Postanesthesia Care Unit

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Postanesthesia Care Unit
(PACU)
to provide close monitoring and care to patients
recovering from anesthesia and sedation.
assuring safety to the transition between
anesthesia and the fully awake state,
before patients are transferred to
unmonitored general wards.
The PACU is staffed by a dedicated team of an
anesthesiologist, nurses and aides.

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 Location
 located close to the operating suite

 good access to immediate radiology,

blood bank, blood gas, and other clinical
laboratory services.

 near the ICU

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size
 determined by the surgical caseload of
the institution.
 Approximately 1.5 PACU beds per
operating room utilized
 An open ward is optimal for patient
observation
 at least one isolation room
 A separate pediatric PACU

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Facilities
 The ward itself should have large
doors, adequate lighting, efficient
environmental control and sufficient
electrical and plumbing facilities.
 the bed spaces
 central nursing station and physician
station
 storage and utility rooms

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 Each bed space should have piped-in
oxygen, air and vacuum for suction
(both intermittent pressure for gastric
suction and high pressure for airway
and chest suction).

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Drugs and equipment for routine care (O2,
suction, and monitors) and advanced
support (mechanical ventilators,
pressure transducers, infusion
pumps, and crash cart) must be
readily available.
A “crash cart” containing
cardiopulmonary resuscitation
equipment and emergency drugs
should be available and fully stocked
at all times.

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The postanesthesia care unit should be well lighted, spacious, and
equipped to deal with any possible postanesthetic emergency. A
central nursing and physician station is useful. Each bedside
should be fully equipped with air, oxygen and suction.
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Personnel
 nursing ratio – 1:3 (one nurse to every
three patients) or 1:2 or 2:1
 A charge nurse should oversee nursing
care.
 Most PACUs are under the medical
direction of the anesthesia department
 The anesthesiologist is usually
responsible for patient discharge to the
postsurgical ward, ICU or home.

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Admission to the PACU

Transport from the OR is carried

out under direct supervision
of the anesthetist.
with the head of the bed elevated
or in the lateral decubitus
position, face mask.

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 Report
 the anesthesiologist should give the
nurse a full report of the events
during surgery.
 This report should include the
patient‘s name, age, surgical
procedure, medical problems,
preoperative medications, allergies,
anesthetic drugs and methods, fluid
and blood replacement, blood loss,
urinary output, gastric output, and
surgical or anesthetic complications
encountered.
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 Monitoring
Close observation of the patient's level of
consciousness, breathing pattern and
peripheral perfusion is most important.
Vital signs should be recorded at least every 15
minutes during the first postoperative
hour.
When monitoring and care requirements are
increasing, plans should be made to
transfer the patient to an intensive care
unit (ICU).

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Discharge Considerations
 Before discharge, the patient who has
undergone general anesthesia should be
arousable and oriented, have stable vital
signs for at least the prior hour and be
comfortable.

 Patients who have had recent large doses
of narcotic analgesics should be observed
for at least 30 minutes.

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The patient should be able to obtain
nursing help while in the surgical ward if
necessary.
Patients discharged without
supplemental oxygen need to have their
arterial oxygen saturation measured by
pulse oximetry while they are breathing
room air.
Discharge of the patient from the
recovery room following regional
anesthesia depends on the type of block
used and sedation administered.
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 Uncomplicated regional blocks do not
require recovery in the PACU.
Postoperative monitoring is indicated
when heavy sedation was administered, a
complication from the block occurred
(e.g., intravascular injection of a local
anesthetic or pneumothorax), or when
required by the nature of the surgery.

 A full description of the patient‘s course
should then be given by the recovery room
nurse to the ward nurse before the patient
is transferred.

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Complications

Complications causing at least

moderate morbidity occur in
approximately 5% to 10% of
PACU admissions.

