Guide to Pain Management in Low-Resource Settings

Are the symptoms a “normal”            
consequence of her fracture?
After the application of a looser cast and the prescription 
of pain medication, the pain was tolerable, even though 
her fi ngers remained swollen. Six weeks later, the cast was 
removed, and physiotherapy commenced. A few days lat-
er, Etta reported an increase in swelling after the removal 
of the cast and said she felt a stinging, partly burning pain 
circularly around the wrist, radiating to the fi ngers. Fur-
thermore, the movement of her fi ngers was reduced; the 
hand was shiny, swollen, and blueish-reddish.
Once again, is this a “normal”            
consequence of her fracture?
Dr. Jones, the attending physician, recommended inten-
sifying the physical treatment and increasing the doses 
of the pain medication. During intensifi cation of physi-
cal therapy, Etta’s fi ngers were trained forcefully, which 
was very painful. With exercise, the pain and swelling 
increased, and the hand was still bluish-reddish colored 
and shiny. Moreover, Etta noticed an increased growth 
of her fi nger nails and the hair on the dorsum of her left 
hand. Although physical therapy was intensifi ed, the lack 
of mobility of the fi ngers worsened, the hand was con-
stantly swollen, and the pain was burning and almost 
unbearable, at rest as well as during movement. Etta be-
came desperate, and Dr. Jones was at the limit of his wis-
dom on how to help her.
What should be done?                                         
Why has Dr. Jones’ therapy failed?
Six weeks passed, and Dr. Jones referred Etta to a pain 
management center. She was still complaining about 
the pain, which at that point was radiating to the fore-
arm and elbow as well. Additionally, she reported strong 
functional defi cits in the hand (it was not possible to 
make a fi st, and the fi nger-palm distance was 10 cm). 
In the past few days, she had also noticed a restriction 
in the shoulder movements (especially abduction). Dr. 
Ndungu, the attending doctor from the pain center, rec-
ognized the problem and recommended an appropriate 
treatment; Etta was lucky.

Complex Regional Pain Syndrome
251
What are Dr. Ndungu’s options                            
for further diagnostic procedures?
Based on the diagnostic criteria defi ned by IASP (see 
below) and the course of the disease, Dr. Ndungu diag-
nosed a complex regional pain syndrome. Upon start of 
the treatment at the pain center, he explained to Etta 
the disease pattern and the principles of therapy, which 
require her active cooperation, understanding, and pa-
tience because progress may be slow, with relapses and 
periods of stagnation. He prescribed Etta a splint and 
recommended that she position the hand and the fore-
arm higher than the heart, until the edema is reduced. 
Coxibs (celecoxib) and anticonvulsants (gabapentin) 
were prescribed as pain medications. Physical and occu-
pational therapy was started one week after the decrease 
of the edema and the pain at rest.
Are there any other therapeutic options?    
What are the main rules for therapy?
At the beginning of physical therapy, focus was put on 
the shoulder, and 2 weeks later, normal mobility was re-
gained. Th
  e progress of improvement in hand function 
was much slower. As soon as Etta exercised too strongly 
with her hand or used it for household tasks, the edema 
developed again and the pain became stronger. After ap-
proximately 3 months, with physical and occupational 
therapy, Etta was able to achieve an improvement in 
hand function and a reduction in pain. It took 6 more 
months before she was able to return to her offi
  ce and op-
erate her computer with her left hand.
Was this a typical course of CRPS?
Th
  is case exemplifi es a typical course of CRPS with re-
spect to sex, age, injury, and symptoms. However, espe-
cially in the early stages of the disease, it is often diffi
  -
cult to diff erentiate between the symptoms of CRPS and 
the normal or slightly delayed fracture healing. Th
 e di-
agnosis of CRPS is possible only after the development 
of typical symptoms, such as an impairment of sensory, 
vasomotor, motor, and sudomotor function. In Etta’s 
case, attention should be focused on two typical clini-
cal phenomena: fi rst, the negative infl uence of forced 
physical exercises on the further course of the disease, 
and second, the commonly observed involvement of the 
shoulder during the course of the disease. Th
 e mobility 
of the elbow joint is mostly unaff ected, whereas abduc-
tion and rotation of the shoulder joint are often dis-
abled. Patience and individually adjusted physical activ-
ity are essential requirements for patients.
