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‫بسم هللا الرحمن الرحيم‬
PAIN MANAGEMENT
1. PHARMACOTHERAPY
Salah N A El-Tallawy
Prof. of Anesthesia and Pain Management,
Faculty of Medicine, Minia University & NCI, Cairo University, Egypt
Associate Prof. KSU, KSA
Objectives

Introduction.

Pain control strategies.

Special painful conditions.

Rules for pharmacotherapy.

Algorithms for pain management.
What’s the definition of pain?
“Pain is a Sensory and Emotional experience,
associated with actual or potential tissue
damage or described in terms of such damage”
(IASP)
Pain is under-treated ???

Lack of Knowledge

Barriers:

in the health care

in the regulatory systems

with the patients
The “Costs” of Uncontrolled Pain







Stress response  Hypothalamo-Pituitary-Adrenal axis:

Disturbed cytokine cascade.

Impairment of immune function.

Increased catabolism.

Negative nitrogen balance.
Pain Chronicity.
Cardiovascular
Respiratory
GIT
Neuro-psychiatric
Impairment of mobility, Gait disturbances.
Peripheral
sensitization
• Tissue damage
Central
Sensitization
•  Nociceptive
input
• Inflammatory
soap
•  Excitability
of DHN
• Sympathetic
stimulation
• Mechanical
allodynia
1ry Hyperalgesia
2ry Hyperalgesia
Causes of Acute Pain

Post-operative

Obstetric - Labor

Burns

Trauma

Infective / Inflammatory conditions

Ischaemic pain

Visceral pain
Causes of Post-Operative Pain

Incisional
skin and subcutaneous tissue

Deep
Positional
IV site
Tubes
Respiratory
Rehab
Surgical
Others
cutting, coagulation, trauma
nerve compression, traction & bed sore.
needle trauma, extravasation, venous irritation
drains, nasogastric tube, ETT
from ETT, coughing, deep breathing
physiotherapy, movement, ambulation
complication of surgery
cast, dressing too tight, urinary retention







Causes of Chronic Pain

Cancer pain




Cancer related
From cancer therapy
Cancer unrelated
Non-cancer



Nociceptive
Neuropathic
Idiopathic
Pain Assessment
S
R
N
Good assessment = Successful management
Pain Assessment
•
Subjective:
• Pain Scores:
•
Unidimentional  Acute pain
•
•
•
Multidimentional  Chronic pain
•
•
VRS, VAS & NRS.
Facial expression.
McGill & Pain Inventory.
Objective:
–
–
–
–
Behavioral: refusal to move, cough & deep breath
Physiological:  PR, RR, ABP, sweatiness & dilated pupils
Neuro-endocrinal: RBS, Stress hormones
Algometry.
Pain Scores
Visual Analogue Scale (VAS)
0
10
Numeric Rating Scale (NRS)
Verbal scale
No
Pain
Mild
Moderate
Severe
Pain
Wong-Baker “Faces Scale”
Questions to Ask about Pain
P A I N

Pattern: onset, course & duration

Area: location

Intensity

Nature: burning, colic, …
Questions to Ask about Pain
P Q R S T
(ECG format)

Provocation

Quality - characters of pain

Referred / Radiating

Severity

Timing
Questions to Ask about Pain
LO CATE S
L – Location.
O – Other Symptoms.
C – Character: deep, burning, throbbing…
A – Aggravating and Alleviating factors.
T – Timing.
E – Effect: your daily routine?
S – Severity.
Personal opinion # Patient self report ?
Pain Control Strategies
–Pharmacotherapy
–
–
–
–
–
–
–
Anesthetic approaches
Implantable devices
Neurostimulation approaches
Alternative approaches
Surgical approaches
Rehabilitative approaches
Lifestyle changes
– Psychological approaches

Non Opioid Analgesics:
– NSAA
– NSAIDs
• Non-selective COX inhibitors
• Selective COX-2 inhibitors

Opioids
– Weak Opioids.
– Strong opioids.
– Mixed agonist – antagonists

Adjuvants
–
–
–
–
–
–
–
–
Antidepressants
Anticonvulsants
Substance P inhibitors
NMDA inhibitors
LA
Drugs for Headache
Drugs for Bone pain
Others .
Drug Strategies
Non-Drug Strategies

