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Objectives. Introduction.Pain control strategies.Special painful conditions.Rules for pharmacotherapy.Algorithms for pain management..
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2. PAIN MANAGEMENT1. 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
3. Objectives Introduction.
Pain control strategies.
Special painful conditions.
Rules for pharmacotherapy.
Algorithms for pain management.
21. Drug Strategies 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 .
22. Alternative medicine:
Acupuncture
TENS
Cupping
Chiropractice
Physical Therapy
ice, heat, massage
Exercise
Psychological therapy
Cognitive-behavioral therapy
Relaxation techniques
Biofeedback
Hypnosis
Non-Drug Strategies
23. WHO step Ladder
24. 1. Drug Therapy * All acidic analgesic / anti inflammatory Ds are highly bound to pp ? high conc in spleen, liver, bone marrow, GIT & especially in inflammed tissue ? almost complete local inhibition of cyclooxygenases.
This explains that only acidic AA & NSAIDs are anitiinflammatory and cause acute side effects in the GIT, -- of platelets aggregation and kidney (fluid and K retention).
Also, chronic inflammation of URT as in asthma, may lead to accummulation of NSAIDs in mucosa “Aspirine Asthma” in asthmatic pts.
* In contrast, acetaminophen with neutral pka values and low pp are equally distributed uniformly throughout the body.
* All acidic analgesic / anti inflammatory Ds are highly bound to pp ? high conc in spleen, liver, bone marrow, GIT & especially in inflammed tissue ? almost complete local inhibition of cyclooxygenases.
This explains that only acidic AA & NSAIDs are anitiinflammatory and cause acute side effects in the GIT, -- of platelets aggregation and kidney (fluid and K retention).
Also, chronic inflammation of URT as in asthma, may lead to accummulation of NSAIDs in mucosa “Aspirine Asthma” in asthmatic pts.
* In contrast, acetaminophen with neutral pka values and low pp are equally distributed uniformly throughout the body.
26. 1.a.) NSAA - Acetaminophen Acetaminophen blocks prostaglandin synthesis centrally , this account for its antipyretic effect.
However, it does not act on prostaglandins peripherally, so it cannot block local inflammation.
Therefore, acetaminophen only lowers temperature and has analgesic properties because of its antiprostaglandin activity in the CNS.
Long-term or large doses are both hepatotoxic and nephrotoxic.
Toxic metabolite: benzoquinones
Antidote: N-acetylcysteine or glutathioneAcetaminophen blocks prostaglandin synthesis centrally , this account for its antipyretic effect.
However, it does not act on prostaglandins peripherally, so it cannot block local inflammation.
Therefore, acetaminophen only lowers temperature and has analgesic properties because of its antiprostaglandin activity in the CNS.
Long-term or large doses are both hepatotoxic and nephrotoxic.
Toxic metabolite: benzoquinones
Antidote: N-acetylcysteine or glutathione
27. NSAA – AcetaminophenCOX-3 inhibitor
28. Salicylates (e.g. aspirin) Aspirine has antipyretic and analgesic effects as well as anticoagulant and anti-inflammatory actions.
Theoretically, these actions result from the antiprostaglandin activity, both centrally and peripherally.
Unfortunately, these additional actions predispose this medication to produce GIT problems, including gastritis, bleeding ulcer, in susceptible individuals.
Despite these problems, aspirin is still the cheapest and most readily available analgesic preparation.Aspirine has antipyretic and analgesic effects as well as anticoagulant and anti-inflammatory actions.
Theoretically, these actions result from the antiprostaglandin activity, both centrally and peripherally.
Unfortunately, these additional actions predispose this medication to produce GIT problems, including gastritis, bleeding ulcer, in susceptible individuals.
Despite these problems, aspirin is still the cheapest and most readily available analgesic preparation.
29. 1.b.) NSAIDs
30. 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
31. 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
32. 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
33. 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 Local haemoregulation of the kidney is dependant on prostaglandins:
PgE2 and PgI2 are medullary vasodilator.
