Transcript Post Anesthesia Recovery Unit - Huntington Beach Oral and

Post Anesthesia Recovery Unit
By David R. Telles, DDS
Diplomate of the American Board of Oral and Maxillofacial
Surgeons
Introduction
Care for pts in the PACU is a vital part of anesthesia practice
 Spans the transition from the OR to the PACU until the
patient is discharged home
 Must be Equipped with monitors
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Pulse Ox
ECG
BP
Thermal monitors
Arterial line if applicable
CO monitors if applicable
AND….
◦ Supplemental Oxygen
◦ Ability to re-intubate
◦ Emergency drugs / crash cart
Admission to the PACU
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Must provide PACU nurse with:
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Patient Hx
Operation performed
Pre-op Vitals
PMHx
Medications
ALL
Anesthesia rendered
EBL
Fluid/Blood Replacement/Urine output
Anesthetic / Surgical Complications
Post-op Pain management
PONV pre-med
Admission to the PACU
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Attention directed at:
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Monitoring Oxygenation (O2 sat)
Ventilation (freq, airway patency, capnography)
Circulation (BP, a line, CVP, ECG, HR)
Supplemental O2
Vital signs: to be taken at least every 15
minutes, recommended every 5 mins
◦ To be documented in the MR
Physiologic Disorders
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Upper Airway Obstruction
Arterial hypoxemia
Hypoventilation
Hypertension
Cardiac Dysrhythmias
Oliguria
Bleeding
Decreased Temperature
Agitation
Delayed Awakening
N/V
Pain
Upper Airway Obstruction
Loss of pharyngeal muscle tone
 Residual Neuromuscular blockade
 Laryngospasm
 Airway Edema
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Loss of pharyngeal muscle tone
May be the result of residual depressant effects of inhaled or
IV anesthetics or persistent Neuromuscular blockade
 In an awake pt – the pharyngeal muscles contract
synchronously with the diaphragm to pull the tongue
forward and tend the airway open against the negative
inspiratory pressure generated
 Collapse of this during inspiration leads to a viscous cycle –
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◦ reflex compensatory increase in respiratory effort
◦ negative inspiratory pressure promotes further airway
obstruction
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Clinically:
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Paradoxical breathing
Retraction of the sternal notch
Exaggerated abdominal muscle activity
Rocking motion progressive
Loss of pharyngeal muscle tone
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Treatment
◦ Opening the airway with a jaw thrust or
Continuous positive pressure ventilation
applied via Face mask
◦ Support of the airway is necessary to allow
the pt to adequately recover
◦ Consider need for placement of an oral/nasal
airway
◦ If non-responsive may require placement of
LMA or be re-intubated
Patients with CPAP
Prone to airway obstruction
 Should not be extubated until fully awake
and following commands
 In the PACU – these pts are sensitive to
Opioids
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◦ Consider placement of pt on CPAP in PACU
◦ Regional anesthesia should be considered
over systemic opioids
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BZD: considered to have a greater effect
on pharyngeal muscle tone than opioids
Hines et. al. “Complications
occurring in the PACU”
Residual Neuromuscular Blockade
Must be considered when a pt received
NMB drugs intraop
 May not be evident on arrival to the
PACU but when the pt is resting
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◦ Diaphragm recovers before the pharyngeal
muscles
◦ During Tracheal extubation pt the is
stimulated as well as during the pt transfer
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MC seen when the pt is resting in the
PACU
Residual Neuromuscular Blockade
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Clinical Assessment
◦ Train of four
 Subjective assessment of neuromusclular blockade
 May not be appreciated until it reaches a value less than 0.4 to 0.5
 Significant Clinical weakness may persist up to a ratio of 0.7
◦ 5 seconds of tetany 100 Hz – most reliable test of adequate
reversal
◦ When residual NMB occurs:
 Presents as pt with inability to breath adequately
 Agitation
◦ Evaluation:
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Grip strength
Tongue protrusion
Ability to lift legs off bed
Head lift > 5 seconds “THE GOLD STANDARD”
Residual Neuromuscular Blockade
