Dolor en Dermatología

CME Article
Submitted: 21.5.2015 DOI: 10.1111/ddg.12822

Accepted: 5.8.2015
Conflict of Interest
None.
Pain and pain management in

dermatology
Ulrike Beiteke1, Stefan Bigge2, Summary

Christina Reichenberger 3, It is estimated that 23 million Germans suffer from chronic pain. A recent survey
Ingrid Gralow4 has revealed that 30 % of chronic pain patients are dissatisfied with their pain ma-
(1) Department of Dermatology, nagement. Furthermore, five million Germans suffer from neuropathic pain, 20 %
Dortmund Hospital of whom are inadequately treated. Pain is also a symptom of many dermatologic
(2) Dermatology Practice, diseases, which is mostly somatic and may be classified as mild in the majority of
Bachemerstraße 1, Hürth cases. Nevertheless, research on the quality of life (QoL) has increasingly shown
(3) Medical student, Würzburg a marked impairment of QoL by moderate pain such as in psoriatic arthritis.
University Severe pain is associated with herpes zoster (shingles), leg ulcers, and pyoderma
(4) Department of Pain Medicine, gangrenosum.
Münster University Hospital This article addresses the basics of pain classification and, in a short excerpt, pain
transduction/transmission and modulation. The use of standardized diagnostic
Section Editor scales is recommended for the purpose of recording and monitoring pain inten-
Prof. Dr. D. Nashan, Dortmund sity, which allows for the optimization of therapy and consistent interdisciplinary
communication.
Any dermatology residency program includes the acquisition of knowledge and
skills in pain management. This review therefore aims to present fundamental the-
rapeutic concepts based on the expanded WHO analgesic ladder, and describes
a step-wise therapeutic approach and combination therapies. The article focuses
on the pain management of the above-mentioned severely painful, conservati-
vely treated dermatoses. Besides well-established therapeutic agents and current
therapeutic standards, it discusses specific options based on guidelines (where
available). Current knowledge on peri- and postoperative pain management is brie-
fly outlined.
This article addresses:
 The fundamentals of the classification and neurophysiology of pain;
 Standards for pain documentation in children and adults;
 General standards for pharmaceutical pain management;
 Current specific treatment options for postherpetic neuralgia, leg ulcers, and
pyoderma gangrenosum in conjunction with the expanded WHO analgesic

ladder.
© 2015 Deutsche Dermatologische Gesellschaft (DDG). Published by John Wiley & Sons Ltd. | JDDG | 1610-0379/2015/1310 967
CME Article
Table 1 Classification and characterization of nociceptive (somatic, visceral) and neuropathic pain.
Somatic pain Visceral pain Neuropathic pain

Location  Skin (superficial pain)  Chest pain  Supply area of affected nerve structures

 Bones, muscles, joints
 Abdominal pain and sometimes beyond
(deep pain)  Pelvic pain
Pain character  Sharp (superficial pain)  Dull  Burning
 Dull (deep pain)  Pressing, dragging  Stabbing
 Stabbing  Colicky  Sharp
 Gnawing
 Lancinating
Sensation  Well-localized
 Poorly localized
 Neurologic disorder, may present with

(superficial pain)  Mostly independent
concomitant vegetative symptoms
 Poorly demarcated
of movement  Sequelae may include hyperalgesia or

(deep pain) allodynia
Classification of pain
The International Association for the Study of Pain (IASP) defines pain as an un-
pleasant sensory or emotional experience associated with actual or potential tissue
damage, or described in terms of such damage.
The classification of pain in acute and chronic pain is primarily based on its
duration. While acute pain can almost always be attributed to a certain cause,
chronic pain lasts longer than six months, or recurs over this period of time. Chro-
nic pain may be present in the absence of any obvious physical alteration and is
mostly due to permanent tissue damage or persistent nerve irritation or damage.
The symptom of “acute pain” can be triggered by mechanical, thermal, or chemi-
cal noxious stimuli, leading to a sensation of pain through the excitation of no-
ciceptive nerve fiber endings. Chronic pain may develop from acute pain, and may
potentially become an independent disease entity. An example thereof is posther-
petic neuralgia, a chronification of pain following an acute herpes zoster infection.
Based on its pathophysiology, pain is classified into nociceptive (somatic and
visceral) and neuropathic pain. Nociceptive pain is a response to mechanical,
chemical, thermal, or electrical noxious events mediated by nociceptors (sensory
receptors). Nociceptors consist of nerve fiber endings of nonmyelinated C fibers
and myelinated Aδ fibers. Nociceptive pain is distinctly localized, and dull or stab-
bing in character (Table 1).
While skin pain is superficial somatic pain, deep somatic pain affects muscles,
joints, tendons, and ligaments. An example of the latter is pain associated with
necrotizing fasciitis; in this condition, marked by rather moderate clinical findings,
the extreme pain represents a significant warning symptom. Somatic pain should
be distinguished from visceral pain (Table 1). Visceral pain originates from inter-
nal organs, and may be associated with “referred” pain in the Head's zones (for
example, pain in the upper arm associated with myocardial infarction). Somatic
pain is well localized, whereas visceral pain is diffuse and thus perceived as poorly
localized.
Neuropathic pain is caused by damage to the peripheral or central nervous sys-
tem, and frequently occurs in postherpetic neuralgia or pyoderma gangrenosum.
Neuropathic pain can be perceived as sharp, nagging, burning, and/or lancinating
968 © 2015 Deutsche Dermatologische Gesellschaft (DDG). Published by John Wiley & Sons Ltd. | JDDG | 1610-0379/2015/1310
CME Article
(Table 1). It may be accompanied by functional disorders and neurovegetative sym-