TxA2 is cortical vasoconstrictor and regulate the renal vascular resistance and Renin secretion.
Accordingly, glumerular filtration rate is greatly dependant on this mechanism.
Both can influence the action of ADH.
Kidney affection by NSAIDs usually due to loss of local haemodynamic regulation.The early sign of affection is plasma sodium disturbance, this is followed by interstitial nephritis, then tubular and papillary necrosis. In early cases this process is recoverable.
This mechanism is important in operative cases when hypotension is present, and NSAIDs are used as analgesic.Local haemoregulation of the kidney is dependant on prostaglandins:
PgE2 and PgI2 are medullary vasodilator.
TxA2 is cortical vasoconstrictor and regulate the renal vascular resistance and Renin secretion.
Accordingly, glumerular filtration rate is greatly dependant on this mechanism.
Both can influence the action of ADH.
Kidney affection by NSAIDs usually due to loss of local haemodynamic regulation.The early sign of affection is plasma sodium disturbance, this is followed by interstitial nephritis, then tubular and papillary necrosis. In early cases this process is recoverable.
This mechanism is important in operative cases when hypotension is present, and NSAIDs are used as analgesic.
34. Choice of NSAIDs 1. NSAIDs with Low Potency & Short t˝
e.g. Ibuprofen
Acute pain: 200 – 800 mg
Chronic pain: 2 – 3 gm/day
35. Choice of NSAIDs 2. NSAIDs with High Potency & Short t˝
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
36. Choice of NSAIDs 3. NSAIDs with Intermittent Potency & t˝
e.g. Naproxen
Clinical use in:
Migraine
Musculoskeletal pain
37. Choice of NSAIDs 4. NSAIDs with High Potency & Long t˝
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 t˝ ? ?? of side effects
GIT & renal.
38. Selective COX-2 Inhibitors
39. 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. Selective COX-2 Inhibitors
40. Drug Therapy2. Opioids- Weak Opioids.- Strong opioids. - Mixed agonist – antagonists
41. 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.
42. 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.
43. 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.
Agonist antagonist opioids are group of drugs that specifically acting on one opioid receptor and antagonize the other opioid eceptor.They are introduced into clinical practice in a trial to get an opioid without famous opioid side effects mainly addiction, respiratory depression, constipation, and tolerance.
Buprenorphine: known as tamgesic, not registered in the Egyptian market, is a parial agonit -antagonist on mu opioid receptor. In clinical concentrations it can produce analgesia,and if the dose increases I turns to be an antagonist.
Butorphanol (Stadol), and Nalbuphine (Nubaine) are k-opioid agonists, mu-opioid antagonists. They can produce spinal analgesia, and sedation without respiratory depression.
They are all having a very high lipid solubility and can pass easily through membranes, and can be used in transmucosal route. Buprenorphine, sublingual tablets are present, but not in the Egyptian market (Dose= 0.4 mg I.M.).
Stadol 1-2 mg., and Nubaine 10 mg. Injectable forms are present in the Egyptian market.
I.M 2 mg stadol, and 10 Nubaine are equipotent to 10 mg. Morphine.
No oral forms are present for this group of drug.
Main side effect is hallucination.Agonist antagonist opioids are group of drugs that specifically acting on one opioid receptor and antagonize the other opioid eceptor.They are introduced into clinical practice in a trial to get an opioid without famous opioid side effects mainly addiction, respiratory depression, constipation, and tolerance.
Buprenorphine: known as tamgesic, not registered in the Egyptian market, is a parial agonit -antagonist on mu opioid receptor. In clinical concentrations it can produce analgesia,and if the dose increases I turns to be an antagonist.
Butorphanol (Stadol), and Nalbuphine (Nubaine) are k-opioid agonists, mu-opioid antagonists. They can produce spinal analgesia, and sedation without respiratory depression.
