Complications and emergencies occur in the postanesthesia care setting including respiratory and cardiovascular complications, thermoregulation,and complications associated with anesthesia medications, techniques, and procedures. The perianesthesia nurse must be prepared to expect the unexpected and observe patients for potential complications and emergent situations. This chapter will review the most common complications experienced in the postanesthesia care setting.
Complications can occur during any phase of the patient’s perianesthesia experience. From allergic reactions to preoperative medications in the holding area to postanesthesia airway obstruction, situations occur that require the perianesthesia nurse’s vigilance, prompt action, and appropriate treatment. The postanesthesia period is a precarious time for the patient; prevention of complications is an essential role for the perianesthesia nurse. The perianesthesia nurse, whether in an inpatient or outpatient setting, must be prepared to respond to rapidly evolving, potentially life-threatening situations. Complications that more commonly occur in the postanesthesia setting are addressed in this chapter including respiratory and cardiovascular complications, thermoregulation, and complications associated with anesthesia medications, techniques, and procedures.
Acute Myocardial InfarctionOccurs when an area of heart muscle dies or is permanently damaged because of an inadequate supply of oxygen to that area.
Anaphylactic ReactionsAnaphylaxis is a severe whole-body allergic reaction that occurs rapidly and causes a life-threatening response.
AspirationThe inhalation of either oropharyngeal or gastric contents into the lungs.
Awareness During AnesthesiaOccurs when a person is aware of some portion of the procedure (sometimes even pain) during general anesthesia; can cause long-term psychological effects and symptoms of post-traumatic stress disorder.
BradycardiaA heart rate of less than 60 bpm (adult) with a regular rhythm and P waves present.
BronchospasmNarrowing of the bronchi and bronchioles from smooth muscle contraction that results in wheezing, coughing, and decreased oxygen exchange.
Delayed Emergence (Awakening)Patient emergence from anesthesia is delayed; failure to emerge can be classified as the result of medication effects, metabolic disorders, or neurologic disorders.
Dilutional HyponatremiaAbsorption of irrigating solutions through open blood vessels (during prostate resection) or perforation of the uterine or bladder wall that leads to circulatory overload from water intoxication. May also be caused by excessive free water intake, excess sodium losses, or inappropriate antidiuretic hormone secretion.
Emergence Excitement/DeliriumA condition characterized by restlessness, disorientation, crying, moaning, irrational talking, and inappropriate behavior.
Hemolytic Transfusion ReactionsAn ABO-incompatible blood reaction that precipitates a hemolytic reaction resulting in agglutination, or clumping, of red blood cells, which blocks the patient’s capillaries and thus obstructs the flow of blood and oxygen to vital organs.
HemorrhageRapid copious blood loss.
HypertensionA blood pressure increased 20% to 30% above the baseline blood pressure.
HyperthermiaA core temperature of more than 38° C.
HypotensionA blood pressure less than 20% to 30% of the baseline blood pressure.
HypothermiaA core temperature of less than 36° C.
HypoventilationA decrease in respiratory rate and tidal volume that leads to an increase in partial pressure of carbon dioxide (Paco2).
HypoxemiaA partial pressure of oxygen (PaO2) of less than 60 mm Hg.
LaryngospasmAn involuntary partial or complete closure of the vocal cords caused by secretions or stimulation or irritation of the laryngeal reflexes during emergence.
Malignant Hyperthermia (MH)A pharmacogenetic (autosomal dominant inheritance) disorder of muscle metabolism involving hypermetabolism that can be triggered by succinylcholine or the volatile anesthetics.
Noncardiogenic Pulmonary EdemaRespiratory disorder that most commonly occurs after an obstructive event resulting in pulmonary capillary leakage and pulmonary edema.
Nonhemolytic Febrile ReactionsMost often caused by sensitivity to leukocytes and platelets and seen most often in patients who have received multiple transfusions.
Perforated ViscusInternal organs perforated during the operative procedure.
Plasma Cholinesterase DeficiencyAn uncommon genetic disorder that renders the patient with an inability to metabolize succinylcholine resulting in prolonged skeletal muscle paralysis and apnea of 2 hours or more.
PneumothoraxAn accumulation of air or gas in the pleural space.
Postdischarge Nausea and Vomiting (PDNV)Nausea or vomiting that occurs after discharge from the health care facility after ambulatory surgery.
Postdural Puncture HeadacheA headache that typically develops 24 to 48 hours after lumbar puncture from a spinal needle placement or unintentional dural puncture during an epidural placement.
Postoperative Nausea and Vomiting (PONV)Nausea or vomiting that occurs within the first 24 hours after inpatient surgery.