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Hemodynamic
complications
 Hypotension  (4% of
admissions)
 Hypertension  (1% to 2%)
 Arrhythmias  (4%)
 Myocardial ischemia and
infarction
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Hypotension
Inadequate venous return
b. True hypovolemia. Ongoing hemorrhage,
inadequate fluid replacement, osmotic
polyuria and fluid sequestration
c. Relative hypovolemia positive pressure
ventilation, intrinsic positive end-
expiratory pressure, pneumothorax,
pericardial tamponade.
Vasodilation
Decreased inotropy
Myocardial ischemia and infarction,
arrhythmias, congestive heart failure,
negative inotropic drugs, sepsis,
hypothyroidism, and malignant
hyperthermia
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 Hypertension
Etiology: preexisting hypertensive
disease, pain, bladder distention,
fluid overload, hypoxemia, increased
intracranial pressure (ICP) and
administration of vasoconstrictive
agents.
Hypertension may present with
headache, visual disturbances,
dyspnea, restlessness, and chest
pain, but is often asymptomatic.
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 Management aims at restoring blood
pressure close to what is normal for each
patient.
 If needed, IV or sublingual drug.
3. Beta-adrenergic blockers:Labetalol,
propranolol and esmolol
4. Calcium-channel blockers: Verapamil,
diltiazem, Nifedipine
5. Hydralazine
6. Nitrates: Nitroglycerin, Sodium nitroprusside
7. Alpha-adrenergic blockers: phentolamine,
labetalol

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Myocardial ischemia and
infarction
T-wave changes

ST-segment elevation or depression.

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Arrhythmias
Increased sympathetic outflow,
hypoxemia, hypercarbia, electrolyte
and acid-base imbalance,
myocardial ischemia, increased ICP,
drug toxicity, and malignant
hyperthermia are possible
etiologies of perioperative
arrhythmias.
In the presence of more worrisome
rhythm disturbances, supplemental
O2 should be delivered and proper
treatment begun while the etiology
is investigated.
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 Respiratory complications

 Hypoxemia (0.9% of
admissions),
 Hypoventilation  (0.2%)
 Upper airway obstruction 
(0.2%)

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Hypoxemia
Causes of hypoxemia include the
following:
2. Atelectasis
3. Hypoventilation
4. Upper airway obstruction
5. Bronchospasm
6. Aspiration of gastric contents
7. Pulmonary edema
8. Pneumothorax
9. Pulmonary embolism
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Hypoventilation
Hypoventilation is an inappropriately low-
minute ventilation and results in
hypercapnea and acute respiratory
acidosis. When severe, hypoventilation
produces hypoxemia, CO2 narcosis, and
ultimately apnea.
Etiologies of postoperative hypoventilation
may be divided in two groups:
n Decreased ventilatory drive
n Pulmonary and respiratory muscle
insufficiency

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Upper airway obstruction
Principal signs are the lack of adequate air
movement, intercostal and suprasternal
retractions, and discoordinate
abdominal and chest wall motion during
inspiration.
Common etiologies include:
3. Incomplete recovery
4. Laryngospasm
5. Airway edema
6. Wound hematoma
7. Vocal cord ( 声带 ) paralysis

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Guidelines for extubation

1. Adequate arterial PaO2.

2. Adequate breathing pattern.
3. Adequate level of consciousness for
cooperation and airway protection.
4. Full recovery of muscle strength.

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• Before proceeding with extubation, the
PACU anesthesiologist should be aware of
preexistent airway problems in the event
that reintubation is necessary.
Supplemental O2 is administered, the
endotracheal tube, mouth, and pharynx
suctioned, and the tube removed
following a positive-pressure breath.

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Renal complications
  Oliguria 
 Polyuria 
 Electrolyte disturbances

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 Oliguria
urine output less than 0.5 mL/kg per hour, but
common sense must be used.
Hypovolemia is the most frequent cause of
postoperative oliguria.
The pre-, post-, and intra-renal causes
4. Prerenal oliguria includes conditions that
decrease renal perfusion pressure. Besides
hypovolemia, other causes of a decreased
cardiac output must be considered.
5. Intrarenal: acute tubular necrosis secondary to
hypoperfusion (e.g., shock or sepsis), toxins
(e.g., nephrotoxic drugs or myoglobinuria) and
trauma.
6. Postrenal: urinary catheter obstruction, trauma,
and iatrogenic damage.