ptoms such as hyperhidrosis or trophic disturbances. Allodynia is defined as the
perception of physiological, non-pain-causing stimuli as pain. Hyperalgesia, on the
other hand, is marked by an exaggerated perception of pain-causing stimuli. With
respect to neuropathy, further terms include negative symptoms such as hypes-
thesia (reduced sensation) or anesthesia (complete loss of sensation), and positive
symptoms such as paresthesia (for example, a tingling sensation) and dysesthesia
(for example. a burning sensation). Nociceptive pain may concur with neuropathic
pain, resulting in mixed pain.
Regarding pain associated with somatoform disorders, patients perceive, for
example, headache or abdominal pain, which may indeed be experienced as ana-
tomically well localized, yet without a sufficient organic correlate. As there is no
apparent tissue damage, an extensive diagnostic workup is required before an un-
derlying psychological disorder may be diagnosed. This, however, does not mean
that it is a mere diagnosis of exclusion; rather, the diagnosis has to be confirmed by
psychological/psychosomatic workup. Possibly, only future research will provide
conclusive pathophysiological explanations.
Pain associated with skin diseases is These and other phenomena such as sensitive skin remain to be elucidated.
mostly nociceptive pain, which can be However, substantial progress has been made in recent years; studies on the tran-
triggered by mechanical, thermal, and/ sient receptor protein (TRP) channels in the skin and on the nerve density in the
or chemical noxious stimuli. Neuropa- skin have facilitated essential diagnostic and therapeutic approaches in disorders
thic pain is caused by damage to the such as pruritus and prurigo. With respect to the regulation of electrolyte channels
peripheral or central nervous system. in synapses, mutations affecting the sodium channels have been shown to be a
This kind of burning, stabbing, and/or significant pathogenetic factor in erythromelalgia [1].
lancinating pain is diagnosed in con- During the chronification process, psychosocial stress factors may significant-
ditions such as postherpetic neuralgia ly affect the perception of pain, even in case of somatic pain; according to ICD 10,
and pyoderma gangrenosum. Nocicep- these patterns are classified as “chronic pain syndrome with somatic and psycho-
tive and neuropathic pain may concur logical factors”.
(mixed pain). Pain does therefore not correspond to a simple stimulus-response principle;
these two variables are not reliably correlated. Frequently modified and quoted,
the statement by McCaffery (1968) still holds true with respect to pain perception:
“pain is whatever the experiencing person says it is, existing whenever the expe-
riencing person says it does”. In this context, the key questions in taking a pain
history include: where does it hurt? When does it hurt? What is the pain like? Do
you have any other symptoms in addition to pain? What makes the pain better
or worse? The perception and assessment of pain is modified in a multifactorial
manner in the context of peripheral and central nervous pain transmission and
processing, but also by affective and cognitive factors on the part of the patient.
Regardless of the cause and type of pain, the patient's subjective perception of pain
determines assessment and therapy.
Pain transduction/transmission and pain modulation

The receptive nerve endings in the skin are Aδ and C fibers, which differ in their
myelination and conduction velocities. Thin myelinated Aδ fibers with a conduc-
tion velocity of up to 25–30 m/s induce an initial intensive, rather sharp, stabbing
pain, followed by a rather dull, burning pain caused by nonmyelinated C fibers
with a conduction velocity of <1.3 m/s [2].
By lowering the stimulus threshold, inflammation contributes to pain sen-
sitization and hyperalgesia. Typical inflammation-induced algogenic mediators
include prostaglandins, serotonin, and bradykinin; in addition, leukotrienes and
interleukins display proinflammatory effects. A recent study by Patruno et al. [3]
CME Article
In the perception of nociceptive pain, has revealed that, in psoriatic skin, interleukin (IL)-33 does not only positively
inflammation lowers the neuronal correlate with psoriatic plaques, but also with a stronger sensation of pain.
stimulus threshold and thus leads to Neuromodulators affect neural conduction via specific receptor molecules.
hyperalgesia. Prostaglandins, serotonin, Associated ion channels cause hyperpolarization or depolarization, an activati-
and bradykinin are examples of algoge- on or inhibition of potentials. Binding of ligands can also lead to the opening of
nic mediators. nonselective cation channels such as TRP channels. Overlapping aspects in pru-
ritus and pain research with respect to TRP channels and neuropeptides open up
new scientific fields, and may help explain the frequently concurrent symptoms of
pruritus and pain [4]. Please refer to the review articles by Bourinet, Julius, and
Baraniuk for further literature on receptors, transmitters, and ion channels [5–7].
Via the respective posterior horn of the spinal cord and the contralateral spinal
cord tract, somatic afferent fibers enter the thalamus, a key control center, from
where they are routed to the sensory cortex, where the location and quality of the
pain is determined.
Pain modulation and control is, among others, exerted by the interaction of
Aδ and C fibers, by inhibitory interneurons at the spinal cord level, and by control
functions of the brain. The system of nociception and antinociception is complex
and controlled, among others, by glutamate binding to N-methyl-D-aspartate
(NMDA) receptors and substance P. The widespread distribution of opioid recep-
tors in the central and peripheral nervous system illustrates the potential inhibition
of the transmission of pain impulses by endogenous opioids [8].
Assessment and documentation of pain

Pain ranks as the fifth vital sign, indicating the significance of this symptom and
the necessity for its documentation in the context of providing medical care. Basic
parameters in pain assessment include pain intensity, location, duration, and quali-
ty. Available recommendations on the use of pain scales and diagnostic approaches
allow for a reliable, reproducible measurement of pain in neonates, infants, child-
ren, adults, elderly, and mentally handicapped patients [9].
The following procedure is recommended for adults:
 Regular documentation of pain intensity in adults using simple one-dimensional
pain intensity scales;
 Self-assessment by the patient;
 Documentation of perceived pain during all painful procedures and pain
management measures;
 Documentation of pain acceptance and extent of pain-related functional
impairment.
In children, the following criteria apply:

 Child-friendly visual analog scales for pain detection;
 Self-assessment by the child;
 Additional consideration of behavioral features such as facial expression,
crying, motor skills, posture, activity, restlessness, apathy, and appearance as
unequivocal evidence for the presence of pain.
The numerical and visual analog scales by Neugebauer are widely used. The
numerical rating scale (NRS) ranges from 0 (no pain) to 10 (worst pain imaginab-
le), while the visual analog scale allows for subjective marking of the perceived pain
intensity on a line using a pen or pointer [9, 10]. For children and patients who can-
not read, smiley cards are used, though their usefulness is questionable since they
are not validated, and the pain-associated facial expressions are not necessarily
CME Article
adequate. In children younger than four years, Buettner's discomfort and pain sca-
le (KUSS, validated for postoperative pain) may be used; and for children between
the ages of five and ten years, the revised Faces Pain Scale. Another option is the
verbal rating scale, with prescribed terms such as “none”, “mild”, “moderate”,
“severe” and “unimaginable pain”. Such qualified pain assessment is also used in
respective guidelines [9, 11].
In addition to these verbal and nonverbal expressions of pain, observation
scales may be used. Examples of these include the Premature Infant Pain Profile
(PIPP) in infants, where facial expressions are used for grading the pain intensity,
or the Comfort Scale in children and cognitively impaired and sedated patients,
which includes organ functions such as heart rate and muscle tension [12]. Other
options have been described by Hechler and Hübner for other age groups, such as
preterm and term newborns [13, 14].
Questionnaires such as the Brief Pain Inventory (BPI) or the West Haven-Yale
Multidimensional Pain Inventory (German: MPI-D) are recommended for a more
Various scales (for example, NRS, VRS, detailed pain documentation. The documentation of chronic pain is possible by
verbal rating scale, PIPP) are used for means of the German Pain Questionnaire as well as corresponding pain logs and
pain documentation/assessment in progress sheets offered by the German Pain Society, in which somatic, psychologi-
adults, children, infants, and cognitively cal, and social influences are taken into account as well.
impaired patients. For a more detailed With respect to neuropathic pain, there are validated questionnaires such as
pain documentation/assessment, painDETECT [15]. In case of persistent pain, pain diaries may be a helpful instru-
various questionnaires are available ment [16]. Standardized pain documentation/assessment facilitates therapy adjust-
(such as MPI-D, painDETECT, German ment and communication with the pain therapist. Specific documentation/assess-
Pain Questionnaire). ment using questionnaires is also recommended in the context of clinical studies.
Pharmaceutical pain management