Alternative medicine:
–
–
–
–

Acupuncture
TENS
Cupping
Chiropractice
Physical Therapy
– ice, heat, massage


Exercise
Psychological therapy
–
–
–
–
Cognitive-behavioral therapy
Relaxation techniques
Biofeedback
Hypnosis
WHO step Ladder
3 severe
Morphine
2 moderate
Codeine
Hydrocodone
1 mild
Oxycodone
Dihydrocodeine
ASA
Acetaminophen
NSAIDs
± Adjuvants
Tramadol
± Adjuvants
Hydromorphone
Methadone
Pethidine
Fentanyl
Oxycodone
± Adjuvants
1. Drug Therapy
1)
Non Opioid Analgesics:
– NSAAs
– Analgesic /Antipyretic e.g.
– Acetaminophen (COX-3 ---) & Antipyrine
– Analgesic/Anti-inflammatory/Antipyretic e.g.
– Salicylic acid
– NSAIDs
• Non-selective COX inhibitors
• Selective COX-2 inhibitors
Commonly Used NSAIDs
Drug Name
Usual Adult Oral
Dose (mg)
Usual dose
interval (Hrs)
Pediatric Dose
(Mg/Kg)
Maximal Daily
Dose (Mg/Day)
Other Comments
Aspirin
325-1000
4-6
10-15 g 4-6
4000
Not for use in children younger than 12
with possible viral illness due to Reye’s
syndrome
Acetaminophen
500-1000
4-6
10-15 q 4-6
4000
Significant liver toxicity in overdose. May
increase INR in patients taking warfarin.
Choline Magnesium
Trisalicylate
1000-1500
12
25 bid
2000-3000
No effect on platelet function. Avoid in
children younger than 12 with possible
viral illness.
Ibuprofen
200-800
6
10 q 6-8
2400-3200
Relatively infrequent GI side effects
Naproxen
250-500
6-12
5 bid
750-1250
May be beneficial for headaches of
migraines
Ketoprofen
12.5-50
6-8
Not recommended
300
Slightly increased GI side effects
Flurbiprofen
50-100
Bid-tid
Not recommended
300
Potent anti-inflammatory properties
Oxaprozin
1200
24
Not recommended
1800
Onset delayed for 3-6 hours
Sulindac
150-200
Bid
Not recommended
400
Prodrug with decreased GI side effects
Etodolac
200-400
6-12
Not recommended
1000
Balanced COX-1/COX-2 with decreased GI
side effects
Indomethacin
25-50
8-12
Not recommended
100
Limit use to 2 weeks if possible
Ketorolac
30 mg IV/IM
6
None
120, except 150
first day
Efficacy similar to 4 mg morphine. Not for
use for more than 5 days
Piroxicam
20
24
Not recommended
20
About half of patients intolerant of GI
effects
Nabumetone
500-1000
12
Not recommended
2000
Low incidence of GI effects
Celecoxib
100-200
12-24
Not recommended
400
Primarily COX-2 inhibitor
Rofecoxib
12.5-50
24
Not recommended
50
Primarily COX-2 inhibitor. Increased
incidence of cardiac events in VIGOR trial
1.a.) NSAA - Acetaminophen
•
Acetaminophen blocks prostaglandin synthesis centrally
 antipyretic effect.
•
However, it does not act on prostaglandins peripherally
 so it cannot block local inflammation.
•
Clinical use:
•
•
•
•
•
•
Fever and mild pain
Can be used in children
Can be used during pregnancy & breast-feeding
May be used in combination with caffeine or propoxyphen
IV forms are available for post-op pain.
Side effects:
•
Long-term or large doses are both hepatotoxic and nephrotoxic.
NSAA – Acetaminophen
COX-3 inhibitor

Recently, COX-3 activity is selectively inhibited by
analgesic/antipyretic drugs such as acetaminophen,
phenacetin and

