Chapter 15 PAIN MANAGEMENT

Eileen Mann

Introduction

This presentation focuses on the healthcare of patients experiencing pain. It adds to the knowledge you will already have gained by reading the book chapter.

Part 1 – Epidural AnalgesiaPart 2 – Postoperative Nausea and

VomitingPart 3 – The Multidimensional Nature of

PainPart 4 - Entonox

PART 1: Epidural Analgesia

Epidural Analgesia

Involves the infusion of a local anaesthetic and commonly an opioid into the epidural space surrounding the spinal cord.

The epidural space extends from the foramen magnum to the sacral canal.

Why Use Epidurals?

• High quality analgesia• Reduced complications/bedstay• Needs much less opioid, resulting in

reduced side effects such as PONV, delayed nutrition, sedation

• Reduced respiratory infections• Increases mobility leading to less

muscle wasting and deep vein thrombosis

Locating the Epidural Space

Spinal

cordSpinal column

Spinal Nerves

Cervical - 8 pairs interconnect to form the cervical plexus and the brachial plexus. These innervate the back of the head, neck, shoulders, arms, hands and diaphragm

Thoracic - directly connected to the muscles between the ribs, deep back muscles, abdomen and thorax

Lumbar - supplies the muscles of the lower limbs and trunk, external genitalia, groin and lower limbs

Sacral - forms the sacral and coccygeal plexus, innervating the thighs, buttocks, legs, feet and the anal/genital area

Coccyx - one pair of nerves supplies the skin in the region of the coccyx

Who may benefit from an epidural?

• Patients recently undergone abdominal incisions

• Serious pelvic & leg fractures

• Major pelvic and leg surgery

• Particularly useful following chest trauma

Epidural is performed with the patient sitting or lying down with their back

curved outwards

Contraindications

• Patient refusal• Coagulopathy• Local infection• Inadequate

facilities, equipment, training, staffing levels

• Anatomical abnormality

•Hypovolaemia•Sepsis/fever•Back problems•Neurological condition

•Allergy

Caudal Analgesia

This involves placing local anaesthetic into a continuation of the epidural space that is located at the lower end of the spine.

It produces a block of the sacral and lumbar nerve roots which is ideal for perineal surgery.

Local Anaesthetics

• Blocks the initiation and spread of action potentials within the nerves

• Blocks conduction in small diameter nerve fibres (A delta & C fibres) more readily than large fibres (A beta)

• Therefore pain sensation is blocked more easily than other sensory modalities (touch etc.)

Opioids

• Thought to bind to opioid receptors in the substansia gelatinosa of the spinal cord interfering with the pain impulse

• Provides analgesia which lasts longer than systemic opioids

• Does not cause motor or sensory blockade, or hypotension

• Fentanyl 50 - 200 mcg will last around 3 - 6 hours

• Diamorphine 0.5 - 5 mg will last 6 - 12 hours

Opioid Side Effects

• Effects receptors in the medullary respiratory centre leading to potential respiratory depression

• Sedation

• Itching

• Nausea

Local Anaesthetic Side Effects

Local anaesthetics block conduction in all types of nerves:

• Sympathetic block - hypotension, urinary retention

• Sensory block - pressure sores

• Motor block - weakness, immobility, falls.

Complications of Combined Local Anaesthetic/Opioid Epidurals

Early: • Hypotension• High sensory and

motor block • Respiratory

depression• Sedation• Cardiovascular

complications• Head/neck/backache• Anaphylaxis

Late:• Haematoma• Epidural

abscess• Infection and

sepsis• Unresolved

motor and sensory loss

• Itching• Leaking

epidural

The Ideal Outcome

A sensory pain block with no motorblock and minimal side effects. An

alertpatient capable of early

mobilisation and able to participate inactive physiotherapy.

Monitoring

• Consciousness level

• Colour

• Heart rate

• Blood Pressure

• Respirations

• Oxygen saturation

• Temperature

• Wound

• Urine output

• Motor/sensory levels

• PAIN

PART 2: Postoperative Nausea and Vomiting (PONV)

Why Treat Nausea and Vomiting?

• Humanitarian reasons• Increase in autonomic activity• Increase in closed compartment

pressure• Delayed hydration and nutrition• Delayed discharge from hospital• Delayed return to work and normal

functioning

P.O.N.V.

A vastly underrated problem.

Many patients fear nausea and vomiting more than postoperative pain.

30% elect to forgo opioids and tolerate pain if this stops the nausea.

