P
P/Q Type Calcium Channel
Definition
Voltage-dependent Ca(
2+) channels not only mediate the entry of Ca(
2+) ions into excitable cells but are also involved in a variety of Ca(
2+)-dependent processes, including muscle contraction, hormone or neurotrans- mitter release, and gene expression. The alpha-1A isoform is abundantly expressed in neuronal tissue and corresponds to the P/Q Ca(
2+) channel type. The P/Q Ca(
2+) channel is responsible for presynaptic neu- rotransmitter release. Abnormalities in this channel could lead to abnormal neurotransmitter release. The affected CACNA1A gene encodes the pore-forming α
1Asubunit of the P/Q-type channel (Ca
V2.1), a pre- dominant mediator of voltage-gated Ca
2+entry and transmitter release at many synapses in the central ner- vous system. Alterations in synaptic signaling are of likely importance for cross-talk between an ascending pain transmission pathway and inhibition by a pow- erful descending modulatory system, interactions that ultimately govern the generation of headache pain.
Migraine, Childhood Syndromes
P1 Receptors
Definition
P1 receptors are seven transmembrane, G protein- coupled receptors that are activated by adenosine.
Purine Receptor Targets in the Treatment of Neuro- pathic Pain
P2X Receptor
Definition
Extracellular adenosine 5’–triphosphate (ATP) evokes cation currents in primary afferent neurons. P2X recep- tors are believed to be ligand-gated cation channels with two membrane spanning domains that are activated by the binding of extracellular ATP. P2X purinoceptors
have been cloned from different tissues and P2X1–7 cDNA have been identified. Among them, P2X3 sub- units have been found to be important receptors that sense peripheral information.
ERK Regulation in Sensory Neurons during Inflam- mation
Purine Receptor Targets in the Treatment of Neuro- pathic Pain
TRPV1 Modulation by p2Y Receptors
P2X3 Receptor
Definition
The P2X
3receptor is a ligand-gated channel activated by adenosine triphosphate (ATP) and mediates fast ex- citatory transmission. The P2X
3channel is selectively expressed by unmyelinated (C-fiber) nociceptors, and exists as either P2X
3homomers or P2X
2/3heteromers.
P2X
3receptor expression overlaps substantiallywith the IB4 positive population of small-diameter sensory neu- rons.
IB4-Positive Neurons, Role in Inflammatory Pain
Nerve Growth Factor, Sensitizing Action on Nocicep- tors
P2Y Receptors
Definition
P2Y Receptors are seven transmembrane, G protein- coupled receptors activated by ATP and other nu- cleotides.
Purine Receptor Targets in the Treatment of Neuro- pathic Pain
TRPV1 Modulation by p2Y Receptors
p38 MAP Kinase
Synonyms
P38 MAPK
1636 p75 Receptor
Definition
p38 mitogen activated protein kinase is involved in intracellular signaling pathways that control both:
(a) the production of proinflammatory cytokines, and (b) cellular activation caused in response to proin- flammatory cytokines binding to their receptors. p38 MAPK is activated by stress signals, such as inflam- matory cytokines, heat shock and ischemia. Although an activity-dependent p38 activation occurs in neu- rons, the contribution of p38 MAPK to nociception and pain hypersensitivity is still under investigation.
Peripheral inflammation induces p38 activation in small DRG neurons and contributes to the maintenance of inflammatory pain hypersensitivity.
ERK Regulation in Sensory Neurons during Inflam- mation
Proinflammatory Cytokines
p75 Receptor
Definition
P75 is the low-affinity nerve growth factor (NGF) re- ceptor that binds and internalizes nerve growth factor (NGF), neurotrophin–3 (NT–3) and brain derived neu- rotrophic factor (BDNF). It is normally expressed in sen- sory neurones, mainly of small diameter, and on the ter- minals of sympathetic and small sensory neurones in pe- ripheral tissues such as skin and vascular muscle. These target tissues produce neurotrophins, which are neces- sary for the maintenance of many sympathetic and sen- sory neurones. After peripheral nerve injury, p75 expres- sion is reduced in neurones and upregulated on satellite glia in dorsal root ganglia.
Nerve Growth Factor, Sensitizing Action on Nocicep- tors
Satellite Cells and Inflammatory Pain
Sympathetic and Sensory Neurons after Nerve Le- sions, Structural Basis for Interactions
PACAP
Definition
PACAP (pituitary adenylate cyclase-activating polypep- tide), a 38-amino acid peptide, was characterized from hypothalamic tissue as a potent stimulator of adenylyl cyclase. PACAP shows a high sequence homology with VIP. It has a wide distribution in the brain and spinal cord, as well as in sensory and autonomic ganglia and in in- hibitory neurons of the enteric nervous system. PACAP in endings that innervate most endocrine glands and lym- phatic tissue acts as an anti-inflammatory peptide. Im- mune cells also contain PACAP.
Neuropeptide Release in the Skin
Pachymeningeal Enhancement
Definition
A distinct MRI picture that, in the setting of an ortho- static headache, is almost diagnostic of a CSF leak. After gadolinium there is diffuse enhancement limited to the pachymeninges without leptomeningeal involvement.
New Daily Persistent Headache
Pachymeningeal Enhancement in MRI with Gadolinium
Definition
Typically linear, thick, and diffuse enhancement of the dura mater in MR images. Whereas the leptomeninges have blood brain barriers, the pachymeninges do not and therefore accumulate the contrast medium.
Headache due to Low Cerebrospinal Fluid Pressure
Paediatric Chronic Pain Management
Complex Chronic Pain in Children, Interdisciplinary Treatment
Paediatric Pain Measures
Pain Assessment in Children
Paediatric Pain Scales
Pain Assessment in Children
Paediatric Procedural Analgesia
Pain and Sedation of Children in the Emergency Set- ting
Paediatric Sedation
Pain and Sedation of Children in the Emergency Set- ting
PAG
Periaqueductal Gray
P
Pain and Sedation of Children in the Emergency Setting 1637
Paget’s Disease
Definition
Paget’s disease is a malfunction in the normal process of bone remodeling.
Chronic Low Back Pain, Definitions and Diagnosis
Pain
Definition
Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or de- scribed in terms of such damage (Definition of the Inter- national Association for the Study of Pain, IASP). The inability to communicate verbally does not negate the possibility that an individual is experiencing pain and is in need of appropriate pain-relieving treatment. Pain is a symptom, not an impairment. A symptom, of itself, is neither exertional nor nonexertional. It is the nature ofthe limitations or restrictions caused by the symptom that are exertional or nonexertional. In a given individual, pain may cause exertional limitations and restrictions, nonex- ertional limitations and restrictions, or a combination of both.
