Transcript Acute Pain and the trauma patient

Multimodal Approach to treating acute
pain in trauma patients
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1. Discussion of the pathophysiology of acute
pain.
2. Discuss opiates and adjuvant medicines.
3. Outline acute pain management in patients
on chronic pain regimens, including
withdrawal avoidance.
4. Discuss relevant regional anesthesia
techniques.
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Caused by noxious stimulation secondary to
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Injury
Disease
Abnormal function
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Pain is nociceptive vs neuropathic
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Pain signals carried by A-delta and C fibers
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Mostly Free Nerve Endings
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High thresholds for activation
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Intensity of stimulation is proportional to rate
of discharge
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Transduction
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Transmission
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Modulation
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Perception
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Three Neuron pathway to get signal from
periphery to brain
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First Order Neurons
 Cell Bodies live in dorsal root ganglia
 Nerve endings connecting to dorsal horn of spine
 May also synapse with interneurons, sympathetic fibers
and motor neurons
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Second Order Neurons
Synapse with First Order Neurons in dorsal horn of
spine
 Cross the midline and connect to thalamus
 Opiates work here
 Many interneurons interact
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Third Order Neurons
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Connect thalamus to postcentral gyrus of cerebral
cortex and others
Interneural connections
 Pain Perception
 Emotional Response
 Feedback (efferent fibers)
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Occurs at:
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Nociceptors
In the spinal cord
Supraspinal structures
These can either suppress or facilitate pain
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Can become sensitized
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Increased frequency of response
Decreased threshold to stimulation
Decreased response latency
Leads to increased Prostiglandin production,
producing hyperalgesia
NSAIDS, ASA, steroids work here
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Function of complex interneuron interaction
“Substance P” increases histamine and
serotonin, and other neuroexcititory peptides
Capsaicin and local anesthetics can work here
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Facilitators
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Produce “wind up” via Wide Dynamic Receptors
Receptor field expansion
Hyperexcitability
Inhibitors
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Gate Theory from different segments confined via
WDRs
GABA drugs work here
 Supraspinal Descending Pathways
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 Interact with first and second order neurons at alpha2,
opiate, and serotonergic receptors
TCAs work here
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Moderate to Severe Pain effects multiple organ
systems
Significant influence of Morbidity and
Mortality
Mediated via increased sympathetic tone and
hypothalamus mediated reflexes
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Cardiovascular
Increased HTN, PVR
 Tachycardia
 Myocardial irritability
 Increased oxygen demand
 Increased CO in normal heart, decreased in diseased
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Leads to MI and dysrhythmia
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Respiratory
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Increased CO2 production
 Increased minute ventilation
 Increased work of breathing
Especially problematic with lung disease
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Decreased chest movement (Splinting)
 Decreased tidal volume and FRC
Atelectasis, intrapleural shunting, hypoxemia
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Decreased cough
Decreased secretion clearance
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GI
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Increased sympathetic tone
 Decreased intestinal motility
 Decreased urinary motility
Ileus and urinary Retention
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Increased Gastric acid production
Risk of aspiration
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Gastric distention
Further decreased FRC
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Endocrine
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Increased catabolic response
 Increased catecholamines, cortisol, glucagon
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Decreased anabolic hormone
 Decreased insulin and testosterone
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Hematologic
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Increased platelet adhesion
Decreased fibrinolysis
Hypercoagulability, DVT, PE
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Immune
Leukocytosis
 Lymphopenia
Infection and poor wound healing
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Psychological
Anxiety, poor sleep, depression
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Opiates have become more commonly used to
treat chronic, non-malignant pain
“Normal” doses ineffective
 Therapeutic dose can vary by 1000%
 Multimodal approach becomes more useful
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Mechanism of action
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Work at mu, kappa, delta, sigma receptors in spine
and supraspinal structures
 Mu receptors in dorsal horn provide bulk of analgesia
 Receptors in medulla produce N/V
 Supratentorial receptors involved in reward/dug
seeking
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Inhibit presynaptic release of, and postsynaptic
response to excitatory neurotransmitters in
nociceptors
 Ach
 sP
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Cardiovascular
No significant impairment
 Bradycardia, vagal mediated
 Decreased sympathetic flow
 Histamine release
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Respiratory
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Depress ventilation
CO2 respiratory drive blunting (brainstem)
Bronchospasm (histamine)
Chest wall rigidity
