dr. Prabowo Wicaksono Y.P.

, SpAn
Anesthesiology Department
UNISSULA Medical Faculty
A. ANALGESIA
INTRODUCTION
Pain: Up to 60-70% patients presenting to the ED; as part of their symptom
Severity : more than 1/3: moderate to severe pain:
Problem: pain is consistenly underestimate by HCP
Pain is commonly:
• Under recognized
• Under treated
• Treatment often delayed
“ ED Oligoanalgesia ” : Internationally recognized problem
Possible reasons:
• Fear of masking symptoms
• Fear that opioid may precipitate hypotension
• Belief the acutey injured patient will not remember painful events
• Pain management is not the highest priority

Recognition and allevation of pain should be a priority when treating the ill and
injured
Pain management in ED:
Start at the triage, monitored during time in the ED, finish with ensuring adequate
analgesia
 WHAT IS PAIN ?
Scientific definition: Merskey : Adopted by IASP in 1979:
Unpleasant sensory and emotional experience
Associated with actual or potential tissue damage, or
describe in term of such damage
Two key point:
1. Unpleasant sensory (physical component)
2. Emotional experience (psychological component)

Clinical definition
Margo Mc Caffery, 1999
“Pain is whatever the patient says”
Addressing patient’s pain is one of the most important contributions ED providers
can make
 SSC FLC

Physiology of pain perception :

Cortex and
Thalamus
VPL MT - Transduksi
- Transmisi
Hypothalamus - Modulasi
and Pituitary
PAG
Sympathetic
Outflow - Persepsi
Hypothalamic-
Pituitary Outflow
Midbrain
LC

Ascending Descending
Peripheral
Pathaways Pathaways
Nociceptor

Brainstem NRM
C-Fiber Sensory
Afferent

NSTT

PSTT Delta Sensory

Afferent

Spinal Cord
Sympathetic
Efferent

A-Alpha Motor
Efferent
prabowo wicaksono 4
 OPIOID Analgesic site of
action
- Systemic
PERCEPTION - Epidural
- Subarach

Pain Ketamin, Tramadol,

α agonist

COX-2,, COX1 LOCAL ANESTHETIC

- Epidural
MODULATION -Subarachnoid
Descending
modulation Dorsal Horn -Peripheral nerve block
Ascending Dorsal root
input ganglion
LA
TRANSMISSION COX-1
COX-2
steroids
Spinothalamic
Peripheral
tract TRANSDUCTION
nerve

Trauma
Peripheral
p
nociceptors

No single drug can produce optimal analgesia without adverse effect

prabowo wicaksono
Adapted from Gottschalk A et al. Am Fam Physician. 2001;63:1981, and Kehlet H et al. Anesth Analg. 1993;77:1049.
5
 12 PRINCIPLES UNDERLYING ED PAIN CARE

1 Pain
1. P i iis often
ft ththe primary
i complaint:
l i t diff
differentt priority
i it b between
t physician
h i i andd patient
ti t
2. ED procedures/ work-up add pain to the patient: explanation is important
3 Improved analgesia facilitates patient care: more cooperative patient
3.
4. Pain should be addressed within a reasonable amount of time: 20-25 minutes
5 Pain relief has medical benefits i.e.
5. i e physiologic advantages
6. Medications: not trying what’s already failed at home
7. Consider targeted analgesia if possible: specific drug, regional block
8. When pain is severe, intravenous analgesia is usually preferable
9. Pain care is ongoing process in the ED; reassessment and repeat therapy is
important
10. Pain care is an ongoing process after ED discharge; make sure adequate post
discharge analgesia
11. Keep it simple; do not move to a “rescue agent” unless sure that the initial drug
already sufficiently dosed. Exception: opioid sparring agents: NSAIDS or ketamine
12. Pain cannot be treated if it cannot be assessed; “zero-to-10 scale” is acceptable for
most acute care patient
i
prabowo wicaksono 8
SELECTED NONOPIOID PHARMACOLOGIC APPROACHES IN THE ED