Cancer Pain Management, Radiotherapy
Disability Evaluation in the Social Security Admin- istration
Disability, Upper Extremity
Ethics of Pain in the Newborn Human
Lateral Thalamic Pain-Related Cells in Humans
Multidimensional Scaling and Cluster Analysis Ap- plication for Assessment of Pain
Pain Assessment in Neonates
Pain Assessment in the Elderly
Pain Treatment, Intracranial Ablative Procedures
Physical Exercise
Statistical Decision Theory Application in Pain As- sessment
Tourniquet Test
Pain Affect
Nociceptive Processing in the Cingulate Cortex, Be- havioral Studies in Animals
Pain Amplification Disability Syndrome
Somatization and Pain Disorders in Children
Pain and Sedation of Children in the Emergency Setting
S
UZANS
CHNEEWEISSThe Hospital for Sick Children and The University of Toronto, Toronto, ON, Canada
suzan.schneeweiss@sickkids.ca Synonyms
Paediatric Procedural Analgesia; Paediatric Sedation Definition
Procedural sedation is a technique of administering sedatives or dissociative agents with or without anal- gesics to induce a state that allows the patient to tolerate unpleasant procedures while maintaining cardiorespi- ratory function. Procedural sedation and analgesia are intended to result in a depressed level of conscious- ness while allowing the patient to maintain airway control independently and continuously. Specifically, the drug doses and techniques used are intended to maintain protective airway reflexes (American College of Emergency Physicians 1998).
Characteristics
In recent years, there has been increasing recognition of the need to provide adequate analgesia and anxiolysis to children undergoing procedures in the Emergency De- partment (Kennedy and Luhmann 1999). Although chil- dren often report fear of a procedure to be the most anxi- ety provoking aspect of their emergency room visit, they often receive less analgesia than their adult counterparts in the emergency setting (Petrack et al. 1997). Fear of adverse events has often prevented the use of sedative and analgesic agents in children (Cote et al. 2000; Pena and Krauss 1999). Emergency physicians, skilled in the care of critically ill children as well as in the manage- ment of the paediatric airway, are increasingly providing children with better pain and anxiety control (Hoffman et al. 2002; Krauss and Green 2000). The Emergency Department provides a unique situation with regards to the patient population and the environment. Most chil- dren presenting with an acute illness or injury requiring an urgent or emergent procedure are healthy.
Although many procedures performed in the Emer-
gency Department are not highly painful, such as an
intravenous cannulation, they may provoke a high de-
gree of anxiety in children and not only warrant pain
relief, but also require some degree of anxiolysis. Even
non-painful diagnostic imaging procedures such as CT
scanning in which the child must lie motionless can
provoke a high degree of anxiety. There are procedures,
however, that are both highly painful and anxiety pro-
voking, requiring both a higher degree of anxiolysis
and analgesia (e.g. fracture reduction).
1638 Pain and Sedation of Children in the Emergency Setting
The therapeutic goals of procedural analgesia and anx- iolysis are:
1. To ensure the patient’s safety and welfare
2. To minimize physical discomfort or pain during a di- agnostic or therapeutic procedure
3. To minimize the negative psychosocial responses to treatment
4. To enhance cooperativeness of the child
5. To return the patient to a state whereby safe discharge, as determined by recognized criteria, is possible.
Guidelines for Procedural Analgesia and Sedation
Guidelines are available from various sources regarding the general practice of procedural sedation and analgesia by non-anaesthetists in order to provide safe, consistent and appropriate sedation to children in the emergency setting undergoing invasive and non-invasive proce- dures (American College of Emergency Physicians 1998, 2004; American Academy of Pediatrics 1992, 2002; American Society of Anesthesiologists 2002;
Innes et al. 1999). Central to these guidelines is the no- tion of a sedation continuum whereby any procedural sedative agent can result in a dose dependent alteration in a child’s level of consciousness from
minimal sedation progressing to
moderate sedation and fi- nally to
deep sedation and general anaesthesia. In the emergency setting, the minimum amount of drug to achieve the desired depth of sedation is achieved by careful intravenous titration of the sedative and analgesic agents.
Agents used for moderate sedation require personnel skilled in management of potentially life threatening airway complications. These children require a thor- ough pre-procedural assessment including a focused history and physical examination including a detailed airway assessment for potential complications. Children deemed high risk should be referred to an anaesthetist for further assessment and management. Generally, children classified as ASA I or ASA II by the American Society of Anaesthesiologists, as shown in Table 1, can undergo moderate sedation by non-anaesthetist physicians. Skilled personnel must be available to deal
Pain and Sedation of Children in the Emergency Setting, Table 1 Classification of the American Society of Anesthesiologists
CLASS DESCRIPTION SUITABILITY FOR SEDATION
1 Normally healthy patient Excellent
2 A patient with mild systemic disease (no functional limitation)
Generally good
3 A patient with severe systemic disease (definite functional impairment) Intermediate to poor; consider benefits relative to risks 4 A patient with severe systemic disease that is a constant threat to life Poor, benefits rarely outweigh risks
5 A moribund patient who is not expected to survive without the operation Extremely poor Adapted from Krauss and Green (2000)
with potential complications. Children should be con- tinuously monitored with frequent vital signs to detect early onset of reversible complications. Practice guide- lines must be established in each individual emergency setting ensuring appropriate training of personnel to recognize potential adverse events and skills necessary to intervene and manage all potential complications.
Suitable monitoring and emergency equipment should be available for children of all ages and sizes being treated. Emergency equipment including oxygen, suc- tion, positive pressure bag-valve-mask and emergency resuscitation drugs should be immediately available and functional during sedation and recovery period. An assessment and documentation of food and fluid intake should be done prior to the procedure. Fasting guide- lines and sound clinical judgment should be exercised by the physician in determining the appropriate time interval between the last oral intake and procedural sedation. In urgent, emergent or other situations where gastric emptying is impaired, the potential for aspiration of gastric contents must be considered in determining the timing of the intervention and the degree of seda- tion / analgesia. If possible, such patients may benefit from delaying the procedure. When proper fasting can- not be assured, the increased risks of sedation must be carefully weighed against its benefits and the lightest sedation should be used. Following the procedure, strict discharge criteria are required, as increased sedation may occur when the painful stimulus is discontinued or if there are prolonged sedative effects because of the pharmacodynamic or pharmacokinetic properties of the medication.
Non-pharmacological Management of Pain and Anxiety
Parents play a key role both in their response to their
child’s pain and in their care of the child in the Emer-
gency Department. Increasingly, parental presence for
procedures is encouraged as a source of comfort and
support for their child (Merritt et al. 1998). Emergency
personnel must be sensitive to parental needs while at
the same time ensuring parents do not interfere with
the procedure. Preparation of the family for the proce-
dure is a key factor in reducing parental anxiety and
P
Pain and Sedation of Children in the Emergency Setting 1639
facilitating the procedure, including an explanation of the procedure to be performed as well as an accurate description of the sensations that children will probably experience. Emphasize the qualitative sensations that a child may experience such as cold, tingling, sharp, so that the child can focus on the sensation rather than only the expectation of hurting. Personnel should avoid using medical jargon when discussing the procedure with the family and explain when they need to attempt a procedure more than once. Age-appropriate distraction techniques are useful adjuncts. Child life specialists bring a wealth of distraction and relaxation techniques into the emergency setting (Aldock et al. 1985). Music, bubbles, puppetry, story and activity books may be very useful for younger children, while older children may benefit from music through headphones, directed breathing and calming self-instruction such as “I can do it” or “I am calm.” More sophisticated methods such as imagery and hypnosis requires skilled personnel and are particularly effective for children who require multiple procedures.