Inhibition of COX -3 could represent a primary central
mechanism by which these drugs decrease pain and
possibly fever
Salicylates (e.g. aspirin)
• Aspirine has:
• Antipyretic and analgesic,
• Anti-inflammatory actions (> 3 gm/d),
• Anticoagulant.
• These actions result from the anti-PGs activity,
• Centrally and Peripherally.
• Unfortunately, these additional actions 
•
GIT problems: gastritis, bleeding ulcer.
1.b.) NSAIDs
NSAIDs
NSAIDs

Blocks the production of Prostaglandin

Very effective in mild – moderate pain

Effective in other types of pain e.g.
– Musculoskeletal pain
– OR & RA
– Cancer Pain

May be used alone or in combination with opioids
Practical guide for NSAID’s
In Postoperative sitting:

Pre-op administration   post-op pain.
– e.g. Leroxicam 8-16 mg IV or Celebrex 400mg, P.O. pre-op

Ketorolac & Leroxicam are effective in acute pain (IV)

Precautions:
– Gastric effects:
• PPI are the drugs of choice to treat gastric complications.
• H2 blockers only mask the disease
– Check the renal function routinely prior to administration
– COX2 inhibitors doesn’t affect the platelet function
Practical guide for NSAID’s Usage (Contin)
All specific or non-specific NSAID’s may cause:

Water retention and edema

Hypertension

Renal dysfunction

May delay bony fusion in chronic usage
Practical guide for NSAID’s Usage (Contin)
Mechanism of Renal dysfunction:
 PGE2 and PGI2 are medullary VD.
 TXA2 is:
– cortical VC,
– regulate the renal vascular resistance and Renin secretion.

Both can influence:
– The action of ADH.
– Loss of local renal Haemo-regulation (e.g. in hypotension)
– Reduction of GFR.


Electrolyte and Na imbalance.
PGDs depletion can result in:
– Acute tubular necrosis & papillary necrosis,
– Interstitial nephritis
Choice of NSAIDs
1. NSAIDs with Low Potency & Short t½
e.g. Ibuprofen
•
Acute pain: 200 – 800 mg
•
Chronic pain: 2 – 3 gm/day
Choice of NSAIDs
2. NSAIDs with High Potency & Short t½
e.g. Diclofenac
•
Less against COX-1 compared to COX-2
– Less GIT side effects.
•
1st pass metabolism 
– oral bioavailability 50%
–  Liver toxicity.
– Other drugs:
•
•
Indomethacin
Ketoprofen
Choice of NSAIDs
3. NSAIDs with Intermittent Potency & t½
e.g. Naproxen
– Clinical use in:
• Migraine
• Musculoskeletal pain
Choice of NSAIDs
4. NSAIDs with High Potency & Long t½
e.g. Oxicams (melo-, piro- & teno-xicam).
– They are not recommended in:
• Acute pain,
• Pain of short duration
– Recommended in:
• Inflammatory pain that persist for longer duration
– Arthritis & bone pain & cancer pain
– The High Potency & Long t½   of side effects
• GIT & renal.
Selective COX-2 Inhibitors
Examples
T-maz
t½
Bioavail.
Daily dose
Celecoxib
2-4 hs
9-15 hs
100
200 – 400 mg
Rofecoxib
2-4 hs
12 hs
100
25 mg







They are poor candidate for acute pain
Effective in chronic pain e.g. OA & RA
They are comparable to non specific NSAIDs
More safe in elderly, GIT pts.
More safe with other medications e.g. steroids & anticoagulants
Less GIT toxicity
~  risk of CV events in pt at risk.
Selective COX-2 Inhibitors

COX-2 inh. & GIT:
– COX-1 confer cytoprotection in the GIT
– COX-2 inhibitors improve risk/benefit regarding GIT safety

COX-2 inh. & Kidney:
– they do not spare kidney ~ edema & HP

COX-2 inh. & CVS:
–
–
–
–
 prostacyclin ++
Do not – platelet COX-1
~ -- throm. /prost. balance  thrombogenic risk
Some studies reported IHD in some pts received celecoxib.
Drug Therapy
2. Opioids
- Weak Opioids.
- Strong opioids.
- Mixed agonist – antagonists
Weak Opioids

e.g. Tramadol hydrochloride
– Potency: 100 mg equivalent to 100 mg pethidine.
– Dose 200 – 400 mg/d.
– Advantages:
•
•
•
•
Less postoperative respiratory depression.
Efficient in reduction of postoperative shivering.
Acute & Chronic pain
Cancer & non cancer pain
– Side effects: Nausea and vomiting.
Strong Opioids

e.g. Morphine, Pethidine and Fentanyl.

