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CHAPTER 1
V O L U M E
T H I R T Y
S E V E N
MANAGEMENT
OF
POSTANESTHESIA CARE
UNIT EMERGENCIES
MAGED ARGALIOUS, M.D., M.B.A.
ASSISTANT PROFESSOR OF ANESTHESIOLOGY
CLEVELAND CLINIC LERNER COLLEGE OF MEDICINE
DIRECTOR, POSTANESTHESIA CARE UNIT AND SAME DAY SURGERY
CLEVELAND CLINIC
CLEVELAND, OHIO
c 2009
PERMISSION TO PHOTOCOPY ARTICLES: This publication is protected by copyright. Permission to reproduce copies of articles for noncommercial use must be obtained from the Copyright
Clearance Center, 222 Rosewood Dr., Danvers, MA 01923; (978) 750-8400, FAX: (978) 750-4470,
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Airway Complications
Airway management is often challenging in the PACU or critical care unit. Factors
including surgery to the airway, intraoperative airway instrumentation or manipulation, previous neck dissection or radiation,3 prolonged surgery in the prone position,
large volumes of intraoperative fluids, and residual anesthetic effects contribute to
these difficulties. Even patients considered as having an easy airway in the
operating room can pose airway challenges in the PACU or critical care unit.
ARGALIOUS
TABLE 1. PACU Emergencies
Respiratory
Apnea
Hypoxemia
Hypercarbia
Airway obstruction (includes pharyngeal obstruction, stridor, laryngospasm, airway edema,
expanding neck hematoma)
Cardiovascular
Hypertension
Hypotension
Arrhythmias
Myocardial ischemia (acute coronary syndromes)
Pulmonary embolism
Cardiac tamponade
Neurologic
Postoperative vision loss
Acute paraplegia
Unexplained coma
Increased intracranial pressure
Status epilepticus
Endocrine/metabolic
Ionized hypocalcemia
Hyperkalemia
Adrenal insufficiency
Thyroid storm
Malignant hyperthermia
Alcohol withdrawal
Environmental
Gas leaks
Fires
Earthquakes
PACU postanesthesia care unit.
Ventilation-perfusion
mismatch
Shunt
Diffusion
impairment
Examples
Alveolar--Arterial
O2 Gradient
Response to
100% O2
Normal
Increased PaO2
Normal
Increased PaO2
Increased
Increased PaO2
Increased
Minimal if any
increase in PaO2
Increased
Increased PaO2
ARDS acute respiratory distress syndrome; COPD chronic obstructive pulmonary disease;
PaO2 partial oxygen tension in arterial blood.
attempts to ventilate the patient, may lead to hemodynamic compromise and render
resuscitation attempts useless.
Hypoventilation
Postoperative hypoventilation and apnea can be caused by residual neuromuscular blockade (as a result of overdose, inadequate reversal dosing, hypothermia, or
metabolic factors [e.g., hypokalemia] that interfere with adequate reversal).4 Opioidinduced respiratory depression is also a frequent cause of postoperative hypoventilation. Opioids not only shift the carbon dioxide response curve to the right (i.e., raise
the apneic threshold), but can also decrease the slope of the carbon dioxide
response curve (i.e., reduce the minute volume response to a high PaCO2). Although
the slope of the carbon dioxide response curve is unchanged by opioids in fully
awake patients, residual anesthetic effect can shift the carbon dioxide response
curve. Splinting resulting from incisional pain can also cause postoperative
hypoventilation.
ARGALIOUS
ability (vs. inability) to ventilate the patient with a facemask or laryngeal mask
airway. If ventilation is unsuccessful or becomes inadequate despite drainage of the
neck hematoma, invasive airway access should proceed.5
Postoperative Airway Management After Cervical Spine Surgery. Patients
undergoing surgery for cervical spine disease have a greater incidence of difficult
intubation than matched control subjects.6 Airway complications are common after
anterior cervical spine surgery and range from acute airway obstruction (1.2%) to
chronic vocal cord dysfunction.7,8 Risk factors associated with airway obstruction
after cervical spine surgery include8,9
advanced age
obesity (greater than 100 kg)
exposure of three or more vertebral bodies or exposure of C2, C3, or C4
estimated blood loss greater than 300 ml
requirement for four or more red cell units
operative time more than 10 hours
combined anteroposterior cervical spine surgery
severe preoperative neurologic deficits
Airway complications may also occur after cervical spine surgery in the prone
position, most commonly macroglossia and laryngeal edema. Decreased venous
return from the face and upper neck is likely because of etiologic factors.10 A plan for
reintubation should be in place before any extubation attempts. The presence of
external stabilization devices complicates airway management. Removal of the
anterior part of a cervical collar during reintubation attempts improves airway
visualization but should be accompanied by manual inline stabilization in patients
with an unstable cervical spine. Manual inline stabilization reduces cervical spine
motion during intubation attempts in patients with an unstable cervical spine.11
Komatsu et al.12 reported a reasonable success rate of intubation with the use of an
intubating laryngeal mask airway in patients with rigid neck collars. A recent study
on postoperative patients after anterior cervical spine surgery showed a reduced
incidence of airway complication with routine postoperative fiberoptic evaluation of
the airway for evidence of airway edema.13 Patients tracheas were only extubated if
there was no reactive swelling or pharyngeal edema. Close communication among
surgeons, anesthesiologists, and respiratory therapists helps in reducing emergency
airway complications.
