and conditions most frequently treated by physiotherapists and where the physiotherapist’s input is vital in monitoring the effects of the prescribed medications. The focus of this chapter will be on the major medications prescribed for specific musculoskeletal disorders and their relevance for the physiotherapist (Table 5.1). As indicated, many of the medications prescribed for musculoskeletal disorders are discussed in detail in other chapters of this handbook.

Each category and the specific subgroup of medications will be reviewed in terms of mechanism of action, route of administration, effects and adverse effects. A range of medication options are available for the treatment and/or management of musculoskeletal disorders and physiotherapists are often involved in discussions regarding treatment options. In addition to the impact of the physiotherapy intervention on the patient, the treating physiotherapist can also monitor the impact of the medications intervention using appropriate outcome measures.

P H Y S I O T H E R A P Y P R A C T I C E P O I N T S : M U S C U L O S K E L E TA L D I S O R D E R S

The main complaints of patients with an MSD are pain, swelling, stiffness and altered functional capacity. An integral component of a physiotherapist’s assessment is to gain an understanding of the severity and irritability of the patient’s symptoms and, through thorough assessment, the underlying disease processes. Understanding the underlying disease processes assists the clinical reasoning of the treating team in relation to the provision and monitoring of medications.

The pathophysiology of pain is addressed in Chapter 7. Figure 5.2 provides a basic understanding of the pathophysiology of inflammation at the organ and tissue level, thus providing valuable information regarding the mechanism of action of medications used to treat inflammation.

TABLE 5.1 Medications used in musculoskeletal disorders

General category Specific group

Relevance for

physiotherapist Where addressed

Medications used for musculoskeletal disorders – symptom orientated

Pain +++ See Chapter 7 for additional information

Inflammation +++ This chapter

Muscle spasm +++ This chapter

Medications used for musculoskeletal disorders – disease orientated

Antibiotics + This chapter

Anti-inflammatories +++ This chapter

Autoimmune ++ This chapter

Osteopenia/porosis ++ Chapter 8

%�&��'()*+)(,��-(��"��*.0 0121).*/��34+/4-2��5

�� !� �� "�#�� "�� $��"

Sample

proofs

@ Else

vier A

ustrali

a


Figure 5.3 highlights the mechanism of action of medications commonly used in the management of inflammation (COX-1 and COX-2 inhibitors). For further information regarding basic pharmacology and pharmacokinetic concepts please see Chapter 1.

Table 5.2 describes the structure, location and signs and symptoms of musculoskeletal disorders in terms of the sites of action for associated medication; disease-specific information and detailed medication management are described in Table 5.3.

Figure 5.2 Acute inflammation. Reproduced with permission from: Kumar, V., Abbas, A.K., Aster, J.C., 2013. Robbins Basic Pathology, ninth ed. Elsevier Sanders, Philadelphia, pp. 29–73.

Extracellular matrix Occasional residentlymphocyte or macrophage

VenuleArteriole

NORMAL

INFLAMED Increased blood flow

Expansion of capillary bedArteriole dilation Venule dilation

1

Neutrophil emigration3 Leakage of plasma2proteins oedema

%�&��'()*+)(,��-(��"��*.2 0121).*/��34+/4-2��5

�� !� �� "�#�� "�� $��"

Sample

proofs

@ Else

vier A

ustrali

a


Figure 5.3 Action of non-steroidal anti-inflammatory drugs (NSAIDs). Adapted with permission from: Stovitz, S.D., Johnson, R.J., 2003. NSAIDs and musculoskeletal treatment: what is the clinical evidence? The Physician and Sports Medicine 31. <http://www.chiro.org/LINKS/FULL/NSAIDs_and_Musculoskeletal_Treatment.html>.

Tissue injury

Phospholipids

Arachidonic acid

Inflammatory prostaglandins• Recruit inflammatory cells• Sensitise skin pain receptors• Regulate hypothalamic temperature control

Cytoprotective prostaglandins• Protect gastric mucosa• Aid platelet aggregation

Leukotrienes• Bronchoconstriction

Inducers• Cytokines• Growth factors

Inhibitors• COX-2 inhibitors• NSAIDS (non–COX-2)• Aspirin

COX-2(Inducible)

COX-1(Constitutional)

Inhibitors• NSAIDS (non–COX-2)• Aspirin

TABLE 5.2 Structure, location, signs and symptoms of medication

action in musculoskeletal disorders

Structure Location Signs and symptoms a

Tissue level Local tissue trauma Pain, swelling and muscle spasm

Central nervous system Dorsal horn Pain, muscle spasm

aSee Table 5.3 for descriptions of the various signs and symptoms.

Depending on the structure(s) affected and the nature of the patient’s condition (e.g. autoimmune) the clinical signs and symptoms will vary. Listed in Table 5.3 are the clinical characteristics, anatomical locations (where applicable) and signs and symptoms for which physiotherapy treatment may be applicable.

Table 5.4 outlines the disease mechanisms of some of the common MDSs treated by physiotherapists – providing further clarity regarding the mechanism of action of the medications used in the treatment of common conditions. This will be explored in greater detail under disease-specific medication regimens later in the chapter.

Conditions will be subdivided according the NICE classification of musculoskeletal disorders and common medication management will be highlighted.

Text continued on p. 115

%�&��'()*+)(,��-(��"��**. 0121).*/��34+64..��5

�� !� �� "�#�� "�� $��"

Sample

proofs

@ Else

vier A

ustrali

a


Mu

scu

loskele

tal

dis

ord

ers

cla

ssifi

cati

on

Sig

ns/s

ym

pto

ms

/sp

ec

ific

dia

gn

osis

Cli

nic

al

ch

ara

cte

ris

tic

sA

na

tom

ic lo

ca

tio

n

Art

hri

tis

Pain

Pain

is th

e m

ost c

omm

only

repo

rted

com

plai

nt o

f pat

ient

s w

ith a

rthrit

is –

rang

ing

from

ac

ute

to c

hron

ic p

ain,

whi

ch c

an b

e m

ild to

sev

ere

in n

atur

eVa

rious

Infla

mm

atio

nSw

ellin

g of

ten

occu

rs in

acu

te fl

ares

of a

rthrit

ic c

ompl

aint

sVa

rious

Stiff

ness

Loss

of m

ovem

ent i

n th

e af

fect

ed jo

ints

, whi

ch m

ay b

e as

soci

ated

with

chr

onic

syn

oviti

sAf

fect

ed jo

ints

Wei

ght g

ain

The

reas

ons

for w

eigh

t gai

n ca

n be

mul

tifac

toria

l, bu

t inc

lude

redu

ced

activ

ity le

vels

(whi

ch

may

be

seco

ndar

y to

pai

n) a

nd c

o-m

orbi

ditie

s (s

uch

as m

etab

olic

dis

ease

)

Mus

cle

wea

knes

sM

uscl

e w

eakn

ess

can

be d

riven

by

alte

red

mov

emen

t pat

tern

s, s

wel

ling

(e.g

. int

raar

ticul

ar

swel

ling

of th

e kn

ee),

redu

ced

activ

ity le

vels

and

co-

mor

bidi

ties

(e.g

. stro

ke)

Infe

ctio

nPa

tient

s w

ith s

eptic

arth

ritis

are

pyr

exia

l, re

port

acut

e se

vere

pai

n, s

wel

ling

and

ofte

n er

ythe

ma

Gen

eral

ly la

rge

join

ts

incl

udin

g kn

ee, s

houl

der

and

elbo

w

Jo

int

co

nd

itio

ns

Adhe

sive

cap

sulit

isPa

tient

s w

ith a

dhes

ive

caps

uliti

s ar

e ge

nera

lly o

ver t

he a

ge o

f 35,

with

pai

n in

the

shou

lder

of

thei

r dom

inan

t arm

that

is g

ener

ally

wor

se a

t nig

htTh

ere

has

been

a g

loba

l los

s of

rang

e of

mov

emen

t; ho

wev

er th

ere

is o

ften

a m

ore

mar

ked

loss

of e

xter

nal r

otat

ion

rang

e (W

alm

sley

, Osm

othe

rly a

nd R

ivet

t 201

4)R

isk

fact

ors

incl

ude:

type

1 o

r 2 d

iabe

tes

mel

litus

, thy

roid

dis

ease

, myo

card

ial i

nfar

ctio

n an

d pr

olon

ged

perio

ds o

f im

mob

ility

(Kel

ley

et a

l. 20

13)

Shou

lder

Rhe

umat

oid

arth

ritis

and

ot

her s

ynov

ial j

oint

di

sord

ers

Rhe

umat

oid

arth

ritis

is a

sys

tem

ic, i

nflam

mat

ory,

aut

oim

mun

e di

sord

er th

at re

sults

in jo

int

dest

ruct

ion

and

pers

iste

nt in

flam

mat

ion

of s

ynov

ial t

issu

e (s

ynov

itis)