Duration of action is:
– Morphine: (10 mg) 3-4 hours.
– Pethidine: (100 mg) 3-4 hours.
– Fentanyl: (100 g) 45- 60 minutes.

Main side effects:
– Nausea and vomiting.
– Respiratory depression.
– Extrapyramidal rigidity.
Agonist Antagonist Opioids

Members are:
– Butorphanol “Stadol” (2 mg)
– Nalbuphine “Nubain” (10 mg)

Duration of action is very short ( 2 hours).

Suitable to be used in infusion pumps and PCA.

Side effects: Hallucination is a famous one.
Opioid / Local Anesthetic Mixture

Epidural Marcaine and fentanyl is a useful mixture:
– Used epidurally
– Can be used in pediatrics.
– High quality of pain relief.
– Potentiation for action and duration.
Positioning of Opioid Therapy
Opioid therapy is the mainstay approach for
• Acute pain
• Cancer pain
• Pain in advanced illnesses
• Moderate - Severe non cancer pain
• AIDS pain
Opioid Therapy in
Chronic Non-Cancer Pain

Under-treatment is a major problem because:
• Published experience of multidisciplinary pain programs
showed that opioids associated with:
• Poor function
• Psychiatric disorders
• Poor outcome

Consider the following:
• Are opioids likely to work well?
• Are there reasonable alternatives?
• Are drug-related behaviors likely to be used?
Opioid Therapy:
Prescribing Principles

Prescribing principles
1. Drug selection
2. Dosing to optimize effects
3. Route of administration
4. Treating side effects
5. Managing the poorly responsive patient
Opioid Therapy: 1. Drug Selection

Immediate-release preparations
– Used mainly
• For acute pain
• For stabilization phase
• For “rescue” dosing
– Can be used for long-term management in select patients
Opioid Therapy: Drug Selection

Immediate-release preparations
– Single-entity drugs e.g.
• Tramadol
• Morphine
– Combination products
• Codeine + ASA
• Propoxene + Acetaminophen.
Opioid Therapy: Drug Selection

Extended-release preparations
– Preferred because of improved pt’s compliance.
– Morphine, oxycodone, hydromorphone, codeine, tramadol,
buprenorphine

Fentanyl-TTS (72 hs).
2. Dose adjustments for opioids

Increase the dose (not the number of opioids) until:
– pain relief is adequate or
– intolerable side effects occur

Only one long acting opioid should be ordered at any
given time.
– (e.g. Oramorph, Oxycontin, Duragesic)

Only one opioid combination should be ordered at any
given time.
3. Poor Opioid Responsiveness

If dose escalation  adverse effects
– Strategy to lower opioid requirement
• + Add non-opioid analgesic
• + Adjuvant analgesic
• + Non-pharmacologic strategy.
– Changes of opioid therapy:
• Change the route: e.g. Spinal opioids
• “Opioid rotation”
4. Opioid Rotation

Based on inter individual variation in response to
different opioids

Reduce equianalgesic dose by 25%–50%:
– Reduce less  if pain is severe
– Reduce less  if same drug by different route
– Reduce less  fentanyl
– Reduce more  methadone (75%–90%)
5. The Equianalgesia
• The amount (mg) required to deliver the same degree of analgesia
varies from one opioid to another
Drug
Oral
IV
Duration
morphine
30mg
10mg
3-4h
hydromorphone
7.5mg
1.5mg
3-4h
codeine
200mg
130mg
3-4h
oxycodone
30mg
-
3-4h
hydrocodone
30mg
-
3-4h
meperidine
300mg
100mg
2-3h
TTS-Fentanyl dose based on oral morphine dose
Oral Morphine (mg/day)
45 - 134
135 - 224
225 - 314
315 - 404
405 - 494
495 - 584
585 - 674
675 -764
765 - 854
855 - 944
945 - 1034
1035 - 1124
TTS Fentanyl Patch
25 g / hour
50 g / hour
75 g / hour
100 g / hour
125 g / hour
150 g / hour
175 g / hour
200 g / hour
225 g / hour
250 g / hour
275 g / hour
300 g / hour
6. Opioid Therapy: Side Effects

