General pain management - Clinical Tree

Essentials

1
Acute pain is the most common symptom in the emergency setting.
2
Pain is a complex, multidimensional, subjective phenomenon.
3
Effective pain management involves both accurate assessment and timely treatment.
4
Patient self-reporting is the most reliable indicator of the presence and intensity of pain.
5
Both pharmacological and non-pharmacological techniques should be employed for the treatment of acute pain. Effective pain relief should always be achievable.
6
In acute abdominal pain, titrated opioid analgesia should never be withheld, pending surgical review; the effect of analgesia on physical signs should not be used as a diagnostic test.

Introduction

Pain is defined by the International Association for the Study of Pain as: ‘An unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage’. Acute pain is defined as: ‘Pain of recent onset and probable limited duration. It usually has an identifiable temporal and causal relationship to injury or disease’. Whereas in some conditions the nature and progression of the pain may be helpful in making the diagnosis of the underlying pathology, too great a reliance has been placed upon this feature, thereby allowing the patient to suffer needlessly for prolonged periods. For example, the notion that analgesia masks clinical signs in the context of abdominal pain is a fallacy; provision of pain relief often enhances a clinician’s diagnostic ability.

It is recognized that failure to adequately treat acute severe pain, in the emergency setting, is associated with adverse biochemical, physiological, metabolic, and psychological sequelae, and in some patients may alter responses to future painful episodes. Thus the timely management of acute pain is a fundamental pillar of good emergency medicine practice to reduce the avoidable suffering to our patients.

Physiology

Pain is one of the most complex aspects of an already intricate nervous system. A number of theories have been developed to explain the physiology of pain, but none is proven or complete.

‘Gate Control Theory’

In 1965, the Melzack–Wall ‘Gate Control Theory’ emphasized mechanisms in the central nervous system that control the perception of a noxious stimulus and thus integrated afferent, upstream processes with downstream modulation from the brain. However, this theory did not incorporate long-term changes in the central nervous system to the noxious input and to other external factors that impinge upon the individual.

Nociceptor function

Most pain originates when specific nerve endings (nociceptors) are stimulated, producing nerve impulses that are transmitted to the brain. Nociception is the detection of tissue damage by specialized transducers. It is now recognized that nociceptor function is altered by the ‘inflammatory soup’ that characterizes a region of tissue injury. The final pain experience is subject to a complex series of facilitatory and inhibitory events that precedes pain awareness, such as past experience, anxiety or expectation. There are two types of nociceptors :

I.
Mechanoreceptors, which are present mainly in the skin (also muscle, joints, viscera, meninges) and respond rapidly to pinprick or heat via Aδ, myelinated afferent neurons.
II.
Polymodal, which are widely distributed throughout most tissues and are the nerve endings of unmyelinated C-type afferent neurons. These respond to tissue damage caused by mechanical, thermal or chemical insults and are responsible for the slow onset, prolonged, poorly localized, aching pain following an injury.

Once transduced into electrical stimuli, conduction of neuronal action potentials is dependent on voltage-gated sodium channels. A number of chemicals are involved in the transmission of pain to the ascending pathways in the spinothalamic tract. These include substance P and calcitonin gene-related peptide, but many others have been identified. Opioid receptors are present in the dorsal horn and it is thought that encephalins (endogenous opioid peptides) are neurotransmitters in the inhibitory interneurons.

Phospholipids released from damaged cell membranes trigger a cascade of reactions, culminating in the production of prostaglandins that sensitize nociceptors to other inflammatory mediators, such as histamine, serotonin and bradykinin.

The threshold for the perception of a painful stimulus is similar in everyone and may be lowered by certain chemicals, such as the mediators of inflammation. The discrete cognitive processes and pathways involved in the interpretation of painful stimuli remain a mystery. The cognitive and emotional reactions to a given painful stimulus are variable among individuals and may be affected by culture, personality, past experiences and underlying emotional state. In addition, intense and ongoing stimuli further increase the excitability of dorsal horn neurons, leading to central sensitization. With increased excitability of central nociceptive neurons, the threshold for activation is reduced and pain can occur in response to low intensity, previously non-painful stimuli known as allodynia. Pain is therefore a complex, multidimensional, subjective phenomenon.