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Factors contributing to Prolonged Nondepolarizing NMB Drugs
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Inhaled Anesthetics
Local anesthetics
Cardiac Antidysrhythmics (procainamide)
Antibiotics (polymyxin, aminoglycosides, lincosamines,
metronidazole, tetracycline)
Corticosteroids
Ca Channel Blockers
Dantrolene
Furosemide
Metabolic and Physiologic States
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Hypermagnesemia
Hypocalcemia
Hypothermia
Respiratory Acidosis
Hepatic/renal failure
Myasthenia syndromes
Residual Neuromuscular Blockade
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Factors contributing to Prolonged
Depolarizing NMB Drugs
1. Excessive Dose of Succinylcholine
2. Reduced plasma cholinesterase activity
1. Decrease levels – extremes of age or disease states
(hepatic Dz, uremia, malnutrition,plasmapheresis)
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Hormonal Changes
Pregnancy
Contraceptives
Glucocorticoids
Inhibited activity
1. Irreversible (echothiophate)
2. Reversible (edrophonium, neostigmine, pyridostigmine)
8. Genetic Variant (atypical plasma cholinesterase)
Residual Neuromuscular Blockade
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Tx:
◦ Reversal of non-depolarizing NMBDs with
Neostigmine + glycopyrolate
◦ If depolarizing: supportive therapy with Pos
pressure ventilation to re-intubation based on
clinical assessment
Laryngospasm
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A sudden spasm of the vocal cords that
completely occludes the laryngeal opening
Typically occurs during emergence from
anesthesia
Tx:
◦ Jaw thrust with CPAP ( up to 40 cm H20) often is
sufficient
◦ If fails then immediate muscle relaxation with
Succinylcholine 1 mg / kg IV or 4 mg / kg IM
◦ DO NOT FORCE ET tube through spasmed VCs
Airway Edema
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Typically seen in pt in the prone or trendelenburg positions
Occurs with the following situations
◦ aggressive fluid resuscitation required
◦ Large amount of Blood loss
◦ Surgical Procedures of the: Tongue, mouth, neck, pharynx
 -- can result in upper airway obstruction due to edema or hematoma compressing
the airway
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Physical signs of external edema is not a predictor of pharyngeal
edema typically
Tx
◦ May require prolonged intubation
◦ If extubation to be attempted – evaluation of airway must precede
extubation –
◦ leak test: suction airway, deflate the cuff of the ET tube, occlude the
proximal end of the ET tube and check pts airway patency around the
ET tube (breathing around the tube)
 Good air movement suggests the pts airway will remain patent after extubation
Airway Edema
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If due to post-surgical edema/hematoma
◦ May require release of clips / sutures from
surgery e.g. with hematoma related to thyroid
or carotid surgery
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If emergency tracheal intubation required
◦ Ensure access to fiberoptic laryngoscope
◦ Ensure surgical back up if surgical airway
emergently required (tracheostomy) for
lifesaving measures
 Typically requires awake technique under LA
Overall Tx of Upper airway obstruction
Jaw thrust with CPAP (5 to 15 cm H20)
 Oral, nasal or laryngeal muscle tone
 After successfully opening the upper
airway the source should be identified
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◦ If Residual Opioid: Reversal with Naloxone (.3 to 0.5 mg/kg q2-3 mins prn
◦ If residual BZD: Flumazenil (0.2 mg IV qmin x
1-5 doses) – may repeat q20min for
resedation
Arterial Hypoxemia
MC causes: Atelectasis + Alveolar
HypOventiation
 Post-op Supplemental O2 blunts the
effect of diffusion hypoxia as a
contributor to arterial hypoxemia
 Factors leading to post-op Arterial
hypoxemia: see next table
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Arterial Hypoxemia
Alveolar Hypoventilation
Hypoventilation alone is sufficient to
cause Art hypox
 A pt with normal lungs will become
hypoxic if allowed to significantly
hyperventilate
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Alveolar Hypoventilation
Percentages indicate the inspired O2 conc required to restore
alveolar Po2 to normal demonstrating why Pulse ox not a reliable
indicator of alveolar hypoventilation
Alveolar Hypoventilation
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Tx:
◦ If 2ndary to hypercapnia can be reversed by
the admin of Supplemenetal O2 or by
normalizing the PCO2
◦ PaCO2 can be normalized by external
stimulation – eval pts wakefullness,
effectiveness of the reversal agents OR if not