Res

ults

in m

uscu

losk

elet

al p

ain

and

swel

ling,

as

a re

sult

of th

e de

stru

ctiv

e er

osio

n of

bon

e an

d a

loss

in jo

int i

nteg

rity

Rep

orte

dly

affe

cts

2% o

f Aus

tralia

ns (A

IHW

201

5)

Vario

us

T

AB

LE

5.3

D

efi

nit

ion

s a

nd

cli

nic

al

fea

ture

s o

f m

ajo

r si

gn

s a

nd

sy

mp

tom

s se

en

in

mu

scu

losk

ele

tal

dis

ord

ers

Cont

inue

d

%�&��'()*+)(,��-(��"��*** 0121).*/��34+64..��5

�� !� �� "�#�� "�� $��"

Sample

proofs

@ Else

vier A

ustrali

a


Mu

scu

loskele

tal

dis

ord

ers

cla

ssifi

cati

on

Sig

ns/s

ym

pto

ms

/sp

ec

ific

dia

gn

osis

Cli

nic

al

ch

ara

cte

ris

tic

sA

na

tom

ic lo

ca

tio

n

Psor

iatic

arth

ritis

Psor

iasi

s is

cha

ract

eris

ed b

y er

ythe

mat

ous,

sca

ly p

atch

es o

f ski

n an

d na

ilsPa

tient

s w

ith p

soria

tic a

rthrit

is (P

sA) m

ay h

ave

spon

dylit

is, o

ligoa

rthrit

is a o

r pol

yarth

ritis

, pr

esen

ting

as p

ain,

stif

fnes

s an

d in

flam

mat

ion,

but

it m

ay a

lso

affe

ct li

gam

ents

, ten

dons

an

d fa

scia

l tis

sue

Vario

us

Cry

stal

arth

ropa

thie

sG

out i

s of

ten

char

acte

rised

by

rapi

d on

set o

f sev

ere

pain

, sw

ellin

g, w

arm

th, e

ryth

ema

and

decr

ease

d ra

nge

of m

ovem

ent i

n th

e af

fect

ed jo

int (

Khan

na e

t al.

2014

)Pa

in is

the

over

ridin

g sy

mpt

om

Knee

, big

toe,

var

ious

Maxil

lofa

cia

l co

nd

itio

ns

Pain

Con

ditio

ns s

uch

as tr

igem

inal

neu

ralg

ia, t

empo

rom

andi

bula

r joi

nt (T

MJ)

dis

orde

rs

(incl

udin

g os

teoa

rthrit

is) a

nd B

ell’s

pal

sy a

re c

omm

only

trea

ted

by p

hysi

othe

rapy

and

are

as

soci

ated

with

pai

n an

d/or

alte

red

sens

atio

n an

d/or

mus

cle

wea

knes

s

TMJ,

ocu

lar p

ain,

ting

ling

in th

e ch

eek/

mou

th

Infla

mm

atio

nAc

ute

inju

ry a

nd fl

are

of a

rthrit

is m

ay b

e as

soci

ated

with

sw

ellin

g to

the

affe

cted

are

aAf

fect

ed a

rea

Stiff

ness

Loss

of m

ovem

ent i

n th

e af

fect

ed jo

ints

, whi

ch m

ay b

e as

soci

ated

with

chr

onic

syn

oviti

sAf

fect

ed a

rea

Infe

ctio

nD

enta

l and

/or i

nfec

tion

is a

diff

eren

tial d

iagn

osis

for p

atie

nts

with

max

illofa

cial

con

ditio

nsAf

fect

ed a

rea

Beni

gn p

arox

ysm

al

posi

tiona

l ver

tigo

Sudd

en o

nset

of s

ever

e po

sitio

nal d

izzi

ness

that

can

be

asso

ciat

ed w

ith n

ause

a an

d vo

miti

ng

So

ft t

issu

e c

on

dit

ion

s

– i

nclu

din

g c

on

necti

ve

tissu

e d

iso

rders

Pain

Spra

ins,

stra

ins

and

cont

usio

ns a

re a

ssoc

iate

d w

ith p

ain

to th

e af

fect

ed a

rea

Affe

cted

are

a

Infla

mm

atio

nSp

rain

s, s

train

s an

d co

ntus

ions

are

ass

ocia

ted

with

sw

ellin

g an

d er

ythe

ma

to th

e af

fect

ed

area

, whi

ch in

som

e ca

ses

may

resu

lt in

ner

ve c

ompr

essi

on a

nd th

eref

ore

be a

ssoc

iate

d w

ith p

arae

sthe

sia,

ting

ling

etc

Affe

cted

are

aN

erve

com

pres

sion

sy

ndro

mes

suc

h as

car

pal

tunn

el s

yndr

ome

T

AB

LE

5.3

D

efi

nit

ion

s a

nd

cli

nic

al

fea

ture

s o

f m

ajo

r si

gn

s a

nd

sy

mp

tom

s se

en

in

mu

scu

losk

ele

tal

dis

ord

ers

—co

nt’

d

Maxil

lofa

cia

l co

nd

itio

ns

%�&��'()*+)(,��-(��"��**) 0121).*/��34+64..��5

�� !� �� "�#�� "�� $��"

Sample

proofs

@ Else

vier A

ustrali

a

113CHAPTER 5 ORTHOPAEDIC AND MUSCULOSKELETAL SYSTEMSM

uscu

loskele

tal

dis

ord

ers

cla

ssifi

cati

on

Sig

ns/s

ym

pto

ms

/sp

ec

ific

dia

gn

osis

Cli

nic

al

ch

ara

cte

ris

tic

sA

na

tom

ic lo

ca

tio

n

Stiff

ness

The

affe

cted

are

a qu

ickl

y be

com

es s

tiff s

econ

dary

to p

ain,

sw

ellin

g an

d al

tere

d fu

nctio

nAf

fect

ed a

rea

Infe

ctio

nPa

in, s

wel

ling

and

eryt

hem

a co

uple

d w

ith fe

ver

Com

mon

aro

und

the

olec

rano

n bu

rsae

Syst

emic

lupu

s er

ythe

mat

osus

A ch

roni

c, in

flam

mat

ory,

mul

tifac

toria

l aut

oim

mun

e co

nnec

tive

tissu

e di

sord

erC

omm

on fe

atur

es o

f the

dis

ease

incl

ude

a bu

tterfl

y ra

sh a

roun

d th

e ey

es, p

olya

rthrit

is,

haem

atol

ogic

al m

anife

stat

ions

, nep

hriti

s an

d ph

otos

ensi

tivity

(Tar

r et a

l. 20

15; Y

eun

& C

unni

ngha

m 2

014)

Cha

ract

eris

ed b

y un

pred

icta

ble

perio

ds o

f exa

cerb

atio

n (fl

ares

) and

rem

issi

on (Y

eun

& C

unni

ngha

m 2

014)

Vario

us

Scle

rode

rma

A ch

roni

c au

toim

mun

e co

nnec

tive

tissu

e di

sord

er, o

f whi

ch th

ere

are

two

maj

or ty

pes:

lo

calis

ed s

cler

oder

ma

and

syst

emic

scl

eros

isBo

th a

re c

hara

cter

ised

by

exce

ss c

olla

gen

in th

e co

nnec

tive

tissu

esLo

calis

ed s

cler

oder

ma

affe

cts

only

the

skin

and

occ

asio

nally

the

tissu

es b

enea

th th

e sk

in,

resu

lting

in s

tiffn

ess

loca

llySy

stem

ic s

cler

osis

als

o af

fect

s th

e sk

in a

nd u

nder

lyin

g tis

sues

, but

add

ition

ally

the

gast

roin

test

inal

trac

t, lu

ngs,

hea

rt an

d ki

dney

s ca

n be

affe

cted

(Arif

et a

l. 20

15) t

hrou

gh

wid

espr

ead

vasc

ular

lesi

ons

and

fibro

sis

of th

e sk

in a

nd in

tern

al o

rgan

s

Sp

inal

co

nd

itio

ns

Pain

The

sym

ptom

s of

mus

culo

skel

etal

spi

nal c

ondi

tions

are

hig

hly

varia

ble

and

have

a

rela

tivel

y lo

w c

orre

latio

n w

ith ra

diog

raph

ic a

nd a

nato

mic

al fi

ndin

gs (G

ibso

n &

Wad

dell

2005

)Pr

esen

ting

com

plai

nts

may

incl

ude

spin

e pa

in, l

eg a

nd/o

r arm

sym

ptom

s (p

ain,

pa

raes

thes

ia),

func

tiona

l im

pairm

ent a

nd h

eada

ches

Cer

vica

l, th

orac

ic o

r lu

mbo

sacr

al s

pine

Stiff

ness

Patie

nts

frequ

ently

repo

rt st

iffne

ss a

nd re

duce

d ra

nge

of m

otio

nC

ervi

cal,

thor

acic

or

lum

bosa

cral

spi

ne

Mus

cle

spas

mAc

ute

or a

cute

-on-

chro

nic

flare

s ar

e of

ten

asso

ciat

ed w

ith m

uscl

e sp

asm

Cer

vica

l, th

orac

ic o

r lu

mbo

sacr

al s

pine

Cont

inue

d

%�&��'()*+)(,��-(��"��**3 0121).*/��34+64..��5

�� !� �� "�#�� "�� $��"