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Cerebral
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Reduction in cerebral oxygen consumption
No change in EEG, no amnesia
GI
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Decreased peristalsis
Sphincter of Oddi contraction
Endocrine
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Blunt stress response hormones
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Use for mod to severe pain when other agents
are ineffective
Monitoring for potential side effects is crucial
Goal is adequate pain control with minimal
side effects
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Typical starting dose for MS is 0.1mg/kg, increase
by 0.05mg/kg
Dosing varies significantly; 10X
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Biggest risk of opioids is Resp Depression
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May or may not be dose dependent
Patient may or may not be tolerant (controversial)
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High risk patients:
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 Elderly
 OSA
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Produce state where injury isn’t bothersome
Dose varies
Decreases spontaneous ventilation and response to
hypercarbia
PCA produces less addiction than RN controlled
prn dosing
Need liver failure >80% for accumulation of drug
Renal impairment increases plasma concentrations
of active metabolites (MS, demerol; not fentanyl)
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Ongoing use activates glial cells
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Release neuroexcititory signals
Release pro inflammatory signals
Oppose analgesia
Enhance tolerance
Enhance Resp depression
Enhance dependence
Promote development of (and maintanace)
pathologic pain pathways
 Via non-opiod receptors
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Anticonvulsants
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Action is to suppress spontaneous neural discharge in
damaged/overactive neurons
Especially useful in neuropathic pain, acute and chronic
Slow onset
Long half-life
Side effects (Gabapentin)
 Sleepiness/dizziness
 Allergic reactions
 Withdrawal precipitated seizure
 Suicidal thoughts
 Pregnancy Class C
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Antidepressants
Action is to block presynaptic reuptake of serotonin
and/or norepi
 Potentiates benefits of opioids
 Help normalize sleep
 Side effects
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 Antimuscarinic (dry mouth, urinary retention)
 Antihistamine (sedation, increased gastric pH)
 Alfa-adrenergic blockade (orthostatic hypotension)
 Suicidal thoughts
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COX inhibitors (NSAIDS, ASA, Tylenol)
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Action is prostaglandin inhibition
Benefits
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Analgesia
Antipyretic
Anti-inflammatory
Enhances opioid effects
Side Effects
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GI upset/ulcers
Platelet inhibition
Bronchospasm (potential)
Renal dysfunction
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COX-2 selective inhibitors (Celebrex)
No platelet inhibition
 Decreased upper GI side effects
 12-24 hr duration
 Analgesia equal in non-selective COX inhibitors
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Key is identifying chronic pain regimen
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Home medicine history (dosing, frequency,
duration)
 Family assistance
 Tox screen
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Social history
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HOME MEDS
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Goal is adequate therapy with minimal side
effects
PCA advantages
Cost effective
 Safe (when used correctly)
 Superior analgesia
 High patient satisfaction
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PCA cont
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Basal rate
 Controversial
 May avoid breakthrough
 May increase Resp Depression
 30-50% of total dose may be via BR
Useful for adding in home dose
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Physical dependence
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Occurs in all patients on large doses of opioids for
prolonged periods
Dependence does not equal addiction
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Avoiding withdrawal: alpha2 agonists
(Clonidine)
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Acts postsynaptically to decrease
norepi/sympathetic outflow presynaptically
 Decreased SVR/BP
 Negative Chronotrope
 Analgesia
 Sedation
 Anxiolysis
 Prolonged duration of peripheral nerve blocks
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Available PO, transdermal, parenteral
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Clonidine side effects
Bradycardia
 Hypotension
 Sedation
 Dry mouth
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Advantages of regional anesthesia
Better pain control
 Better preserved pulmonary function
 Early ambulation
 Early PT
 Decreased M&M
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Risks:
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Local anesthetic toxicity
Damage to nerve/other structures
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Trauma is a leading cause of death and
disability
Thoracic trauma accounts for 10 to 15% of
trauma admissions
25% of annual traumatic deaths result from
chest trauma
Rib fractures are the most common injury
associated with chest trauma.
Trauma associated with rib fractures results in
significant morbidity and mortality
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7147 trauma patients reviewed Level 1 Trauma
Center
10% had rib fractures
Only 6% of patients had isolated rib fractures,
94% had associated injuries
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32% had HTX/PTX
26% had Lung Contusion
Ziegler, D.. The morbidity and mortality of Rib Fractures.The
Journal of Trauma, 1994.
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Conclude that rib fractures are a marker of severe
injury
Mortality rate of 12%, with most deaths (69%) occurring
within first 24 hours
 55% patients required immediate operation or ICU
admission
 35% patients required ECF upon discharge
 35% developed pulmonary complications, 6% of these
patients died
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A lower ISS in elderly that died compared to younger
patients, suggests it takes a lesser injury to be lethal in
elderly
Increased severity of injury and mortality with
increasing number of rib fractures
Ziegler, D.. The morbidity and mortality of Rib Fractures.The Journal of
Trauma, 1994.