Pain and Sedation of Children in the Emergency Setting, Table 2 Commonly used sedative and analgesic agents in the emergency department AGENT / ROUTE OF
ADMINISTRATION
CLINICAL EFFECT
PRECAUTIONS INDICATIONS
SEDATIVE-HYPNOTIC
MIDAZOLAM Sedation
Motion control Anxiolysis
No analgesia
May not immobilize patient Paradoxical reactions
Synergistic with opioid analgesic Reversible with flumazenil
Procedures requiring anxiolysis
PENTOBARBITAL Sedation Motion control Anxiolysis
No analgesia Not reversible
Diagnostic Imaging
ANALGESIC AGENTS
MORPHINE Analgesia Concomitant administration of other respiratory depressants, including benzodiazepines, increases the risk of respiratory depression and prolongs the period of sedation
Reversible with naloxone
Procedures with moderate to severe pain
FENTANYL Analgesia Apnea, skeletal muscle rigidity, chest wall rigidity with higher doses Synergistic effect with benzodiazepines
Reversible with naloxone
Procedures with moderate to severe pain
KETAMINE Analgesia, Dissociation Amnesia
Motion control
Not reversible
Not for use if potential raised ICP, cardiovascular disorder, airway instability, active pulmonary infection or disease, procedures resulting in increased secretions, infants<3 months, psychiatric disorder, glaucoma
Procedures with moderate to severe pain, anxiety or requiring immobilization
NITROUS OXIDE Anxiolysis Analgesia Sedation
Amnesia
Avoid in pneumothorax, bowel obstruction, otitis media
Deep sedation may occur if used in conjunction with opioids or other sedatives and may progress to a state of deep sedation / general anaesthesia
Procedures requiring mild sedation and analgesia
REVERSAL AGENTS
FLUMAZENIL Benzodiazepine reversal
May require repeated doses due to short duration of action Benzodiazepine overdose NALOXONE Opioid reversal May require repeated doses due to short duration of action Opioid overdose
Pharmacological Management of Pain and Anxiety
The practitioner must be familiar with the various pharmacological agents available and their side effect profiles as well as possible synergistic effects occurring when more than one agent is used (American College of Emergency Physicians 2004). Commonly used agents and drug dosages are listed in Table 2 and Table 3 respectively. Some agents such as ketamine provide both analgesia and anxiolysis while other agents may provide only analgesia (e.g. morphine) or anxiolysis (e.g. midazolam). Shorter acting opioid agents such as fentanyl are preferred to the traditional long acting morphine or meperidine because they have a faster onset of action and shorter duration of action and involve no histamine release. The dissociative agent, ketamine is commonly used because it is characterized by profound analgesia, sedation, amnesia and immobilization, while preserving upper-airway muscular tone and protective airway reflexes.
A key to minimizing complications of procedural se-
dation and analgesia is the slow titration of drugs to the
1640 Pain and Sedation of Children in the Emergency Setting
Pain and Sedation of Children in the Emergency Setting, Table 3 Recommended drug dosages for paediatric procedural sedation
DRUG ROUTE OF ADMINISTRATION DOSAGE
Sedatives
Midazolam Oral
Intranasal Intravenous
Wt.<20 kg: 0.5–0.75 mg/kg Wt.≥20 kg 0.3–0.5 mg kg−1 maximum 20 mg;
Administer 20–45 min prior to procedure 0.1–0.2 mg/kg (maximum 5 mg)
(0.5–5 years) initially 0.05–0.1 mg/kg, titrate to maximum of 0.15 mg/kg (maximum 10 mg)
Pentobarbital Intravenous Intramuscular
2.5 mg/kg over 1 min,
Wait 1 min then 1.25 mg/kg over 30 s Wait 1 min then 1.25 mg/kg over 30 s
Wait 1 min., then if required give additional 1.0 mg/kg to a total dose of 4.0–6.0 mg/kg (maximum 200 mg), titrated to effect
If no intravenous access:
6 mg/kg for children<15 kg 5 mg/kg for children≥15 kg
Administer 20–30 min prior to procedure (maximum 200 mg)
Analgesics
Fentanyl Intravenous 0.5–1 mcg kg−1, administered slowly in incremental doses every 1–2 min to desired effect, maximum 3 mcg kg−1; maximum initial dose 100 mcg When used with midazolam, reduce dosages of both drugs
Morphine Oral
Intravenous
0.3 mg/kg; Administer 30–60 min prior to procedure 0.05–0.1 mg/kg over 1 min (maximum 15 mg) Dose may be repeated once at 15 min
Ketamine Intravenous
Intramuscular
0.5–1.5 mg/kg slowly over 1–2 min May repeat 0.5 mg/kg× 1 in 10 min (maximum 100 mg)
4 mg/kg; may repeat half the dose in 10 min (maximum 100 mg)
Nitrous Oxide Inhalation A self-administration of no more than 50% nitrous oxide in oxygen Reversal Agents
Naloxone Intravenous
Intramuscular Endotracheal
0.001 mg/kg, titrate to maximum of 0.01 mg/kg May repeat every 2 min as required
maximum dose 1 mg / dose
Flumazenil Intravenous 0.01 mg/kg over 15 s; repeated every 1–3 min to a maximum of 5 doses
≤20 kg: 0.05 mg/kg total dose
>20 kg: 0.2 mg / dose; 1 mg total dose
Adapted from Kowalczyk (2004) Sedation and Analgesia Guidelines. The 2004–2005 Formulary of Drugs. The Hospital For Sick Children, 23rdedn. The Graphics Centre: The Hospital for Sick Children: Toronto;2
desired effect. Combination of drugs may accentuate the potential side effects of each drug individually.
Each agent is administered individually in small in- cremental doses to the desired effect. Sufficient time must elapse between doses to allow the effect of each dose to be assessed before subsequent drug administra- tion. The propensity for combinations of sedative and analgesic agents to potentiate respiratory depression emphasizes the need to appropriately reduce the dose of each component, as well as the need to continually monitor respiratory function. Specific benzodiazepine and opioid antagonists (reversal agents) are available
to reverse possible respiratory depression from over sedation, improving the safety of procedural sedation.
Local and regional anaesthesia may be useful adjuncts to procedural analgesia. They have no systemic effects and do not result in compromises to the airway. Newer top- ical agents are now available and are particularly useful anaesthetics for wound closure and intravenous inser- tion (Bishai et al. 1999).
References
1. Aldock DS, Feldman W, Goodman JT et al. (1985) Evaluation of child life intervention in emergency department suturing. Pediatr Emerg Care 1:111–115
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Pain as a Cause of Psychiatric Illness 1641
2. American Academy of Pediatrics (1992) Guidelines for mon- itoring and management of pediatric patients during and after sedation for diagnostic and therapeutic procedures. Pediatrics 89:1110–1115
3. American Academy of Pediatrics (2002) Guidelines for mon- itoring and management of pediatric patients during and after sedation for diagnostic and therapeutic procedures: addendum.
Pediatrics 110:836–838
4. American College of Emergency Physicians (2004) Clinical pol- icy: Evidence-based approach to pharmacologic agents used in pediatric sedation and analgesia in the emergency department.