Important principles of pain management are:
 Treat in as simple a manner as possible, preferably selecting oral agents so that
the patient can self-administer them.
 Provide a regular dose regimen for the individual dose and controlled dose
adjustment; avoid prescribing on a PRN basis.
Pain management requires a rigid treatment plan in order to achieve effective

analgesia and a reduced need for analgesics [17]. Table 2 summarizes the general
rules for the use of opioids. Regimens have to consider side effects and interac-
tions. Due to their synergistic effects, specific combinations allow for lower doses
of individual substances such as NSAIDs and opioids, as well as of coanalgesics
such as anticonvulsants and antidepressants. The expected side effects of opioids,
notably nausea and constipation, must be specifically addressed. While patients
become tolerant to the emetic effects over time, this is not true for constipation,
Pain management should preferably be which may require the regular use of laxatives. Myoclonus as a sign of an overdo-
conducted using oral agents and a fixed se, for example in the context of renal failure, should not be overlooked. Regular
time regimen. Combinations frequently monitoring of symptoms is mandatory. Depending on the type of pain and its in-
allow for lower doses of individual tensity, pharmaceutical agents are to be selected according to the expanded WHO
substances. analgesic ladder (Table 3).
WHO level I
WHO level I nonopioid analgesics include the nonacidic antipyretic agents aceta-
minophen (paracetamol) and metamizole (dipyrone) (Table 3). The maximum daily
dose of acetaminophen is about 4 g. In patients with liver damage, acetaminophen
CME Article
Table 2 Fundamental rules for the use of opioids, for example, in severe acute pain. In case of complex drug regimens, a pain
therapist has to be consulted.
Fundamental rules for the use of opioids

1 Selection of the analgesic is based, among others, on contraindications, route of administration, and side effects
2 Preferably sustained-release formulations and long duration of action
3 Rigid schedule
4 Starting with low doses
5 Optimal dose and treatment response are based on formulated treatment goals and side effects
6 Usual maximum dose 120 mg of oral morphine equivalent every day
7 > 3 months of therapy only in responders
8 Institute antiemetic therapy early on, and review the indication after 2–4 weeks
9 Prophylactic use of laxatives; in most patients, continue checking the indication during the entire treatment period
10 Switching to another opioid or changing the route of administration have to take pharmacokinetics and pharmacodynamics
into account
11 After six months, discuss dosage and treatment pause
12 Regular therapy monitoring
Table 3 Expanded WHO analgesic ladder adapted from [17]. Treatment concepts are geared towards the pathophysiology
(nociceptive/neuropathic) as well as the increase in pain intensity from level I to III with the addition of coanalgesics and adjuvants.
Level III Nonopioid + highly potent opioid (e.g. morphine, fentanyl, + Coanalgesics (e.g. anticonvulsants,
buprenorphine) antidepressants, corticosteroids)
Level II Nonopioid + low-potency opioid (e.g. tramadol, tilidine)
+ Adjuvants (e.g. laxatives, proton pump
Level I Nonopioid (e.g. metamizole (dipyrone), acetaminophen, inhibitors, antiemetics)
ibuprofen, diclofenac)
is contraindicated due to its hepatotoxic effects. Allergic agranulocytosis should

be emphasized as a side effect of the frequently used analgesic metamizole (dipy-
rone). Although the incidence in Western Europe is likely to be less than 0.01 %,
regular CBC monitoring is necessary. Oral administration is recommended. Intra-
venous use may lead to acute circulatory dysregulation including shock. Hence, as
a precaution, intravenous metamizole (dipyrone) should be slowly administered by
short infusion.
The acidic antiinflammatory, antipyretic analgesics diclofenac and ibuprofen
are grouped under the term NSAIDs (nonsteroidal antiinflammatory drugs). Their
effects and side effects can be explained by nonselective COX inhibition. The en-
zyme cyclooxygenase is involved in the synthesis of prostaglandins, thromboxane
A2, and antithrombogenic prostacyclins. The inhibition of enzymatic reactions
results in analgesic, antipyretic, and antiinflammatory effects not only at the site
of tissue damage (pain location), but it also affects the protective function of pro-
staglandins in the gastrointestinal tract and the kidneys (protective prostaglandin
PGE2). The inhibition of this isoenzyme limits the long-term use of these agents,
which may subsequently result in gastrointestinal ulcers and renal impairment.
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Gastrointestinal ulcers cannot be categorically avoided by the prophylactic use of

