Management of 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.
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