What are the clinical           
symptoms of CRPS?
Th
  e clinical pattern of CRPS is characterized by sen-
sory, motor, and autonomic impairment. Additionally, 
patients with CRPS often feel as if the hand or the foot 
does not belong to them anymore or as if it is not per-
ceptible or controllable; movements can only be per-
formed under direct visual control (“neglect-like syn-
drome”). Furthermore, the following features occur in 
almost all cases:
• Th
  e impairment due to CRPS is disproportionate 
to the inciting event.
• Th
 ere is a tendency for a distal generalization 
for all symptoms, i.e., not a single fi nger, but the 
whole hand is aff ected, and the hand is more 
strongly aff ected than the forearm.
• Th
  e joint and soft tissue structures are also aff ect-
ed, with according mobility impairment.
•  An edema, depending on position and physi-
cal activity, usually occurs, especially in the early 
stages of the disease.
Sensory impairment: Spontaneous pain and hy-
peralgesia in the hand or foot, which is not restricted to 
the supply area of a single peripheral nerve, are main 
characteristics of the clinical pattern of CRPS. Th
 e pain 
is described as burning and is felt in the deep tissues; 
additionally, sudden pain attacks, described like electri-
cal shocks, are often present. A periarticular pressure 
pain of the fi nger joints is almost always present. As a 
rule, strong hypersensitivity to mild painful stimuli (hy-
peralgesia) or pain following usually nonpainful stimuli 
(allodynia) can be observed.
Motor impairment: In 90% of all cases, the vol-
untary motor function of all distal muscles is impaired. 
Complex movements, such as fi st closure or fi nger-
thumb opposition, are restricted. Th
  ese movements are 
only possible under visual control. Approximately 50% 
of patients with involvement of the upper limb develop 
a tremor; dystonia or spasticity is seldom found.
Autonomic impairment: Skin temperature dif-
ferences of more than 2°C between the aff ected  and 
the unaff ected extremity are often present (the aff ected 
side is warmer in about 75% of cases), and they corre-
spond to an altered skin blood fl ow. About 60% of pa-
tients have hyperhidrosis, and 20% have hypohidrosis. 
In the early stages, hair and nail growth on the aff ected 
extremity is often increased, in the further course of the 
disease it is often decreased. Dystrophic symptoms (i.e., 

252
Andreas Schwarzer and Christoph Maier
skin and muscle atrophy, connective tissue fi brosis) are 
typical for the later stages of the disease; however, they 
are not always found.
What are the diagnostic           
criteria for CRPS?
CRPS is a clinical diagnosis. Th
 ere are no laboratory 
parameters that confi rm the presence or absence of the 
disease. Patchy demineralization especially in the peri-
articular regions appears in the radiography some weeks 
or months after the disease begins, but it can be seen in 
less than 50% of patients with CRPS. CT and MRI ex-
aminations are not specifi c for the diagnosis of CRPS. 
However, triple-phase bone scintigraphy plays an im-
portant role for the diagnosis of CRPS during the fi rst 
year after trauma. Band-shaped increased radionuclide 
accumulation in the metacarpophalangeal and interpha-
langeal joints of the aff ected extremity during the min-
eralization phase is a very specifi c diagnostic criterion.
Th
  e current diagnostic criteria are listed below 
according to Harden and Bruehl [3]. Aside from diff er-
entiation between sensory, vasomotor, sudomotor, and 
motor impairment, the physician should discriminate 
between anamnestic hints (symptoms) and current clin-
ical signs during the physical examination.
What is the diff erential       
diagnosis for CRPS?
In the clinical routine, it is most essential to diff erenti-
ate between CRPS and a delayed healing of a trauma 
or complaints after long-term immobilization. In the 
case of CRPS, not only an increase in pain intensity, 
but also a change in the characteristics of pain usually 
occurs. Diff erential diagnosis is nerve or plexus injury, 
especially after an operation to treat nerve entrapment 
syndromes (carpal tunnel syndrome). However, in these 
cases, the symptoms are limited to the area supplied 
by the injured nerve. Autonomic impairment does not 
prove the diagnosis of CRPS. Furthermore, self-injuri-
ous behavior is another diff erential diagnosis to CRPS.
What are the treatment          
options for CRPS?