Ann Emerg Med 44:4:342–377
5. American College of Emergency Physicians (1998) Clinical pol- icy for procedural sedation and analgesia in the emergency de- partment. Ann Emerg Med 31:663–677
6. American Society of Anesthesiologists Task Force on Sedation and Analgesia by Non-Anesthesiologists (2002) Practice guide- lines for sedation and analgesia by non-anesthesiologists. Anes- thesiology 96:1004–1017
7. Bishai R, Taddio A, Bar-Oz B et al. (1999) Relative efficacy of lignocaine-prilocaine cream and amethocaine gel for local anal- gesia before venipuncture in children. Pediatrics 104:e31 8. Cote CJ, Notterman DA, Karl HW et al. (2000) Adverse sedation
events in pediatrics: a critical incident analysis of contributing factors. Pediatrics 105:805–814
9. Hoffman GM, Nowakowski R, Troshynski TJ et al. (2002) Risk reduction in pediatric procedural sedation by application of an American Academy of Pediatrics / American Society of Anes- thesiologists. Pediatrics 109:236–243
10. Innes G, Murphy M, Nijssen-Jorden C et al. (1999) Procedural sedation and analgesia in the emergency department. Canadian consensus guidelines. J Emerg Med 17:145–156
11. Kennedy RM, Luhmann JD (1999) The ouchless emergency de- partment. Getting closer: Advances in decreasing distress during painful procedures in the emergency department. Pediatr Clin North Am 46:1215–1247
12. Krauss B, Green SM (2000) Sedation and analgesia for proce- dures in children. N Engl J Med 342:938–945
13. Merritt KA, Sargent JR, Osborn LM (1998) Attitudes regarding parental presence during medical procedures. AmJ Dis Child 144:270–271
14. Pena BM, Krauss B (1999) Adverse events of procedural se- dation and analgesia in pediatric emergency department. Ann EmergMed 34:4:483–491
15. Petrack EM, Christopher NC, Kriwinsky J (1997) Pain manage- ment in the emergency department: Patterns of analgesic utiliza- tion. Pediatrics 99:711–714
Pain as a Cause of Psychiatric Illness
T
IPUA
AMIR, R
OBERTG. L
ARGEThe Auckland Regional Pain Service, Auckland Hospital, Auckland, New Zealand
bobl@adhb.govt.nz Synonyms
Psychopathology caused by pain; Pain as a Stressor; Psy- chological Consequences of Pain; Psychiatric Illness Definition
The title suggests a linear model of causality from pain to psychiatric illness. Careful reading of the studies ad- dressing this issue, however, suggests that it is not that simple.
Pain cannot be fully explained in terms of a pure sen- sory phenomenon. Wall and Melzack’s (1965) gate con- trol theory of pain proposed a balance between sensory and central inputs, with a tonic input to the gating sys- tems in the spinal cord from higher centres. At around the same time, various explanations based on psychoan- alytic principles started to dominate the literature. The assumption, underlying the psychoanalytic principles, is that pain is a defence against unconscious psychic con- flict. Most of the literature was based on anecdotal ac- counts (Merskey and Spear 1967).
In the 1970s (Gamsa 1994),
behavioural therapies and
cognitive theories were employed to explain the relationship of psychological factors and pain. Fordyce looked at pain as a reflexive response to an antecedent stimulus (tissue damage). He also postulated that pain behaviours depend on contingent reinforcement and can be learned by observing ‘pain models’. In this be- havioural model, factors like emotional state and other psychosocial variables are not considered. Cognitive approaches to pain look at the meaning of pain to the patients themselves. This cognitive model also looks at the beliefs, self-efficacy, problem solving, and coping abilities of the person. In the last 25 years, both cogni- tive and behavioural approaches have been combined and used extensively in pain management programmes.
This brief overview highlights the shift from a linear to a multicausal model. In a biopsychosocial model, psycho- logical and emotional factors play an important role in the continual experience of pain. The fact that psychoso- cial factors are considered so important in maintaining pain, leads to the assumption that psychiatric illnesses will be more common in patients with pain.
Characteristics
Relationship between Pain and Psychiatric Disorder
Studies of psychiatric diagnoses in pain populations have revealed a high incidence of
psychiatric disorder.
In one study, 94% of chronic pain patients suffered from a psychiatric disorder; 30% of these were diagnosed as suffering from depression (Large 1980). Polatin et al.
(1996) showed that, after excluding
somatoform pain disorder, 77% of patients met lifetime diagnostic crite- ria and 59% showed current symptoms for at least one psychiatric diagnosis. The most common diagnoses were of major depressive disorder, substance abuse, and anxiety disorders. 51% of patients in this study met criteria for at least one
personality disorder. The prevalence rates were significantly higher compared to the rates in the general population. This study also showed that, out of the patients with a life time diagnosis of a psychiatric disorder, 54% with major depressive disorder, 94% with substance abuse disorder and 95%
with anxiety disorder, had experienced the disorders
before the onset of their back pain. Hotopf et al. (1998)
showed a robust link between psychiatric disorder and
1642 Pain as a Cause of Psychiatric Illness
presence of physical symptoms. “Psychiatric disorder was associated with 2.9–6.9- fold increase in the odds of each physical symptom. Back pain, abdominal pain and chest pain were all associated with an increased likelihood of new onset psychiatric symptoms aged 43 years.” The best estimate of
1-year prevalence of any psychiatric disorder between age group 18–54 years, diagnosed using DSM III R, is 21.0%. The rate of Major Depressive episode is 6.5%. Hence there is a definite association between psychiatric disorder and pain.
Proposed Model of Development of Psychopathology
Gatchel (1996) has proposed a model of the develop- ment of psychopathology in low back pain over a period of time. This model looks at pain in three stages. Stage 1 represents the initial psychological distress, which is associated with fear and anxiety. This is a natural emotional reaction. When the pain continues beyond the acute period (2–4 months), it leads into stage 2. This stage is associated with phenomena like depression, distress, anger, somatization and learned helplessness.
Stage 3 is the acceptance of the “
sick role” and consolidation of “
abnormal illness behaviour”.
Gatchel (1996) hypothesises that the specific nature of the psychological problems that develop in stage 2, depend on the individual’s pre-morbid personality and psychological characteristics. They suggest that there is no specific “
pain prone personality”. The patient who suffers from persistent emotional problems passes onto stage 3, where the “sick role” is established and the patient is excused from his/her duties. This reinforces the sick role. This situation can be further complicated by compensation issues, which can become critical in the persistence of disability.
Banks and Kerns (1996) proposed a
Diathesis-Stress framework for the development of depression in patients suffering from chronic pain. Diathesis refers to consti- tutional, biological or psychological vulnerability. The stressors are any environmental or life event perceived by the individual as threatening to his or her physical or psychological well being, and exceeding his or her capacities to cope. This model hypothesizes that a con- stitutional vulnerability in the presence of
stress can perpetuate chronic pain and trigger a depressive disor- der.
Pain as a Stressor
Pain, unlike some other chronic conditions, for example hypertension, is symptomatic (Banks and Kerns 1996).
This quality of pain makes it noxious and aversive. The experience of pain is closely associated with affective distress. This may range through anxiety, fear, anger and depression. Pain becomes an overriding and ever present part of a person’s life.
At a psychological level, pain signifies danger. This is an instinctive phenomenon, which is ingrained in animals to propel them into self-preservation behaviour. This be-
haviour includes retraction from danger, reduced activ- ity and rest. The fact that pain represents danger raises the level of anxiety. In the longer term, pain promotes
impairment and
disability.
Impairment and disability lead to the restriction of a per- son’s ability to participate in day-to-day social activities.
Over a period of time cumulative effects of ongoing im- pairment and disability lead to a series of events nomi- nated as secondary losses (Banks and Kerns 1996).