Match the marking of the AEC with the centimeter markings on the ETT to
avoid excessive advancement of the AEC, which can irritate the carina and
cause bronchial trauma and bleeding
Use an AEC with an inner hollow lumen that allows oxygen insufflation,
whether by jet ventilation or a bag valve device. Two adapters Rapi-Fits
adaptors (Cook Medical, Bloomington, IN) usually accompany the AEC for this
purpose
If resistance is encountered during the advancement of the ETT over the AEC,
oral laryngoscopy (if feasible) can aid tube advancement. Rotation of the ETT in
90-degree increments also helps to pass the ETT tip past the arytenoids. ETTs
with flexible tips (Parker Flex-Tip) serve the same purpose in that the tube tip is
prevented from becoming caught against the arytenoids
Avoid using force in advancing the AEC and the ETT because it may traumatize
airway structures19
Applying a silicone-based spray or a lubricant gel on the outside of the AEC can
facilitate tube advancement
The position of the new ETT should be confirmed before the AEC is withdrawn.
This can be done by end-tidal capnography through a flexible bronchoscope
adapter16
Longer AECs are available for double-lumen tubes and can be used with the
same precautions
ARGALIOUS
APH
Acute ischemic stroke/intracerebral bleed
Esmolol may be appropriate for patients who will also benefit from
b-blockade
7. Avoid abrupt reduction of blood pressure (greater than 20%), especially in
patients at no immediate risk (hypertensive urgencies)
8. Resume oral antihypertensive therapy as soon as possible postoperatively to
reduce the occurrence of rebound hypertension, especially in patients taking
centrally acting a-2 agonists or b-blockers. Initiate additional agents as needed.
ARGALIOUS
TABLE 5. Causes of Hypotension in the Postanesthesia Care Unit
Hypovolemia
Inadequate fluid replacement (for dehydration or third space losses)
Hemorrhage (external or internal)
Temporary: high neuraxial block
Mechanical (obstructive): pneumothorax, pericardial effusion, abdominal tamponade,
excessive PEEP, superior vena cava syndrome, or atrial occlusion
Cardiogenic
Chronic heart failure
Acute pulmonary edema
Acute myocardial infarction
Pulmonary embolism
Distributive
Septic shock, anaphylaxis
PEEP positive end-expiratory pressure.
Volume Responsiveness
One of the most frequently encountered management dilemmas in the PACU
is deciding whether additional intravenous fluid should be administered to a
postoperative patient with acute circulatory failure. Most postoperative patients will
have a positive fluid balance. A fluid challenge may result in acute pulmonary edema,
especially in patients with increased capillary permeability.
Static markers of cardiac preload, especially central venous pressure or pulmonary
artery occlusion pressure, but also left ventricular end-diastolic area and early/late
diastolic wave ratio do not identify fluid responders from nonresponders.37 These
static markers, especially those derived from echocardiography, can identify whether
a cardiac chamber is full or empty; they do not reliably predict the hemodynamic
response to a subsequent fluid bolus administration. The reason why cardiac preload
is not synonymous with fluid responsiveness is shown in Figure 1.
The physiologic benefit of a fluid bolus is based on the Frank--Starling relationship
whereby an increase in cardiac preload results in an increased stroke volume and
subsequently an increased cardiac output. This concept assumes that a patients
preload is on the steep portion of the Frank--Starling curve. However, there are
several curves that rely on stroke volume and cardiac preload, depending on the
ventricular function. A given value of cardiac preload can be associated with an
increase in stroke volume and the presence of preload reserve in patients with good
FIG. 1. Frank--Starling curve and its relationship to fluid responsiveness. Reprinted with
permission from Monnet et al.37
ventricular function, whereas the same value of preload will not be associated with
an increase in stroke volume (no preload reserve) in patients with poor ventricular
function. Thus, it is the actual interaction among the three parameters --- preload,
stroke volume, and cardiac contractility --- which determines fluid responsiveness.
10
ARGALIOUS
TABLE 6. Steps for Assessment of Fluid Responsiveness
Conclusions
Prompt recognition, diagnosis, and treatment of various PACU emergencies and
also the knowledge of potential complications unique to certain surgical procedures
are essential for improving postoperative morbidity and mortality outcomes. The role
of anesthesiologists as perioperative physicians is emphasized in the management
of PACU emergencies and requires familiarity with a variety of diagnostic and
monitoring tools.
11
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