Th
  e treatment of CRPS should be based on a multidisci-
plinary approach. Next to pain treatment, the recovery 
of limb function should play an important role.
Pharmacological options: Traditional NSAIDs 
(ibuprofen 3 × 600 mg) or COX-2 inhibitors (celecox-
ib 2 × 200 mg) can be taken temporarily for treatment 
of CRPS pain. Additionally, metamizol (4 × 1000 mg) 
Table 1
Diagnostic criteria for CRPS (according to Harden and Bruehl [3])
1
Persistent pain, which is disproportionate to any known inciting event
2
Th
  e patient must report at least one symptom in three of the following categories (anamnestic hints):
2.1
Sensory
Reports of hyperesthesia and/or allodynia
2.2
Vasomotor
Reports of temperature asymmetry and/or skin color changes and/or skin 
color asymmetry
2.3
Sudomotor/edema
Reports of edema and/or sweating changes and/or sweating asymmetry
2.4
Motor/trophic
Reports of decreased range of motion and/or motor dysfunction (weakness, 
tremor, dystonia) and/or trophic changes (hair, nails, skin)
3
Th
  e patient must display at least one sign in two or more of the following categories during the current 
physical examination:
3.1
Sensory
Evidence of hyperesthesia and/or allodynia
3.2
Vasomotor
Evidence of temperature asymmetry and/or skin color changes and/or skin 
color asymmetry
3.3
Sudomotor/edema
Evidence of edema and/or sweating changes and/or sweating asymmetry
3.4
Motor/trophic
Evidence of decreased range of motion and/or motor dysfunction (weakness, 
tremor, dystonia) and/or trophic changes (hair, nails, skin)
4
Th
  ere is no other diagnosis that would otherwise account for the signs and symptoms and the degree of 
pain and dysfunction. 

Complex Regional Pain Syndrome
253
and opioids (controlled-release) can be prescribed. Th
 e 
most important adjuvants for the treatment of neuro-
pathic pain are tricyclic antidepressants (amitriptyline) 
and anticonvulsive drugs (gabapentin). After taking into 
consideration their possible contraindications and their 
anticholinergic eff ects, the physician should increase 
the dose slowly. Furthermore, the dose should be high 
enough before its effi
  cacy is evaluated. Th
  e dose of ami-
triptyline should be initially 25 mg in the evening (alter-
natively 10 mg). Th
  e dose can be increased every seven 
days in 25-mg steps up to a maximal dose of 75 mg. Th
 e 
starting dose of gabapentin is 3 × 100 mg, and the dose 
should be increased in 300-mg steps every three days. 
A dose of at least 1800 mg/d should be achieved. Espe-
cially in cases of arthrogenic pain (particularly during 
physical examination), oral glucocorticoids are indicat-
ed (prednisolone in decreasing doses of 90/60/30/10/5 
mg for 14 days).
Invasive therapies:  Th
 e  sympathetic  nervous 
system can be blocked either by unilateral anesthetic 
blockades of the lower cervical sympathetic ganglion 
(stellate ganglion) (10–15 mL bupivacaine 0,5%) or by 
blocks of the lumbar or thoracic sympathetic chain (5 
mL bupivacaine 0.5%). Intravenous regional anesthe-
sia blocks are seldom performed because of poor eff ect 
and painful procedures. Th
 e indication for a sympa-
thetic block is pain at rest despite immobilization and/
or pronounced allodynia. Sympathetic blocks not only 
reduce the pain, but can often also improve the motor 
and autonomic impairment. However, it is important to 
prove that the sympatholysis was technically successful 
by noting a signifi cant skin temperature increase in the 
supplying area.
Nonpharmacological options: As long as pain 
at rest prevails, therapy should be restricted to consis-
tent immobilization of the aff ected extremity in a po-
sition higher than the heart, supported by a splint and 
by lymphatic drainage. After a distinct decrease of the 
pain, physical and occupational therapy come to the 
fore. Initially, the proximal joints of the aff ected and the 
contralateral extremity should be treated. Especially in 
cases of sensory impairment and allodynia, desensitiza-
tion exercises are indicated. Th
  e main treatment prin-
ciple should start with stimulus adaptation, followed by 
exercises aiming at pain-free mobility and improvement 
of fi ne motor skills, and ultimately movements against 
strong resistance.