They are all having a very high lipid solubility and can pass easily through membranes, and can be used in transmucosal route. Buprenorphine, sublingual tablets are present, but not in the Egyptian market (Dose= 0.4 mg I.M.).
Stadol 1-2 mg., and Nubaine 10 mg. Injectable forms are present in the Egyptian market.
I.M 2 mg stadol, and 10 Nubaine are equipotent to 10 mg. Morphine.
No oral forms are present for this group of drug.
Main side effect is hallucination.
44. 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.
45. 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
The broad international consensus is that opioid therapy serves as the mainstay approach for treatment of pain associated with acute pain and pain due to serious illnesses, such as cancer. Notwithstanding, we have abundant evidence that undertreatment is common, even in these populations.
The broad international consensus is that opioid therapy serves as the mainstay approach for treatment of pain associated with acute pain and pain due to serious illnesses, such as cancer. Notwithstanding, we have abundant evidence that undertreatment is common, even in these populations.
46. 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?
We have no consensus about the role of opioid therapy in nonmalignant pain—and, hence, no certain data about the degree of undertreatment that exists. However, the individual and systemic barriers to opioid use, as well as the bias against opioid therapy that developed from the experience of multidisciplinary pain management programs, make undertreatment likely. The data published from the aforementioned programs do reveal associations between opioid use and negative characteristics and outcomes, and they suggest the potential for adverse responses to this therapy. However, because of the selection biases inherent in these programs, which attracted the most difficult patients, this experience cannot be used to evaluate the larger role of opioid therapy.
We have no consensus about the role of opioid therapy in nonmalignant pain—and, hence, no certain data about the degree of undertreatment that exists. However, the individual and systemic barriers to opioid use, as well as the bias against opioid therapy that developed from the experience of multidisciplinary pain management programs, make undertreatment likely. The data published from the aforementioned programs do reveal associations between opioid use and negative characteristics and outcomes, and they suggest the potential for adverse responses to this therapy. However, because of the selection biases inherent in these programs, which attracted the most difficult patients, this experience cannot be used to evaluate the larger role of opioid therapy.
47. Opioid Therapy: Prescribing Principles Prescribing principles
Drug selection
Dosing to optimize effects
Route of administration
Treating side effects
Managing the poorly responsive patient Many published guidelines reflect consensus views about the best approaches for management of long-term opioid therapy. The principles in these guidelines must be understood to optimize the likelihood of successful outcomes.Many published guidelines reflect consensus views about the best approaches for management of long-term opioid therapy. The principles in these guidelines must be understood to optimize the likelihood of successful outcomes.
48. 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
Immediate-release opioids are usually used for a limited period to treat acute pain or to help identify a useful starting dose for a long-acting drug. These drugs can be administered on a long-term basis as well, usually as supplemental doses given “as needed” to patients who are receiving a concomitant long-acting drug (an approach known as “rescue” dosing). Immediate-release opioids are usually used for a limited period to treat acute pain or to help identify a useful starting dose for a long-acting drug. These drugs can be administered on a long-term basis as well, usually as supplemental doses given “as needed” to patients who are receiving a concomitant long-acting drug (an approach known as “rescue” dosing).
49. Immediate-release preparations
Single-entity drugs e.g.
Tramadol
Morphine
Combination products
Codeine + ASA
Propoxene + Acetaminophen. Opioid Therapy: Drug Selection Short-acting opioids include the combination products, single-entity pure mu-agonists, and tramadol. Dose escalation of the combination products is subject to the limits of safe dosing with the nonopioid constituent. Acetaminophen-containing combinations, for example, generally should not be given at doses that deliver more than 4 grams of acetaminophen per day. Single-entity drugs, such as morphine, oxycodone, and hydromorphone, have no such top doses. Tramadol is a unique centrally-acting analgesic that acts via both an opioid mechanism and a nonopioid, monoaminergic mechanism. Short-acting opioids include the combination products, single-entity pure mu-agonists, and tramadol. Dose escalation of the combination products is subject to the limits of safe dosing with the nonopioid constituent. Acetaminophen-containing combinations, for example, generally should not be given at doses that deliver more than 4 grams of acetaminophen per day. Single-entity drugs, such as morphine, oxycodone, and hydromorphone, have no such top doses. Tramadol is a unique centrally-acting analgesic that acts via both an opioid mechanism and a nonopioid, monoaminergic mechanism.