responsive then mechanical ventilation
Ventilation to perfusion mismatch
and shunt
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Hypoxic pulmonary vasoconstriction
◦ An attempt of normal lungs to optimally match
ventilation/perfusion
◦ Response constricts vessels in poorly ventilated
regions of the lung and directs pulmonary blood flow
to well ventilated alveoli
◦ Inhibited by:
 Pneumonia
 Sepsis
 Vasodilators
◦ In the PACU: inhaled anesthetics and systemic
vasodilators (e.g. nitroprusside and dobutamine) –
typically used to Tx HTN can blunt HPV and
contribute to arterial hypoxemia
Ventilation to perfusion mismatch
and shunt
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Shunt:
◦ Will no respond to supplemental O2
◦ Causes:
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Atelectasis ** MC
Pulmonary edema
Gastric aspiration
Pulmonary emboli
Pneumonia
◦ Tx:
 Mobilization of the Pt to the sitting position
 Incentive spirometry
 Positive airway pressure
Increased Venous Admixture
Typically occurs in low cardiac output
states
 Normally 2 – 5% of CO is shunted
through the lungs with minimal effect on
PaO2
 Low Cardiac output states:
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◦ Blood returns to the heart severely
desaturated
◦ Mixing of desaturated shunted blood with
saturated arterial blood decreases the PaO2
Pulmonary Edema
leads to impaired gas exchange and may
cause respiratory failure
 Either due to failure of the heart to remove
fluid from the lung circulation ("cardiogenic
pulmonary edema")
 OR a direct injury to the lung parenchyma
("noncardiogenic pulmonary edema")
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◦ intravascular fluid volume overload
◦ CHF
◦ Non-cardiogenic edema e.g. sepsis
Pulmonary Edema
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Symptoms
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difficulty breathing
coughing up blood
excessive sweating
Anxiety
pale skin
classic sign = production of pink frothy
sputum
Can lead to coma and even death
Pulmonary Edema
Pulmonary Edema
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Post-Obstructive
◦ Def: a transudative edema produced by the
exaggerated negative pressure generated by
inspiration against a closed glottis
◦ Exaggerated negative intrathoracic pressure
increases venous return – promoting
transudation of fluid
◦ MC cause: laryngospams
◦ Arterial hypoxemia seen 90 mins after
UAObstruction with Bilateral fluffy infiltrates on
the CXR
◦ Tx: supportive + supplemental O2 + diuresis +
possibly positive pressure ventilation
Pulmonary Edema
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Transfusion related lung injury
◦ Can occur in any pt who received blood, coagulation
factor or Platelet transfusions intraop
◦ Manifests 1-2 hours after the transfusion of plasmacontaining blood products
◦ Reactions can occur up to 6 hours after transfusion
◦ Often associated with Fever + Chills + Systemic
Hypotension
◦ If CBC taken: initially may seen acute leukopenia
 Reflects the sequestration of granulocytes within the lung and
exudative fluid
◦ Dx: made clinically + CXR (bilateral pulm. Infiltrates) +
increased alveolar to arterial oxygen difference related to
transfusion
◦ Tx: supportive + supplemental O2 + diuresis
Hemodynamic Instability
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Hypotension
Hypertension
Tachycardia
Bradycardia
MI
Hemodynamic instability – has a negative
impact on long-term outcome
Post-op hypertension/tachycardia are more
predictable than hypotension/bradycardia
Hypertension
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Factors leading to post-op Hypertension
◦ Arterial Hypoxemia
◦ Preop essential HTN
◦ Enhanced Sympathetic tone (hypercapnia from
hypoventilation, pain, gastric distension, bladder
distension)
◦ PONV
◦ Hypervolemia
◦ Emergence Excitement
◦ Shivering
◦ Drug rebound
◦ Increased intracranial pressure
Hypotension
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Types
◦ Hypovolemic (depressed pre-load)
◦ Cardiogenic ( intrinsic pump failure)
◦ Distributive (decreased afterload)
Hypotension - causes
Hypotension
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Hypovolemic (depressed pre-load)
◦ Responds favorably to IV fluids
◦ MC causes:
 ongoing third-space translocation of fluid
 Inadequate replacement of IV fluids intraop
 E.g. pts undergoing abdominal Sx or who had bowel preps
 Loss of sympathetic tone – e.g. due to neuraxial
blockade
 On going bleeding – can take an H&H bedside
 Tachycardia not reliable indicator of hypovolemia
esp if pt taking Beta blocker
Hypotension