Patients at Risk from PONV

• History of PONV and/or motion sickness

• Females > males (pre menopause)

• Young > old

• Type of procedure performed

• Use of opioids

Chemical Receptors in the Vomiting Centre in the Brain

Acetylcholine: • cyclizine, hyoscine

Dopamine antagonist: • droperidol, metoclopramide,

phenothiazines

5 Hydroxytryptamine (serotonin):• ondansetron

Histamine

Antiemetics

All give 30-45% reduction of symptoms at best

May reduce vomiting more than nauseaPharmacodynamics/kinetics poorly

understood for older drugsMultimodal antiemetic therapy?Cyclizine, prochlorperazine and

ondansetron all have more or less equal efficacy.

Metoclopramide has no antiemetic action in the postoperative setting.

The role of steroids?

Antiemetics

Ondansetron available as i.v.+ melts• Cyclizine i.v.i ( side effect

problems)• Prochlorperazine P.O

Buccastem (i.m., p.r.)

Best evidence :• Ondansetron 8mg i.v. PLUSPLUS• Dexamethasone 8mg i.v.

Summary

• Carry out a risk assessment• Prophylaxis• Avoid emetogenic drugs if possible• Combination therapies • Complementary therapies• Educate patients and staff

PART 3: The Multidimensional Nature of Pain

Definition of Pain

“An unpleasant sensory and emotional experience associated with actual or

potential tissue damage, or described in terms of such damage”

IASP 1986

‘Pain of recent onset and probably limited duration. It usually has an identifiable temporal and causal

relationship to injury and disease’.IASP 1986

Acute pain will always respond to analgesia

Definition of Acute Pain

‘Pain lasting for long periods of time. It usually persists beyond the

time of healing of an injury and frequently there may not be any

clearly identifiable cause’.

IASP 1986

Chronic pain may or may not be opioid responsive and other

analgesic regimes may also be ineffective

Definition of Chronic Pain

The Acute/Chronic Debate

Q. Where does acute pain end and chronic pain begin? Do changes happen much earlier than previously thought?

Q. What is the biological mechanism that is driving pain?

Q, What are the impact of psychosocial factors?

Acute AND Chronic Pain

• Acute – nociceptive (biologically active)• Chronic – nociceptive/neuropathic,

mixed• Acute on Chronic episodic/background• Visceral• Idiopathic

Acute TO Chronic Pain

Pain is usually event related and starts as an acute episode with a high level of biological activity. The pain is initially reversible.

Changes tend to become fixed depending upon: the nature and duration of the original cause of pain, age of the patient, psychosocial influences such as pain memory, culture, pain affect and possibly genetic susceptibility.

Types of Pain Syndromes (IASP 1986)

• Chronic pain

• Cancer related pain

• Somatic pain (superficial & deep)

• Visceral pain

• Neuropathic pain

Theories of Pain

• Specificity theory • Pattern theory

• Neuromatrix

• Gate Control Theory

The Gate Control Theory

• Modulating ‘gating’ mechanism

• Large diameter fibres (touch) ‘closed’ the gate

• Small diameter fibres (nociceptors) ‘opened’ the gate

• Affective/cognitive descending ‘modulation’

• Pain is multidimensional

Nociceptors

Two types of afferent fibres:

A DELTA: Mylenated, fast (>30m/s) “fast” painBright, sharpSomatic

C FIBRES: Unmyelenated, slow (.5-2 m/s)

“slow” painDull diffuse, continuous, deep

Cross Section of the Spinal Cord

A Beta

A Delta

C FibresSubstantia Gelatinosa

“GATING” MECHANISMS

Located within the dorsal horn of the spinal cord, but also found within the brain stem, hypothalamus and thalamus

Somatosensory cortex

ThalamusHypothalamus

Brainstem

Substantia gelatinosa

Sensory input from the periphery

Ascending mechanism

Descending mechanism

Autonomic response

Limbic system

1

2

3

4

5

Physiology (Sensory)

1. Nociceptors A-delta, B-delta, C fibres2. Chemicals – histamine, bradykinin3. Neurochemical mediators 4. Ascending transmission5. Descending transmission6. Pain systems dynamic and “plastic” 7. Pain perception can be modulated by

both pharmacological and non pharmacological strategies at all levels of the nervous system.

8. Changes may become fixed - remapping

Primary Hyperalgesia

• Reduction in the pain threshold in the area of damage. e.g. skin burn, pharyngitis, sprained ankle

• Locally released chemical inflammatory mediators: potassium, histamine, bradykinin, leukotrienes, serotonin, histamine, substance P, arachadonic acid metabolites (prostaglandins etc)

Secondary Hyperalgesia

• Non-nociceptors acquire capacity to evoke pain

• Central pain pathways adjust and change – pain memory?