gastroprotective agents; nevertheless, prophylactic administration of proton pump
inhibitors such as omeprazole as first-line agent or misoprostol as second-line agent
is recommended in high-risk patients with gastrointestinal complaints.
Approved for the symptomatic treatment of degenerative inflammatory joint
diseases, the selective COX-2 inhibitors etoricoxib and celecoxib, as well as pare-
coxib (approved for postoperative pain management), are increasingly being used
in inflammatory pain of other origin. They had been expected to be associated
with a significant reduction in gastrointestinal side effects. However, metaanalyses
have revealed an increased incidence of adverse cardiovascular events including
myocardial infarction and stroke during long-term use. According to international
recommendations, this group of agents is contraindicated in patients with relevant
preexisting conditions such as coronary artery disease, stroke, heart failure, and
peripheral artery disease [18].
However, recent studies have shown similar cardiovascular side effects also for
conventional NSAIDs as well, and with respect to renal side effects, both NSAIDs
and coxibs warrant critical scrutiny [19]. According to the consensus of the In-
ternational Committee for Medicinal Products for Human Use, both groups of
agents should therefore be used for the shortest amount of time possible and using
the lowest therapeutically required dose. In case of other significant risk factors
such as poorly controlled hypertension, diabetes mellitus, or dyslipidemia, careful
weighing between increased cardiovascular and gastrointestinal risk is warranted.
Therapeutic options at level 1 of the Therapeutic options at level 1 of the expanded WHO analgesic ladder are gea-
expanded WHO analgesic ladder are red towards mild to moderate pain. They show good efficacy in nociceptive pain, for
geared towards mild to moderate pain. example, of inflammatory origin. While NSAIDs are the mainstay for skeletal pain,
They show good efficacy in nociceptive metamizole (dipyrone) is a preferable choice in the treatment of visceral pain because
pain. The combination of these nonopi- of its antispasmodic effects. Given that studies have not shown any additive thera-
oid analgesics is associated with increa- peutic effects, concurrent use of NSAIDs and metamizole (dipyrone) is not recom-
sed side effects. mended as side effects increase and both agents compete for elimination pathways.
WHO level II
Level II of the expanded WHO analgesic ladder provides for the treatment of mo-
derate and severe pain, primarily using nonopioid analgesics in combination with
low-potency opioids. Common side effects of opioids include nausea, vomiting,
somnolence, respiratory depression, spastic constipation, and micturition prob-
lems including urinary retention.
Tramadol and tilidine/naloxone are examples of low-potency opioids (Table 3).
A prodrug activated by hepatic cytochrome enzymes, tramadol is a pure μ ago-
nist and also inhibits the reuptake of serotonin and norepinephrine. Exaggerated
serotonergic effects may include side effects such as confusion, agitation, sweating,
tachycardia, and gastrointestinal symptoms. Tilidine unfolds its analgesic effects
in the central nervous system via the metabolite nortilidine. When given intra-
venously and at a high dose, the antagonist naloxone starts to exert its effects, thus
preventing an overdose and side effects such as sensory disturbances, insomnia,
depression, and loss of appetite. An impaired ability to drive and the potential for
abuse must be considered in both drugs, which may be prescribed as oral medica-
tion without a special narcotic prescription form.
If adequate pain reduction cannot be achieved by means of combined level II
therapy, the patient is switched to potent opioids (Tables 3, 4). When switching
the patient, it is recommended that the specified equianalgesic dose be reduced by
30–50 %, followed by rapid uptitration using the immediate-release form.
CME Article
Table 4 Summary of the analgesic potency of common opioids compared with

morphine [8, 17].
Opioid Analgesic potency compared with morphine ( = 1)

Tilidine + Naloxone 0.1–1
Tramadol 0.1–0.2
Morphine 1
Oxycodone 2
Hydromorphone 7.5
Buprenorphine 30–40
Fentanyl 125
The selection of the opioid is guided by its analgesic potency, the maximum
nalgesia attainable, and the composition of agonist and antagonist. The term ‘cei-
a
ling effect’ refers to the phenomenon that, from a certain dose on upward, no greater
analgesic effect can be achieved; at the same time, however, side effects may still in-
crease. For example, this saturation effect is observed with buprenorphine, a partial
When switching opioids, it is recom- agonist, but not with oxycodone, a κ receptor agonists. Oxycodone, whose dose may
mended that the specified equianalge- be 50 % lower than that of morphine due to its superior bioavailability, displays a
sic dose be reduced by 30–50 %, with similar side effect spectrum as morphine. The combination of oxycodone and nalo-
rapid uptitration using immediate- xone (antagonist) is supposed to reduce the risk of constipation, explaining the ratio-
release opioids. Advanced patient age nale behind its frequent use. The combined use of pure μ agonists such as tramadol or
and renal impairment require specific morphine with partial antagonists such as buprenorphine should be avoided. Hydro-
considerations. morphone is recommended in polymedicated patients due to the fewest pharmacolo-
gical interactions. For additional details, please refer to the relevant literature [8, 17].
WHO level III

Highly potent opioids (WHO level III) are listed in Table 5. Even at level III may
the use of NSAIDs lead to improved analgesia and a reduced need for opioids.
Other comedications include anticonvulsants such as gabapentin or pregabalin,
the latter also displaying anxiolytic effects. With respect the anticonvulsant dose,
both a gradual increase as well as subsequent tapering over the course of at least
one week is necessary. Major side effects include dizziness, ataxia, nausea, and dry
mouth. In patients with renal failure, the dose must be adjusted.
In neuropathic pain marked by a severe burning sensation, nonselective antide-
With neuropathic pain being the pri- pressants such as mirtazapine and amitriptyline, which inhibit the reuptake of the
mary indication, combination therapies neurotransmitters norepinephrine and serotonin, are suitable, also in combination
using gabapentin and pregabalin are with anticonvulsants and opioids. Research on pruritus has made the use of selec-
suitable in order to improve analgesia tive serotonin reuptake inhibitors (SSRIs) and serotonin norepinephrine reuptake
and reduce the need for opioids. inhibitors (SSNRIs) standard practice in dermatology. Compared with nonselec-
tive antidepressants, this group of agents represented by venlafaxine, citalopram,
and fluoxetine displays considerably weaker analgesic effects.
Perioperative and postoperative pain

Analysis performed by a pain clinic at a teaching hospital with respect to referring
departments has shown that 10.6 % of consults are dermatologic patients. The
CME Article
Table 5 Immediate-release and sustained-release opioids with their respective individual doses, dose intervals (in mg), and
possible transdermal and sublingual products (dose calculation in μg/h for patches and μg for lozenges).
Agent Individual dose Dosing interval

Tilidine: naloxone 50 : 4–100 : 8 4h
Tilidine: naloxone (sustained-release) 50 : 4/100 : 8/150 : 12/200 : 16 8–12 h
Tramadol 50–100 4h
Tramadol (sustained release) 50/100/150/200 8–12 h
Morphine HCL 5–40 4h
Morphine sulfate (sustained-release) 10–200 8–12 h
Long-term morphine sulfate 30/60 24 h
Oxycodone (immediate-release) 5/10/20 4
Oxycodone (sustained-release) 5/10/20/40/80 8–12 h
Oxycodone : naloxone (sustained-release) 5 : 2.5/10 : 5/20 : 10/40 : 20 8–12 h
Hydromorphone
 Immediate-release 1.3/2.6 4
 Sustained release 4/8/16/24 8–12 h
 Sustained release 8/16/32/64 24 h
Fentanyl transdermal 12.5–125 μg/h 3 days
Fentanyl citrate: Buccal, sublingual/lozenge 100–1 600 μg ≤ 60 min
Buprenorphine
 sublingual 0.2–0.4 6–8 h
 transdermal 5/10/20/35/52.5/70 μg/h 4–7 days
r equests for a consult primarily pertained to postoperative pain management and