Secondary loss refers to the effect of pain in various do- mains of daily life. These include loss of work and leisure activities, interference in and loss of intimate relation- ships, financial strife, unemployment and loss of self- esteem. Thus, it can be inferred that pain is not an iso- lated phenomenon; rather it affects a person globally.
A consideration of the models above, together with the fact that pain can act as a stressor in its own right, en- ables us to postulate a model in which all these factors can interrelate (Fig. 1). An individual can have under- lying vulnerabilities. These vulnerabilities can be a bi- ological predisposition to various psychiatric disorders or premorbid personality traits e.g. paranoid, antisocial, borderline, histrionic, narcissistic, dependent etc. Peo- ple during their lifetime can pass through various life events e.g. physical/sexual abuses, deprivation, loss, fi- nancial difficulties etc. In an individual with premorbid vulnerability, any of these life events can become a pre- cipitating factor for psychiatric disorder. When such a vulnerable individual suffers from pain, it can act as a strong stressor as described above, and can precipitate or magnify a mental disorder. Thus, pain acts as a magnify- ing lens. This relationship works both ways. Conditions like depression, anxiety and somatization can increase pain, which can lead to an increase in stress and fur- ther deterioration of mental state. The underlying mech- anisms at work are both cognitive and behavioural.
Relationship of Individual Psychiatric Disorders and Pain
Pain and Substance Related Disorders
The relationship between substance-related disorders and pain has been widely reported in the literature.
The rate of current substance related disorders range between 15–28%, and the lifetime rate lies between 23–41%. Lifetime prevalence in the general population is 16.7% (Dersh et al. 2002). These disorders are more prevalent in males in both the pain sufferers and the general population.
Various pathways have been suggested to show the un- derlying interaction between the two conditions. Polatin et al. (1993) showed that 94% of chronic pain patients with lifetime substance related disorder had the onset of these disorders before the start of the pain disorder.
This has been explained by an increased risk of accidents
leading to chronic pain. Brown et al. (1996) have ob-
served an increased risk for new substance related dis-
order 5 years after the onset of chronic pain. It can be due
P
Pain as a Cause of Psychiatric Illness 1643
Pain as a Cause of Psychiatric Illness, Figure 1 The conceptualisation of pain as a magnifying lens in development in psychopathology.
to iatrogenic reasons. This risk is greater in individuals with a previous history of substance related disorder.
Pain and Depressive Disorder
The relationship between pain and depression has gener- ated quite a lot of interest, yet research on this subject is fraught with problems. These problems have arisen due to the different criteria used to define depression. Fur- thermore, DSM criteria of depression consist of a num- ber of somatic features of depression e.g. sleep distur- bance, sexual dysfunction etc. These features can also be symptomatic of organic illnesses (Dersh et al. 2002).
However, despite these methodological difficulties, var- ious hypotheses regarding the relationship between pain and depression have been studied.
Fishbain et al. (1997) conducted a literature review exploring the relationship between pain and depressive disorder. They considered the following hypothe- ses:
1. Antecedent: This hypothesis was very weakly sup- ported by the literature
2. Consequence: This was very strongly supported by the literature.
3. Scar: This hypothesis suggested the episode of de- pression before the onset of pain predisposing to de- pression. Literature supporting this hypothesis was not consistent.
4. Cognitive-behavioural mediation model: This hy- pothesis presupposes the role of cognitive distortions mediating the relationship between depression and chronic pain. This model was supported by the literature.
Based on the currently available evidence, depression can be seen as a consequence of chronic pain in patients.
Pain and Anxiety Disorder
Dersh et al. (2002) have highlighted the high rates of anx- iety disorders in chronic pain patients. Rates between 16.5–28.8% have been observed. Factors leading to anx- iety disorders can be premorbid vulnerability and anxi- ety in stage I (Gatchel 1996), Kinesophobia and operant conditioning (avoidance of feared situation reinforcing the disability) can maintain the disorder. Anxiety disor- ders can be explained on
diathesis-stress model. Anx- iety disorders have high rates in both acute and chronic pain states.
Pain and Somatoform Disorders
Pain and somatoform disorders are closely related. Re- cently, literature has suggested an increased focus on internal stimuli. There has been no study published re- cently on this relationship using DSM IV. However, stud- ies in the past suggested a rate of 73% (Dersh et al. 2002).
Pain and Personality Disorder
The literature shows a high rate of personality disor- ders in chronic pain patients. The prevalence ranges from 31–81% (Dersh et al. 2002). However no specific personality disorder predicts chronicity. Research has shown that parameters on various personality assess- ments change from pre to post treatment in chronic pain subjects, with a reduction in personality disorder diagnoses being made post treatment. It may be that the stress of pain can exacerbate the patient’s vulnerability, leading to the expression of psychopathology.
Conclusion
The existing body of research shows that there is a
definite association between psychiatric disorders and
pain. The relationship between these conditions is
complicated and efforts are being made to unravel the
1644 Pain as a Stressor
complexities of their interaction. It is important for clinicians to be aware of this relationship, because fail- ure to identify psychopathology can adversely affect the outcome of treatment and our patients’ overall well being.
References
1. Banks SM, Kerns RD (1996) Explaining High Rates of Depres- sion Chronic Pain: A Diathesis-Stress Framework. Psychol Bull 119:95–110
2. Brown RL, Patterson JJ, Rounds LA, Papasouliotis O (1996) Substance use Among Patients with Chronic Back Pain. J Family Practice 43:152–160
3. Dersh J, Polatin PB, Gatchel RJ (2002) Chronic Pain and Psychopathology: Research Findings and Theoretical Consid- erations. Psychosom Med 64:773–786
4. Fishbain DA, Cutler R, Rosomoff HL, Rosomoff RS (1997) Chronic Pain-Associated Depression: Antecedent or Conse- quence of Chronic Pain? A review. Clin J Pain 13:116–137 5. Gamsa A (1994) The Role of Psychological Factors in Chronic
Pain. I. A Half-Century of Study. Pain 57:5–15
6. Gatchel RJ (1996) Psychological Disorders and Chronic Pain:
Cause-and-Effect Relationships. In. Gatchel RJ, Turk DC (eds) Psychological Approaches to Pain Management: A Practioner’s Handbook, chapter 2, pp 33–52
7. Hotopf M, Mayou R, Wadsworth M, Wessely S (1998) Tempo- ral Relationships Between Physical Symptoms and Psychiatric Disorder. Results from a National Birth Cohort. Br J Psychiatry 173:255–61
8. Large RG (1980) The Psychiatrist and the Chronic Pain Patient:
172 anecdotes. Pain 9:253–263
9. Melzack R, Wall PD (1965) Pain Mechanisms: A New Theory.
Science 150:971–979
10. Merskey H, Spear FG (1967) The Concept of Pain. J Psychosom Res 11:59–67
11. Polatin PB, Kinney PK, Gatchel RJ, Lillo E, Mayer TG (1993) Psychiatric Illness and Chronic Low-Back Pain. The Mind and the Spine - Which Goes First? Spine 18:66–71
12. Polatin PB, Mayer TG (1996) Occupational Disorders and the Management of Chronic Pain. Orthop Clin North Am 27:881–890
Pain as a Stressor
Pain as a Cause of Psychiatric Illness
Pain Assessment
Definition
Pain assessment is the systematic process of evaluating and making pain treatment decisions, obtained either through the use of self report or by proxy (a person other than the person experiencing pain, e.g. health care professional). The process incorporates the consistent use of standardized pain assessment tools to obtain a valid and reliable measure of pain and takes into con- sideration contextual, situational and familial factors.