Sample

proofs

@ Else

vier A

ustrali

a


Mu

scu

loskele

tal

dis

ord

ers

cla

ssifi

cati

on

Sig

ns/s

ym

pto

ms

/sp

ec

ific

dia

gn

osis

Cli

nic

al

ch

ara

cte

ris

tic

sA

na

tom

ic lo

ca

tio

n

Infe

ctio

nPa

tient

s w

ith s

eptic

arth

ritis

and

/or d

isci

tis a

re p

yrex

ial,

repo

rt ac

ute

seve

re p

ain

Cer

vica

l, th

orac

ic o

r lu

mbo

sacr

al s

pine

Anky

losi

ng s

pond

yliti

sPa

tient

s pr

esen

t with

pai

n, s

tiffn

ess

and

redu

ced

mob

ility

in th

e lu

mba

r spi

ne a

nd

sacr

oilia

c jo

ints

Com

mon

ly a

ssoc

iate

d w

ith p

erip

hera

l arth

ritis

, ent

hesi

tis a

nd a

cute

ant

erio

r uve

itis

(Dag

finru

d, K

vien

& H

agen

200

8)

Lum

bosa

cral

spi

ne is

mos

t co

mm

only

affe

cted

Tra

um

a –

fra

ctu

res a

nd

dis

locati

on

Pain

Dep

endi

ng o

n th

e se

verit

y of

the

inju

ry th

is is

ofte

n as

soci

ated

with

mod

erat

e to

sev

ere

pain

of t

he a

ffect

ed a

rea

In th

e ca

se o

f bot

h fra

ctur

e an

d di

sloc

atio

n th

e po

ssib

ility

of n

euro

vasc

ular

com

prom

ise

is

high

, res

ultin

g in

par

aest

hesi

a, ti

nglin

g et

c

Vario

us

Infla

mm

atio

nD

epen

ding

on

the

seve

rity

of th

e in

jury

this

is o

ften

asso

ciat

ed w

ith m

oder

ate

to s

ever

e sw

ellin

g of

the

affe

cted

are

aVa

rious

Mus

cle

spas

mAc

ute

fract

ures

and

dis

loca

tions

are

ofte

n as

soci

ated

with

mus

cle

spas

mVa

rious

Infe

ctio

n (p

roph

ylac

tic

med

icat

ion)

Ope

n fra

ctur

es a

nd d

islo

catio

ns re

quire

pro

phyl

actic

trea

tmen

t for

infe

ctio

nVa

rious

Vascu

liti

sPa

in a

nd in

flam

mat

ion

The

sym

ptom

s of

vas

culit

is a

re h

ighl

y va

riabl

e an

d de

pend

ent o

n th

e af

fect

ed a

rea,

ho

wev

er th

ey m

ay in

clud

e:•

feve

r•

loss

of a

ppet

ite•

wei

ght l

oss

• fa

tigue

• ge

nera

l ach

es a

nd p

ains

Vario

us

a Olig

oarth

ritis

is a

rthrit

is a

ffect

ing

one

to fo

ur jo

ints

dur

ing

the

first

6 m

onth

s of

dis

ease

.

Mu

scu

los

kele

tal

dis

ord

ers

cla

ss

ificati

on

Vascu

liti

s T

AB

LE

5.3

D

efi

nit

ion

s a

nd

cli

nic

al

fea

ture

s o

f m

ajo

r si

gn

s a

nd

sy

mp

tom

s se

en

in

mu

scu

losk

ele

tal

dis

ord

ers

—co

nt’

d

%�&��'()*+)(,��-(��"��**+ 0121).*/��34+64..��5

�� !� �� "�#�� "�� $��"

Sample

proofs

@ Else

vier A

ustrali

a


TABLE 5.4 Disease mechanisms in musculoskeletal disorders and

examples of disease states for each category

Mechanism(s) Disorder(s)

Vascular HaematomaAvascular necrosisDeep vein thrombosis

Inflammatory/autoimmune Rheumatoid arthritisSystemic lupus erythematosusPsoriatic arthritisAnkylosing spondylitis

Infections OsteomyelitisSeptic arthritisInfective bursitis

Degenerative/genetic Osteoarthritis

Neoplastic Sarcoma (Ewing’s, chondrosarcoma and osteosarcoma)Soft tissue sarcoma

Trauma Fracture, soft tissue sprain, strain and contusion

Metabolic/nutritious/toxic Osteopenia

Arthritis

Osteoarthritis

Osteoarthritis (OA) is one of the primary causes of illness in the world, affecting 8% of the Australian population (AIHW 2015); hip and knee arthritis alone is a leading cause of global disability (Cross et al. 2014; Reid et al. 2014; Woolf & Pfleger 2003).

Pharmacological management

Oral treatment

Regular paracetamol is currently the recommended first-line treatment (see Table 5.11 later), and is combined with NSAIDs (see Table 5.12 later) if symptoms are not controlled with paracetamol alone. An anti-inflammatory dose of fish oil may also have benefit in osteoarthritis (Therapeutic Guidelines Limited 2010a).

However, a recent meta-analysis has indicated that the evidence for single therapy paracetamol is lacking, and has questioned its role as single therapy in the treatment of OA (da Costa et al. 2015).Topical treatment

Topical NSAIDs and capsaicin treatments (see Table 5.14 later) have been shown to improve short-term (up to 10 days) pain when compared to placebo rubs (Therapeutic Guidelines Limited 2010a).Intraarticular treatment

A single intraarticular corticosteroid injection can provide symptomatic relief for up to 4 weeks and up to 12 weeks in hip and trapeziometacarpal joint

%�&��'()*+)(,��-(��"��**- 0121).*/��34+64.*��5

�� !� �� "�#�� "�� $��"

Sample

proofs

@ Else

vier A

ustrali

a


osteoarthritis (see Table 5.15 later). The effect of repeated doses appears to be less successful, and a general guide is that an individual joint should not be injected more than 4 times per year (Therapeutic Guidelines Limited 2010a).

These injections should only be given by, or under the supervision of, experienced clinicians. Local anaesthetic may be used before, or mixed with, the corticosteroid.

Only corticosteroids specifically formulated for the purpose should be used for intraarticular injection or injection into soft tissue.

Table 5.5 gives examples of appropriate doses. The dose must be adjusted to the specific requirements of the patient according to the size of the joint or soft tissue lesion, the severity of the condition, the response obtained and the patient’s tolerance of the corticosteroid. The total volume of the injection administered will vary depending on the amount of local anaesthetic (see Table 5.15).Other treatment

Patient uptake of the use of glucosamine sulfate and chondroitin sulfate for symptomatic benefit in osteoarthritis has been widespread despite limited

TABLE 5.5 Examples of doses of local corticosteroid injections

Corticosteroid

Dose

Comments

Small joint

(e.g. hand)

Medium

sized joint

(e.g. wrist)

Large joint

(e.g. knee)

Soft tissue

(e.g. bursa)

Betamethasone sodium phosphate + betamethasone acetate 5.7 mg/mL

0.5–1 mL 1 mL 1–2 mL 1–2 mL Usually used for injection into smaller joints

Methylprednisolone acetate 40 mg/mL

n/a 1 mL 1–2 mL 1–2 mL Methyprednisolone is crystalline and is formulated as a suspensionIt is not suitable for injection into small joints or superficial soft tissue sites, where it may cause fat atrophy and can be an irritantIt could be used in a large bursa such as a trochanteric bursa

Triamcinolone acetonide 10 mg/mL

0.5–1 mL 1 mL 1–2 mL 1–2 mL Triamcinolone acetonide is the least soluble injection and provides the longest duration of action (up to 21 weeks)

Triamcinolone acetonide 40 mg/mL

n/a n/a 0.5 mL n/a

Adapted from: Therapeutic Guidelines Limited, 2010. Joint aspiration and injection, Table 12.6. In: eTG complete [Internet]. Therapeutic Guidelines Limited, Melbourne.

%�&��'()*+)(,��-(��"��**/ 0121).*/��34+64.*��5

�� !� �� "�#�� "�� $��"

Sample

proofs

@ Else

vier A

ustrali

a


evidence (see Table 5.14 later). For patients with osteoarthritis of the knee who want to try alternative therapies a 3–6 month trial of glucosamine sulfate either with or without chondroitin sulfate may be indicated, although not strongly supported by evidence (Therapeutic Guidelines Limited 2010a; Towheed et al. 2005).