• Brief stimulation of nociceptors can cause major changes in the receptive fields in the spinal cord.

• Repetitive peripheral stimulation causes response to progressively increase.

• Possibly due to loss of central inhibition.

• Acute gene expression altering receptors.

• Remapping at cord and brain level.

“Pain Windup”

Pain continuing or worsening when the cause is stable or

improving.

FEATURES: • Reduced threshold• Augmented response• Ongoing activity• Pain adjacent to but beyond the

limits of tissue injury.

Pain Management

ACUTE PAIN

Relatively easy to treat but needs effective early therapy to reduce the risk of wind up/cortical remapping. A narrow therapeutic window. **

**At one year following hernia surgery 29% of patients reported pain in the area of the hernia, 11% reported that it impaired their work or leisure activity but only 4.5% had sought medical advice (Bay Nielsen et al 2001)

CHRONIC PAIN

Once established often relatively difficult to treat.

Can be resistant to ordinary analgesia. Psychosocial interventions needed, central changes, autoimmune components.

Recent Developments

• Better understanding of the mechanisms

• Improved use of assessment tools • Advances in imaging – CAT, PET and

fMRI• Evidence based health care –

improved guidelines and algorithms• New drugs for pain management • New modes of delivery & more

appropriate use• The role of non pharmacological

therapy - cognitive and behavioural strategies

Summary

• Pain is multidimensional

• The assessment and management of pain should reflect the sensory, affective and cognitive components

• Sociocultural components are important

• Future developments are likely to focus on genetic variability

PART 4: Entonox

Identification

Presented in cylinders that are painted blue with a white and blue shoulder.

The gas is pressurised and is self administered by the patient via a pressure regulator and demand valve.

Mechanism of Action

True mechanism of analgesia is not known.

The effects of Entonox take place within the pain centres of the brain and spinal cord.

The gas forms an essential ingredient in general anaesthesia.

Pharmacokinetics

Entonox is an analgesic agent that is composed of 50% nitrous oxide and 50% oxygen.

It offers rapid onset of potent analgesia with speedy reversal of effects.

It is inhaled, absorbed through the lungs into the blood within which it is carried to the brain where analgesia occurs.

The effects of Entonox are felt within three to four breaths and maximised after 2 minutes.

The effects rapidly disappear once Entonox inhalation is discontinued.

Residual effects are hard to display after 30-40 minutes. Despite this patients are usually advised not to drive for 12 hours.

Pharmacodynamics

Metabolism and Excretion

Entonox is rapidly excreted from the body.

It is excreted, largely unchanged, by the lungs into the surrounding air.

Toxicity

Prolonged use of Entonox in an enclosed space may subject staff to undue exposure.

Prolonged use (exceeding 6-8 hours) may have an adverse effect on vitamin synthesis.

Use over 6 hours may also interfere with folate metabolism and DNA synthesis which can impair bone marrow function.

Use of Entonox

Ideal for situations where pain is of short duration.

Can be used in combination with other analgesics such as paracetamol, NSAIDs and opioids.

A mouthpiece/face-mask and bacterial filter is required for individual patient use.

The gas is safe for any age group as long as they are able to comprehend and physically operate the system.

• Changing dressings, packs and removing drains

• Suturing and removing sutures• Redressing burns• Invasive procedures : catheterisation,

cannulation, sigmoidoscopy• Changing and removing clothing• Applying traction; removing skeletal

pins• Physiotherapy• Renal colic; constipation• Lifting and moving patient

Clinical Uses of Entonox

Precautions

Patient refusal or known allergy

Entonox will cause an enclosed air pocket in the body to expand rapidly in volume as the gas mixture is absorbed from the blood into the space. Therefore Entonox is contra-indicated in all cases where there is air trapped within a body space.

Contraindications • Artificial, spontaneous or traumatic

pneumothorax• Intestinal obstruction• Air embolism, following a recent

underwater dive/ decompression sickness• Myringoplasty• Intoxication• Severe bullous emphysema• Head injuries with impaired consciousness.• Maxillofacial injuries with a risk of inhaling

blood• Patient non-compliance

Drug Interactions

There are no major incompatibilities with other drugs and Entonox, when used with other analgesics, can form

part of an effective multimodal approach to pain control.

Side Effects

• May cause drowsiness

• Allergic and sensitivity reactions are rare

• Minor effects on the heart and cardiovascular system

• Minimal effects on respiration

• Can cause nausea