As it pertains to newborns, frequent assessment of pain and associated stress is required and especially relevant when newborns are on analgesics or sedatives.
Pain Assessment in Children
Pain Assessment in Neonates
Pain Assessment in the Elderly
Pain Assessment in Children
P
ATRICIAA. M
CG
RATHPain Research Center, The Hospital for Sick Children, University of Toronto, Toronto, ON, Canada
patricia.mcgrath@sickkids.ca Synonyms
Paediatric Pain Measures; Paediatric Pain Scales Definition
Pain assessment is an integral component of pain man- agement. At diagnosis, we need a reliable measure of a child’s pain and an understanding of the factors that cause or contribute to pain and disability. Subsequent as- sessments of pain intensity enable us to determine when treatments are effective and to identify those children for whom they are most effective. Thus, pain assessment is a dynamic process that begins with a diagnostic examina- tion and culminates with a clinical decision that a child’s pain has improved sufficiently. Although the key aspects of assessment are the same throughout a treatment pro- gram, the assessment tools or specific measures differ depending on the treatment phase – diagnosis, routine clinical monitoring of treatment efficacy and evaluation at discharge to define whether a child has achieved the treatment objectives (McGrath and Koster 2001).
Characteristics
The criteria for an accurate pain measure for children are similar to those required for any measuring instru- ment. A pain measure must be
valid, in that it unequiv- ocally measures a specific dimension of a child’s pain so that changes in pain ratings reflect meaningful differ- ences in a child’s pain experience. The measure must be
reliable, in that it provides consistent and trustworthy pain ratings regardless of the time of testing, the clinical setting or who is administering the measure. The mea- sure must be relatively
free from bias in that children should be able to use it similarly, regardless of differ- ences in how they may wish to please adults. The pain measure should be practical and versatile for assessing different types of pain (e.g. disease-related, procedural pain) in many different children (according to age, cog- nitive level, cultural background) and for use in diverse clinical and home settings.
An extensive array of pain measures have been de- veloped and validated for use with infants, children, and adolescents (Gaffney et al. 2003; McGrath and Gillespie 2001; RCN Institute 1999; Stevens et al.
2000). Children’s pain measures are classified as
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Pain Assessment in Children 1645
physiological (
physiological pain measure), be- havioural (
behavioral pain scale) and psychological (
psychological pain measures) depending on what is monitored: physical parameters, such as heart or respi- ration rate, distress behaviours, such as crying or facial expression or children’s own descriptions of what they are experiencing. Both physiological and behavioural measures provide indirect estimates of pain because the presence or strength of pain is inferred solely from the type and magnitude of responses to a noxious stimulus.
In contrast, psychological measures can provide direct estimates for many different dimensions of pain (i.e.
intensity, quality, affect, duration and frequency) and provide valuable information on the impact of pain.
Behavioural Pain Scales
Most behavioural pain scales include checklists of the different distress behaviours (e.g. crying, grimacing, guarding) that children exhibit when they experience a certain type of pain (McGrath 1998; McGrath and Gille- spie 2001; Stevens et al. 2000). Health care providers complete such pain scales by noting which of the listed behaviours they see and by ranking their intensity. Most behavioural scales were developed to measure acute procedural or post-operative pain in otherwise healthy children. More recently, attention is focusing on val- idating pain scales for children with developmental disabilities (Breau et al. 2002; Hadden and von Bayer 2002; Hunt et al. 1999; Oberlander and Craig 2003;
Stallard et al. 2002; Terstegen et al. 2003).
Physiological Pain Scales
Physiological parameters that have been monitored in infants and children as potential pain measures in- clude heart rate, respiration rate, blood pressure, palmar sweating, cortisol and cortisone levels, O
2levels, vagal tone and endorphin concentrations (Sweet and McGrath 1998). Although physiological responses can provide valuable information about a child’s distress state, more research is required to develop a sensitive system for interpreting how these parameters reflect the quality or intensity of a child’s pain. At present, physiological pa- rameters do not constitute valid clinical pain measures for children.
Psychological Pain Scales
Psychological or self-report pain scales directly capture a child’s subjective experience of pain. Interviews, ques- tionnaires, adjective checklists and numerous pain inten- sity scales are available for children, each with some ev- idence of validity and reliability (Champion et al. 1998;
McGrath and Gillespie 2001). These self-report mea- sures can provide valuable diagnostic information about the causes and contributing factors for a child’s pain, as well as provide practical tools for regularly assessing pain intensity to ensure that children receive adequate pain control.
When possible, health care providers should ask children directly about the location, quality, intensity, duration or frequency of pain using a semi-structured format (a few basic questions asked in a consistent manner with different follow-up questions depending on the child’s responses). Clinical interviews are ideally suited for learning about the sensory characteristics of pain, the aversive component and contributing cognitive, be- havioural and emotional factors. Interviews should also include a simple rating scale to document pain strength.
Children can use many analogue, facial and verbal rating scales (samples shown in Fig. 1). Children select a level on the scale (i.e., a number, a mark on a visual analogue scale, a face from a series of faces varying in emotional expression or a particular word from an adjective list) to match the strength of their own pain. These scales are easy to administer, requiring only a few seconds once children understand how to use them. Table 1 lists some analogue scales developed for children, along with the type of pain used to initially develop the scale, the scale type, pain feature measured and the resulting pain score.
Pain Ratings –What Do the Numbers Mean?
Although children can use many pain scales, the result- ing pain scores from the different scales are not neces- sarily equivalent. Thus, it is important to know what the pain scores mean on different scales. Some scales simply use numbers to represent different pain intensity levels (e.g. no pain equals 0, mild pain equals 1, moderate pain equals 2 and strong pain equals 3). The numbers are of- ten interpreted as if they represent absolute and accurate amounts of pain. But, unless an investigator studies the relationship between a child’s pain level and the num- bers he or she uses to rate – the psychometric proper- ties – we only know that larger numbers mean stronger pain and we do not know how much stronger. As a re- sult, when evaluating treatment effects, we cannot as- sume that a child who reports that a treatment lessened a pain from a score of 2 to 1 (moderate to mild) is equiv- alent to a reduction from 3 to 2 (strong to moderate) for another child. Similarly, when a child rates a pain as a 3, the pain level may not really be 3 × the strength of the pain he / she rates as a 1. Nevertheless, most pain scores are interpreted as if they represent numbers on equal interval or ratio scales.
The four types of measurement scales (nominal, as in the
numbers designating players on a sports team, ordinal, as
in the rank-ordering of children according to height, in-
terval, as in the Fahrenheit temperature scale and ratio,
as in a yardstick) refer to 4 different relationships be-
tween the properties of an event or perception (e.g. pain
intensity score) and the number or metric system. Ratio
scales have all the properties of the 3 other scales; they
represent a set position or order between numbers, they
show the magnitude of the difference between numbers
and the numbers reflect true ratios of magnitude. Each
1646 Pain Assessment in Children
Pain Assessment in Children, Figure 1 Three scales for assessing children’s pain: word descriptor scale, facial affective scale and colored analog scale.