For patients who have uncontrolled pain and where surgery is pending or not possible, oral opioids may be tried (see Table 5.13 later). The risk of adverse effects is high and the benefit is minimal, so this approach must be made with caution (Therapeutic Guidelines Limited 2010a).

For further information see Chapter 7.

P H Y S I O T H E R A P Y P R A C T I C E P O I N T S : O S T E O A R T H R I T I S

It is common practice for corticosteroid injections to be used in conjunction with physiotherapy as a means of improving functional status, strength and range of movement while the patient is experiencing lower pain levels (Hawkins & Ghazi 2012; Jowett et al. 2013; Roddy et al. 2014). Physiotherapists are therefore directly involved in the care of patients post-injection. Patients are commonly advised to undertake gentle range of movement exercises of the injected joint 0–48 hours after the injection as this will assist with the circulation of the corticosteroid around the joint. There is variability in the post-injection advice, depending on site/structure injected, however generally patients should be advised to avoid any heavy activity for 5–7 days post-injection (Brukner & Khan 2012). This is particularly important as it is possible that patients will feel significantly better post-injection and therefore are likely to increase their activity levels. Outcomes from corticosteroid injections are mixed: they are used to provide short-term relief (1–6 weeks), but no long-term benefit is evident in the majority of cases (Jüni et al. 2015).

It is widely accepted that exercise is an essential component of OA management, in which physiotherapists play a significant role (French et al. 2013). Depending on the pain medication of the patient, the physiotherapist can provide guidance regarding the best time to undertake exercise in accordance with the efficacy of the pain medication – for specific information regarding the duration of action of pain medications see Tables 5.11, 5.12, 5.13 and 5.14.

Septic arthritis

Definition

Septic arthritis is an infection of a joint that may be bacterial, fungal, mycobacterial or viral in origin (Carpenter et al. 2011).

Clinical significance

Permanent disability and increased mortality are associated with a delayed diagnosis of septic arthritis. In the presence of infection the cartilage of the joint can be destroyed in a matter of days if antibiotic management is not commenced (Carpenter et al. 2011).


Diagnostic specimens should always be taken before starting antibiotic therapy. Pus should be drained and the joint irrigated to reduce the pathogen load, protect the articular surface and improve the diffusion of the antibiotic into the joint.

%�&��'()*+)(,��-(��"��**6 0121).*/��34+64.*��5

�� !� �� "�#�� "�� $��"

Sample

proofs

@ Else

vier A

ustrali

a


Empirical therapy is the same as what would be used in long bone osteomyelitis (see ‘Osteomyelitis’ below). Directed therapy should then be guided by microbiology results of cultures and susceptibility testing from the aspirate.

Once directed therapy starts, antibiotic therapy must continue for the following duration (Therapeutic Guidelines Limited 2010c):◆ neonate – 3 weeks (all IV therapy)◆ child – 3 weeks (minimum of 3 days of IV therapy)◆ adult – 4 weeks (minimum of 2 weeks of IV therapy).

Rheumatoid arthritis and other synovial joint disorders

Rheumatoid arthritis

Definition

Rheumatoid arthritis (RA) is a chronic, systemic, inflammatory, progressive, autoimmune disease, with joint synovitis as its predominant clinical manifestation (Breedland et al. 2011; Iversen, Chhabriya & Shadick 2011).

Clinical significance

RA affects around 400,000 Australians and is the second most common type of arthritis, after osteoarthritis. The disease is more common among females and in older age groups (AIHW 2009). Further tests including blood tests and imaging are required to confirm a diagnosis of RA.


Rheumatoid arthritis treatment can be described in four groups as listed in Table 5.6 below.

Recommendations for treatment of early RA are described in Figure 5.4. For further pain management information see Chapter 7.

Figures 5.4 and 5.5 detail recommendations for the progression of medications in the management of early RA (under 6 months), first-line treatments and when medications should be increased or changed according to the patient’s prognosis and the disease activity. Specifically, Figure 5.5 highlights the ‘2012 update of the 2008 American College of Rheumatology recommendations for the use of disease-modifying antirheumatic drugs and biologic agents in the treatment of rheumatoid arthritis’ (Singh et al. 2012).

Psoriatic arthritis

Definition and clinical significance

Psoriatic arthritis (PsA) is a chronic, systemic inflammatory disease, classified as a seronegative spondyloarthropathy (Cinar et al. 2015). Sufferers of psoriasis include 1–3% of the population of the world, and 42% go on to develop psoriatic arthritis. It is therefore estimated that PsA has a prevalence of 0.1–1.0% in the general population (Mease & Armstrong 2014).

%�&��'()*+)(,��-(��"��**0 0121).*/��34+64.*��5

�� !� �� "�#�� "�� $��"

Sample

proofs

@ Else

vier A

ustrali

a


TABLE 5.6 Medication management of rheumatoid arthritis (RA)

Class of treatment

Examples of

medications used Place in therapy, extra information

Disease-modifying antirheumatic drugs (DMARDs)

Methotrexate (MTX)Hydroxychloroquine (HCQ)SulfasalazineLeflunomide (LEF)Cyclosporin

Reduce or resolve synovial inflammation and therefore prevent joint damageCan be used alone or in combination and all have dose limiting side effectsChoice depends on arthritis severity, patient’s age, childrearing status and coexisting conditions

Corticosteroids Prednisolone/prednisone (prednis(ol)one)HydrocortisoneBetamethoasoneOrtisoneDexamethasoneMethylprednisoloneTriamcinolone

Used while waiting for a response from a DMARD or to achieve remission quickly, either as pulse oral, intravenous or intramuscular therapy or as intraarticular therapyLong-term significant adverse effects (e.g. cardiovascular and osteoporosis) that limit long-term use

Biological disease-modifying antirheumatic drugs (DMARDs)

AbataceptAdalimumabCertolizumabEtanerceptGolimumabInfliximabTocilizumabAnakinra

Are considered if remission is not achieved with the appropriate use of DMARDsShould only be used under the supervision of experienced specialists, and the Australian Rheumatology Association has specific recommendations for when and how they are to be used (Australian Rheumatology Association 2011)Before commencing treatment patients must be screened for tuberculosis and hepatitis B and C as the immunosuppression caused by DMARDs can cause these diseases to re-emerge

Symptom management NSAIDs NSAIDs improve symptoms of RA, but do not reduce joint damage and have significant adverse effectsUsed before DMARD therapy is started or intermittently during flare-ups

Fish oil Has been shown to reduce symptoms and the need for NSAIDs and may also give cardiovascular protection

Analgesia (paracetamol and opiates)

Should be used to facilitate activity rather than to relieve painParacetamol should be used to reduce the NSAID loadOpiates should only be added if paracetamol and NSAIDS do not adequately control pain or ability to function or exercise and should only be used for a fixed short period of time such as 3 weeksSee Chapter 7 for more detail

NSAIDs, non-steroidal anti-inflammatory drugs.Adapted from: Therapeutic Guidelines Limited, 2010. Rheumatoid arthritis: pharmacological management. In: eTG complete [Internet]. Therapeutic Guidelines Limited, Melbourne. See Table 5.19 later for further information.

%�&��'()*+)(,��-(��"��**2 0121).*/��34+64.*��5

�� !� �� "�#�� "�� $��"

Sample

proofs

@ Else

vier A

ustrali

a


Figure 5.4 American College of Rheumatology recommendations in the treatment of early rheumatoid arthritis (disease duration less than 6 months). Adapted with permission from: Singh, J.A., Furst, D.E., Bharat, A., et al., 2012. 2012 update of the 2008 American College of Rheumatology recommendations for the use of disease-modifying antirheumatic drugs and biologic agents in the treatment of rheumatoid arthritis (RA). Arthritis Care and Research 64 (5), 625–639.

DMARDmonotherapy

CombinationDMARDtherapy

(double andtriple therapy)

DMARDmonotherapy

OrHCQ and MTX

Anti-TNF with orwithout MTX

OrCombination

DMARD therapy(double and triple

therapy)

Targetlow

diseaseactivity orremission

Low High

Moderate

WithWithout WithWithoutFeatures of poorprognosis

Disease activityEarly RA

Features of poorprognosis


NSAIDs and intraarticular corticosteroid injections are usually first line, with DMARDs used in resistant cases (see Tables 5.12 and 5.15). In polyarticular cases DMARDs are always used (see Tables 5.18 and 5.19 later). Fish oil is also used as an NSAID-sparing agent, as recommended in the Australian Therapeutic Guidelines (Therapeutic Guidelines Limited 2010e).

Methotrexate is the DMARD of choice in psoriatic arthritis as it benefits both the arthritis and the skin. It is given either orally, subcutaneously or intramuscularly, but always with folic acid supplementation (see Table 5.18 later for further information). There is also evidence to support the use of sulfasalazine, leflunomide and cyclosporin for this indication.