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 Polyuria
urine output disproportionately high for
a given fluid intake.
2. Excessive volume administration.
3. Pharmacologic diuresis.
4. Nonoliguric renal failure.
5. Osmotic diuresis may be caused by
hyperglycemia, alcohol intoxication,
and administration of hypertonic
saline, mannitol, or parenteral
nutrition.

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Electrolyte disturbances

hyperkalemia and acidemia.

Hypokalemia and alkalemia
Hypomagnesemia

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Neurologic complications

  Delayed awakening 
 Neurologic damage 
 Emergence delirium 
 Peripheral neurologic lesions

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 Delayed awakening

2. The most frequent cause is the

persistent effect of anesthesia.
3. Decreased cerebral perfusion
4. Metabolic causes of delayed
awakening include hypoglycemia,
sepsis, preexisting
encephalopathies, and electrolyte
or acid-base derangements.

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Neurologic damage
Neurologic damage may occur from a stroke
and may be initially difficult to diagnose
because of residual anesthesia.
Strokes can be thromboembolic or
hemorrhagic.
Strokes are more frequent following intracranial
surgery or multiple trauma.

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 Emergence delirium
is characterized by excitement alternating with
lethargy 无生气 , disorientation, and
inappropriate behavior.
Delirium may more frequently occur in the
elderly and in those with a history of drug
dependency or psychiatric disorders.
Many drugs used perioperatively may precipitate
delirium: ketamine, opioids,
benzodiazepines, large doses of atropine.

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Delirium may be a symptom of
ongoing pathology (e.g.,
hypoxemia, acidemia,
hypoglycemia, intracranial injury,
sepsis, severe pain, and alcohol
withdrawal).
Treatment is symptomatic:
supplemental O2, fluid and
electrolyte replacement, and
adequate analgesia. An
antipsychotic medication such as
haloperidol, Benzodiazepines may
be added.
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Peripheral neurologic
lesions
may follow direct surgical
damage and improper
intraoperative positioning.
Early neurological consultation
for diagnosis and
rehabilitation are crucial for a
full recovery.

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Principles of pain
management
 Opioids 
 Nonsteroidal 
 Adjuvant analgesics 
 Regional sensory blocks 
 Patient-controlled

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Principles of pain
management
Adequate analgesia begins in the OR and continues
in the PACU.
Opioids (IV or peridural) are the mainstay of
postoperative analgesia. Intramuscular
injections, ordered on an “as needed” basis,
have essentially no indication in adult PACU
patients.
Fentanyl, Morphine, Meperidine
Nonsteroidal anti-inflammatory drugs (NSAIDs):
Ketorolac,ibuprofen, acetaminophen
Regional sensory blocks
Patient-controlled and continuous epidural
analgesia
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Postoperative nausea and
vomiting (PONV)
 PONV typically occurs in 20 to 30%
of surgical cases.
 aspiration of emesis, gastric
bleeding, and wound hematomas
may occur with protracted or
vigorous retching or vomiting.
 Troublesome PONV can prolong
recovery room stay and
hospitalization.

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Body temperature
changes
  Hypothermia 

 Hyperthermia

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 ACUTE
POSTOPERATIVE
PAIN MANAGEMENT

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 Definition and History
 Acute pain: a normal, predicted, physiological response to an
adverse chemical, thermal or mechanical stimulus
-Surgery, trauma and acute illness…
-Short duration, recent onset, poss. prolong or chronic
 Consequences of surgical procedure
-Cardiopulmonary compression
-Autonomic hyper-stimulation
-Increased blood clotting
-Water retention and delayed GI function
-Immune dysfunction
-Pain:
 Surgical injuries and emotional reactions

 Fear of pain (59%) and postponing surgery (8%)

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 Definition and History
 Consequences of acute postop pain
-Increased M&M
 Cardiovascular : HTN, ischemia, MI, arrhythmia, DVT

 Pulmonary: atlectasis, pneumonia, bronchospasm

 CNS: agitation, elevated ICP, stroke
 GI/GU: ileum, constipation, N/V, urinary
retention
 Surgical site: poor healing, tissue breakdown, bleeding
-Prolonged hospital staying
-High health care cost
-Chronic pain syndrome
-Negative physical and psychological effects 45
 Definition and History