Pain Assessment in Children, Table 1 Analog Pain Scales for Children
Name Pain Type Method Pain
Characteristic
Scale Type/Pain Score
Comments
Eland Colour Tool Eland and Anderson 1977
Post-operative Projective rating scale on body outline
Intensity, location
Quantitative (probably interval)
Children select colours to represent 3 levels of pain and shade body outline
Poker Chip Tool Hester et al. 1990
Acute pain (immunization)
Object scale compriset of 4 poker chips
Intensity Quantitative, interval scale pain scores 0–4
Children ages 4–7 yrs
Pain Thermometer Syzfelbein et al.
1985
Treatment (Burn dressing change)
Analogue scale, shaped like thermometer
Intensity Quantitative, may be interval or ratio scale, pain scores 0–10
Children and adolescents, ages 8–17
Coloured Analogue Scale (CAS) McGrath et al. 1996
Acute trauma, postoperative, recurrent, chronic pain
Analogue scale, varying in length, hue, and area
Intensity Quantitative, ratio scale properties, pain scores 0–10.0
Psychometric properties demonstrated
Children ages 5 yrs and older, versatility demonstrated for clinical and home use Multiple Size Poker
Chip Tool (MSPCT) St. Laurent-Gagnon et al 1999
Procedural (immunization)
Object scale compriset of 4 poker chips, varying in size (2–3.8 cm)
Intensity Quantitative, interval scale pain scores 0–4
Children ages 4–6 yrs
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Pain Assessment in Children 1647
scale has a certain number of permissible mathematical calculations, so it is important to understand which type of scale one is using when measuring a child’s pain or evaluating analgesic efficacy.
Guidelines for Selecting a Pain Scale for Children
More than 50 pain scales have been developed for chil- dren. Yet, no one scale is appropriate for all children and for all situations in which they experience pain. The crit- ical issue is how to select the most appropriate measure for the age and cognitive level of the child and one that satisfies your clinical objectives. Many simple, easy to use pain scales provide meaningful values that reflect a child’s pain intensity and are ideal measures for evalu- ating treatment effectiveness throughout a child’s treat- ment. But, they are not adequate for teaching us about the nature of a child’s pain or for identifying the primary and secondary situational factors that affect pain.
Health care providers must first consider the age and cognitive ability of a child when selecting a pain scale.
Behavioural scales and physiological distress indices are required for infants and for children who are unable to communicate verbally. Although caution must al- ways be used when interpreting children’s pain solely from their scores on these scales because children’s behaviours are not simply passive reflections of their pain intensity, these scales can provide valuable in- formation. Because a child’s pain behaviours naturally vary in relation to the type of pain experienced, different behavioural scales are usually required for acute and chronic pain.
Pain Assessment in Children, Table 2 Primary components of pain assessment
Sensory characteristics: Cognitive factors:
Onset Location Intensity Quality Duration
Spread to other sites (consistent with neurological pattern) Temporal pattern
Accompanying symptoms
Understanding of pain source
Understanding of diagnosis, treatment, and prognosis Expectations
Perceived control
Relevance of disease or painful treatments Knowledge of pain control
Medical/Surgical: Behavioural factors:
Investigations conducted Radiological and laboratory results Consult results
Analgesic and adjuvant medications (type, dose, frequency, route)
General coping style Learned pain behaviours Overt distress level Parent’s behaviours
Physical activities and limitations Social activities and limitations
Clinical factors: Emotional factors:
Environmental features
Roles of medical and associated health professionals Nature of interventions
Documentation of pain
Criteria for determining analgesic effectiveness
Frustration Anxiety Fear Denial Sadness Anger Depression
Most toddlers (approximately two years of age) first express the “hurting” aspect of pain using a few words learned from their parents to describe the sensations they feel when they hurt themselves. Gradually children learn to differentiate and describe three levels of pain intensity –"a little, some or medium and a lot” By the age of five, most children can differentiate a wide range of pain intensities and many children at this age can use simple quantitative scales to rate their pain intensity.
These pain scales can provide meaningful values that reflect a child’s pain intensity and are ideal measures for evaluating treatment effectiveness throughout a child’s treatment.
But, pain intensity scales alone can not teach us about the nature of a child’s pain or enable us to identify the primary and secondary situational factors that affect pain (McGrath and Hillier 2003). Health care providers who treat a wide range of children’s pain problems need a flexible pain measurement inventory comprised of a more comprehensive assessment instrument and pain diaries, as well as simple pain intensity scales.
Diaries are particularly useful for treating children with recurrent or chronic pain; children record prospectively the frequency, intensity, quality and duration of pain, as well as what they do to reduce the pain and its effective- ness. Diaries can be flexible instruments to fit the needs of the specific therapy program; health care providers may monitor school attendance, physical activity, peer activities, medication use and use of non-drug strategies using simple observation forms.
In summary, evaluating a child’s pain requires an inte-
grated approach. Health care providers should always
1648 Pain Assessment in Neonates
ask a child directly about his or her pain experience and evaluate the sensory characteristics to facilitate an accurate diagnosis. Pain onset, location, frequency (if recurring), quality, intensity, accompanying physical symptoms and pain related disability should be assessed as part of a child’s clinical examination. Health care providers should also assess relevant situational fac- tors in order to modify their pain-exacerbating impact, especially the factors listed in Table 2. Then, health care providers should assess pain intensity or pain be- haviours regularly using brief quantitative scales to monitor the effectiveness of their therapy. Only pre- viously validated pain scales should be used, unless clinicians are willing to conduct the rigorous research necessary to prove that a measure is valid and reliable and to determine its psychometric properties.
References
1. Breau LM, McGrath PJ, Camfield CS et al. (2002) Psychometric properties of the non-communicating children’s pain checklist- revised. Pain 99:349–357
2. Champion GD, Goodenough B, von Baeyer CL et al. (1998) Measurement of pain by self-report. In: Finley GA, McGrath PJ (eds) Measurement of pain in infants and children. Progress in Pain Research and Management. IASP Press, Seattle, pp 123–160 3. Eland JM, Anderson JE (1977) The experience of pain in children.
In: Jacox, AK (ed) Pain: A source book for nurses and other health professionals. Little, Brown, Boston, pp 453–471
4. Gaffney A, McGrath PJ, Dick B (2003) Measuring pain in chil- dren: Developmental and instrument issues. In: Schechter NL, Berde CB, Yaster M (eds) Pain in Infants, Children and Adoles- cents, 2nd edn. Lippincott, Williams and Wilkins, Philadelphia, pp 128–141
5. Hadden KL, von Baeyer CL (2002) Pain in children with cerebral palsy: common triggers and expressive behaviors. Pain 99:281–288
6. Hester NO, Foster R, Kristensen K (1990) Measurement of Pain in Children: Generalizability and Validity of the Pain Ladder and the Poker Chip Tool. In: Tyler DC, Krane EJ (eds) Pediatric Pain.
Raven Press, New York, pp 79–84
7. Hunt AM, Goldman A, Seers K, Crichton N, Mastroyannopoulou K, et al. (2004) Clinical validation of the paediatric pain profile.
Dev Med Child Neurol 46:9–18
8. McGrath PJ (1998) Behavioral measures of pain. In: Finley GA, McGrath PJ (eds) Measurement of pain in infants and children.