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Retrospective analysis at Level 1 trauma center
Identified High-Risk rib fractures to be those
associated with intrathoracic injury, increased
morbidity and mortality
Factors indicating a high-risk rib fracture
include
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High energy trauma
Extremes of age
> 3 rib fractures Perils of rib fractures. Sharma OP, Oswanski MF, Jolly S, Lauer SK,
Associated injuriesDressel R, Stombaugh HA American Surgeon, 2008
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The population 65 years of age and older currently
represents approximately 12% of the population in
the United States
The most common mechanism for rib fractures are
motor vehicle crashes
Low velocity falls increase with increasing age
Trauma patients older than 65 are more likely to die
or have significant complications after chest trauma
than similarly injured younger patients
Bergeron, E et al. Elderly Trauma Patients with Rib Fractures Are at greater risk
of Death and Pneumonia. J of Trauma. 54:3, 478-484. March 2003.
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Also found that severity of trauma morbidity
and mortality increase with increasing number
of rib fractures
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The pain associated with rib fractures leads to:
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respiratory compromise
impairment of pulmonary mechanics including:
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hypoventilation
atelectasis
decreased pulmonary compliance
poor pulmonary drainage
hypoxia
This can be further complicated by pre-existing
lung disease, underlying pulmonary contusion
and development of pneumonia
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70% long term dyspnea
49% had persistent chest wall pain
Paradoxical chest movement
Landercasper JL, Cogbill TH, Lindesmith LA:
Long-term Disability after Flail Chest Injury.J
trauma. 24:410-14, 1984
1. Pain Control
2. Pulmonary Toilet
3. Management of
associated Injuries
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Pain management is critical in these patients
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Despite multiple approaches to pain control including:
 anti-inflammatory medications
 systemic narcotics
 intrapleural blocks
 intercostal nerve blocks
 epidurals
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There is no single method satisfactory to all patients.
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Think MULTIMODAL
Acute Pain Management of Patients with Multiple Fractured Ribs
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Medline search 1966-2002
Summarized the various analgesic techniques
used in patients with multiple fractured ribs
No single method that can be safely and
effectively used for analgesia in all
circumstances.
Karmakar, M, et al. 54:3.
615-625. March 2003
PROS
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Systemic opioids are
readily available and
are minimally
invasive.
CONS
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Respiratory
Depression
Sedation
Constipation
Hypotension
Nausea/Vomiting
Urticaria/Pruritus
PROS
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May be the gold standard
for analgesia in rib
fractures allowing
treatment of multiple
levels as well as bilateral
fractures.
No CNS depression
Prolonger duration
CONS
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Hypotension
Urinary Retention
Altered Neuro exam
Avoid anticoagulation
Risk of
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Infection
Epidural hematoma
Spinal cord injury (rare)
CONS
PROS
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Highly effective for
8-24 hours
No CNS depression
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Require multiple
injections at multiple
levels
Risk of Pneumothorax
Risk of toxicity
Risk of vascular
puncture and injection
Short duration
PROS
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Effective for
multiple rib
fractures, bilateral
No CNS depression
No altered neuro
exam
Can be discharged
home/rehab
Anticoagulation OK
CONS
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Risks of systemic
toxicity with local
Pneumothorax
Hematoma
CATHETERS
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Good prep of the area
Pain score not revealing in multiple trauma
patients
Incentive spirometry-focus specifically on the
pain associated with deep breathing
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reduce the incidence of pneumonia often seen in
multi-level rib fracture patients
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Reviewed patients who received an ON-Q Catheter
system from July 2005-Feb 2008
41 trauma patients with ON-Q placement identified
Age range 18-88 years
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average age 61 years old
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Mean # rib fx 7.61
VAS pre insertion 9.4 VAS post insertion 4.8 p<0.001
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Halm, Shapira Presented ACS Annual Meeting 2008
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In the absence of a universal modality for the management of
pain associated with rib fractures, the “over the ribs”
ON-Q catheter pain system provides a safe and effective method
for pain relief in the injured patient with rib fractures.
It enables minimization of opiates utilization, early ambulation
and effective pulmonary toilet.
Patients can continue treatment after discharge from hospital.
The placement is a simple bedside technique and does not
require a specialized practitioner for placement.
Associated Trauma
Sternal fracture
Bilateral parasternal
insertion
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Goal: Block the femoral and lateral femoral
cutaneous nerves, ideally with proximal spread
into the lumbosacral plexus
Technique:
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Ultra sound guidance
Medial to ASIC and sartorius muscle, lateral to fascia
over psoas and femoral nerve/artery
Just deep to fascia iliaca
30-40mL dilute local anes (0.2% ropivacaine)
Single shot vs catheter infusion
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Pathophysiology of pain
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Complex interneural interactions
Opioids
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Mainstay of Rx
PCA safe and effective
Adjuvant meds
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Improve pain control
Help avoid opioid side effects
Acute on chronic pain
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Requires multimodal approach
Regional Anesthetic techniques
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Improve outcomes and patient satisfaction