Management of Complications
RESPIRATORY COMPLICATIONS
Respiratory problems are the most frequently
encountered serious complications in theCU. The overwhelming majority are
related to airway obstruction, hypoventilation, or hypoxemia. Because hypoxemia
is the final common pathway to serious morbidity and mortality, routine monitoring
of pulse oximetry in the PACU leads to earlier rec-ognition of these
complications and fewer adverse outcomes.
Airway obstruction in unconscious patients is
most commonly due to the tongue falling back against the posterior pharynx .
Other causes include laryngospasm, glottic edema, secretions, vomitus, a
retained throat pack or blood in the airway, or external pressure on the
trachea (most commonly from a neck hematoma). Partial airway obstruction
usually presents as sonorous respira-tion. Near-total or total obstruction
causes cessa-tion of airflow and an absence of breath sounds and may be
accompanied by paradoxic (rocking) move-ment of the chest. The abdomen and
chest should normally rise together during inspiration; however, with airway
obstruction, the chest descends as the abdomen rises during each inspiration
(paradoxic chest movement). Patients with airway obstruc-tion should receive
supplemental oxygen while corrective measures are undertaken. A combined
jaw-thrust and head-tilt maneuver pulls the tongue forward and opens the
airway, and insertion of an oral or nasal airway often alleviates the problem.
Nasal airways may be better tolerated than oral air-ways by patients emerging
from anesthesia and may decrease the likelihood of trauma to the teeth when the
patient bites down.
If the above maneuvers fail to reestablish an
open airway, laryngospasm should be considered. Laryngospasm is usually
characterized by high-pitched crowing noises, but may be silent with com-plete
glottic closure. Spasm of the vocal cords is more apt to occur following airway
trauma, repeated instrumentation, or stimulation from secretions or blood in
the airway. The jaw-thrust maneuver, par-ticularly when combined with gentle
positive airway pressure via a tight-fitting face mask, usually breaks
laryngospasm. Insertion of an oral or nasal airway is also helpful in ensuring
a patent airway down to the level of the vocal cords. Any secretions or blood
in the hypopharynx should be suctioned to prevent recurrence. Refractory
laryngospasm should be treated with a small dose of intravenous
succinyl-choline (10–20 mg in adults) and positive-pressure ventilation with
100% oxygen. Endotracheal intu-bation may occasionally be necessary to
reestablish ventilation; cricothyrotomy or transtracheal jet ven-tilation is
indicated if intubation is unsuccessful in such instances.
Glottic edema following airway
instrumenta-tion is an important cause of airway obstruction in infants and
young children because of the relatively small airway lumen. Intravenous
corticosteroids (dexamethasone, 0.5 mg/kg, 10 mg dose maximum) or aerosolized
racemic epinephrine (0.5 mL of a 2.25% solution with 3 mL of normal saline) may
be useful in such cases. Postoperative wound hemato-mas following thyroid,
carotid artery, and other neck procedures can quickly compromise the airway,
and opening the wound immediately relieves tracheal compression in most cases.
Rarely, gauze packing may be unintentionally left in the hypopharynx following
oral surgery and can cause immediate or delayed complete airway obstruction,
especially in patients with intermaxillary fixation.
Accidental or intentional decannulation of a fresh tracheostomy is
hazardous because the vari-ous tissue planes have not yet organized into a
well-formed track, thereby often making recannulation very difficult or
impossible. In cases of tracheos-tomy performed within the previous 3–4 weeks,
intentional replacement of a tracheostomy cannula should only be performed with
a qualified surgeon at the bedside and a surgical tracheostomy instru-ment set,
along with other appropriate airway equip-ment, immediately available.
Hypoventilation, which is generally defined as a Paco2>45 mm Hg, is common following
general anesthesia. In most instances, the hypoventilation is mild, and most
cases are undiagnosed. Signifi-cant hypoventilation is usually clinically
apparent when the Paco2 is >60 mm Hg or arterial blood pH is <7.25. Signs are varied and
include excessive somnolence, airway obstruction, slow respiratory rate,
tachypnea with shallow breathing, or labored breathing. Mild to moderate
respiratory acidosis may cause tachycardia, hypertension, and cardiac
irritability (via sympathetic stimulation), but more severe
acidosis produces circulatory depression. If significant hypoventilation is
suspected, assessment and management is facili-tated by capnography and/or
arterial blood gas measurement.Hypoventilation in the PACU is most com-monly
due to the residual depressant effectsof anesthetics on respiratory drive.
Opioid-induced respiratory depression characteristically produces a slow
respiratory rate, often with large tidal volumes. Excessive sedation is usually
present, but the patient is often responsive and able to breathe on com-mand.