50. Extended-release preparations
Preferred because of improved pt’s compliance.
Morphine, oxycodone, hydromorphone, codeine, tramadol, buprenorphine
Fentanyl-TTS (72 hs). Opioid Therapy: Drug Selection Numerous extended-release formulations are available in different countries. The oral drugs allow dosing 1 to 3 times per day and the transdermal drugs allow dosing every 2 to 3 days. Usually, steady-state is approached with these formulations within a few days and dose adjustments are best made in this time frame. Numerous extended-release formulations are available in different countries. The oral drugs allow dosing 1 to 3 times per day and the transdermal drugs allow dosing every 2 to 3 days. Usually, steady-state is approached with these formulations within a few days and dose adjustments are best made in this time frame.
51. 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. Opioid responsiveness can be defined as the likelihood that a favorable balance between analgesia and side effects will be attained as the opioid dose is slowly titrated. A patient cannot be said to be a “nonresponder” unless the dose has been increased to the point of treatment-limiting side effects. Responsiveness varies with characteristics of a particular patient and his or her particular pain. Studies have suggested that responsiveness is inversely related to neuropathic mechanism, breakthrough pain, previous opioid exposure, cognitive impairment, and psychologic distress. However, no evidence exists that any characteristic imparts opioid resistance.
Opioid responsiveness can be defined as the likelihood that a favorable balance between analgesia and side effects will be attained as the opioid dose is slowly titrated. A patient cannot be said to be a “nonresponder” unless the dose has been increased to the point of treatment-limiting side effects. Responsiveness varies with characteristics of a particular patient and his or her particular pain. Studies have suggested that responsiveness is inversely related to neuropathic mechanism, breakthrough pain, previous opioid exposure, cognitive impairment, and psychologic distress. However, no evidence exists that any characteristic imparts opioid resistance.
52. 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” Surveys in the cancer population suggest that 10% to 30% of patients will experience a poor response to an optimally titrated opioid regimen. Poorly-responsive patients can be considered for a variety of alternative opioid strategies. These include: 1) more sophisticated management of opioid side effects (eg, a psychostimulant for opioid-induced sedation or mental clouding), 2) use of a pharmacologic approach to reduce the systemic opioid requirement (either a trial of intraspinal therapy or coadministration of a nonopioid or adjuvant analgesic), 3) opioid rotation, or 4) a trial of a nonpharmacologic approach to reduce the opioid requirement (eg, a stimulatory, rehabilitative, anesthesiologic, surgical, or complementary approach). Comparative studies of these strategies have been conducted, and selection of one over another involves a detailed assessment, careful judgments about risks and benefits, and discussion of patient preferences.
Surveys in the cancer population suggest that 10% to 30% of patients will experience a poor response to an optimally titrated opioid regimen. Poorly-responsive patients can be considered for a variety of alternative opioid strategies. These include: 1) more sophisticated management of opioid side effects (eg, a psychostimulant for opioid-induced sedation or mental clouding), 2) use of a pharmacologic approach to reduce the systemic opioid requirement (either a trial of intraspinal therapy or coadministration of a nonopioid or adjuvant analgesic), 3) opioid rotation, or 4) a trial of a nonpharmacologic approach to reduce the opioid requirement (eg, a stimulatory, rehabilitative, anesthesiologic, surgical, or complementary approach). Comparative studies of these strategies have been conducted, and selection of one over another involves a detailed assessment, careful judgments about risks and benefits, and discussion of patient preferences.
53. 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%) Opioid rotation is common practice and is based on the clinical observation of large individual variation in the response to different opioids. Guidelines for switching drugs assure safety and yield a reasonable starting dose of the new drug, which then must be titrated.