Common
– Constipation
– Somnolence, mental clouding

Less common
–
–
–
–
N/V
Myoclonus
Itch
Urinary retention
– Sweating
– Amenorrhea
– Sexual dysfunction
– Headache
Prevention # management of constipation
“The hand that writes the “opioid order”
 also writes the bowel regimen”

In every patient receiving opioids
– Increase fluids and fibers
– Scheduled stool softeners/stimulant laxatives
Addiction
•
It is associated with:
•
•
Genetic, psychosocial, and environmental factors.
It is characterized by behavioral changes:
•
impaired control over drug use,
•
compulsive use,
•
continued use despite harm & craving.
•
Quality of life is not improved
Tolerance
Tolerance is a state of adaptation; in which exposure
to a drug results in a diminution of the drug's effects
over time.
- 1st in duration of action;
- 2nd in overall effectiveness.
Pseudotolerance
Pseudotolerance is the need to increase due to other
factors such as:
•
disease progression,
•
new disease,
•
increased physical activity,
•
lack of compliance,
•
change in medication formulation,
•
drug interaction.
Physical Dependence
Physical dependence is a state of adaptation that is
manifested specific withdrawal syndrome that can
be produced:
•
by abrupt withdrawal,
•
rapid dose reduction,
•
decreasing blood level of the drug,
•
or administration of an antagonist.
Opioid Pseudoaddiction
An iatrogenic syndrome in which patients develop
certain behavioral characteristics of psychological
dependence as a consequence of inadequate pain
treatment.
Drug Therapy
3. Adjuvant's Therapy
3. Adjuvant Therapy
Clonidine
 Anxiolytic drugs
 Anticonvulsants
 Antidepressants
 Ketamine
 LA
 Corticosteroids
 Others

Clonidine

Alpha-2 agonist.

Routes of adminstration: Oral, neuraxial & TTS

Pain control properties by itself

Excellent adjuvant for opioid dependent patients

Decrease the requirement of opioids

Decrease tolerance

Effective control for neuropathic pain

Caudal block for children 1g/kg  pain relief / 24h
Ketamine

NMDA receptors antagonist  Neuropathic pain

Potent analgesic effect

Small doses in combination of opioids   pain control

Post-op in chronic opioid users:
– Bolus dose of 100 g/kg followed by a continuous drip of 1-3
g/kg/min.
Anti-Convulsant Drugs in Pain
 Gabapentin
 Carbamazipine
 Phenytoin
 Depakine
Mechanisms of Anti-Convulsant Drugs in Pain
Usage of Anti-Convulsants Drugs in Acute Pain
Gabapentin:

Mainly for neuropathic pain

Studies showed that:
– giving 600-1200 mg of Gabapentin 1 h pre-op.:
• decreases the opioids requirement post-op &
• better pain relief without increased sedation
– Combining Gabapentin + opioids is ideal for:
• re-do back surgery cases
• with chronic opioids usage

These class of drugs are also mode stabilizers
Antidepressant Drugs in Pain Managements
This type of drug may be divided into 4 categories:
1.
Drugs that inhibit synaptic neurotransmitter
reuptake.
2.
Drugs that have direct receptor stimulation.
3.
Drugs that produce receptor blockade.
4.
Drugs that inhibit the activity of enzymes such as monoamine
oxidase.
Mechanism of Action of Antidepressants
Name
Dosage
Presynaptic
Mechanism of
Action
Fluoxetine (Prozac)
“SSRI”
20–80 mg
Inhibits serotonin
reuptake
Paroxetine (Paxil)
SSRI
20–50 mg
Inhibits serotonin
reuptake
Mirtazapine (Remeron)
15–45 mg
Stimulates
norepinephrine and
serotonin release
Tricyclic
antidepressant
10 – 50 mg
inhibiting reuptake
of catecholamines, as
well as indolamines
Postsynaptic
Mechanism of
Action
Blocks 5-HT2 and 5HT3 receptors
Adjuvant Analgesics for Musculoskeletal Pain
“Muscle relaxants”

