Pain Management for the Pectus Nuss Patient: A Journey

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1. Concept of Evidence Based Practice
 2. Anatomy of Pectus Procedures and
pain
 3. Importance of Pectus pain
management
 4. Pectus Nuss procedure
 5. Ravitch procedure

6. Post op goals of care
 7. History of prior treatment
 8. Establishment of a pain protocol
 9. Team effort
 10. Drugs of protocol
 11. Results
 12. Solutions

Idea of using a protocol for pain
management
 Witnessing the amount of pain post op
 Wanting to provide adequate pain
management and improve patient
outcomes
 Improving patient experience and
satisfaction

Successful management of a post
procedural pain requires the use of
numerous methods of pain control.
 These include epidural, PCA, NSAIDs and
systemic opioids.
 This is the top priority and in turn effects
patient satisfaction and can increase
complication rates.


By definition is using the best evidence
possible with the most appropriate
information available to make clinical
decisions for individual patients and
improve outcomes.
Steps:
1. Formulate the question/s that need
answers to satisfy the specific patient
needs.
2. Retrieval of the necessary information to
answer the question
3. Reading and assessing the retrieved
information to answer the question
4. Carry out a decision.
5. Evaluation of the process to determine if
optimal outcomes were achieved.
A strong pain stimuli activates NMethyl-D aspartate (NMDA) receptors and
produce hyperexcitibility of dorsal root
neurons. This trigger induces central
sensitization leading to the wind up
phenomenon and pain memory thus
causing pain.
Adaptation of the WHO Analgesic Ladder
First performed in 1987 by Donald Nuss to
correct the deformity of Pectus Excavatum
or “sunken chest”
Involves insertion of a metal bar into the
chest under the defect and then flipping it
causing the chest to be popped up into a
more anatomical position.
This causes a dislocation and realignment
of the costovertebral joints with the chest
reposition.
By abruptly elevating the sternum
anteriorly a substantial amount of pain in
the chest and back is generated in a
skeletally mature adolescent.
The pressure of the bar holding the chest in
a new elevated position increases the
magnitude of pain involving the
dermatomes of T1-T10.
A transverse incision is made between the
nipples, and the offending costal cartilage
is removed with remodeling of the sternum
and then placement of the bar for
stabilization. Sutures are then placed
around the bar to secure it to the ribs. The
bar remains in place for about 12 months.
You are not able to see the bar on the
outside of the chest.
POD 0
 Ketorolac (Toradol)
 Methocarbamol
(Robaxin) IV
 Ondansetron (Zofran)
 Famotidine (Pepcid)
 Epidural
POD 2
 Oxycodone/acetamin
ophen (Percocet)
 oxycodone
(Oxycontin)
 Ibuprofen
 Methocarbamol
(Robaxin) po
 Famotidine (Pepcid)
po

Miralax
Prophylaxis: for gastric upset due to
NSAID therapy
 Duration of therapy: 1 month post op
 Adverse Rx: dizziness, headache,
constipation, diarrhea
 Dose 20 mg BID for 1 month

MOA: inhibits histamine at H2 receptors
and gastric parietal cells inhibiting gastric
secretion
 Onset: 1 hour
 Max: 30 minutes (IV) 1-4 hours (oral)
 Duration: 10-12 hours

Anti inflammatory Nsaid
 Duration of therapy: 1 month post op
 Adverse Rx: increased risk of
gastrointestinal bleeding and perforation
 Dose: 10 mg/kg Q 6 hours

MOA: inhibits cyclooxygenase 1&2 (Cox
1&2) enzymes decreasing the formation
of prostaglandin precursors, has
antipyretic, analgesic and anti
inflammatory effects
 Onset 1 hour
 Max: 2-4 hours
 Duration: 6-8 hours (dose related)

Non narcotic anti inflammatory agent,
Nsaid
 Duration of therapy: POD 0 and POD 1
 Adverse Rx: edema, hypotension,
dizziness, drowsiness, headache
 Dose: every 6 hours for 24 hours post op
then replaced with ibuprofen every 6
hours

MOA: inhibits Cox 1&2 enzymes,
decreases formation of prostaglandin
precursors, antipyretic, analgesic, anti
inflammatory
 Onset: 30 minutes (IV)
 Max: 2-3 hours (IV)
 Duration: 4-6 hours

Treatment of muscle spasms associated
with acute painful musculoskeletal
conditions
 Duration of therapy: 1 month post op
 Adverse Rx: bradycardia, flushing,
hypotension, syncope, dizziness,
drowsiness, fever, headache
 Dose:15mg/kg/dose IV Q 6 hours
POD0&1 then po

MOA: causes skeletal muscle relaxation
by general CNS depression
 Onset: 30 minutes
 Max: 1-2 hours
 Duration: 1-2 hours

Used for around the clock management of
moderate to severe pain when analgesic is
needed for long period of time
 Duration of therapy: starts POD 2 and
continues for 1 week after discharge
 Adverse Rx: orthostatic hypotension,
drowsiness, dizziness, anxiety, chills,
confusion, nervousness, twitching,
abdominal pain, gastritis, vomiting and
constipation

Dose: 10 mg Q 12 hours
 MOA: binds to opiate receptors in CNS,
inhibiting ascending pain pathways,
altering perception and response to pain
produces generalized CNS depression
 Onset: 12 hours
 Max: 12 hours
 Duration: 12 hours

Percocet
Percocet
Pain spike
Oxycontin
Pain spike
Relief of moderate to moderately severe
pain
 Duration of therapy: 1 week post op
 Adverse Rx: circulatory depression,
hypotension, dizziness, drowsiness,
fatigue, headache, insomnia, skin rash,
constipation, nausea and vomiting
 Dose: 1-2 Norco 5 Q 4-6 hours prn

MOA: blocks pain perception in cerebral
cortex by binding to specific receptor
molecules and opiate receptors within
neuronal receptors decreasing synaptic
chemical transmission throughout CNS
inhibiting flow of pain sensations in the
higher centers
 Onset: 10-15 minutes
 Max: 60 minutes
 Duration: 3-6 hours

Use as an osmotic laxative, prophylactic
with narcotic use
 Duration of therapy: 1 month post op
 Adverse Rx: urticaria, abdominal
bloating, cramping, diarrhea, flatulence,
nausea
 Dose: 17gm daily

MOA: osmotic agent causes water
retention into stool increasing stool
frequency
 Onset: 1-3 days

Management of severe acute pain
 Duration of therapy: during
hospitalization as PCA or prn dosing
 Adverse Rx: bradycardia, flushing,
syncope, amnesia, agitation, anxiety,
drowsiness, slurred speech, pruritus, rash,
urticaria, constipation, nausea, vomiting,
urinary retention, respiratory depression

Dose: PCA or 2 mg Q 2-3 prn
 MOA: binds to opioid receptors in CNS
causing inhibition of ascending pain
pathways altering perception and
response to pain producing generalized
CNS depression
 Onset: 20 minutes
 Duration: 3-5 hours

The degree of pain affects all
measureable objective outcomes during
their hospitalization
 Parents during hospitalization are asked
about the control of their child’s pain
and for 2015 the average is 88%
controlled
 In patients less than age 12 or 40 kg
Oxycontin is not used

If they have a reaction to Oxycontin it is
discontinued and the patient is
monitored closely and alternate
methods are use to control pain
 A future study is being researched at the
present time
 If the Oxycontin causes over sedation it is
held and other meds are added as
needed

Have only had 2 patients who
developed gastric upset with the
ibuprofen, so Pepcid became standard
 Constipation is averted with Miralax and
if problems MOM is given and if no results
suppository is next step

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
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
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