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Cardiogenic ( intrinsic pump failure)
◦ Can occur with
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Myocardial ischemia or infarction
Cardiomyopathy
Cardiac dysrhythmias
May require
 CVP line
 Echocardiogram to ID the source of the hypotension
Hypotension
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Distributive (decreased afterload)
◦ Iatrogenic Sympathectomy
 High sympathetic block (to T4) will decrease vascular tone
and block cardioaccelerator fibers
◦ Critically ill patients
 May rely on exaggerated sympathetic nervous system tone to
maintain BP
◦ Allergic reactions
 Can check serum tryptase concentrations to confirm -- must
be obtained 30 – 120 mins after the Rxn
 Tx: epi
◦ Sepsis
 Blood cultures
 Emperical Antibiotics
 Pressors: Levophed or Neo-synephrine
MI
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ECG monitoring typically influence by pts
cardiac Hx and risk index
Low Risk
◦ < 45 yo, no known cardiac Dz, onlyone risk factor
◦ Post-op ST changes on ECG doesn’t typically
indicate post-op MI
 Due to Anxiety, GERD, Hyperventilation, hypokalemia
◦ Further work up warranted when ST changes on
ECG + hemodynamic instability
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High Risk
MI
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Low Risk
High risk
◦ ST and T wave changes on ECG can be significant
even if S / Sx not present
◦ ANY ST or T wave changes are compatible with
myocardial ischemia and warrant investigation
◦ Determine Serum troponin levels + MB fraction
of creatinine phosphokinase + 12 Lead ECG
◦ Prompt cardiology f/u + possible admission to
telemetry
Cardiac Monitoring
In the PACU: MI is rarely accompanied by
chest pain
 Combined leads II and V5 reflect 80% of
ischemic events on a 12 lead ECG
 American college of Cardiology:
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◦ Recommend Computerized ST segment
analysis to monitor high risk pts in the PACU
◦ Routine post-op 12 lead ECG: recommended
for pts with known or suspected CAD who
have undergone intermediate or high risk Sx
Cardiac Dysrhythmias
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Typically transient and multifactorial
Types
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Tachy
Atrial
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Ventricular
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Brady
MC causes:
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Hypoxemia
Hypoventilation
Hypercapnia
Endogenous/exogenous catecholamines
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Anticholingergics
MI
HTN
Digitalis Intoxication
Electrolyte abnormalities
Acidemia
Fluid overload
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Anemia
Substance withdrawal
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Pre-op cardiac dysrhythmias
Tachydysrhythmias
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MC causes:
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Less common causes:
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Pain
Agitation
Hypoventilation associated with hypercapnia
Hypovolemia
Shivering
Presence of ET tube
Cardiogenic or septic shock
PE
Thyroid storm
Malignant hyperthermia
Result: decreases diastolic and coronary perfusion time and
increases myocardial oxygen consumption
◦ Most harmful with CAD pts
Atrial Dysrhythmias
May be as high as 10% of cases
 MC:
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◦ Atrial fibrillation
May require immediate electrical
cardioconversion
 Most pt can be Tx with:
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◦ IV B-blocker (e.g. esmolol [short acting] or Ca
Channel blocker (Diltiazem)
◦ If goal is chemical cardioversion:
 Administer Amiodarone
Ventricular Dysrhythmias
Vtach is uncommon
 MC:
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◦ PVCs and Ventricular bigeminy
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True Vtach – indicative of true cardiac
pathology
Bradydysrhythmias
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Causes:
◦ Drug related (Beta blocker, anticholinesterase
reversal of NDNMBD, opiods,
Dexmedetomidate)
◦ Procedure/Pt related causes
 Bowel distension
 Increased intracranial/intraocular pressures
 High spinal block
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Has a more deleterious effect on pts with
fixed Stroke Volumes: infants / restrictive
pericardial disease / cardiac tamponade
Delirium
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10% of adult pts older than 50 will experience delirium in the first
5 post-op days who undergo elective Sx