Refers to numerous drugs: e.g.


cyclobenzaprine, orphenadrine, methocarbamol.
Centrally-acting analgesics.
Adjuvant Analgesics for Cancer Pain

For bone pain
– Bisphosphonates (e.g. pamidronate, clodronate),
– Calcitonin,
– Radiopharmaceuticals (e.g. Sr89, Sm153)

For bowel obstruction pain
– Anticholinergics, octreotide
Adjuvant Analgesics for Chronic Headache

Beta blockers

Anticonvulsants

Antidepressants

Alpha-2 adrenergic agonists

Vasoactive drugs

Triptans


Mimic 5-HT involved in migraine
Only indicated for migraine pain
Other Adjuvant Analgesics
Miscellaneous drugs
 Calcitonin
– RCTs in CRPS and phantom pain
– Bone pain

Baclofen
– RCT in trigeminal neuralgia
– 30–200 mg/d or higher
– Taper before discontinuation
Other Adjuvant Analgesics
NMDA-receptor antagonists

N-methyl-D-aspartate receptor involved in
neuropathic pain

Commercially-available drugs are analgesic:
ketamine, amantadine, dextromethorpan.
Topical Adjuvant Analgesics

For neuropathic pain
- Local anesthetics
• Lidocaine patch
• Cream: lidocaine 5%, EMLA
- Capsaicin

For musculoskeletal pains
• NSAIDs
Routes of Drug Administration
Oral
 Rectal
 SQ
 IM
 IV
 TTS
 Neuraxial.
 Others

Routes of Administrations

Use the oral route whenever possible
– Except e.g. post op period,
– Try other routes e.g.
• buccal, sublingual, or rectal routes before initiating parenteral routes

Parenteral:
– SQ and IV preferred &
– feasible for short-term therapy

Always avoid IM.

Oral and transdermal: preferred
Routes of Administrations

I.M. not recommended but it is commonly used:
– Painful
– Serum levels are unpredictable.

Rectal route:
– For pediatric patients.
– Simple procedures.
– Slow absorption: longer duration.

Neuraxial:
– Intrathecal generally preferred for long-term use
– Epidural for a shorter periods.
Routes of Administrations
Intravenous Route

Desired.

Easy titrated.

Serum level is controllable.

Can be used in:
– drip form ,
– by pumps ,
– best is by PCA.
Routes of Administrations - PCA
 Used for IV, SC & Epidural.
 Pre-set by the physician.
 Activated by the patient.
 Programming modalities include:
1.
2.
3.
4.
5.
Loading dose or infusion.
Demand bolus dose.
Constant background infusion rate.
Lock-out interval.
Maximum hourly dose.
} Safety
Routes of Administrations - PCA