Th
  erapy for CRPS, with regard to the use of medi-
cal and nonmedical treatment, does not require any 
particular setting and meets the standards of a com-
munity or primary care level. Th
  e application of nerve 
block techniques should be reserved for specialized pain 
management centers (“referral hospital level”). Th
 e ad-
vantage of treatment in specialized pain management 
centers is, besides the reliability of making the diagnosis 
of CRPS and the use of sympathetic blocks, the greater 
experience in dosing the physical and the occupational 
treatment—fi nally, it is perhaps the most essential issue 
for the function recovery of the aff ected extremity.
What are today’s insights about      
the pathophysiology of CRPS?
Currently, there is no global pathophysiological concept 
that explains all the symptoms in CRPS. Th
  ere are sev-
eral possible explanations. Next to hints for a genetic 
predisposition, infl ammation seems to play an impor-
tant role. In the context of a neurogenic infl ammation, 
C fi bers and some receptors may release neuropeptides, 
inducing clinical signs such as vasodilatation and ede-
ma. Additionally, experts are discussing the concept of a 
disease of the central nervous system, in which changes 
of the aff erent neurons, such as pathological connec-
tions with the sympathetic nervous system, may cause 
spontaneous and evoked pain. Th
  e pattern of symptom 
spread resembles that of diseases of the central nervous 
system. Th
  e central nervous dysregulation is assumed 
to result in maladaptation, for example a change in the 
ambient temperature induces an inadequate reaction of 
skin blood fl ow and sudomotor function. Furthermore, 
cortical reorganization processes seem to play an im-
portant role, wherein the degree of the reorganization 
correlates positively with the spread of the mechanical 
hyperalgesia and the pain, which in turn is reversible us-
ing the appropriate treatment.
Pearls of wisdom
• Th
 ree important aspects account for the diag-
nosis of CRPS: pain or functional impairment, 
which is disproportionate to the inciting event; 
hints of sensory, vasomotor, sudomotor, or motor 
impairment in the past; and current fi ndings  of 
sensory, vasomotor, sudomotor, or motor impair-
ment in the clinical examination
• Th
  e treatment must not induce pain. If a treat-
ment procedure leads to escalation of pain, this 
procedure must be given up. Th
  e following three 

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Andreas Schwarzer and Christoph Maier
therapeutic steps should be followed: fi rst, treat-
ment of the pain and edema; second, treatment 
of the pain, allowing movement; and third, treat-
ment of the functional orthopedic impairment.
• Th
  e intensity of physiotherapy must be reduced if 
pain increases again or after a new physical trau-
ma.
References
[1]  Baron R, Schattschneider J, Binder A, Siebrecht D, Wasner G. Relation 
between sympathetic vasoconstrictor activity and pain and hyperalge-
sia in complex regional pain syndromes: a case-control study. Lancet 
2002;359:1655–60.
[2]  Birklein F, Schmelz M. Neuropeptide, neurogenic infl ammation  and 
complex regional pain syndrome (CRPS). Neurosci Lett 2008;437:199–
202.
[3]  Harden RN, Bruehl S. Diagnostic criteria: the statistical derivation of 
the four criterion factors. In: Wilson PR, Stanton-Hicks M, Harden RN, 
editors. CRPS: current diagnosis and therapy, Progress in pain research 
and management, vol. 32. Seattle: IASP Press; 2005.
[4]  Maihöfner C, Handwerker HO, Neundörfer B, Birklein F. Patterns of 
cortical reorganisation in complex regional pain syndrome. Neurology 
2003;61:1707–15.
[5]  Moseley GL. Graded motor imagery for pathologic pain: a randomized 
controlled trial. Neurology 2006;67: 2129–34.
[6]  Nelson DV, Brett RS. Interventional therapies in the management of 
complex regional pain syndrome. Clin J Pain 2006;22:438–42.
[7]  Pleger B, Ragert P, Schwenkreis P, Förster AF, Wilimzig C, Dinse H, 
Nicolas V, Maier C, Tegenthoff  M. Patterns of cortical reorganization 
parallel impaired tactile discrimination and pain intensity in complex 
regional pain syndrome. Neuroimage 2006;32:503–10.
[8]  Rowbotham MC. Pharmacological management of complex regional 
pain syndrome. Clin J Pain 2006;22:425–9.