Assessment of pain and pain scales

Pain intensity may be assessed subjectively (i.e. as reported by the patient) or by some objective measures. In daily clinical practice, health care providers employ a combination of tools to estimate the degree of physical patient distress including subjective assessment, for example, not only by asking the patient to rate the intensity of their pain, but also by the nature of the illness or injury, the patient’s appearance, behaviour and physiological concomitants. No single method has proved to be 100% reliable.

Pain scales have been developed because there are no reliable physiological or clinical signs to measure pain objectively. Ultimately the perception of pain is an individual experience. Three scales have become popular tools to quantify pain intensity as follows:

Visual analogue scale (VAS),
Numeric rating scale and
Verbal rating scale.

Visual analogue scale

The VAS usually consists of a 100-mm line with one end indicating ‘no pain’ and the other end indicating the ‘worst pain imaginable’. The patient simply indicates a point on the line that best indicates the amount of pain experienced. The minimum clinically significant change in patient pain severity measured with a 100-mm VAS is 13 mm. Studies of pain experience suggest that less than a 13 mm change in pain severity, although statistically significant, is not clinically significant.

Numeric rating scale

The patient is asked in the numeric rating scale to choose a number from a range (usually 0 to 10) that best describes the amount of pain experienced, with zero being ‘no pain’ and 10 being the ‘worst pain imaginable’.

Verbal rating scale

The verbal rating scale simply asks a patient to choose a phrase that best describes the pain, usually ‘mild’, ‘moderate’ or ‘severe’.

Pain intensity is generally accepted to fall into one of three categories, as follows: mild pain (1–3/10), moderate pain (4–6/10), and severe pain (7 or greater/10)

In the clinical setting, anxiety, sleep disruption and illness burden also contribute to the burden of pain. It is difficult to use a unidimensional pain scale to measure a multidimensional process. Using pain intensity alone will often fail to capture the many other qualities of pain and the overall pain experience. The best illustration of this problem is that the same pain stimulus can be applied to two different people with dramatically different pain scores and analgesic requirements. At best, the use of pain scales is an indirect reflection of ‘real’ pain, with patient self-reporting still being the most reliable indicator of the existence and intensity of pain. Indeed some authorities have suggested that simply asking the patient ‘Do you require medication to relieve your pain?’ may be all that is required to trigger initiation of analgesic therapy.

Nevertheless, pain scales are simple and easy to use. They are now routine in many emergency departments (EDs), often being a standard part of the triage process, which leads to substantially faster provision of initial analgesia.

General principles

Patients in pain should receive timely, effective and appropriate analgesia, titrated according to response. The following points should be stressed:

The correct analgesic dose is ‘enough’; that is, whatever amount is needed to achieve appropriate pain relief.
A patient’s analgesic requirements should be reviewed frequently. Do not wait for pain to return to its previous level before re-dosing with analgesia. Larger early doses and more frequent doses of analgesia are associated with lower total doses and shorter duration of analgesic use. Some patients have been misled into believing that pain medicine is dangerous, so it is important to explain the safety and efficacy of this approach.
EDs should have specific policies relating to pain and analgesia.
Senior clinicians should lead by example.

Routes of administration

Analgesic agents may be administered by many routes including oral, intranasal, subcutaneous, intramuscularly, intravenous, epidural, nebulized, intra-pleural, intra-articular and transdermal. All may have a role in a specific clinical situation. There is a good rationale for the use of the intravenous route in moderate-to-severe pain and titration of intravenous opioids remains the standard of care for acute severe pain. However, in the presence of severe pain, and in patients where immediate vascular access is problematic, the intramuscular (e.g. morphine or ketamine), oral transmucosal (e.g. fentanyl citrate), or intranasal routes may provide a useful alternative in delivering timely and effective analgesia (e.g. intranasal diamorphine/fentanyl/ketamine).

Specific agents

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