ACETAMINOPHEN
Key points:
• Mild to moderate analgesic;
g comparable
p to aspirin
p
• Antipyretics
• Weak anti-inflammatory
• Now available an an IV analgesic
• Patient with contraindication to NSAID
• Patient with fever
• Opioid sparring effect
• One of the safer analgesic in the ED
NSAIDs
Analgesic mechanism: COX inhibition: COX-1 (constitutive) and COX-2 (inducible)
COX-1: platelet aggregation and GI mucosal integrity : side effects
COX-2: prostaglandin, mediator of inflammation and pain : analgesia
Key points:
• Route of administration: when given in equipotent doses, analgesic efficacy
almost the same: IV vs PO
• Differences in side effects between COX-2 selective inhibitor and non selective
NSAIDs: risk and benefits on individual basis. Longer prescription duration, more
co-morbidities: higher the NSAID risk
• When an NSAID does not appear to be working, it is reasonable to switch to an
NSAID off a different
diff t class
l
• NSIAIDs are best for inflammatory pain: renal colic, menstrual cramps
• Opioid sparring effect
KETAMINE
Most complicated but also most useful of ED analgesics.
Full dose: 1.5-2.0 mg/kg BW : true dissociative: trance like cataleptic state
Sub dissociative doses: 0.1- 0,5 mg /kgBW. Half life: 10-15 minutes.
Property:
• Induce analgesia
• Reduce hyperalgesia: anti NMDA receptor: prevent central sensitization
• Opioid sparring effect: 0,1 mg/kg BW/hour
• Preservation of airway reflexes
• Sympathomimetic
S h i i effect
ff h hemodynamically:
d i ll iincrease HR and
d BP
Side effects:
• Hyper salivation
• Laryngospasm
• Unpleasant emergence reaction (bad dream)
• Vomiting
Prevention: premedication with
Midazolam: 0.05 mg/kg BW
Sulfas atropin: 0.5 mg/kg BW
SELECTED OPIOID APPROACHES TO ED ANALGESIA
Benchmark for analgesic in the ED
Analgesia mechanism:
Receptor mediated blockade of neurotransmitter release (GABA) that will increase
descendingg inhibitoryy pathway;
p y; less pain
p transmission
Blockade of pain transmission in the dorsal horn of spinal cord.
Opioid
p receptor:
p μ
μ, κ, δ and σ
Most opioid: relatively selective to μ receptor
μ receptor: analgesia, euphoria, respiratory depression, miosis and constipation
Κ receptor: analgesia, sedation, dysphoria
δ receptor: spinal analgesia, antinociception for thermal stimuli
σ receptor: monotherapy for neuropathic pain
As opioid doses increases, μ selectivity decreases: effects from other receptor increases
MORPHINE
Excellent safety and efficacy when used appropriately
Concern: histamine release, hypotension , respiratory depression
Mayy be combined with ketamine.
Dosage: 0.1-0.15 mg/kg BW intravenous. ( 7-10 mg for 70 kg BW adult)
IM route not recommended: delayed onset and titration difficulties
FENTANYL
Most potent opioid routinely used in ED
Advantage:
g equipotent
q p analgesic
g potency,
p y, significant
g faster onset time
Dosage: start titration from 1-2 mcg/kg BW, continuous dose start from 0.5
mcg/kgBW/hour.
SPECIAL ISSUES WITH OPIOID
Analgesia for patient with undifferianted abdominal pain: covering the physical
findings?
Existing evidence: patient don’t have to suffer to preserve physical examination

Analgesia for trauma patient: risking of physiologic compromise from opioid:

respiratory and hemodynamic depression
Existing evidence: trauma analgesia can be safely provided with judicious
medication use

prabowo wicaksono 16
Continuous use of meperidine (petidine): the risk of normeperidine build up: seizure
Opioids can be used safely in the ED setting
Side effect can be prevented or treated
• Close monitoring: SpO2
• Airway repositioning
• Rapid stimulation

