9 The Post Anesthesia Care Unit

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

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good access to immediate radiology, blood bank, blood gas, and other clinical laboratory services.

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near the ICU

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size 

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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 

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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. 7

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. 8

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 

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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. 11

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.

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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. 14



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.

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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 

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Hypotension  (4% of admissions) Hypertension  (1% to 2%) Arrhythmias  (4%) Myocardial ischemia and infarction 17

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 endexpiratory pressure, pneumothorax, pericardial tamponade. Vasodilation Decreased inotropy Myocardial ischemia and infarction, arrhythmias, congestive heart failure, negative inotropic drugs, sepsis, hypothyroidism, and malignant hyperthermia 18

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. 19

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 3. 4. 5. 6. 7.

Management aims at restoring blood pressure close to what is normal for each patient. If needed, IV or sublingual drug. Beta-adrenergic blockers:Labetalol, propranolol and esmolol Calcium-channel blockers: Verapamil, diltiazem, Nifedipine Hydralazine Nitrates: Nitroglycerin, Sodium nitroprusside 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. 22

Respiratory complications 

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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 24

Hypoventilation Hypoventilation is an inappropriately lowminute 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 26

Guidelines for extubation 1.

Adequate arterial PaO2.

2.

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

3.

4.

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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. 30

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. 3. 4.

The most frequent cause is the persistent effect of anesthesia. Decreased cerebral perfusion 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. 37

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. 38

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 40

Postoperative nausea and vomiting (PONV)  

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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. 41

Body temperature changes 

 Hypothermia 

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Hyperthermia

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ACUTE POSTOPERATIVE PAIN MANAGEMENT

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Definition and History 

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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%) 44

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: -1995/APS: -2000/JCAHO: -2003/NPCPA:

comfort & pain relief in dying patient pain scale as the fifth vital sign pain assess and mgt as a patient’s right “the decade of pain control and research” 46

Professional Guidelines for Pain Management  Agency/year

-ASA/95’,04’ -APS/03’ -EAU/03’ -VHADD/02’ -JCAHO/00’ -AHCPR/93’ -IASP/92’

Guideline Practice guidelines for acute pain management in the perioperative setting Principles of analgesic use in the treatment of acute pain and cancer pain Guidelines on pain management Clinical practice guideline for the management of postoperative pain Pain assessment and management: an organizational approach Acute pain management Task force on acute pain 47

Acute Pain Service Models 

APS with Anesthesiologists and other care providers  

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Multi-models with more aggressive ways  

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Comprehensive techniques New pharmacological agents

Reliable assessment of pain  

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24–hr availability Personal training via up-to-date knowledge/skills/techniques

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 48

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 49

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

Surgery

Pain

Minor Inguinal Hernia Breast Biopsy Varicose veins Closed reduction Knee arthroscopy Gyn laparoscopy mild-moderate

Intermediate Fem/Hip ORIF Hysterectomy Exp. Lap Lower abd. Maxillofacial Cesarean section moderate-severe

Major Thoracotomy Nephrectomy Colectomy Upper abd. TKR/THR AAA 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

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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:



Out-patient:

PCA or PCEA Epidural or PNB catheter IV, IM or PO PO opioid, NSAIDs, Durogenic patch

 Frequently Assessment of pain/satisfaction – Adjustment management – Treatment of adverse reactions

scale

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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

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NSAIDs Others

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Systemic Opioids -Type   

Hydrophilic: Lipophilic: Mixed:

Morphine, Hydromorphone, Meperidine Sufentanil, Fentanyl 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: Intermittent: Long-acting: Transdermal: Transmucosal:

Fentanyl, Sufentanil, Remifentanil… Meperidine, Hydromorphone Morphine, Duromorphine Duragesic patch (Fentanyl) ACTIQ (Fentanyl) 56

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 Hydromorphone 0.1-0.5 Meperidine 50-100 Fentanyl 0.015-0.05 Methadone 0.5-3

5-10 5-15 5-15 3-10 10-20

0.5-1 0.2-0.5 5-50 0.02-0.1

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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 58

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 59

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  Sufentanil 5-15 mcg 2-5  Fentanyl 10-50 mcg 2-5 Solubility Lipophilic Onset /Duration rapid/short CSF sol./spread low/minimal Resp.depression early Systemic absorb. high Adverse effects low Analgesia/area PCEA,infusion/limited 

8-24 2-4 1-3 Hydrophilic slow/long high/extensive later low high bolus/spread

– Local anesthetics  

0.5-0.75% Bupivacaine 5% Lidocaine 60

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.(%) Duration  Lidocaine  Mepivacaine intermittent  Bupivacaine 

Ropivacaine

Onset

1-2 1-2 0.1-0.125 (T) <0.5 (L) 0.2

quick quick

short

slow

long

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

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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 No consent/refuse Sepsis or bacteremia Elevated ICP Infection at site L.A allergy Coagulopathy

Relative Around area infection Demyelinating CNS diseases Dementia Hypovolemia LBP/Prior spinal surgery Drugs (ASA) 63

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 64

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)

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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 66

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.(%) Onset (min) Duration(min) Max dose(mg) Spinal/epidural PNB/infiltra. IVor <12yo Motor block

1-2 1 5-10 >10 30-120 45-90 300/500 300/500 +/+ -/+ +/+ +/+ +/+ -/>2%,epi >1%

.25-.5 10-15 120-240 175/225 +/+ +/+ -/>.5%

.2 10-15 120-360 200/ -/+ +/+ -/>.5% 68

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 71

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 72

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 74

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

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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 76

Thanks for your attention!

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