> 30% occurrence if undergoes certain procedures e.g. hip
replacement or bilateral knee replacement
RFs
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Advanced age
Pre-op cognitive impairment
Decreased functional status
Alcohol abuse
Previous Hx of delirium
Intraop RFs
◦ Surgical blood loss
◦ Hct < 30
◦ # of intraoperative blood transfusions
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Management
◦ Restraints
◦ Additional personnel
◦ May require higher doses of Opioids and prevent alcohol withdrawal
DDx of Delirium
Arterial Hypoxemia
 Pre-existing cognitive disorder
 Metabolic derangements
 Drugs
 Electrolyte abnormalities
 Seizures
 Acute CNS event (stroke, hemorrhage)
 Infection
 Emergence Excitement
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Renal Dysfunction
In the PACU Identification and Tx of
readily reversible cause of oliguria ( urine
output < 0.5 ml/kg/hr)
 MC Causes:
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◦ Catheter obstruction / dislodgement
◦ Intravascular volume depletion  can result
in hepatorenal syndrome or ATN caused by
sepsis
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Other causes: see table
Renal Dysfunction
Body Temperature / Shivering
Incidence may be as high as 65% after GA and 33 % after epidural
anesthesia
 Can lead to inhibited platelet fxn/coagulation factor/drug metabolism
 RFs: male, drug admin (propofol > than thiopental)
 Levels:
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◦ Mild to moderate: 33 – 35 C
◦ Severe < 33 C
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Mechanism
◦ Not always associated with decreased body temp
◦ In hypothermic pt – thermoregulatory mech responsible
◦ In normothermic pt:
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Theory: brain and spinal cord do not recover at the same rate – more rapid recovery of the
spinal cord results in uninhibited spinal reflex and clonic activity
Tx:
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Accurate body core temperature: Tympanic membrane best
Forced air warmers
Opioids + clonidine – effective @ abolishing shivering once it starts
Meperidine (12.5 – 25 mg IV) is the most effective Tx
PONV
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1/3 of pts in the PACU will develop PONV
RFs:
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Female
Hx of motion sickness or PONV
Non-smoker
Use of post-op Opioids
Cost effective management of PONV based on
pts underlying risk
 Prevention / Tx
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◦ Use of propofol decreases incidence by 19%
◦ Admin of antiemetic – e.g. ondansetron /
dexamethasone / droperidol decrease risk by 26%
PONV
Bleeding Abnormalities
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Possible causes
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Most often due to inadequate surgical hemostasis
May be due to unknown coagulopathy
ASA administration
Consumption e.g. DIC
 DIC – thrombocytopenia, prolonged PT, decreased serum conc of
fibrinogen and increased levels of fibrin split products
◦ Dilution of factors V and VIII due to massive transfusions of
whole blood or inadequate reversal of heparin – cause
prolonged PTT
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FFP:
◦ Can help mitigate decrease PT and PTT when abnormalities are
due to liver Dz or factor V or VIII deficiency
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Protamine reverses heparin induced prolonged PTT
Delayed Awakening
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Seen commonly in prolong Sx/Anesthesia
Eval VS, ECG, arterial O2, body temp
Eval electrolytes + possible metabolic disturbances
Radiologic examinations:
◦ eval for intracranial/intrathoracic abnormalities
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Possible explanations for delayed awakening
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Residual drug effects
Hypothermia
Hypoglycemia
Electrolyte abn
Arterial hypoxemia
Increased intracranial pressure
Air embolism
Hysteria
Bleeding
Discharge criteria
Requires escort always – no exception
 Stable VS for last 2-3 times
 Requiring urination prior to discharge is
not necessary in all pts except those at
risk for renal complication
 No Minimum mandatory stay required
 Assessment of pt to determine no long at
risk for cardiorespiratory depression +
mental status returned to baseline
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Discharge criteria
Patients who are determined
to have a score of 9 or better
are acceptable for discharge
Reference

Stoelting and Miller. Basics of anesthesia
5th edition. “ Post-anesthesia recovery
unit” pp. 563-577