In cases where DMARDs are poorly tolerated or not effective, good evidence supports the use of the tumour necrosis factor (TNF) inhibitors adalimumab, etanercept, golimumab and infliximab – see Table 5.19 (Therapeutic Guidelines Limited 2010f).

For further pain management information see Chapter 7.

%�&��'()*+)(,��-(��"��*). 0121).*/��34+64.*��5

�� !� �� "�#�� "�� $��"

Sample

proofs

@ Else

vier A

ustrali

a


Figure 5.5 Recommendations for the use of disease-modifying anti-rheumatic medications and biologic agents in the treatment of RA. DMARD, disease-modifying anti rheumatic drugs; HCQ, hydroxychloroquine; LEF, leflunomide; MTX, methotrexate; TNF, tumour necrosis factor. Adapted with permission from: Singh, J.A., Furst, D.E., Bharat, A., et al., 2012. 2012 update of the 2008 American College of Rheumatology recommendations for the use of disease-modifying antirheumatic drugs and biologic agents in the treatment of rheumatoid arthritis (RA). Arthritis Care and Research 64 (5), 625–639.

Switch to anti-TNF biologics or non-TNF biologics

Reassess orif any adverse

event

Reassess orif non-seriousadverse event

Add or switch toabatacept orrituximab

MTX monotherapy or combination DMARD therapy(including double or triple therapy)

DMARD monotherapy

Reassess

Add MTX, HCQ orLEF

(as appropriate)

Add orswitch toanotherDMARD

Switch to another type or category of anti-TNF or non-TNF biologics

Switch to a non-TNFbiologic

Add or switch to anti-TNF biologics

If seriousadverse event

Reassess

Low disease activitywith poor prognosis or

moderate/highdisease activity

Low disease activitywithout

poor prognosis

Reassess

Reassess

Reassess

Crystal arthropathies

Gout

Definition

Gout is an inflammatory disorder characterised by the deposition of monosodium urate (MSU) crystals in articular and peri-articular structures (Punzi et al. 2012). It is often associated with co-morbidities such as cardiovascular disease, chronic kidney disease, obesity and type 2 diabetes (Robinson & Horsburgh 2014).

%�&��'()*+)(,��-(��"��*)* 0121).*/��34+64.)��5

�� !� �� "�#�� "�� $��"

Sample

proofs

@ Else

vier A

ustrali

a


Further tests to confirm diagnosis include blood tests to ascertain the presence of raised urate and analysis of joint aspirate.Pharmacological management

Management involves providing rapid pain relief for acute attacks, preventing further attacks and preventing the complications of gout such as the formation of gouty tophi and destructive arthritis.

Acute gout treatment focuses on treating the inflammation only, with the following agents used:◆ NSAIDs with indomethacin being the agent of choice (see Table 5.12 later)◆ colchicine – use is limited by adverse effects (see Table 5.17 later)◆ corticosteoids, oral or intraarticular (if more than one joint is involved or

NSAIDs are contraindicated) – see Table 5.15.Any changes to allourinol or probenecid therapy must be avoided during an

attack, as sudden changes in uric acid concentrations can precipitate further acute attacks.

Urate lowering therapy with allopurinol can be commenced once the attack has settled and appropriate lifestyle factors or medication changes have been made. The aim is to reduce the plasma urate level to <0.3 mmol/L, and monthly blood test are recommended to allow appropriate dose adjustment. During the initiation and dose titration period, concurrent treatment with cholchicine or an NSAID is recommended to prevent an acute exacerbation. Oral prednis(ol)one can be used in patients in whom NSAID or colchicine is contraindicated (Therapeutic Guidelines Limited 2010g).

Some patients do develop an asymptomatic hyperuricaemia due to genetic factors, medication or concurrent medical problems. These patients should not be treated with urate lowering therapy unless they develop gout symptoms (Therapeutic Guidelines Limited 2010g).

For further pain management information see Chapter 7.

Joint conditions

Adhesive capsulitis

Definition

A disorder that affects the capsule of the glenohumeral joint, it is generally accepted that adhesive capsulitis is divided into three stages: 1) the painful stage, 2) the adhesive phase and 3) the resolution stage (Walmsley, Osmotherly & Rivett 2014).


Analgesia

Simple oral analgesic such as paracetamol and NSAIDs should be used first line (see Tables 5.11 and 5.12). Limited evidence suggests that topical NSAIDs are not effective in adhesive capsulitis. If pain persists despite simple analgesia, and it is interfering with the activities of daily living, immediate release opioids (codeine, tramadol or oxycodone) can be considered for short-term use, with an active

%�&��'()*+)(,��-(��"��*)) 0121).*/��34+64.)��5

�� !� �� "�#�� "�� $��"

Sample

proofs

@ Else

vier A

ustrali

a


Med

icati

on

Mech

an

ism

of

acti

on

Ind

ica

tio

ns

fo

r

the

rap

eu

tic

us

eC

om

mo

n s

ide

eff

ec

tsP

rac

tic

e p

oin

tsC

om

mo

n a

du

lt, c

hild

do

sa

ge

ra

ng

es

Para

ceta

mol

(T

hera

peut

ic

Gui

delin

es L

imite

d 20

10a,

201

2a)

Inhi

bits

syn

thes

is o

f pr

osta

glan

dins

in th

e hy

poth

alam

us a

nd

spin

e an

d in

hibi

ts

indu

cibl

e ni

tric

oxid

e sy

nthe

sis

in

mac

roph

ages

Trea

tmen

t of m

ild to

m

oder

ate

pain

, pa

rticu

larly

pai

n or

igin

atin

g in

sof

t tis

sue

and

mus

culo

skel

etal

sy

stem

sM

ay a

lso

be u

sed

in

conj

unct

ion

to re

duce

th

e ov

eral

l dai

ly d

oses

of

NSA

IDs

or o

pioi

ds

requ

ired,

and

thus

the

risk

of th

eir a

dver

se

effe

cts

Rai

sed

amin

otra

nsfe

rase

sH

epat

otox

icity

hype

rsen

sitiv

ity

reac

tions

,ne

utro

peni

a,

thro

mbo

cyto

peni

a,

panc

ytop

enia

, acu

te

hepa

titis

If pa

race

tam

ol a

lone

is

inad

equa

te fo

r tre

atin

g pa

in,

addi

ng a

n N

SAID

may

pro

vide

ad

ditio

nal a

nalg

esia

and

allo

w

use

of lo

wer

or i

nter

mitt

ent d

oses

of

NSA

IDAv

aila

ble

in m

any

diffe

rent

form

s an

d in

com

bina

tion

with

man

y ot

her a

nalg

esic

sAl

way

s ta

ke c

are

not t

o du

plic

ate

ther

apy

or e

xcee

d m

axim

um

reco

mm

ende

d da

ily d

ose

of

para

ceta

mol

Adul

t, ch

ild >

12 y

ears

, ora

l/rec

tal:

0.5–

1 g

ever

y 4–

6 ho

urs

(max

imum

4 g

da

ily)

Con

trolle

d re

leas

e 13

30 m

g ev

ery

6–8

hour

s (m

axim

um 3

990

mg/

day)

Chi

ldre

n, o

ral/r

ecta

l:15

mg/

kg e

very

4–6

hou

rs

Not

e: A

lso

avai

labl

e as

IV p

repa

ratio

n –

dose

d at

the

sam

e do

seO

nset

of p

ain

relie

f is:

• 30

min

utes

afte

r ora

l dos

ing

• 5–

10 m

inut

es a

fter s

tarti

ng IV

infu

sion

Rec

tal a

bsor

ptio

n ca

n be

var

iabl

e

NSA

ID, n

on-s

tero

idal

ant

i-infl

amm

ator

y.Ad

apte

d fro

m: A

ustra

lian

Med

icin

es H

andb

ook

Pty

Ltd,

201

5. A

ustra

lian

Med

icin

es H

andb

ook

(onl

ine)

. Aus

tralia

n M

edic

ines

Han

dboo

k Pt

y Lt

d, A

dela

ide.

<ht

tp://

amho

nlin

e.am

h.ne

t.au/>.