Websites
http://www.mayoclinic.com/health/complex-regional-pain-syndrome/
DS00265
http://www.iasp-pain.org/AM/Template.cfm?Section=WHO2&Template=/
CM/ContentDisplay.cfm&ContentID=4174

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Guide to Pain Management in Low-Resource Settings, edited by Andreas Kopf and Nilesh B. Patel. IASP, Seattle, © 2010. All rights reserved. Th
  is material may be used for educational 
and training purposes with proper citation of the source. Not for sale or commercial use. No responsibility is assumed by IASP for any injury and/or damage to persons or property 
as a matter of product liability, negligence, or from any use of any methods, products, instruction, or ideas contained in the material herein. Because of the rapid advances in the 
medical sciences, the publisher recommends that there should be independent verifi cation of diagnoses and drug dosages. Th
  e mention of specifi c pharmaceutical products and any 
medical procedure does not imply endorsement or recommendation by the editors, authors, or IASP in favor of other medical products or procedures that are not covered in the text.
Guide to Pain Management in Low-Resource Settings
Dilip Pawar and Lars Garten
Chapter 34
Pain Management in Children
Th
  is chapter will cover the diffi
  culties in treating pain in 
children and provide you with an overview of pharma-
cological and nonpharmacological interventions for ef-
fective pain control in acute pain (injury/trauma-related 
and postoperative pain) and chronic pain (cancer and 
HIV-related pain) in children.
Do children feel pain?
Until recently, many believed that children do not feel 
pain, a belief based on lack of understanding, and on 
fear of using narcotics with potential respiratory depres-
sion and addiction in children, rather than on any sci-
entifi c rationale. Today it is well known that the sensory 
nervous system and pain pathways develop around mid-
gestation, with connections and function maturing over 
the fi rst 3 months after birth.
Th
  ere is no evidence to support the view that pain is 
less intense in neonates and young children due to their 
developing nervous system. However, pain is subjec-
tive, and the pain response is individual and is modifi ed 
through social learning and experience. Early pain expe-
rience plays an important role in shaping an individual’s 
later pain response by alternation in the stress-axis and 
antinociceptive circuitry.
Aren’t children just “little adults”?
Th
  e pediatric age group is heterogeneous, ranging from 
the newborn to the adolescent. Children’s pain percep-
tion and responses are diff erent both qualitatively and 
quantitatively compared to adults. Th
  e pain response is 
more intense at the beginning, but wears off  much ear-
lier than in adults. Hence, no single formula is going to 
work for everyone, and customized pain relief measures 
are required.
Parental understanding and support is helpful be-
cause of their emotional attachment. As children may 
not ask for analgesia as adults can or do, an eff ort has 
to be made to anticipate pain, especially in infants and 
children who cannot express themselves verbally.
Most of the general principles of analgesia can be 
applied to children, but there are some signifi cant physi-
ological diff erences between adults and children that 
can cause problems, especially in neonates and small in-
fants. Just look at the case reports and imagine you have 
to deal with these clinical situations.
Case reports
You are in a small rural hospital with limited drugs. 
Consider the following real-life cases. How might you 
manage them?
Case report 1 (“acute trauma”)
Ahmed, a 3-year-old boy, with acute burns over a large 
part (more than 20%) of his body, has been admitted. 
He is in severe pain. How will you manage analgesia in 
this child?
Th
  e boy suff ers from severe post-traumatic pain, 
so he needs fast analgesia. Use morphine as an intra-
venous (i.v.) bolus (if not possible, substitute enteral 

256
Dilip Pawar and Lars Garten
morphine) followed by enteral morphine (if the child 
needs to be ventilated, use morphine i.v. infusion) on a 
regular basis for ongoing background pain. For any ad-
ditional procedures, e.g., change of dressing, use an ad-
ditional morphine bolus as necessary. Th
  ink also about 
anxiety management, which plays an important role in 
children with burns. Often the use of benzodiazepines 
such as oral lorazepam or i.v. midazolam is benefi cial. 
Combine medication with nonpharmacological methods 
(see below). Use a behavioral pain assessment scale (e.g., 
the FLACC scale) for monitoring pain severity and as-
sessing the eff ect of your therapy. When pain decreases, 
wean the patient off  the medication.