the treatment of neuropathic pain. Although dermatooncologic surgery is an essen-
tial and major part of dermatology, hardly any comprehensive data or studies exist.
As part of a doctoral thesis at the Department of Dermatology of the Univer-
sity of Freiburg, pain profiles of 203 patients hospitalized on a surgical ward were
generated by means of a systematic survey (NRS scale). The average time spent as
an inpatient was six days. The survey period was three months. Forty-five patients
reported no pain, 132 patients did experience pain, and information was missing in
26 patients. Of the 132 individuals who reported pain, 81 patients reported grade
1 pain; 43 patients, grade 2; and eight patients, grade 3. There was evidence of the
significance of painful comorbidities such as underlying rheumatologic diseases in
this cohort, affecting 13 % of individuals with moderate and severe pain (NRS > 4).
New-onset and surgery-related pain not adequately treated by the routine
administration of pain medication displayed surprisingly high incidence rates,

more strongly associated with basal cell carcinoma surgeries. Thirty-four of 117
reported cases of pain were in the range of NRS 4–7; four, NRS 8–10 (Figure 1).
Differences in pain severity are a function of the location and the extent of sur-
gery; thus, surgery of basal cell carcinoma in the nasal region was more frequently
perceived as painful [20]. By contrast, following sentinel lymph node dissection
(SLND) and extensive lymphadenectomy (LAD), four of 27 patients reported
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Figure 1 Distribution of pain intensity with respect to surgery of various tumors;

repeated reports of pain are considered in the columns.
s evere pain (NRS 8–10) and 14 patients NRS 4–7. In a review, Slagelse et al. [21]
found persistent postoperative pain after SLND in 1–14 % of cases (6-34 % after
LAD), and concluded that prospective studies on the prevalence and differentiation
of pain and the predisposition thereto were needed.
Limthongkul et al. reported pain on days 0 and 1 in the majority of cancer pa-
tients treated with Mohs micrographic surgery, followed by with a steady decrease
in pain. Nevertheless, 16 % of patients still reported pain on the 7th postoperative
day [22]. This article described an increased prevalence of pain in association with
head surgery and multiple invasive surgical procedures performed on the same day.
In addition to the extent of the surgical procedure and the individual attitu-
de, ethnic differences, preexisting pain medication, and a history of pain-relevant
preexisting conditions have to be taken into account as well. The situation may
be optimized by choosing adequate local anesthesia techniques and, if necessary,
employing using preoperative pharmacotherapy [23].
The AWMF guidelines on the “Management of acute perioperative and post-
traumatic pain“ [9] can be used as a basis for better comparability of data as well as
for data collection and studies. It is recommended that postoperative pain be mea-
Using the measures outlined in the sured at two-hour intervals for 24 hours. Pain measurements should be reinitiated
AWMF guidelines on the “Management in case of new-onset pain and an increase in pain intensity. It should be conducted
of acute perioperative and posttrau- before and 30 minutes after a nonpharmacologic intervention as well as after the
matic pain” allows for the optimization use of analgesics; analogous to the duration of action of the drugs, this is generally
of pain assessment and management. 10–30 minutes after intravenous administration or 30–60 minutes after oral admi-
nistration. The maximum interval between individual pain measurements should
not exceed eight hours.
Pain in skin diseases

Skin diseases stigmatize, they are burdensome, and they are often painful. Pain
represents a considerable burden and reduces the quality of life. An overview of the
pain spectrum in conservative as well as surgical dermatology is largely missing. In
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Figure 2 Distribution of pain categories according to the NRS with respect to

various dermatologic diagnoses.
melanoma patients, on the other hand, data on pain as partial aspect of the quality
of life is more frequently collected. The perception and management of cancer-as-
sociated pain is an independent topic, which is beyond the scope of this article.
Pain in inpatients of a conservative dermatology ward (at the Department of
Dermatology of the University of Freiburg) was the focus of a study conducted in
the context of a doctoral thesis [24]. Two hundred-seventeen patients (111 men,
106 women) who reported pain on admission were evaluated (Figure 2). In addi-
tion to epidemiological data, pain severity and frequency with respect to various
dermatoses were examined. Generally speaking, patients with bullous and pruri-
ginous diseases, atopic dermatitis, psoriasis vulgaris, and erysipelas reported pain
in an unequivocal manner; however, patients with leg ulcers, zoster, and pyoderma
gangrenosum stand out from other potential pain patients due to the intensity of
pain (frequently pain categories II and III). For this reason, these disorders are
discussed separately.
Leg ulcer
In Germany, about one million people suffer from lower leg ulcers (Figure 3), eigh-
ty percent of which are of venous origin. Clinically diverse and frequently compli-
cated by comorbidities and – in case of longer duration – also recurrent erysipelas/
cellulitis and contact allergies, venous leg ulcers are a common problem in daily
practice. Apart from antiseptic and antibiotic treatment as well as wound dressings
and stimulation of granulation, pain assessment and management are important
elements in the care of these patients, which is also reflected in current guidelines
[25]. Studies show that – especially due to pronounced pain – two-thirds of patients
with venous leg ulcers experience a significant reduction in the quality of life [26].
Less than 5 % of lower leg ulcers are of arterial origin, and 10 % are classified
as mixed forms. Besides the actual wound pain, arterial ulcers, which primarily
occur in the context of peripheral artery disease (PAD), are characterized by exer-
tional pain induced by hypoxia [27].
CME Article
Figure 3 Leg ulcer.
Etiologically, leg ulcers may be caused by a wide variety of disorders, thus

requiring a targeted differential diagnostic workup [28]. In addition to pyoderma
gangrenosum, which is separately discussed below, the painful hypertensive ulcer
should be mentioned in this context. Developing as a sequela of long-standing and
inadequately controlled arterial hypertension and clinically marked by polycyclic,
sharply demarcated borders, the latter is frequently located unilaterally or bila-
terally on the distal lower leg above the lateral malleolus, rarely over the Achilles'
tendon or on the dorsum of the foot. It is characterized by a sudden onset, severe
pain (in part explained by ischemic infarction), and necrosis. Histologic analysis
should focus on finding evidence of calcified atherosclerosis.
In its initial stages, calciphylaxis is already marked by an extremely painful
induration of the skin, which is followed by a red-livid reticular pattern on which
deep necrotic ulcers develop. The origin of pain is thought to be ischemic and
neuropathic. Other differential diagnoses include ecthyma, drug-induced ulcers
CME Article
(for example, hydroxyurea), and ulcers with an underlying metabolic, neuropathic,