Antidote:
Naloxon: 0.4-2 mg/dose IV/IM/SC
May repeat every 2-3 minutes as needed
Continuous infusion: 0.005 mg/kg loading dose, followed by an infusion
0.00025/mg/kg/hour
B. SEDATION
Definition of Procedural Sedation and Analgesia (PSA): The American College of
Emergency Physicians (ACEP):
• A technique of administering sedatives or dissociative agents
• With or without analgesia
• Induce a state that allows the patient to tolerate unpleasant procedures
• Maintaining cardiorespiratory function independently
ASA SEDATION DEPTHS
Minimal sedation
• Response to verbal stimulation: normal
• Cognitive function and coordination: impaired
• Ventilatory and CV function: unaffected

Moderate sedation (conscious sedation)

• Level of consciousness: depressed (drug induced)
• Response to verbal commands: purposefully
• Airway patent, adequate spontaneous ventilation, CV unaffected
Deep Sedation
• Level of consciousness: depressed (drug induced)
• Not easily aroused, respond purposefully to painful stimulation
• Ventilation function: may be impaired
• Patent airway: may require assistance
• Spontaneous ventilation inadequate
• CV function: maintained
DRUG CHOICES FOR PSA
Most frequently used: a short acting benzodiazepines
Alone or in combination with opioid analgesics
(fentanyl, morphine)
Combination with opioid:
• longer duration
• Increased risk of SpO2 desaturation and CV complication
• Reversal drug must be readily available (flumazenil and naloxone)
BENZODIAZEPINES
Beneficial effects:
• Amnesia
• Anticonvulsant
• Anxiolytics
• Sedation
Mechanism: bind to receptor in GABA: inhibitory effects of CNS
First line DOC: Midazolam
• Faster sedation onset
• Duration:
D ti 30 60 minutes
30-60 i t
• Better amnesia
• Less painful on injection
• Improved awakening compared with diazepam
OPIATES
Analgesia and sedation during painful procedures
First line DOC:
Fentanyl
• Benefit:
• Prompt onset, short duration
• Mechanism:
• Increases pain threshold,
• alter pain reception, inhibits ascending pain pathways
• Minimal CV depressive effects
Pethidine: not first line DOC; active metabolite, accumulation in poor renal
clearance: seizures
KETAMINE
• Profound dissociative and amnestic action
• Dissociative: cataleptic, can not speak or respond to verbal commands
• Maintain airway reflexes: patent airway and spontaneous respiration
• Caution: increases orophyaryngeal secretions; laryngospasm
Premedication:
Sulfas atropin (reduce secretions)
Midazolam (reduce dissociation, emergence delirium: vivid imagery, hallucinations,
confusion, excitement, irrational behavior)
• Beneficial in non fasting patient
• CV and respiratory stimulation;
• contraindication in hypertension
• Active metabolite, 1/3 potency.
Intravenous (IV):
Onset: 1 minute
Duration: 10-15 minutes
Intramuscular (IM):
Onset: 3-5 minutes
Duration: 20-30 minutes

I adult:
In d l combination
bi i ketamin
k i and
d propofol
f l : 1:1
11
Example: in one 20 cc syringe (10 cc ketamine 10 mg/cc + 10 cc propofol 10 mg/cc)
Overall dose: 0.5
0 5 mg/kg
PROPOFOL
Potent, ultra short acting sedation and anesthesia
Shorter recovery than midazolam
No analgesic properties
Rapid deepening of sedation level to that of general anesthesia
Intravenous injection
j
Onset: 90-100 seconds
Duration: 5-10 minutes
Dose dependent decrease in arterial blood pressure and cardiac output
Contraindication in hemodynamically unstable patient
Painful on injection, especially in small vein
Reduced by combination with lidocaine or ketamine

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