Advantages:
– Patients can titrate their own analgesia
– Improved:
• Pain relief
• Pulmonary function.
– Decreased:
• Total daily dose.
• Over sedation.
• Postoperative complications.
Transdermal Therapeutic System TTS
“Fentanyl-TTS”
Non-permeable protective cover
Drug Reservoir
- Alcohol is added
- Hydroxy-ethyl
cellulose matrix
Rate controlling
membrane
Adhesive
layer
Protective Liner
TTS- Fentanyl
Character of the patch:
Dose
Patch size
Cmax
Tmax
ng/ml
Range in hours
25g/hour
10 cm2
0.3-1.2
26-78
50g/hour
20 cm2
0.6-1.8
24-72
75 g/hour
30 cm2
1.1-2.6
24-48
100g/hour
40 cm2
1.9-3.8
25-72
• The composition of the patch/unit area is fixed (2.5 mg/10 cm2).
• The dose is dependent upon the patch size.
Advantages of the TTS route
1. Reduction in the variability of in the plasma levels.
2. Avoidance of 1st pass metabolism.
3. Bioavailability: 92 %
4. Prolonged duration of action: 72 hrs.
5. Improved compliance.
6. Less side effects e.g. constipation.
Disadvantages of TTS-fentanyl
-
It has a delayed onset of action (12-17 hours).
- The time to reach Cmax. is ranged from 26-72 hours.
-
Followed by residual effects after removal of the patch
up to 17 hours.
Pain Management Algorithm
Algorithm for Management of Neuropathic Pain
Initial Assessment
History
•
•
•
•
•
•
•
•
•
Quality of pain.
Distribution of pain
Course.
Sleep disturbances
Mental changes
Drugs, toxins.
Alcoholism
Systemic illness
Trigger points
Physical / Neurologic
examination
• Sensory examination:
Pin prick, pain, T, Position,
vibration.
• Allodynia or Hyperalgesia
• Motor examination:
Strength, atrophy,
fascisulations
• Reflexes
• Vasomotor changes
Investigations
• EMG & NC study
• Blood: CBC, FBS, ESR,
B12, folate, heavy
metals, immune fixation,
• Electrophoresis.
• Radiological.
• Lumbar puncture
• Nerve biopsy.
Algorithm for Management of Neuropathic Pain
Central Pain
Trigeminal Neuralgia
Other Neuropathies
1st line therapy
1st line therapy
1st line therapy
• Amitryptiline
2nd line therapy
• Mexiletine
3rd line therapy
Anticonvusants:
• Carbamazepine
• Gapapentine
• Valporate
• Carbamazepine
2nd line therapy
• Baclofen
• Gabapentin
• Lamotrigine
• Valporate
• Phenytoin
• Gabapentin/TCA
2nd line therapy
• Carbamazepine
• Tramadol
• Capsaicin,lidocain
3rd line therapy
• Mexiletine
• SSRIs
• Phenytoin
• Lamotrigine
4th line therapy
El-Tallawy
• Opioids
Trauma pain management Algorithm
HeadInjury
injury
Head
patients
Clear mental
status
Unclear mental
status
Treat with any
modalities
Small doses of
opioids(codeine)
or/with Ketorolac
Trauma pain management Algorithm
Extremity
Injury
Extremity injury
Bone injury
Peripheral nerve or vascular
injury
Epidural analgesia
opioids or
local anesthetics
Nerve function
monitoring
yes
Epidural analgesia
Opioids only
No
PCA
Epidural opioids
with or without
local anesthetics
Peripheral
nerve block
Trauma pain management Algorithm
Abdominal
Abdominal Injury
injury
Surgery required
Surgery not rquired
Epidural analgesia
PCA
Trauma pain management Algorithm
Neurologic
Injury
Neurologic injuries
Spinal cord injury
Neuropathic
nerve injury
PCA
CRPS I
CRPS II
Epidural analgesia
with local anesthetics
(Very effective)
PO/IV Narcotics
Antidepressants
Anticonvulsants
Trauma pain management Algorithm
Thoracic Injury
Thoracic trauma
Intubated
patients
IV narcotics
PCA
Not Intubated
patients
Thoracic epidural
analgesia
Ready for
extubation
Thoracic epidural
analgesia
Intercostal
nerve block
PCA
Intercostal
nerve block
PCA
Summary of Pain Management
…the basics
Do Not Use Placebos!

Unethical

They don’t work

Not helpful in diagnosis

Effect is short lived

Destroys trust
Match the therapy to the type of pain

Intensity of pain
– Mild, moderate or severe.

Type of pain e.g.
– Somatic & Visceral pain # Neuropathic pain

Duration of pain
– Continuous # intermittent pain.


Acute # chronic
Drug combinations
– Never order more than one SR preparation at a time
– Only one combination analgesic should be ordered at a time
Basics of Pain Management

1st step: is the good pain assessment.

Pain medications must be taken:
 when the pain is first perceived.

Doses of opioids are increased:
 with the patient’s report of pain

Adjuvant medications are used for:
 opioid non-responsive & neuropathic pain.

Non-pharmacologic approaches are always a part of
 any pain management protocol.
Pain Management in the late 18th century
“By any reasonable code, freedom from pain
should be a basic human right, limited
only by our knowledge to achieve it ...”
Wall P & Melzack R 1987