 Historically, postop pain mgt has been inadequately

-Patient education and communication
-Staff training/knowledge on acute pain management
-Pain assessment before and after analgesia
-Timely evaluation and follow-up
 Recently, more attention to the pain
-1992/ANA: comfort & pain relief in dying patient
-1995/APS: pain scale as the fifth vital sign
-2000/JCAHO: pain assess and mgt as a patient’s right
-2003/NPCPA: “the decade of pain control and research”
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 Professional Guidelines for Pain Management
 Agency/year Guideline
-ASA/95’,04’ Practice guidelines for acute pain management
in the perioperative setting
-APS/03’ Principles of analgesic use in the treatment of
acute pain and cancer pain
-EAU/03’ Guidelines on pain management
-VHADD/02’ Clinical practice guideline for the management
of postoperative pain
-JCAHO/00’ Pain assessment and management:
an organizational approach
-AHCPR/93’ Acute pain management
-IASP/92’ Task force on acute pain

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 Acute Pain Service Models
 APS with Anesthesiologists and other care providers
 24–hr availability
 Personal training via up-to-date knowledge/skills/techniques
 Multi-models with more aggressive ways
 Comprehensive techniques
 New pharmacological agents
 Reliable assessment of pain
 Pre/intra/postoperative evaluation
 Timely monitoring and management
– Pain scale, response and adverse reactions to treatment
– Life-threaten emergency
 Outcome
 A score of 3 or below without adverse reactions
 Patient’s satisfied and early discharged
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 Assessment of Pain & Management

 Subjective report by patient

-Pain score: 0-10 (no pain to worst pain in life)
-Satisfaction score
-Anxiety, fear, culture/religious influence, communication
 Objective report by APS
-General condition
 Vital signs, mental status

-Clinical functions
 Deep breath, cough, ambulation…

-Monitoring response to therapy and adverse reactions

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 Preoperative Patient Evaluation & Planning
 Proactive individualized APS planning
 Type of surgery
 Expected severity of acute pain

 Patient’s previous experience with pain

– Type of analgesia (PO,IV,IM, PCA, epidural…)

– Response to the treatment
– Any adverse reactions
– Any surgical complications
 Co-existing conditions

– Cardiac, pulmonary, renal, diabetic neuropathy,

sickle cell anemia, mental status…
– Allergies and drugs (anticoagulation, pain pills)
 Risk-benefit ratio for the available techniques
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 Type of Surgery & Severity of Pain

Minor Intermediate Major

Surgery Inguinal Hernia Fem/Hip ORIF Thoracotomy
Breast Biopsy Hysterectomy Nephrectomy
Varicose veins Exp. Lap Colectomy
Closed reduction Lower abd. Upper abd.
Knee arthroscopy Maxillofacial TKR/THR
Gyn laparoscopy Cesarean section AAA
Pain mild-moderate moderate-severe very severe

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Preoperative Preparation of the Patient
 Adjustment or continuation of medications
 Withdrawal syndrome
 Surgical-related stress/physiological reactions

 Optimizing patient’s conditions

 Premedication prior to surgery

 Initiation of analgesic pain management program
 Reduction of preexisting pain and anxiety

 Patient and family education

 Behavioral pain control techniques/communication
 Emotional/stress relief and support