and/or a physical cause.
Evidence-based therapies and comprehensive treatment concepts for chronic
leg ulcers have been published [29]. Special forms require specific treatments. Pain
management has to take the root cause into account. Here, nociceptive wound pain
comes to the fore, however, ischemic – in terms of nociceptive-inflammatory pain
– and neuropathic pain may occur as well.
With respect to pain prevention, the S3 guidelines for the “Treatment of
Chronic Wounds in CVI, PAD, and Diabetes Mellitus” recommend the following
three measures: (1) avoidance of any material that adheres to the wound or dries
it out, (2) avoidance of irritating wound irrigation solutions, and (3) avoidance of
unnecessary manipulation [30]. The recommendations for Good Clinical Practice
(GCP) call for adequate pain management in the treatment of leg ulcers [31], given
that up to 87.5 % of patients report pain during dressing changes. Upon comple-
tion of dressing changes, 84.4 % of those affected still complain of persistent pain
[32, 33]. Measures should be taken to prevent pain during therapeutic procedures
as well as during wound debridement and dressing changes [34]. Although the-
re has been a growing number publications addressing the subject of “ulcer and
pain”, further studies on the impact of interventions on pain are desirable. This is
also formulated in the Cochrane review on “Compression Therapy for Venous Leg
Ulcers” [35].
Given the ever-increasing repertoire of available wound dressings, some
research on “wound dressings and ulcer-related pain” has also been publis-

hed in randomized trials. Various professional societies are working towards
improving the evidence base for stage-adapted wound care [36]. Pain reducti-
on is one of the requirements for wound dressings. For hydrocolloid and foam
dressings, there is strong evidence of their ability to meet this requirement (evi-
dence level IA) [29]. A randomized trial has demonstrated that treatment with
larvae, though having some advantages, nevertheless does cause significant local
pain [37].
Topical therapies are a domain of dermatologic treatment. In daily clinical
practice, ibuprofen-containing dressings and anesthetizing lidocaine-containing
gels or lidocaine-containing transdermal systems, as well as morphine gel, may be
used for pain relief [38]. Huptas et al. [38] published an improved formulation of
the morphine gel and a summary of their experience with it. Instead of 20 % pro-
pylene glycol, the gel (with HEC300 from the New Prescription Formulary guide-
lines (2008)) uses a 0.2 % Lavasept ® concentrate as antiseptic with low allergenic
potency. Oral pain medication is given in accordance with the expanded WHO
analgesic ladder; in case of a “pain emergency”, a single bolus of 5 mg morphine
or 1 mg hydromorphone IV is suitable, if necessary repeated after 10–20 minutes.
Adequate monitoring and particular caution in opioid-naive and elderly patients
is warranted.
Up to 87.5 % of patients with leg Palliative pain management, often extending over several months, is part of the
ulcers report pain during dressing interdisciplinary care of calciphylaxis [39]. The use of opioids (e.g. hydromorpho-
changes. Upon completion of dressing ne) in addition to other agents such as anticonvulsants, antidepressants, NSAIDs,
change, 84.4 % of those affected still and NMDA receptor antagonists is determined by the patients’ risk profile as well
complain of persistent pain. Prior to as disease progression. There are individual case reports on possible combination
any intervention, measures aimed at therapies. Analogous to pain management in mixed nociceptive and neuropathic
preventing pain are recommended. A pain of other causes, combination therapy is always recommended. Therapeutic
therapeutic concept for chronic pain is attempts using lumbar sympathetic block, hyperbaric oxygen, and patient-cont-
also frequently required in addition to rolled intravenous analgesia (morphine pump) reflect the quest for optimal pain
stage-adapted wound care. management in this disease.
CME Article
Figure 4 Pyoderma gangrenosum.
Pyoderma gangrenosum
A neutrophilic dermatosis, pyoderma gangrenosum is part of the group of auto-
inflammatory skin disorders (Figure 4). Pyoderma gangrenosum is one of the dif-
ferential diagnoses in lower leg ulcers. More than 50 % of affected patients have
a systemic disease, predominantly chronic inflammatory bowel disease. Hemato-
logic disorders, solid tumors, as well as endocrinopathies and rheumatic diseases
may also be associated with pyoderma gangrenosum. The characteristic clinical
presentation of an ulcer with distinctly erythematous, undermined borders is often
preceded by only minimal local trauma (pathergy phenomenon); subsequently, one
or more, slowly progressive ulcers develop, partly with a moth-eaten appearance.
In predisposed individuals, pyoderma gangrenosum may even occur following in-
vasive medical procedures, thus warranting caution when planning biopsies and
especially elective surgery. Most commonly affected areas include the lower legs,
forearms, and sometimes shoulders, abdomen, and chest.
Pyoderma gangrenosum ranks among the most painful skin disorders. Various
causes regarding the development of pain in this condition have been implicated.
The depth of the ulcerations with concomitant nerve damage plays a role. Wound
healing with regeneration of nerve fibers results in hypersensitivity. Similar to all
ulcers, local measures such as dressing changes and wound debridement also lead
to local neuronal and inflammatory irritation of axons located in deeper tissue
layers.
Apart from the requirements of wound management already mentioned
in the section on “Leg Ulcers”, treatment involves topical measures, sometimes
also antibiotic and immunosuppressive agents, primarily corticosteroids and cy-
closporine. Pain management focuses in particular on opioids [40]. Modified
according to guidelines for “Diagnosis and Therapy in Neurology”, a clinical
pathway for the treatment of neuropathic pain is presented in Table 6. The pati-
ent must be informed about pharmaceutical agents, side effects, initial dose and
CME Article
Table 6 A brief summary is shown as a clinical pathway for the treatment of neuropathic pain. Depending on the underlying
disease and specific diagnosis such as zoster, possible alternative therapies include serotonin reuptake inhibitors, capsaicin, and
lidocaine patches.
Consultation Decision Course of action

Analgesics, Severe pain and/or Opioids Pain reduction < 3 NRS Continue
therapeutic goal, the need for rapid Pain reduction > 30 % Switch
treatment duration, onset of action but NRS > 4
side effects, dosing/
Mixed nociceptive, Nonopioid analgesics ± opioid Pain reduction < 30 % Switch
uptitration
neuropathic pain + and NRS > 4
Anticonvulsants/antidepressants, Inadequate Pain
possible additions and alternatives therapist
Pyoderma gangrenosum ranks among ptitration, treatment duration, and treatment goal. In neuropathic pain, complete
u
the most painful skin disorders, and relief of pain can never be promised as the ultimate treatment goal. As listed in
often requires combination therapies column 3, a combination of opioids and an additional agent such as anticonvul-
consisting of opioids, antidepressants, sants is frequently required. Topical application of 0.1 % morphine gel – as adjunct
and anticonvulsants to combat neuro- to systemic therapies – has been reported to reduce severe neuropathic pain [40].
pathic pain.
Herpes zoster and postherpetic neuralgia