Delayed occurrence of respiratory depres-sion have been reported with all
opioids. Proposed mechanisms include variations in the intensity of stimulation
during recovery and delayed release of the opioid from peripheral compartments,
such as skeletal muscle (or possibly the lungs with fentanyl), as the patient
rewarms or begins to move.
Causes of residual muscle paralysis in the
PACU include inadequate reversal, pharmacological inter-actions, altered
pharmacokinetics (due to hypother-mia, altered volumes of distribution, and
renal or hepatic dysfunction), and metabolic factors (such as hypokalemia or
respiratory acidosis). Regard-less of the cause, generalized weakness,
dyscoordi-nated movements (“fish out of water”), shallow tidal volumes, and
tachypnea are usually apparent. The diagnosis can be made with a nerve
stimulator in unconscious patients; head lift and grip strength can be assessed
in awake patients. The ability to sustain a head-lift for 5 sec may be the most
sensitive test for assessing the adequacy of reversal.
Splinting due to incisional pain, diaphragmatic dysfunction following
upper abdominal or thoracic surgery, abdominal distention, and tight abdomi-nal
dressings are other factors that can contribute to hypoventilation. Increased
CO 2 production from shivering, hyperthermia, or sepsis can also increase
Paco2, even in normal patients recovering from general anesthesia. Marked
hypoventilation and respiratory acidosis can result when these factors are
superimposed on an impaired ventilatory reserve due to underlying pulmonary,
neuromuscular, or neurological disease.
Treatment should generally be directed at the
underlying cause, but marked hypoventilation always requires assisted or
controlled ventilation until causalfactors are identified and corrected.
Obtundation, circulatory depression, and severe acido-sis (arterial blood pH
7.15) are indications for immediate and aggressive respiratory and hemody-namic
intervention, including airway and inotropic support as needed. Antagonism of
opioid-induced depression with large doses of naloxone often results in sudden
pain and marked increase in sympathetic tone. The latter can precipitate a
hypertensive crisis, pulmonary edema, and myocardial ischemia or infarction. If
naloxone is used to reverse opioid-induced respiratory depression, titration in
small increments (80 mcg in adults) usually avoids compli-cations by reversal
of hypoventilation without significant reversal of analgesia. Following
naloxone administration, patients should beobserved closely for recurrence of
opioid-induced respiratory depression (“renarcotization”), as nalox-one has a
shorter duration than most opioids. If residual muscle paralysis is present,
additional cho-linesterase inhibitor may be given. Residual paralysis in spite
of a full dose of a cholinesterase inhibitor necessitates controlled
ventilation under close obser-vation until spontaneous recovery occurs.
Hypoven-tilation due to pain and splinting following upper abdominal or
thoracic procedures should be treated with intravenous or intraspinal opioid
administra-tion, intravenous ketorolac, epidural anesthesia, or intercostal
nerve blocks.
Mild hypoxemia is common in patients
recovering from anesthesia when supplemental oxygen is not given. Mild to
moderate hypoxemia (Pao2 50–60 mm Hg) in young healthy patients may be well tolerated initially,
but with increasing duration or severity, the initial sympathetic stimulation
often seen is replaced with progressive acidosis and circulatory depression.
Obvious cyanosis may be absent if the hemoglobin concentration is reduced.
Hypoxemia may also be suspected from restlessness, tachycardia, or cardiac
irritability (ventricular or atrial). Obtundation, bra-dycardia, hypotension,
and cardiac arrest are late signs. Pulse oximetry facilitates early detection
of hypoxemia and must be routinely utilized in the PACU. Arterial blood gas
measurements may be per-formed to confirm the diagnosis and guide therapy.
