Pain MX

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SCENARIO: Patient with severe post-operative pain.

Drug chart: received only


Panadol and Arcoxia (selective COX2 inhibitor)

Define pain?

Unpleasant Sensory and emotional experience associated with actual or


potential tissue damage

What to do after seeing this drug chart?

• Investigate why PRN medications were not given


• File an incident report

How will you manage this patient after this drug chart?

Immediate management: In the critically ill patient in pain, patient assessment is vital. It
should follow the same CCrISP system of assessment as in any other circumstance.

A. Airway: Start at the beginning by checking that the patient has a patent airway.
B. Breathing: Check the respiratory rate, pattern and depth of breathing. Is your
patient’s respiratory function impaired by inadequate analgesia? Can he or she cough and
expectorate properly to avoid problems later?
C. Circulation: Tachycardia should not automatically be assumed to be caused by
pain–there is commonly an underlying cause. A persistent tachycardia or hypertension
caused by inadequate analgesia may potentiate the development of myocardial ischemia,
particularly in the patient who is already hypoxemic.
D. Disability: It is important to assess whether the method of analgesia is
contributing to the patient’s clinical deterioration. Particular attention should be paid to the
patient’s level of consciousness as decreasing conscious level is an early indicator of opioid
toxicity.
Full patient assessment:
• Chart review: If pain relief is felt to be contributing to the patient’s deterioration, the
drug charts should be reviewed with the following questions in mind:
o Is effective analgesia prescribed?
o Is effective analgesia being given?
o Is the treatment appropriate for this patient?
• History and systemic examination

• Investigations:
serial ABG analysis and chest X-rays
• Decide and plan: If pain relief is adequate and the patient is improving then continue and
review. If pain relief is inadequate determine why:
o Is it due to failure of the method of analgesia?
o Is it due to incorrect implementation of the method chosen?
o Is it due to the development of a surgical complication?
• Liaise with acute pain multi-disciplinary team (acute pain services): multidisciplinary acute
pain team consisting of surgeons, anaesthetists, nursing staff and pharmacists

What are the Side effects of opioids?

Adverse Effects with Acute Use:


• Respiratory depression • Nausea / vomiting • Pruritus • Urticaria •
Constipation • Urinary retention • Delirium • Sedation • Myoclonus • Seizures
Adverse Effects with Chronic Use:
• Hypogonadism • Immunosuppression • Increased feeding • Increased
growth hormone • Withdrawal effects • Tolerance, dependence • Abuse,
addiction • Hyperalgesia • Impairment while driving
Can you please describe pain Intensity and Management? C

Pain intensity escalation and management:


Mild: Paracetamol or NSAID
Mild-to-moderate: Combination analgesic ± NSAID
Moderate: Oral opioid OR combination analgesic ± NSAID
Moderate-to-severe: Oral opioid + paracetamol ± NSAID
Severe: Parenteral opioid (IV, IM or SC) + paracetamol ± NSAID OR epidural (local anaesthetic
± opioid)
Combination analgesics are a mixture of weak oral opioid and paracetamol

What is the pain pathway?

Pain is transmitted via fast A-delta fibres (sharp pain) and slower C fibres
(dull pain) to lateral spinothalamic tract then to the thalamus

Ascending tracts carrying sensory information from peripheral receptors to the


cerebral cortex.
A) Dorsal column pathway mediates touch, vibratory sense, and
proprioception. Sensory fibres ascend ipsilaterally via the spinal dorsal columns
to medullary gracilus and cuneate nuclei; from there the fibres cross the
midline and ascend in the medial lemniscus to the contralateral thalamic
ventral posterior lateral (VPL) and then to the primary somatosensory cortex.
B) Ventrolateral spinothalamic tract mediates pain and temperature. These
sensory fibres terminate in the dorsal horn and projections from there cross
the midline and ascend in the ventrolateral quadrant of the spinal cord to the
VPL and then to the primary somatosensory cortex.
Describe Patient controlled analgesia: (PCA)??

• It's a syringe pump connected IV to allow the patient to self-administer


boluses of morphine
• Overdosage is avoided by limiting both the size of the bolus and the
frequency of administration
• A lock-out time is set within which pressing the button again will not result in
a bolus of analgesia
• One-way valve preventing backflow of opiates into the infusion chamber
which may lead to overdose when redelivered
Normal dose of morphine (PCA)?

0.5-2 mg bolus

What problems may arise while using syringe pumps?

• Patient must be alert and oriented to be able to use it


• Can break down, run out of battery
• Sleep disturbance
• Not suitable for patients who are confused or who are unable to press the
demand button for physical reasons.
• Limits patient mobility

What are the complications of pain?

• CVS: Increased HR, BP, and myocardial consumption → MI, DVT from
immobility.
• GIT: Delayed gastric emptying, Reduced bowel motility, Paralytic ileus.
• Respiratory: Limit chest movements leading to atelectasis, retained
secretions, pneumonia.

How would you manage his pain initially?

After ABCDE assessment, I will assess the severity of the pain with
one of the pain scales then I will consult the Pain Team if available, if no pain
team l will give analgesics according to the WHO analgesic ladder with the
regular assessment.
• Non-pharmacological methods: Preoperative explanation and education,
relaxation therapy, hypnosis, cold or heat, splinting of wounds, Transcutaneous
Electrical Nerve Stimulation (TENS).
• Pharmacological methods: Simple analgesia (paracetamol), NSAIDs, Opiates,
LA (epidural & local infiltration).

Give examples of the opioids in common use. Which agents are synthetic and
which ones are non-synthetic?

• Non-synthetic: morphine, codeine (10% of this is metabolized to Morphine)


• Semi-synthetic: diamorphine, dihydrocodeine.
• Synthetic: pethidine, fentanyl.

Why is codeine bad?

• Drowsiness, constipation, itching, nausea, vomiting, dry mouth, miosis,


orthostatic hypotension, urinary retention, euphoria, dysphoria, and coughing.
• Rare anaphylaxis, seizure, acute pancreatitis, and respiratory depression.
• CYP2D6 (cytochrome P450 enzyme) converts codeine into morphine in the
liver. Some Patients (Ultra-rapid Metabolizers) who have high level of CYP2D6
resulting in rapid formation of morphine in them causing life threatening
intoxication, including respiratory depression requiring intubation, can develop
over a matter of days. Other patients (10%) lack this enzyme, they lose the
analgesic effect of codeine (poor metabolizers) but suffer its side effects.

What is the mechanism of action of Paracetamol?


Mechanism of action of paracetamol (acetaminophen) is not completely
understood. But it’s generally considered to be a weak inhibitor of the
synthesis of prostaglandins (PGs). However, the in vivo effects of paracetamol
are similar to those of the selective cyclooxygenase-2 (COX-2) inhibitors.
How do you manage paracetamol toxicity?
• Gastric decontamination:
➢ Gastric lavage, within 60 minutes of ingestion.
➢ Activated charcoal: 30 minutes to 2 hours of ingestion.
• Acetylcysteine (N-acetylcysteine): Antidote replenishing body stores of
the antioxidant glutathione.
• Liver transplant in acute liver failure

Please describe pain scoring systems?

Verbal descriptor scale: Is your pain: 0, absent; 1, mild; 2, discomforting; 3,


distressing; 4, excruciating
Verbal Numerical rating scale: Which number describes your pain: 0, no pain;
10, worst imaginable
Visual Analogue Scale (VAS): No pain to Worst imaginable
Wong-Baker FACES: For children
Functional assessment: Can you move? Can you cough?
WILDA: Word to describe, Intensity, Location, Duration, Aggravating/alleviating
factors

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