 Optimal use of PCA and PCEA

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Intraoperative Evaluation & Management
 Preemptive analgesia (Reducing sensitization)
-Local infiltration
-IV opioids
-Epidural bolus or continued infusion
 Lower sympathetic tone
-SBp 20-30% below base-line
-HR 50-70’s
 Emergence or spontaneous breath
-RR is key (12-15/min)
-Adequate oxygenation and ventilation 53
Postoperative Evaluation & Management
 PACU
– Rapid control pain score to 3-4 or below
 IV Toradol or PO weak opioid for mild pain
 IV bolus of Morphine for mod-severe pain
 Fontanels or combined Morphine for very severe pain
 Peripheral nerve blockade
– Then continue multi-model pain management
 In-patient: PCA or PCEA
Epidural or PNB catheter
IV, IM or PO
 Out-patient: PO opioid, NSAIDs,
Durogenic patch
 Frequently Assessment of pain/satisfaction scale
– Adjustment management
– Treatment of adverse reactions
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 Therapeutic Models for Acute Pain
 Systemic opioids
-Enteral
 Oral (PO): via digestion, absorption, liver metabolism then to blood
 Rectal, Sublingual (SL): directly into vein
-Parenteral
 Transdermal/Transmucosal/Subcutaneous (SQ): slow absorption
 Intramuscular (IM): 15-30 min reach peak blood concentration
 Intravenous (IV): bolus or infusion/PCA
 Neuroaxial (intrathecal/epidural)
 Afferent neural block with L.A. (+/- opioid)
-Neuraxial (intrathecal or epidural)
-Peripheral plexus/nerve & incision
 NSAIDs
 Others 55
 Systemic Opioids
-Type
 Hydrophilic: Morphine, Hydromorphone, Meperidine
 Lipophilic: Sufentanil, Fentanyl
 Mixed: DepoDur (liposome slow-release morphine)
-Enteral:
 Short-acting: Codeine, Hydrocodone, Oxycodone, Hydromorphone
 Long-acting: MsContin, OxyContin, Methadone…
 Newer agents: Avinza, Kadian (longer-acting morphine)
-Parenteral:
 Short-acting: Fentanyl, Sufentanil, Remifentanil…
 Intermittent: Meperidine, Hydromorphone
 Long-acting: Morphine, Duromorphine
 Transdermal: Duragesic patch (Fentanyl)
 Transmucosal: ACTIQ (Fentanyl)
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 Therapeutic Models for Acute Pain

 IV-PCA
-Potential efficacy for most in-house patients with
moderate to severe pain procedures
-Improving pain scores & patient satisfaction
-Equivocal to PCEA
-Better or more constant analgesia with basal infusion
Agents: bolus(mg) lockout(min) basal(mg/hr)
Morphine 0.5-3 5-10 0.5-1
Hydromorphone 0.1-0.5 5-15 0.2-0.5
Meperidine 50-100 5-15 5-50
Fentanyl 0.015-0.05 3-10 0.02-0.1
Methadone 0.5-3 10-20

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Therapeutic Models for Acute Pain
 IV-PCA overdose
– Clinical symptom and sign
 Hypotension
 Asleep, drowsing, and seizure (Meperidine)
 Respiratory depression, apnea and death
 Estimated death rate: 1in 10,000-30,000
– Programming errors of PCA machine
– Drug prep errors
 Error drug
 Error concentration
– Basal infusion
– Patient conditions and co-exited morbidities
– Inadequate observation from care provider
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 Therapeutic Models for Acute Pain

 Inadequate IV-PCA
– Usually managed by non-anesthesiologists
– Lack of understanding of adverse physiologic
squealer
– Myths about opioid risks persist
 Addiction, dependence
– Lack of application on multimodal therapy
 Bolus or breakthrough

 Regional techniques

– Analgesic gap in transition to oral route

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 Therapeutic Models for Acute Pain
 Intrathecal analgesia via single shout or continuous catheter
– Narcotics Dose Onset(min) Duration(hr)
 Morphine 0.2-0.5 mg 15-45 8-24
 Sufentanil 5-15 mcg 2-5 2-4
 Fentanyl 10-50 mcg 2-5 1-3
Solubility Lipophilic Hydrophilic
Onset /Duration rapid/short slow/long
CSF sol./spread low/minimal high/extensive
Resp.depression early later
Systemic absorb. high low
Adverse effects low high
Analgesia/area PCEA,infusion/limited bolus/spread
– Local anesthetics
 0.5-0.75% Bupivacaine
 5% Lidocaine