Herpes zoster (Figure 5) is triggered by reactivation of the latent varicella zoster
virus. In Europe, 95 % of young adults are seropositive for varicella zoster virus
[41]. The spread over one or more dermatomes is possible on the entire integument,
as well as in special cases – for example, in immunosuppressed patients – wides-
pread dissemination. Patients experience pain in the head and genital region as
extremely severe and burdensome. Besides aseptic meningitis (cranial nerve V),
paralysis (cranial nerve VII, VIII), ocular involvement (cranial nerve II, III, V), ear
involvement including deafness (cranial nerve VIII), postherpetic neuralgia per-
sisting over months to years represents the primary complication [42]. It must be
distinguished from transverse myelitis with the involvement of vertebral ganglia,
which may result in paraparesis and loss of sensation.
The lifetime prevalence of herpes zoster is approximately 30 %; 50 %, in
patients older than 85 years [43]. The hallmark of acute herpes zoster is stabbing,
episodic or continuous pain, usually appearing 1–2 days – but also up to a week
– prior to initial skin lesions. Approximately 10–50 % of herpes zoster patients
develop postherpetic neuralgia [42]. Postherpetic neuralgia is defined as pain per-
sisting for 90 days after the acute onset [41]. In approximately 15 % of patients,
the pain persists for up to two years. Clinical experience has shown that neuralgia
often develops in cases of inadequate initial pain management and thus also in-
creased pain intensity. Immunocompromised patients and elderly individuals are
at an increased risk of postherpetic neuralgia [43]. Factors contributing to pain
chronicity are thought to include sensitization of peripheral nociceptive C fibers
with subsequent sensitization of nociceptive neurons in the dorsal horn of the spi-
nal cord. Moreover, degeneration of nociceptive C fibers as well as a secondary
anatomic reorganization of synaptic structures in the dorsal horn of the spinal cord
are deemed to be involved [44].
In addition to antiviral medication, pain management is paramount at the on-
set of the disease. Antivirals are credited with pain reduction and possible complete
CME Article
Figure 5 Herpes zoster.
relief of acute pain. Likewise, pain reduction is assumed to be achieved by a short

course of corticosteroids at the onset of the disease [42]. However, the development
of postherpetic neuralgia is not completely prevented by antivirals or corticoste-
roids [45, 46].
In the acute phase, NSAIDs and/or acetaminophen are recommended for mild
to moderate pain. For more severe pain, opioids are indicated. Here, following tit-
ration with immediate-release tramadol, the patient may be switched to sustained-
release tramadol at a dose of 50 (100) mg twice a day (maximum 600 mg every
day). In case of excruciating pain, immediate-release oxycodone 5 mg may be given
every four hours, with a possible further increase by additional 5 mg every four
hours – as tolerated – every other day. If prolonged use is indicated, switching the
patient to the corresponding sustained-release form (administration every 12 hours)
is recommended [42]. The anticonvulsants gabapentin or pregabalin are further
options besides opioids. The benefit of the use of anticonvulsant drugs in neuro-
pathic pain is corroborated by a current systematic review and meta-analysis of
CME Article
pharmacotherapy of neuropathic pain in adults [47]. Therapy can be started with

gabapentin 100–300 mg in the evening. Uptitration using the usual 100 mg three
time a day takes place at two to three-day intervals up to a maximum of 600 (900)
mg three times a day. Pregabalin is started with 25–75 mg in the evening, and
gradually increased every three days up to a maximum dose of 300 mg twice every
day. Amitriptyline, an antidepressant, may be integrated into the long-term treat-
ment of postherpetic neuralgia, e.g. in combination with anticonvulsants or opi-
oids. Please note the fundamental rules for the administration of opioids (Table 2).
Interactions with other drugs as well as dependent organ functions have to be
observed as well. The patient should be informed about potential effects on the
About 10–50 % of herpes zoster patients ability to drive, possible other impairments, occupational risks, and loss of libido.
develop postherpetic neuralgia. This Available topical therapies include lidocaine and capsaicin patches; the latter
most frequently occurs in case of inade- are approved for the treatment of peripheral neuropathic pain [48]. In a small
quate pain management, in severe acute group of patients, topical application of a cannabinoid receptor agonist resulted in
pain, as well as in immunocompromised pain reduction by more than 80 % [49]. Interventional pain management requires
patients and elderly individuals. For the cooperation with pain specialists. As a general rule, interventional procedu-
severe pain, early use of gabapentin or res relieve acute pain, but do not prevent the transition to postherpetic neuralgia.
pregabalin at gradually increased doses Comprehensive efforts are needed as patients suffering from postherpetic neuralgia
as well as antidepressants should be are burdened by a reduced quality of life due to both physical and psychological
considered in addition to opioids. impairments [41].
Conclusions for daily clinical practice

In dermatology, pain management is an essential component of optimal patient
care. Following diagnostic pain workup and standardized documentation of the
subjective pain intensity, pain medication is initiated in a differential and graded
manner according to the expanded WHO analgesic ladder. Topical therapies are
primarily reserved for acute mild to moderate pain; morphine gel has a broader
range of use, while capsaicin patches should be considered in localized neuropathic
pain such as postherpetic neuralgia. Oral combination therapies achieve optimal
analgesia while minimizing side effects. Opioids are used in the management of
severe pain; in neuropathic pain, in combination with anticonvulsants and antide-
pressants. Given the increasing chronification and complex etiology of pain syn-
dromes, an interdisciplinary approach is recommended; this particularly includes
consulting a pain therapist.
Pain management is part of the core curriculum of residency training in der-
matology. The President of the German Pain Society, Prof. Schäfer (Charité Berlin),
voiced the following plea: “The care of patients suffering from pain must be im-
proved”. Presenting primarily relevant indications and the corresponding course of
action, this article is supposed to contribute to achieving this goal.
Correspondence to
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Fragen zur Zertifizierung durch die DDA