Hypoxemia in the PACU is usually caused by
hypoventilation, increased right-to-left intrapulmo-nary shunting, or both. A
decrease in cardiac output or an increase in oxygen consumption (as with
shiv-ering) will accentuate hypoxemia. Diffusion hypoxia is an uncommon cause of hypox-emia when
recovering patients are given supple-mental oxygen. Hypoxemia due exclusively
to hypoventilation is also unusual in patients receiving supplemental oxygen,
unless marked hypercapnia or a concomitant increase in intrapulmonary shuntin is present. Increased intrapulmonary shunting from a decreased
functional residual capacity(FRC) relative to
closing capacity is the most com-mon cause of hypoxemia following general
anesthe-sia. The greatest reductions in FRC occur following upper abdominal and
thoracic surgery. The loss of lung volume is often attributed to
microatelectasis, as atelectasis is often not identified on a chest
radio-graph. A semi-upright position helps maintain FRC. Marked right-to-left
intrapulmonary shunting (Qs/Qt 15%) is usually associated with radio-graphic
findings, such as pulmonary atelectasis, parenchymal infiltrates, or a large
pneumothorax. Causes include prolonged intraoperative hypoventi-lation with low
tidal volumes, unintentional endo-bronchial intubation, lobar collapse from
bronchial obstruction by secretions or blood, pulmonary aspi-ration, or
pulmonary edema. Postoperative pulmo-nary edema most often presents as wheezing
within the first 60 min after surgery, and, to a lesser extent, pink frothy
fluid in the airway, and may be due to left ventricular failure (cardiogenic),
acute respiratory distress syndrome, or relief of prolonged airway obstruction
(negative pressure pulmonary edema). In contrast to wheezing associated with
pulmonary edema, wheezing due to primary obstructive lung disease, which also
often results in large increases in intrapulmonary shunting, is not associated
with edema fluid in the airway or infiltrates on the chest radiograph. The possibility of a postoperative pneumothorax should
always be consideredfollowing central line placement,
supraclavicular or intercostal blocks, abdominal or chest trauma (including rib
fractures), neck dissection, tracheos-tomy, nephrectomy, or other
retroperitoneal or intraabdominal procedures (including laparoscopy),
especially if the diaphragm may have been pene-trated or disrupted. Patients
with subpleural blebs or large bullae can also develop pneumothorax during
positive-pressure ventilation.
Oxygen therapy with or without positive
airway pressure is the cornerstone of treatment for hypox-emia. Routine
administration of 30% to 60% oxy-gen is usually enough to prevent hypoxemia
with even moderate hypoventilation and hypercapnia (conversely, clinical signs
of hypoventilation and hypercapnia may be masked by routine oxygen
administration). Patients with underlying pulmo-nary or cardiac disease may
require higher concen-trations of oxygen; oxygen therapy should be guided by
Spo2
or arterial blood gas measurements. Oxygen concentration must be closely
controlled in patients with chronic CO2 retention to avoid precipitating acute respiratory failure. Patients
with severe or per-sistent hypoxemia should be given 100% oxygen
vianonrebreathing mask or an endotracheal tube until the cause is established
and other therapies are insti-tuted; controlled or assisted mechanical
ventilation may also be necessary. The chest radiograph (prefer-ably with the
patient positioned sitting upright) is valuable in assessing lung volume and
heart size and in demonstrating a pneumothorax or pulmonary infiltrates.
However, in cases of pulmonary aspira-tion, infiltrates are usually initially
absent. If pneu-mothorax is suspected, a chest radiograph taken at
end-expiration helps highlight the pneumothorax by providing the greatest
contrast between lung tis-sue and adjacent air in the pleural space. In the
situa-tion of an intubated patient with hypoxemia, a chest radiograph provides
additional usefulness to breath sound assessment in verifying endotracheal tube
position, especially when the tube is inadvertently positioned immediately
above the carina, with resul-tant intermittent migration into a main bronchus.
Additional treatment of hypoxemia should be directed at the underlying
cause. A chest tube or Heimlich valve should be inserted for any symptomatic
pneumothorax or one that is greater than 15% to 20%. An asymptomatic
pneumotho-rax may be aspirated using a intercostal catheter or followed by
observation. Bronchospasm should be treated with aerosolized bronchodilator
therapy. Diuretics should be given for circulatory fluid over-load and cardiac
function should be optimized. Per-sistent hypoxemia in spite of 50% oxygen
generally is an indication for positive end-expiratory pressure ventilation or
CPAP. Bronchoscopy is often useful in reexpanding lobar atelectasis caused by
bron-chial plugs or particulate aspiration. In the setting of an intubated
patient, secretions or debris must be removed by suction and also by lavage, if
neces-sary, and a malpositioned endotracheal tube must be appropriately
repositioned.symptomatic pneumothorax or one that is greater than 15% to 20%.
An asymptomatic pneumotho-rax may be aspirated using a intercostal catheter or
followed by observation. Bronchospasm should be treated with aerosolized
bronchodilator therapy. Diuretics should be given for circulatory fluid
over-load and cardiac function should be optimized. Per-sistent hypoxemia in
spite of 50% oxygen generally is an indication for positive end-expiratory
pressure ventilation or CPAP. Bronchoscopy is often useful in reexpanding lobar
atelectasis caused by bron-chial plugs or particulate aspiration. In the
setting of an intubated patient, secretions or debris must be removed by
suction and also by lavage, if neces-sary, and a malpositioned endotracheal
tube must be appropriately repositioned.
Related Topics
Privacy Policy, Terms and Conditions, DMCA Policy and Compliant
Copyright © 2018-2024 BrainKart.com; All Rights Reserved. Developed by Therithal info, Chennai.