T

AB

LE

5.1

1

De

tail

ed

de

scri

pti

on

of

pa

race

tam

ol

%�&��'()*+)(,��-(��"��*32 0121).*/��34+64.3��5

�� !� �� "�#�� "�� $��"

Sample

proofs

@ Else

vier A

ustrali

a


Med

icati

on

Mech

an

ism

of

acti

on

Ind

ica

tio

ns

fo

r

the

rap

eu

tic

us

eC

om

mo

n s

ide

eff

ec

tsP

rac

tic

e p

oin

tsC

om

mo

n a

du

lt, c

hild

do

sa

ge

ra

ng

es

CL

AS

S:

No

n-s

tero

idal

an

ti-i

nfl

am

mato

ry

(NS

AID

s) (

Ther

apeu

tic

Gui

delin

es L

imite

d 20

10a)

No

n-s

ele

cti

ve N

SA

IDs

Dic

lofe

nac

Ibup

rofe

nIn

dom

etha

cin

Keto

prof

enKe

toro

lac

Mef

enam

ic a

cid

Nap

roxe

nPi

roxi

cam

Sulin

dac

Sele

cti

ve N

SA

IDs

(CO

X-2

in

hib

ito

rs)

Cel

ecox

ibEt

oric

oxib

Mel

oxic

amPa

reco

xib

Prev

ent p

rodu

ctio

n of

pro

stag

land

ins

by in

hibi

ting

cycl

o-ox

ygen

ase

(CO

X) to

pro

duce

an

ti-in

flam

mat

ory,

an

alge

sic

and

antip

yret

ic

func

tions

CO

X is

pre

sent

as

CO

X-1

and

CO

X-2

CO

X-1

inhi

bitio

n ca

uses

impa

ired

gast

ric p

rote

ctio

n an

d an

tipla

tele

t ef

fect

sC

OX-

2 in

hibi

tion

caus

es

anti-

infla

mm

ator

y an

d an

alge

sic

actio

nA

redu

ctio

n in

re

nal f

unct

ion

occu

rs w

ith b

oth

CO

X-1

and

CO

X-2

inhi

bitio

nM

ost N

SAID

s ar

e no

n-se

lect

ive

(inhi

bitin

g bo

th

CO

X-1

and

CO

X-2)

Pain

due

to

infla

mm

atio

n,

tissu

e in

jury

and

in

flam

mat

ory

arth

ropa

thie

s

Nau

sea,

dys

peps

ia, G

I ul

cera

tion

or b

leed

ing,

ra

ised

live

r enz

ymes

(e

spec

ially

dic

lofe

nac)

, di

arrh

oea,

hea

dach

e,

dizz

ines

s, s

alt a

nd fl

uid

rete

ntio

n, h

yper

tens

ion

Use

pre

caut

ion

in p

atie

nts

with

th

e fo

llow

ing:

• ca

rdio

or c

ereb

rova

scul

ar

dise

ase

• ac

tive

GIT

dis

ease

• hi

stor

y of

NSA

ID-in

duce

d hy

pers

ensi

tivity

reac

tions

• pr

e-ex

istin

g re

nal d

isea

se, o

r co

ncur

rent

use

of n

ephr

otoc

xic

med

icat

ions

• he

patic

• el

derly

• de

hydr

atio

n•

asth

ma

• co

agul

atio

n di

sord

ers

or

conc

urre

nt a

ntic

oagu

lant

or

antip

late

let m

edic

atio

ns•

preg

nanc

y an

d br

east

feed

ing

Dos

e re

duct

ion

may

be

re

quire

d in

:•

rena

l dis

ease

• he

patic

dis

ease

• el

derly

Very

littl

e di

ffere

nce

in

anti-

infla

mm

ator

y re

spon

se

betw

een

diffe

rent

NSA

IDs,

so

choi

ce o

f age

nt d

epen

ds o

n in

divi

dual

resp

onse

and

tole

ranc

eTh

ere

is n

o ra

tiona

le fo

r usi

ng

mor

e th

an o

ne N

SAID

at a

tim

e (e

xclu

ding

low

-dos

e as

pirin

)

Ce

lec

ox

ib

Adul

t ora

l:20

0–30

0 m

g da

ily in

1–2

dos

esD

o no

t use

>20

0 m

g da

ily lo

ng te

rmH

alf-l

ife: 4

–15

hour

sD

iclo

fen

ac

Adul

t ora

l/rec

tal:

75–1

50 m

g da

ily in

2 o

r 3 d

oses

(max

imum

20

0 m

g da

ily)

Chi

ld >

1 ye

ar o

ral/r

ecta

l:0.

5–1

mg/

kg (m

axim

um 5

0 m

g) 2

or 3

tim

es

daily

Topi

cal:

1% g

el, r

ub in

to th

e af

fect

ed a

rea

3 or

4

times

dai

lyH

alf-l

ife:1

–2 h

ours

Eto

ric

ox

ib

Adul

t ora

l:30

–120

mg

once

dai

lyH

alf-l

ife: 2

2 ho

urs

Ibu

pro

fen

Adul

t ora

l:20

0–40

0 m

g 3

or 4

tim

es a

day

(max

imum

2.

4 g

daily

)C

hild

>3

mon

ths,

ora

l:5–

10 m

g/kg

(max

imum

400

mg)

3 o

r 4

times

a d

ay.

Topi

cal a

dult,

chi

ld >

12 y

ears

:ru

b 4–

10 c

m in

to th

e af

fect

ed a

rea

if ne

eded

, up

to 4

tim

es d

aily

T

AB

LE

5.1

2

De

tail

ed

de

scri

pti

on

of

no

n-s

tero

ida

l a

nti

-in

fla

mm

ato

rie

s (N

SA

IDS

)

%�&��'()*+)(,��-(��"��*+. 0121).*/��34+64.3��5

�� !� �� "�#�� "�� $��"

Sample

proofs

@ Else

vier A

ustrali

a


Cont

inue

d

Med

icati

on

Mech

an

ism

of

acti

on

Ind

ica

tio

ns

fo

r

the

rap

eu

tic

us

eC

om

mo

n s

ide

eff

ec

tsP

rac

tic

e p

oin

tsC

om

mo

n a

du

lt, c

hild

do

sa

ge

ra

ng

es

CO

X-2

sele

ctiv

e in

hibi

tors

hav

e m

inim

al e

ffect

on

CO

X-1,

but

they

ar

e st

ill as

soci

ated

w

ith G

I sid

e ef

fect

s at

ther

apeu

tic

dose

s

Abou

t 60%

of p

atie

nts

will

resp

ond

to a

ny N

SAID

; tho

se

who

do

not r

espo

nd to

one

may

re

spon

d to

ano

ther

To re

duce

com

plic

atio

ns:

• try

a to

pica

l NSA

ID b

efor

e us

ing

one

oral

ly•

use

the

low

est e

ffect

ive

dose

fo

r the

sho

rtest

per

iod

of ti

me

• us

e pa

race

tam

ol to

ena

ble

low

er d

oses

of N

SAID

Hal

f-life

:2–2

.5 h

ours

Ind

om

eth

ac

in

Adul

t ora

l:25

–50

mg

2–4

times

dai

lyAd

ult r

ecta

l:10

0 m

g on

ce o

r tw

ice

daily

Chi

ld o

ral:

Initi

ally

0.5

–1 m

g/kg

twic

e da

ily (m

axim

um

of 4

mg/

kg)

Hal

f-life

: 4.5

–6 h

ours

Ke

top

rofe

n

Adul

t, or

al:

200

mg

once

dai

lyAd

ult,

rect

al:

100

mg

at b

edtim

eTo

pica

l:Ap

ply

to th

e af

fect

ed a

rea

2–4

times

dai

lyH

alf-l

ife: 1

.5–2

hou

rsK

eto

rala

c

Adul

t, IM

/IV:

10 m

g fo

llow

ed b

y 10

–30

mg

ever

y 4–

6 ho

urs

(max

imum

90

mg

daily

)Ad

ult,

oral

:10

mg

ever

y 4–

6 ho

urs

(max

imum

40

mg

daily

)H

alf-l

ife: 4

–6 h

ours

Me

fen

am

ic a

cid

Adul

t, or

al:

Up

to 5

00 m

g 3

times

dai

lyH

alf-l

ife: 3

–4 h

ours

%�&��'()*+)(,��-(��"��*+* 0121).*/��34+64.3��5

�� !� �� "�#�� "�� $��"

Sample

proofs

@ Else

vier A

ustrali

a


Med

icati

on

Mech

an

ism

of

acti

on

Ind

ica

tio

ns

fo

r

the

rap

eu

tic

us

eC

om

mo

n s

ide

eff

ec

tsP

rac

tic

e p

oin

tsC

om

mo

n a

du

lt, c

hild

do

sa

ge

ra

ng

es

Me

lox

ica

m

Adul

t, or

al:

7.5–

15 m

g on

ce d

aily

Hal

f-life

: 20

hour

sN

ap

rox

en

Adul

t, or

al:

Con

vent

iona

l pro

duct

, 250

–500

mg

twic

e da

ilyC

ontro

lled

rele

ase

prod

uct,

750–

1000

mg

once

dai

ly (u

p to

a m

axim

um o

f 125

0 m

g da

ily)

Chi

ld >

2 ye

ars,

ora

l:5–

7.5

mg/

kg (m

axim

um 5

00 m

g) tw

ice

daily

Hal

f-life

: 12–

15 h

ours

Pa

rec

ox

ib

Adul

t, IM

/IV:

40 m

g si

ngle

dos

eH

alf-l

ife: 6

.5–7

hou

rs (a

ctiv

e m

etab

olite

)P

iro

xic

am

Adul

t, or

al:

10–2

0 m

g on

ce d

aily

, usu

ally

for n

o m

ore

than

14

days

Topi

cal:

Appl

y to

the

affe

cted

are

a 3

or 4

tim

es

daily

.H

alf-l

ife: 3

0–50

hou

rsS

ulin

da

c

Adul

t, or

al:

200–

400

mg

daily

in 1

or 2

dos

esH

alf-l

ife:1

6 ho

urs

(act

ive

met

abol

ite)

Adap

ted

from

: Aus

tralia

n M

edic

ines

Han

dboo

k Pt

y Lt

d, 2

015.