1. Welche Antwort zum Schmerz ist 4. Bei der Gabe von Opioiden ist was 7. Für Schmerzmessungen im
falsch? zu beachten? Eine Antwort ist falsch. Rahmen operativer Verfahren
a) Schmerzen werden in nozizeptive a) Die Gabe von Laxantien ist empfehlen sich nicht?
und neuropathische Schmerzen konsequent zu überprüfen. a) Postoperative Schmerzmessungen
unterteilt. b) Eine antiemetische Therapie ist alle zwei Stunden über 24 Stunden.
b) Schmerzen der Haut werden vorrangig zu Beginn notwendig. b) Nach oraler Gabe eines Schmerzmit-
den somatisch tiefen Schmerzen c) Eine regelmäßige Applikation tels Schmerzerfassung nach 30-60
zugeordnet. der Opioide ist in einem Zeitplan Minuten.
c) Chronische Schmerzen entste- festzulegen. c) Nach intravenöser Applikation eines
hen u. a. durch eine dauerhafte d) Die Höchstdosis der Opioidäquiva- Schmerzmittels Schmerzerfassung
Gewebeschädigung. lenzen beträgt 500 mg/d. nach 10–30 Minuten.
d) Neuropathische Schmerzen können e) Zur Titration eignen sich nichtretar- d) Ein Tag postoperativ kann man
von neurovegetativen Symptomen dierte Opioide. damit grundsätzlich aufhören.
begleitet sein. e) Präoperative Schmerzerfassungen
e) Nozizeptive Schmerzen sind klar zu sind sinnvoll.
lokalisieren. 5. Welche Antwort ist richtig?
a) Dünne myelinisierte Aδ-Fasern
induzieren eher einen scharfen 8. Was ist bei Schmerzen und
2. Welche Antwort ist richtig? stechenden Schmerz. Hauterkrankungen korrekt?
a) Das erweiterte WHO-Schema b) Aδ-Fasern haben eine Leitgeschwin- a) Hauterkrankungen sind immer
kategorisiert Substanzgruppen digkeit von < 1,3 m/sec. schmerzhaft und stigmatisieren.
entsprechend ihrer c) Afferente Nervenfasern gelangen b) Eine typische schmerzhafte
Nebenwirkungen. über ein jeweiliges Hinterhorn und Hauterkrankung ist das Pyoderma
b) Das WHO-Schema zur den lateralen Rückenmarksstrang gangraenosum.
Schmerzbehandlung ist nicht zum Thalamus. c) 5 % der Ulcera-cruris-Patienten
alltagstauglich. d) Der Thalamus ist für die Schmerzlo- beklagen eine Minderung ihrer
c) Das erweiterte WHO-Schema kalisation verantwortlich. Lebensqualität.
gestaltet die Schmerzthera- e) Bei der Schmerzanamnese ist d) Morphingele sind zur Schmerz-
pie in drei Stufen und richtet die subjektive Wahrnehmung behandlung von Ulzerationen
sich nach einer zunehmenden unwichtig. ungeeignet.
Schmerzintensität. e) Die Calciphylaxie erfordert nur eine
d) Entsprechend des erweiterten akute Schmerztherapie.
WHO-Schemas werden bevorzugt 6. Für neuropathische Schmerzen
Opioide eingesetzt. gilt welches Statement nicht?
e) Niedrigpotente und hochpotente a) Neuropathische Schmerzen sind
9. Welche Antwort zur Dokumenta-
Opioide gehören in eine Stufe des häufig stark schneidend, einschie-
tion und Evaluation von Schmerz ist
erweiterten WHO-Schemas. ßend.
falsch?
b) Neuropathische Schmerzen sind
a) Zur Schmerzbeurteilung sind
häufig > 5 auf der nummerischen
3. Welche Schmerzsubstanzen nummerische und visuelle Analogs-
Rating-Skala.
kalen weit verbreitet.
werden bevorzugt kombiniert? c) Neuropathische Schmerzen sind
b) Bei der Schmerzbeurteilung ist die
Eine Antwort ist falsch. sehr gut zu therapieren.
Gesichtsmimik des Patienten unwe-
a) NSAIDs und Opioide d) In einem Stufenplan empfiehlt sich
sentlich.
b) NSAIDs und Laxantien die Gabe von Opioiden und z. B.
c) Der Brief Pain Inventory (BPI) dient
c) Metamizol und Opioide Antikonvulsiva.
zu einer detaillierten Schmerzerfas-
d) Opioide und Antikonvulsiva e) Antidepressiva sind eine mögliche
sung.
e) Metamizol und Tramadol weitere Komedikation.
d) Eine standardisierte Schmerzerfas-
sung dient der Therapieanpassung.
CME Article
e) Empfehlenswert ist eine Erfassung b) Die Prävalenz für einen Zoster-

der empfundenen Schmerzen bei neuralgie steigt mit höherem Alter
Liebe Leserinnen und Leser,
allen schmerzverursachenden Pro- deutlich an.
der Einsendeschluss an die DDA für
zeduren. c) Die Schmerzsymptomatik persistiert
diese Ausgabe ist der 18. November 2015.
über Monate bis Jahre.
Die richtige Lösung zum Thema „Häufige
d) Eine Zosterneuralgie kann durch
bakterielle Infektionen der Haut- und
10. Für den Herpes zoster trifft welche eine frühe Steroidgabe vermieden
Weichgewebe: Klinik, Diagnostik und
Aussagen nicht zu? werden.
a) Die Lebenszeitprävalenz liegt bei e) Nicht selten ist einen multimodale Therapie“ in Heft 7 ( Juli 2015) ist: 1b, 2a,
30 %. Schmerztherapie notwendig. 3e, 4d, 5a, 6a, 7a, 8d, 9d, 10b
Bitte verwenden Sie für Ihre Einsen-

dung das aktuelle Formblatt auf der
folgenden Seite oder aber geben Sie
Ihre Lösung online unter http://jddg.
akademie-dda.de ein.

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CME Article

Submitted: 21.5.2015 DOI: 10.1111/ddg.12822

Pain and pain management in

Ulrike Beiteke1, Stefan Bigge2, Summary

Somatic pain Visceral pain Neuropathic pain

(Table 1). It may be accompanied by functional disorders and neurovegetative sym-

Pain transduction/transmission and pain modulation

Assessment and documentation of pain

In children, the following criteria apply:

Pharmaceutical pain management

Pain management requires a rigid treatment plan in order to achieve effective

Fundamental rules for the use of opioids

is contraindicated due to its hepatotoxic effects. Allergic agranulocytosis should

Gastrointestinal ulcers cannot be categorically avoided by the prophylactic use of

Table 4 Summary of the analgesic potency of common opioids compared with

Opioid Analgesic potency compared with morphine ( = 1)

WHO level III

Perioperative and postoperative pain

Agent Individual dose Dosing interval

r­ equests for a consult primarily pertained to postoperative pain management and

Figure 1 Distribution of pain intensity with respect to surgery of various tumors;

Pain in skin diseases

Figure 2 Distribution of pain categories according to the NRS with respect to

Figure 3 Leg ulcer.

Etiologically, leg ulcers may be caused by a wide variety of disorders, thus

(for example, hydroxyurea), and ulcers with an underlying metabolic, neuropathic,

Figure 4 Pyoderma gangrenosum.

Consultation Decision Course of action

Herpes zoster and postherpetic neuralgia

Figure 5 Herpes zoster.

relief of acute pain. Likewise, pain reduction is assumed to be achieved by a short

pharmacotherapy of neuropathic pain in adults [47]. Therapy can be started with

Conclusions for daily clinical practice

Fragen zur Zertifizierung durch die DDA

e) Empfehlenswert ist eine Erfassung b) Die Prävalenz für einen Zoster-

Bitte verwenden Sie für Ihre Einsen-

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r equests for a consult primarily pertained to postoperative pain management and