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 Therapeutic Models for Acute Pain
 Epidural analgesia
Opioid Bolus(mg) Onset(min) Duration(hr) Conc.(mg/ml) Rate(ml/h)
Morphine 5 10-20 12-24 0.1 1-6
Fentanyl 100 mcg 4-10 2-4 4 mcg 4-12
Dilaudid 1 10-15 10-12 0.05 6-8
Meperidine 25-100 5-10 4-6 1 10-20
Sufentanil 30-50mcg 5-7 3-4 5 mcg 8-10
DepoDur 15-20 48
-More thoracic epidurals for thoracic, abdominal cases
-Lumbar epidural for lower abdominal/extremities cases
-Increasing PCEA(30-40%), less sedated than PCA
-Epidural opioid analgesia more effective than IM or IV
-Preemptive opioid
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 Therapeutic Models for Acute Pain
 Epidural analgesia with L.A.
-Local anesthetics Conc.(%) Onset
Duration
 Lidocaine 1-2 quick short
 Mepivacaine 1-2 quick
intermittent
 Bupivacaine 0.1-0.125 (T) slow long
<0.5 (L)
 Ropivacaine 0.2 slow long
-Motor block occurs latest to all L.A.
 2-3 segments below the sensory level
 Lidocaine, Bupivacaine >> Ropivacaine
-Vasoconstrictor: Epinephrine, Phenylephrine
 Lowing systemic absorption
 Enhancing blockade and prolonging duration
 Testing dose 62
Pros and Cons of Neuraxial Analgesia
– Advantages
 Improving postop pain control
 Reducing pulmonary complication & GI motility
 Reducing incidence of postop myocardial infarction (T>L)
 Reducing hypercoagulability & DVT (L.A.>opioid)
 Better patient’s satisfaction/life-quality & early discharge
– Contraindications
Absolute Relative
No consent/refuse Around area infection
Sepsis or bacteremia Demyelinating CNS diseases
Elevated ICP Dementia
Infection at site Hypovolemia
L.A allergy LBP/Prior spinal surgery
Coagulopathy Drugs (ASA)

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Complications of Neuraxial Analgesia
-L.A. allergy & toxicity
 Hypersensitivity: skin rashes to anaphylaxis
 Toxic symptoms:

CV CNS
dysrhythmia circumoral numbness
bradycardia tinnitus, blurred vision
hypotension agitation, confusion
asystole seizure
-Narcotics
 Pruritus, ileum, urinary retention, N/V

 Respiratory depression and apnea

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Complications of Neuraxial Analgesia
-Headache
 Spinal H/A, Co-existed H/A, Meningitis, Pneumocepheral
-Infections
 Epidural abscess, Arachnoiditis
 Risk factor: Steroids dependent, Sepsis, Localized lesions
-Hematoma
 Blood tap or vascular injury
 Anticoagulopathy:
-Drugs: Coumadine, Plavix, LMWH, ASA, Herbs
-Congenital disease: vw disease, hemophyllis
 Prevention:
-Stopping anticoagulators and rechecking coax profiles

5d for Coumadine, 12d for Plavix, 12hr for LMWH
-Correcting coagulopathy before giving/withdrawing

FFP, DDAVP, cryoprecipitate, specific factor(VIII) 65
Complications of Neuraxial Analgesia
-Hypotension
 Dehydration

 Vasodilatation via sympathetic blockade

 Co-existing cardiac, pulmonary, metabolic problems

-High spinal
 Slurred speech, agitated or drowsing

 SOB with above T4 block

 Apnea with C3-C5 block (nearly total spinal)

-Backache and nerve injuries

 Difficult placement: multiple puncture/directed damage

 Muscle spasm and poor position

 Co-existing LBP, herniated discs, spinal stenosis, etc

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Regional Analgesia Techniques
– Peripheral nerve blocks (PNB)
 Intercostal, Interpleural
 Ilioinguinal and 3-in-1 block
 Plexus: Interscalene, Axillary, Brachial, Femoral, Ankle block
 Penile and dorsal nerve block
– IV block: Bier Block
– Field infiltration
– Intraartricular block (peripheral opoid receptor)
 1-5 mg morphine +/- bupivacaine(0.25%)
– Systemic absorptive rate:
Intercostal>caudal/spinal>epidural>brachial plexus>SQ
– Adjuvant (clonidine, epinephrine, opioids)
 Reducing L.A. dose with less motor block
 Improving analgesia
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 Regional Analgesia Techniques
 Local anesthetics
Neural blockade sequence:
 Sympathetic block: temp. elevation/vasodilatation