Aus

tralia

n M

edic

ines

Han

dboo

k (o

nlin

e). A

ustra

lian

Med

icin

es H

andb

ook

Pty

Ltd,

Ade

laid

e. <

http

://am

honl

ine.

amh.

net.a

u/>.

T

AB

LE

5.1

2

De

tail

ed

de

scri

pti

on

of

no

n-s

tero

ida

l a

nti

-in

fla

mm

ato

rie

s (N

SA

IDS

)—co

nt’

d

%�&��'()*+)(,��-(��"��*+) 0121).*/��34+64.3��5

�� !� �� "�#�� "�� $��"

Sample

proofs

@ Else

vier A

ustrali

a


Med

icati

on

Mech

an

ism

of

acti

on

Ind

ica

tio

ns

fo

r

the

rap

eu

tic

us

e

Co

mm

on

sid

e

eff

ec

tsP

rac

tic

e p

oin

tsC

om

mo

n a

du

lt, c

hild

do

sa

ge

ra

ng

es

CL

AS

S:

Op

ioid

s

Op

ioid

s u

sed

in

MS

K

co

nd

itio

ns:

Cod

eine

Dex

tropr

opox

yphe

neFe

ntan

ylM

orph

ine

Oxy

codo

neTr

amad

ol

Activ

ate

opio

id

rece

ptor

s in

the

cent

ral a

nd

perip

hera

l ne

rvou

s sy

stem

s to

pr

oduc

e an

alge

sia,

re

spira

tory

de

pres

sion

, se

datio

n an

d co

nstip

atio

n

Acut

e or

chr

onic

pa

inN

ause

a an

d vo

miti

ng,

dysp

epsi

a,

drow

sine

ss,

dizz

ines

s,

head

ache

, or

thos

tatic

hy

pote

nsio

n,

itch,

dry

mou

th,

mio

sis,

urin

ary

rete

ntio

n,

cons

tipat

ion

Use

with

cau

tion

in th

e fo

llow

ing

patie

nt g

roup

s:•

unco

rrect

ed e

ndoc

rine

abno

rmal

ities

, hy

poth

yroi

dism

, adr

enoc

ortic

al

insu

ffici

ency

, acu

te a

lcoh

olis

m,

mya

sthe

nia

grav

is, C

NS

depr

essi

on•

epile

psy

or a

reco

gnis

ed ri

sk fo

r se

izur

e•

rais

ed in

tracr

ania

l pre

ssur

e•

hypo

tens

ion,

sho

ck•

phae

ochr

omoc

ytom

a•

gast

roin

test

inal

ileu

s•

resp

irato

ry d

epre

ssio

n•

rena

l im

pairm

ent

• he

patic

impa

irmen

t•

elde

rly•

preg

nanc

y an

d br

east

feed

ing

Avai

labl

e in

man

y di

ffere

nt d

ose

form

s (im

med

iate

rele

ase,

slo

w re

leas

e,

mix

ture

s, ta

blet

s, s

ache

ts, c

apsu

les)

; ta

ke c

are

to a

lway

s se

lect

the

corre

ct

dose

form

Alw

ays

use

a re

gula

r lax

ativ

e fo

r pe

ople

requ

iring

regu

lar o

pioi

ds to

pr

even

t con

stip

atio

nPh

ysic

al d

epen

denc

e is

com

mon

Rec

omm

ende

d do

ses

are

for t

hose

th

at a

re o

pioi

d na

ive

Patie

nts

with

a h

isto

ry o

f opi

oid

use

may

requ

ire h

ighe

r dos

es

Co

de

ine

Adul

t, or

al:

30–6

0 m

g ev

ery

4 ho

urs

if ne

eded

(max

imum

24

0 m

g in

24

hour

s)C

hild

>1

year

, ora

l:0.

5–1

mg/

kg e

very

4–6

hou

rs if

nee

ded

(max

imum

24

0 m

g in

24

hour

s)D

urat

ion

of a

ctio

n: 3

–4 h

ours

Prac

tice

poin

ts:

• av

aila

ble

in fi

xed

dose

com

bina

tions

with

asp

irin,

ib

upro

fen

and

para

ceta

mol

• co

dein

e (a

pro

drug

) is

met

abol

ised

to m

orph

ine;

pe

ople

with

nor

mal

cod

eine

met

abol

ism

m

etab

olis

e 30

mg

of c

odei

ne to

app

roxi

mat

ely

4.5

mg

of m

orph

ine

• m

etab

olis

ed b

y C

YP2D

6 w

hich

has

gen

etic

va

riatio

n, re

sulti

ng in

som

e pa

tient

s be

ing

ultra

-rapi

d m

etab

olis

ers

incr

easi

ng th

eir r

isk

of

toxi

city

and

som

e be

ing

slow

met

abol

iser

s w

ho

do n

ot m

etab

olis

e su

ffici

ent c

odei

ne to

hav

e a

bene

ficia

l effe

ct

T

AB

LE

5.1

3

De

tail

ed

de

scri

pti

on

of

op

ioid

s

Cont

inue

d

%�&��'()*+)(,��-(��"��*+3 0121).*/��34+64.3��5

�� !� �� "�#�� "�� $��"

Sample

proofs

@ Else

vier A

ustrali

a


Med

icati

on

Mech

an

ism

of

acti

on

Ind

ica

tio

ns

fo

r

the

rap

eu

tic

us

e

Co

mm

on

sid

e

eff

ec

tsP

rac

tic

e p

oin

tsC

om

mo

n a

du

lt, c

hild

do

sa

ge

ra

ng

es

De

xtr

op

rop

ox

yp

he

ne

pra

cti

ce

po

ints

Do

not u

se b

ecau

se:

• ev

iden

ce fo

r use

is la

ckin

g; n

o be

nefit

ove

r reg

ular

par

acet

amol

w

hen

used

in c

ombi

natio

n w

ith

regu

lar p

arac

etam

ol•

regu

lar u

se m

ay le

ad to

ac

cum

ulat

ion

of a

nd th

e ca

rdio

toxi

c no

rdex

tropr

opox

yphe

ne•

very

toxi

c in

acu

te o

verd

osag

e•

regu

lar m

onito

ring

of re

nal f

unct

ion

and

ECG

s m

ust b

e pe

rform

ed

De

xtr

op

rop

ox

yp

he

ne

:Ad

ult,

oral

:10

0 m

g ev

ery

4 ho

urs

whe

n ne

cess

ary

(max

imum

60

0 m

g da

ily)

All p

rodu

cts

have

bee

n w

ithdr

awn

from

the

mar

ket

in s

ever

al c

ount

ries

due

to s

afet

y co

ncer

ns; i

t is

still

avai

labl

e in

Aus

tralia

, but

rest

rictio

ns fo

r pre

scrib

ing

exis

t (ht

tp://

ww

w.tg

a.go

v.au

.atla

ntis

2.an

u.ed

u.au

:204

8/al

ert/

dext

ropr

opox

yphe

ne-p

ain-

kille

rs-c

onta

inin

g-de

xtro

prop

oxyp

hene

-di-g

esic

-and

-dol

oxen

e-10

-oc

tobe

r-201

3)

Fe

nta

ny

l p

rac

tic

e p

oin

ts

Also

ava

ilabl

e in

pat

ch a

nd lo

zeng

e fo

rm, w

hich

are

use

d in

chr

onic

pai

n

Fe

nta

ny

l – a

cu

te p

ain

:Fo

r use

in c

hron

ic p

ain

(see

Cha

pter

7)

Adul

t, su

bcut

aneo

us:

Ag

e (

ye

ars

)In

itia

l d

os

e (

in m

cg

)

ev

ery

4 h

ou

rs a

s r

eq

uir

ed

<39

100–

200

40–5

975

–150

60–6

940

–100

70–8

540

–75

>85

year

s30

–50

Intra

nasa

l, ch

ild 1

–12

year

s:1.