Opioid rotation is common practice and is based on the clinical observation of large individual variation in the response to different opioids. Guidelines for switching drugs assure safety and yield a reasonable starting dose of the new drug, which then must be titrated.
54. 5. The Equianalgesia
56. 6. Opioid Therapy: Side Effects Common
Constipation
Somnolence, mental clouding
Less common
N / V – Sweating
Myoclonus – Amenorrhea
Itch – Sexual dysfunction
Urinary retention – Headache
For most patients, the goal during long-term therapy is to identify a favorable balance between analgesia and opioid side effects. The common side effects are constipation and mental clouding. Other side effects occur less often. For most patients, the goal during long-term therapy is to identify a favorable balance between analgesia and opioid side effects. The common side effects are constipation and mental clouding. Other side effects occur less often.
57. 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
63. Drug Therapy3. Adjuvant's Therapy
64. 3. Adjuvant Therapy
Clonidine
Anxiolytic drugs
Anticonvulsants
Antidepressants
Ketamine
LA
Corticosteroids
Others
65. 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
66. 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.
67. Anti-Convulsant Drugs in Pain Gabapentin
Carbamazipine
Phenytoin
Depakine
68. Mechanisms of Anti-Convulsant Drugs in Pain
69. 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
Every surgical incisional pain has Neuropathic component
Studies showed giving 1200 mg of Gabapentin 1 h prior to surgery:
decreases the opioids requirement post-op &
better pain relieg without increased sedation
Combining Gabapentin with opioids is ideal for re-do back surgery cases with chronic opioids usage
These class of drugs are also mode stabilizersEvery surgical incisional pain has Neuropathic component
Studies showed giving 1200 mg of Gabapentin 1 h prior to surgery:
decreases the opioids requirement post-op &
better pain relieg without increased sedation
Combining Gabapentin with opioids is ideal for re-do back surgery cases with chronic opioids usage
These class of drugs are also mode stabilizers
70. Antidepressant Drugs in Pain Managements This type of drug may be divided into 4 categories:
Drugs that inhibit synaptic neurotransmitter reuptake.
Drugs that have direct receptor stimulation.
Drugs that produce receptor blockade.
Drugs that inhibit the activity of enzymes such as monoamine oxidase.
71. Mechanism of Action of Antidepressants
73. Adjuvant Analgesics for Cancer Pain
74. Adjuvant Analgesics for Chronic Headache
75. Other Adjuvant Analgesics
79. 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
80. 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
81. Intravenous Route Desired.
Easy titrated.
Serum level is controllable.
Can be used in:
drip form ,
by pumps ,
best is by PCA.
82. Used for IV, SC & Epidural.
Pre-set by the physician.
Activated by the patient.
Programming modalities include:
Loading dose or infusion.
Demand bolus dose.
Constant background infusion rate.
Lock-out interval.
Maximum hourly dose.
83. Advantages:
Patients can titrate their own analgesia
Improved:
Pain relief
Pulmonary function.
Decreased:
Total daily dose.
Over sedation.
Postoperative complications.
88. Pain Management Algorithm
91. Trauma pain management Algorithm
92. Trauma pain management Algorithm
93. Trauma pain management Algorithm
94. Trauma pain management Algorithm
95. Trauma pain management Algorithm
96. Summary of Pain Management …the basics
97. Do Not Use Placebos! Unethical
They don’t work
Not helpful in diagnosis
Effect is short lived
Destroys trust
98. 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
99. 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.
The pain assessment: so the pain syndrome can be identified and appropriately treated.
The oral route is used whenever possible.
If the patient is unable, buccal, sublingual, rectal, and TTS routes are considered before parenteral routes.
IM route is avoided.
The pain assessment: so the pain syndrome can be identified and appropriately treated.
The oral route is used whenever possible.
If the patient is unable, buccal, sublingual, rectal, and TTS routes are considered before parenteral routes.
IM route is avoided.
101. “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