 Loss of pain and temp. sensation

 Loss of proprioception, touch and pressure sensation

 Motor block

Agents Lido Mepiv Bupiv Ropiv

Conc.(%) 1-2 1 .25-.5 .2
Onset (min) 5-10 >10 10-15 10-15
Duration(min) 30-120 45-90 120-240 120-360
Max dose(mg) 300/500 300/500 175/225 200/
Spinal/epidural +/+ -/+ +/+ -/+
PNB/infiltra. +/+ +/+ +/+ +/+
IVor <12yo +/+ -/- -/- -/-
Motor block >2%,epi >1% >.5% >.5%
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Regional Analgesia Techniques
-Advantages
 Patient satisfaction, fully function
 Better & prolonged analgesia

 Lower opioid consumption

 Lower adverse reactions: opioid via L.A.

 Early discharge

-Disadvantages
 Experienced, high skillful provider
 Difficult position for certain blocks

 Potential nerve injuries

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 Therapeutic Models for Acute Pain
 NSAIDS
– Inhibiting cyclooxygenase (COX), low prostaglandins
 COX-1 in various tissues with normal physiologic regulations
 COX-2 only induced by pain & inflammation
 COX-2 inhibitors (Vioxx, Celebrex):
Analgesia/anti-inflammation
No side effects of opioid, steroids and other NSAIDS (COX1&2)
Increase risk of AMI, CVA in patients with cardiovascular disease
– Precautious
 PUD, GI or CNS hemorrhage; kidney, liver, or platelet dysfunction
– Acetaminophen alone or combined with opioid
 Mild to moderate pain
– Ketorolac (Toradol): only parenteral form
 Potent analgesia: 30 mg = 10mg morphine, same onset & duration
 Loading: 30-60 mg, then 15-30 mg q6h for up to 5 days 70
 Therapeutic Models for Acute Pain

 Others
-NMDA antagonist:
 Reducing hyperalgesia, allodynia and chronic pain
 Ketamine, Dextromethorphan, Methadone
 Ketamine (.5-1mg/kg): preemptive analgesia & few side effects
-Alpha 2 agonist:
 Clonidine, Dexmetodomidine
 Effective in reducing postoperative opioid requirements
-Physical therapy, behavior relaxants, TENS
-Specific:
 Adequate drainage of urine, bloody and fluids
 Surgical re-exploration
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Multi-Model Techniques for Pain Management
 Most effective analgesic technique (single one)
-Afferent neural blockade with local anesthetics
 Neuroaxial (spinal or epidural) block
 Peripheral nerve block
 Local infiltration
-Intrathecal opioids
-Epidural opioids and clonidine
-PCA with opioids
-NSAIDS and other agents
 Multi-drugs are more potent than single one
 Multi-routes are more potent than single route

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Multimodal Techniques for Acute Pain Control
 Two or more analgesic agents via a single agent
-Epidural or intrathecal opioids combined with
 L.A. via epidural opioid

 L.A. via epidural L.A.

 Clonidine via epidural opioid

-IV opioids combined with

 Clonidine

 Ketorolac

 Ketamine

-Oral opioid combined

 NSAIDs, COXIBs, or acetaminophen
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Cost of Postoperative Pain Management
 Cost of medications
 Health care providers
-Physician
-Nurse
 Cost of instruments & equipments
-PCA pump and tubes
-Epidural and spinal trays
-Peripheral nerve block kits
 Length of hospitalization
 Pain related complications
 Outcomes
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Challenge of Comprehensive APS
-Increasing demands of anesthesiologists
 Anesthesiologist shortage
 Increased surgical loading

 Patient population change

-Hospital staff shortage

-Financial Limitation
 Lower or no reimbursement for IV-PCA
 Lower reimbursement for continuous PNBs

 O.K. for Epidurals

-Malpractice risks
 Epidural, intrathecal > PNB > IV, IM, PO 75
Future in Acute Pain Management

A role of anesthesiologists
 Proliferation of regional techniques
 Training surgical colleagues
 Implementing multimodals
 Integrating economical manner
 Developing new agents and techniques

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Thanks for your attention!

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