5 m

cg/k

g (m

axim

um 1

00 m

cg);

if ne

eded

, a

seco

nd d

ose

of 0

.75–

1.5

mcg

/kg

(max

imum

10

0 m

cg) m

ay b

e gi

ven

afte

r 5–1

0 m

inut

esD

urat

ion

of a

ctio

n: 0

.5–2

hou

rs

T

AB

LE

5.1

3

De

tail

ed

de

scri

pti

on

of

op

ioid

s—co

nt’

d

%�&��'()*+)(,��-(��"��*++ 0121).*/��34+64.3��5

�� !� �� "�#�� "�� $��"

Sample

proofs

@ Else

vier A

ustrali

a


ed

icati

on

Mech

an

ism

of

acti

on

Ind

ica

tio

ns

fo

r

the

rap

eu

tic

us

e

Co

mm

on

sid

e

eff

ec

tsP

rac

tic

e p

oin

tsC

om

mo

n a

du

lt, c

hild

do

sa

ge

ra

ng

es

Mo

rph

ine

pra

cti

ce

po

ints

Peak

ana

lges

ia fo

llow

ing

a do

se o

f m

orph

ine

occu

rs w

ithin

:•

60 m

inut

es a

fter c

onve

ntio

nal o

ral

liqui

d•

50–9

0 m

inut

es a

fter S

C in

ject

ion

(30–

60 m

inut

es a

fter I

M)

• 20

min

utes

afte

r IV

inje

ctio

nD

o no

t use

con

trolle

d re

leas

e pr

oduc

ts

for a

cute

pai

n m

anag

emen

tAv

oid

use

in re

nal i

mpa

irmen

t due

to

accu

mul

atio

n of

toxi

c m

etab

olite

Mo

rph

ine

– a

cu

te p

ain

:Fo

r use

in c

hron

ic p

ain

(see

Cha

pter

7)

Adul

t, ch

ild >

50 k

g, IV

:In

itial

ly, 0

.5–2

mg;

repe

at e

very

3–5

min

utes

and

tit

rate

as

abov

eAd

ult,

child

>50

kg,

SC

/IM:

Ag

e (

ye

ars

)In

itia

l d

os

e (

in m

g)

ev

ery

2 h

ou

rs a

s r

eq

uir

ed

<39

7.5–

12.5

40–5

95–

10

60–6

92.

5–7.

5

70–8

52.

5–5

>85

year

s2–

3

Adul

t, or

al:

Do

not u

se c

ontro

lled

rele

ase

prod

ucts

for t

reat

men

t of

acu

te p

ain

Con

vent

iona

l ora

l pro

duct

, ini

tially

5–1

5 m

g ev

ery

4 ho

urs

Chi

ld (1

–12

year

s an

d <5

0 kg

):IV

infu

sion

: ini

tially

0.0

2–0.

04 m

g/kg

/hou

rIV

bol

us: i

nitia

lly 0

.05

mg/

kg (o

ver a

t lea

st 5

m

inut

es) e

very

2 h

ours

Subc

utan

eous

: 0.1

–0.2

mg/

kg e

very

4 h

ours

Dur

atio

n of

act

ion:

2–4

hour

s (in

ject

ion,

imm

edia

te re

leas

e ta

blet

and

liq

uid)

12–2

4 ho

urs (

mod

ified

rele

ase

tabl

ets a

nd su

spen

sion)

Cont

inue

d

%�&��'()*+)(,��-(��"��*+- 0121).*/��34+64.+��5

�� !� �� "�#�� "�� $��"

Sample

proofs

@ Else

vier A

ustrali

a


Med

icati

on

Mech

an

ism

of

acti

on

Ind

ica

tio

ns

fo

r

the

rap

eu

tic

us

e

Co

mm

on

sid

e

eff

ec

tsP

rac

tic

e p

oin

tsC

om

mo

n a

du

lt, c

hild

do

sa

ge

ra

ng

es

Ox

yc

od

on

e p

rac

tic

e p

oin

ts

May

be

tried

as

an a

ltern

ativ

e op

ioid

fo

r pat

ient

s in

tole

rant

of m

orph

ine

Do

not u

se c

ontro

lled

rele

ase

tabl

ets

for a

cute

pai

n as

slo

w o

nset

and

offs

et

mak

e ra

pid,

saf

e tit

ratio

n im

poss

ible

Ox

yc

od

on

e –

ac

ute

pa

in:

(For

use

in c

hron

ic p

ain

see

Cha

pter

7)

Adul

t IV:

0.5–

2 m

g; re

peat

eve

ry 3

–5 m

inut

esAd

ult,

subc

utan

eous

:

Ag

e (

ye

ars

)In

itia

l d

os

e (

in

mg

) e

ve

ry 2

ho

urs

<39

7.5–

12.5

40–5

95–

10

60–6

92.

5–7.

5

70–8

52.

5–5

>85

year

s2–

3

Adul

t, or

al:

Do

not u

se c

ontro

lled

rele

ase

tabl

ets

for t

reat

men

t of

acu

te p

ain

Con

vent

iona

l ora

l pro

duct

: ini

tially

5–1

5 m

g ev

ery

4 ho

urs

Acut

e pa

in: c

hild

>1

year

,C

onve

ntio

nal o

ral p

rodu

ct: i

nitia

lly 0

.1–0

.2 m

g/kg

(m

axim

um 5

mg)

eve

ry 4

–6 h

ours

Dur

atio

n of

act

ion:

3–4

hour

s (in

ject

ion,

imm

edia

te re

leas

e ta

blet

s,

caps

ules

and

ora

l liq

uid)

12 h

ours

mod

ified

rele

ase

prod

ucts

T

AB

LE

5.1

3

De

tail

ed

de

scri

pti

on

of

op

ioid

s—co

nt’

d

%�&��'()*+)(,��-(��"��*+/ 0121).*/��34+64.+��5

�� !� �� "�#�� "�� $��"

Sample

proofs

@ Else

vier A

ustrali

a


ed

icati

on

Mech

an

ism

of

acti

on

Ind

ica

tio

ns

fo

r

the

rap

eu

tic

us

e

Co

mm

on

sid

e

eff

ec

tsP

rac

tic

e p

oin

tsC

om

mo

n a

du

lt, c

hild

do

sa

ge

ra

ng

es

Tra

ma

do

l p

rac

tic

e p

oin

ts

Anal

gesi

c ef

fect

sta

rts w

ithin

1 h

our o

f or

al a

dmin

istra

tion

and

peak

s at

2–

4 ho

urs

Do

not u

se c

ontro

lled

rele

ase

prod

ucts

fo

r acu

te p

ain

man

agem

ent

6–10

% o

f Cau

casi

ans

and

1–2%

of

Asia

ns la

ck th

e en

zym

e C

YP2D

6;

thes

e pe

ople

may

obt

ain

redu

ced

anal

gesi

a w

ith tr

amad

olR

educ

e do

se in

rena

l, he

patic

im

pairm

ent a

nd th

e el

derly

Tra

ma

do

l

Adul

t, IV

/IM:

50–1

00 m

g ev

ery

4–6

hour

s, u

p to

a to

tal d

aily

dos

e of

600

mg

Adul

t, or

al (c

onve

ntio

nal p

rodu

ct):

50–1

00 m

g ev

ery

4–6

hour

s w

hen

nece

ssar

y (m

axim

um 4

00 m

g da

ily o

r 300

mg

daily

if

>75

year

s)Ad

ult,

oral

(12-

hour

con

trolle

d re

leas

e pr

oduc

t):50

–200

mg

ever

y 12

hou

rs (m

axim

um 4

00 m

g )

Chi

ld >

1 ye

ar, o

ral (

conv

entio

nal p

rodu

ct:

On

ly u

se

d in

ch

ild

ren

un

de

r s

pe

cia

lis

t

su

pe

rvis

ion

1–2

mg/

kg e

very

4 h

ours

whe

n ne

cess

ary

(max

imum

400

mg)

Dur

atio

n of

act

ion:

3–6

hour

s (im

med

iate

rele

ase

caps

ules

and

in

ject

ions

)12

–24

hour

s m

odifi

ed re

leas

e ta

blet

s

CN

S, c

entra

l ner

vous

sys

tem

; MSK

, mus

culo

skel

etal

.Ad

apte

d fro

m: A

ustra

lian

Med

icin

es H

andb

ook

Pty

Ltd,

201

5. A

ustra

lian

Med

icin

es H

andb

ook

(onl

ine)

. Aus

tralia

n M

edic

ines

Han

dboo

k Pt

y Lt

d, A

dela

ide.

<ht

tp://

amho

nlin

e.am

h.ne

t.au/>.

%�&��'()*+)(,��-(��"��*+6 0121).*/��34+64.+��5

�� !� �� "�#�� "�� $��"

Sample

proofs

@ Else

vier A

ustrali

a

Australia Elsevier proofs...

Documents

Transcript of Australia Elsevier proofs...