Acute Pain Flashcards
Acute Pain
Why do we need to treat acute pain?
● Pain of recent onset and probable limited duration
● Usually has an identifiable temporal and causal relationship
to injury or disease
● Has a physiologic protective function
● ↓ complications
● ↓ likelihood of acute-to-chronic pain conversion
● Improve outcome
○ ↑ speed of recovery → ↓ length of stay → ↓ health care costs
● ↑ patient satisfaction
● Make the period of disease accompanied by pain less unpleasant
● ↑ productivity
● ↑ quality of life
Physical Consequences of Poor Pain Management
Cardiovascular Tachycardia, hypertension, ↑ cardiac workload
Pulmonary Respiratory muscle spasm, atelectasis, hypoxia
Gastrointestinal Post-operative ileus
Renal ↑ risk of oliguria and urinary retention
Coagulation ↑ risk of thromboembolism
Immunologic Impaired immune function
Muscular Muscle weakness and fatigue
Psychological Anxiety, fear, frustration, poor patient satisfaction
Pathophysiology - Revisited
acute pain tends to be more of nociceptive
can have a component of inflamm with some spontaneous pain and pain from normally nor painful stimuli
Assessment
Perform a pain assessment
● Solicit pain description from patient (SCHOLAR or other; pain scales)
● Inquire about prior work-up, diagnostic and lab tests, prior self-treatment
● Medical history (including allergies)
● Current medications
● Physical exam
cause for pain
Differential Diagnosis and Red Flags - Examples
● Fractures or degenerative disease
● Cardiovascular disease
● Infection
● Cancer
● Visceral disease (i.e., referred pain), endometriosis, pelvic inflam
● GI disease (pUD, pancreatitis, acute cholecystis)
NIFTI: neurologyical, inflamm, fractures, tumors, infections
Goals of Therapy
● Reduce or eliminate the pain
● Identify and treat the cause
● Prevent progression to chronic pain
● Minimize or prevent adverse effects associated
with treatment
Therapeutic Alternatives
Non-pharmacologic
Pharmacologic
● Acetaminophen
● NSAIDs
● Opioids
● Other
Non-pharmacologic Treatment
always employed
(P): Protection
R: Rest (often 48 hours)
I: Ice (10-20 min q2-3h x 48h or until swelling improves)
C: Compression (snug, not tight)
E: Elevation (above level of the heart)
● Activity as tolerated
● Physiotherapy, range of motion exercises
● External supports (e.g., bandages, tape, braces)
● Cold/heat therapy
● Massage, acupuncture
● Self-management education and support
complete bed rest is rarely recommended
Non-opioid Analgesics
Benefits:
● Provide pain relief
● More readily available
● May eliminate need for opioids
● May enhance opioid analgesia
● Varied mechanism of action from opioids
WHO Analgesic Ladder
- mild: nonopioid +/- adjuvant tx
- weak: weak opioid (codeine) +/- nonopioid +/- adjuvant
- strong: strong opioid +/- nonopioid +/- adjuvant
not used that much
weak opioids are not used as much, stronger ones used with lower dose
mild pain 1-3 on scale
mod 4-6
severe 7-10
Acetaminophen
Analgesic and antipyretic
Well-tolerated and “safe”
May be useful for mild-moderate nociceptive pain
Commonly dosed at 650 mg PO q4-6h or 1000 mg PO q6h (adults)
● May be given with (or in addition to) other analgesics
● Max per day: 4 g from all sources
dont need to know dosing just max dose
650 mg → NNT = 4.6 (3.9-5.5), N = 1886
1000 mg → NNT = 3.8 (3.4-4.4), N = 2759
(For a 50% ↓ in nociceptive pain over 4-6 hours compared to placebo)
Acetaminopherm raises INR - interaction with warfarin
Keep lvls of aceta consistent do warfairin dose can be adjusted for it
Phenytoin increase actaminphen toxiictiy
Isoniazid additive hepatotoxicity
NSAIDs
Analgesic, antipyretic, and anti-inflammatory (if adequately and routinely dosed)
Generally more effective and more toxic than acetaminophen
Adverse effects (oral):
● Gastrointestinal
● Cardiovascular
● Renal
● Central nervous system
more ae with higher doses with prolonged exposure
min effective dose for shortest duration
NSAIDs - Analgesic Effectiveness
shouldnt say onne is more effective than antoher
all have comparable effectiveness
Are NSAIDs safe in a patient with a history of cardiovascular
disease?
CV events:
celecoxib vs diclofenac
no diff in major vascualar events
celecoxib vs naproxen - risk higher with celecoxib
similar for all cause mortality
GI complications:
celecoxib COX 2 selective, better than ibuprofen and naprox
similar to diclofenac
less fx on GI mucosa
celecoxib and diclofenac very similar on these fronts (both COX2 selective)
naproxen only one that is CV neutral (crosses line of no diff)
NSAIDs and ASA
Pharmacodynamic interaction
theoretical but not a cliknical interaction
● ASA and some NSAIDs compete for COX-1 binding site
○ Ibuprofen in particular causes steric hindrance of ASAʼs binding
A Post-hoc analysis of the TARGET trial (N = 18 325):
● Looked at CV outcomes in patients taking ASA with ibuprofen, naproxen, or
lumiracoxib.
● In patients with high CV risk not taking ASA:
○ Naproxen, and not ibuprofen, associated with lower CV risk than lumiracoxib
● In patients with high CV risk taking low-dose ASA:
○ Ibuprofen associated with greater CV risk at 1 year than lumiracoxib and naproxen