Progress in Pain Research and Management. IASP Press, Seattle, pp 83–102
9. McGrath PA, Gillespie JM (2001) Pain Assessment in Children and Adolescents. In: Turk DC, Melzack R (eds) Handbook of Pain Assessment. Guilford Press, New York, pp 97–118 10. McGrath PA, Hillier LM (2003) Modifying the psychological
factors that intensify children’s pain and prolong disability. In:
Schechter NL, Berde CB, Yaster M (eds) Pain in infants, chil- dren, and adolescents. Lippincott Williams & Wilkins, Baltimore, pp 85–104
11. McGrath PA, Koster AL (2001) Headache measures for children:
a practical approach. In: McGrath PA, Hillier LM (eds) The Child with Headache: Diagnosis and Treatment. IASP Press, Seattle, pp 29–56
12. McGrath PA, Seifert CE, Speechley KN et al. (1996) A new analogue scale for assessing children’s pain: an initial validation study. Pain 64:435–443
13. Oberlander TF, Craig KD (2003) Pain and children with develop- mental disabilities. In: Schechter NL, Berde CB, Yaster M (eds) Pain in Infants, Children and Adolescents, 2ndedn. Lippincott Williams & Wilkins, Philadelphia, pp 599–619
14. RCN Institute (1999) Clinical Guideline for the Recognition and Assessment of Acute Pain in Children: Recommendations. RCN Publishing, London
15. Szyfelbein SK, Osgood PF, Carr DB (1985) The assessment of pain and plasma beta-endorphin immunoactivity in burned chil- dren. Pain 22:173–82
16. Stallard P, Williams L, Velleman R et al (2002) The develop- ment and evaluation of the pain indicator for communicatively impaired children (PICIC). Pain 98:145–149
17. Stevens BJ, Johnston CC, Gibbins S (2000) Pain assessment in neonates. In: Anand KJS, Stevens BJ, McGrath PJ (eds) Pain in Neonates, 2nd edn. Elsevier, Amsterdam, pp 101–134 18. St-Laurent-Gagnon T, Bernard-Bonnin AC, Villeneuve E (1999)
Pain evaluation in preschool children and by their parents. Acta Paediatr 88:422–427
19. Sweet S, McGrath PJ (1998) Physiological Measures of Pain.
In: Finley GA, McGrath PJ (eds) Measurement of pain in infants and children. Progress in Pain Research and Management. IASP Press, Seattle, pp 59–82
20. Terstegen C, Koot HM, de Boer JB et al. (2003) Measuring pain in children with cognitive impairment: pain response to surgical procedures. Pain 103:187–98
Pain Assessment in Neonates
F
AYW
ARNOCKChildren’s and Women’s Hospital and The University of British Columbia, Vancouver, BC, Canada
warnock@nursing.ubc.ca Synonyms
Infant Composite Pain Measures; Infant Pain Instru- ments; Pain Evaluation
Definition
Pain assessment is the basis of all
pain management for the rapidly developing
neonate. Assessment is the evaluation of the presence, and if possible the severity, of a neonate’s pain experience. Early and significant exposure to
pain has far-reaching developmental and psychosocial implications for neonates and long term economic costs for society, especially if pain is not treated at critical epochs of infant development (Anand and Scalzo 2000). A neonate’s expression of pain, and the ability of others to recognize and respond appropriately to those expressions, determines whether pain is treated (Craig 1998), and likely influences the future development or survival of that neonate. The assessment of pain during the newborn period is thus crucial, and is especially important for premature and full term newborns born at-risk (e.g. infants who have been prenatally exposed to illicit drugs (cocaine, alco- hol). Such infants are at particular risk because prior exposure to stressors may make them more vulnerable to the harmful effects of subsequent stress and pain stimulation (which is often unavoidable owing to the medical needs of these babies) (Schneider 1998).
Pain assessment enables health care providers to make
judicious pain management decisions using reliable
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Pain Assessment in Neonates 1649
and valid measures and to make use of relevant behav- ioral and environmental information about potential pain
modifying factors for neonates. Yet, assessing pain and gauging the adequacy of pain treatment are particularly challenging in the newborn. For exam- ple, distinguishing newborns’ responses to a noxious (painful) event, from their responses to a non-noxious but distress-inducing event (such as hunger) remains difficult due to lack of scientific data. In addition, healthcare provider attitude, lack of knowledge, and hospital organizational factors that hamper regular pain assessment as a part of care compound the difficulty of evaluating newborns who are still developing their ability to inhibit incoming sensory inputs and who cannot communicate their pain verbally.
Thus, while newborns are highly vulnerable to the neg- ative developmental effects of pain stimulation, they are also entirely dependent upon their
caregivers, and the process of pain assessment is a demanding and highly complex process. For these reasons we require
valid and
reliable measures of newborn pain in order to fur- ther theoretical understanding, and to help promote the development and practice of unbiased pain assessment approaches and best practice guidelines. We also need to be alert to the everyday factors that cause, intensify or prolong newborn pain in order to assess the newborn’s pain comprehensively.
Characteristics
The unbiased assessment of newborn pain requires pain assessment tools that meet universally acknowledged criteria pertinent to any measuring instrument. The pain tool must be reliable in that it is reproducible and stable under the different conditions in which it is likely to be used. A pain tool must also be valid in that it is rooted in theoretical understanding of the construct under study (e.g. newborns and their pain), it measures what it is intended to measure and it predicts what it is intended to predict. The tool must also have clinical utility, be
feasible to use (if it is designed for clini- cal application), and it should allow quantification of both pain intensity and pain duration. In addition, the unbiased assessment of newborn pain requires that the act or process of assessment itself be
systematic and based on
objective judgment rather than
subjective judgment.
At least 20 pain assessment tools have been developed for newborns (Mathew and Mathew 2003), including physiological, behavioral, and biochemical indica- tors (measures). These measures are categorized as
unidimensional or
multidimensional (composite) depending on the number of pain indictors included.
At present, no biological measure of pain exists, so that these three pain indicators are ‘indirect” estimates of newborn pain because we infer pain based on the type and frequency of responses made by the newborn to a noxious stimulus.
Heart rate is the most widely used physiological measure of newborn pain. Changes in heart rate can be assessed easily and continuously with an electrocardiograph.
Other physical measures include blood pressure, respi- ratory rate, oxygen consumption, mean airway pressure, palmar sweat, flushing, pallor, intracranial pressure and cerebral blood volume. Behavioral measures include crying, grimacing, change in facial action (using the neonatal facial action coding system), body move- ment, infant state, and a lack of pain response (noted in premature infants). Some biochemical measures include increased secretion of cortisol, catecholamines, glucagons, growth hormone and decreased section of insulin. Behavioral measures provide the most direct information, because behavior enables the pre-verbal neonate to communicate their pain. Increase in heart rate and change in facial action are generally suggested to correlate with intensity of pain, with facial action being the most consistent (Craig 1998), and it has been found to be applicable for bedside application (Harrison et al. 2002). More recently, researchers investigating pain response in premature infants have added gestational age, prior pain experience and lack of response as im- portant adjuncts to newborn pain assessment (Stevens et al. 1994). Of the tools published, the majority have been developed for research purposes rather than for direct clinical application.
Application of Pain Assessment Tools for Research and for Clin- ical Purposes