Pulmonary EdemaIncrease in lung fluid as a result of leakage from pulmonary capillaries into the interstitium and alveoli of the lung; leads to impaired gas exchange and may cause respiratory failure.
Pulmonary EmbolismA sudden blockage of an artery in the lungs by fat, air, clumped tumor cells, or a blood clot; usually a blood clot that traveled to the lung from the leg.
Spinal Epidural HematomaA hematoma after spinal procedures or surgery; blood accumulates between the spinal dura and bone compressing nerves; without prompt treatment, it can cause permanent neurologic deficits.
TachycardiaA heart rate greater than 100 bpm (adult) with a regular rhythm and P waves present.
Transfusion-Related Acute Lung Injury (TRALI)Rare but devastating complication of blood component therapy; findings are similar to adult respiratory distress syndrome and consist of hypotension, fever, dyspnea, and tachycardia.
Unplanned/Unwanted SedationSedation occurring as the result of treatment of pain, residual effects of anesthesia, or co-morbidities that is unexpected or undesired.
Airway management and respiratory care are first in the mind of the perianesthesia nurse when patients arrive in the postanesthesia care unit (PACU). Avoidance of postoperative pulmonary complications, including atelectasis, pneumonia, respiratory failure, and exacerbation of respiratory disease (e.g., asthma), helps to reduce patient morbidity and mortality rates. The perianesthesia nurse works to prevent these serious longer-term complications by maintaining and improving the patient’s respiratory function in the immediate postanesthesia period of care. Some patients are at greater risk for developing these complications. Primarily, these risk factors are related to the patient or the procedure. Box 29.1 lists the most common risk factors supported by evidence.1–3
Data from Lakshminarasimhachar A, Smetana GW. Preoperative evaluation: estimation of pulmonary risk. Anesthesiol Clin 2016;34(1):71-88; Miskovic A, Lumb AB. Postoperative pulmonary complications. Br J Anaesth. 2017;118(3):317-334.
One of the most commonly occurring complications in the postanesthesia care setting is airway obstruction. Airway obstruction can be upper or lower in origin, from the simple problem of the tongue falling back and obstructing the upper airway to complete laryngospasm with no air movement.
Upper airway obstruction can be caused by tongue relaxation, which is most common, and it is often seen in the patient who has not fully recovered from anesthesia, who has received opioid or sedative medications, or who has residual neuromuscular blocking agents on board. Other causes include swelling or edema of the airway, airway injury, bleeding (hemorrhage), obstructive sleep apnea, or preexisting neurologic or muscular weakness. Treatment includes verbal or tactile stimulation of the patient, airway repositioning with chin lift or jaw thrust (Fig. 29.1), placement of an oral or nasopharyngeal airway adjunct, and application of positive pressure with a bag-valve-mask device. If the patient’s airway cannot be maintained with these methods, oral or nasal placement of an endotracheal tube may be necessary, or emergency cricothyroidotomy or tracheostomy may be performed. Positioning the patient in the recovery position (side-lying with head down to facilitate drainage) can also help to maintain a patent airway in the patient at risk for soft tissue obstruction or significant oral drainage that interferes with the airway. See Chapter 30 for more information on management of the airway.
Laryngospasm is an involuntary partial or complete closure of the vocal cords caused by secretions, stimulation, or irritation of the laryngeal reflexes during emergence. Wheezing, reduced compliance, stridor (partial), paradoxical chest or abdominal movements, and absence of ventilation (complete) are signs and symptoms of laryngospasm. Ventilation is decreased or absent, and oxygenation of the patient is difficult as carbon dioxide builds (Paco2 increases). Treatment may include airway maneuvers (chin lift/jaw thrust), elevation of the head of bed to maximize respiratory excursion, and application of a bag-valve-mask for continuous positive pressure with oxygen. Secretions need to be carefully removed with suction. The patient may need reintubation to secure the airway if mask ventilation is difficult. Medications may include succinylcholine and can include other neuromuscular blocking agents and lidocaine. When the patient has received a neuromuscular blocking agent, the patient may need sedation to reduce anxiety related to apnea, muscle relaxation, and awareness.
The primary complication of postextubation laryngeal edema is subglottic edema. For the pediatric patient, this obstruction is typically observed in children 1 to 4 years of age. Traumatic intubation, tight fit of the endotracheal tube, coughing with the tube in place, position change with the tube inserted, surgery of the head or neck, and procedures that last more than 1 hour can result in subglottic edema. Crowing respirations, stridor, and rocking chest wall respiratory attempts may signal subglottic edema. Postoperative supplemental humidified oxygen can diminish airway swelling. Initial treatment includes humidified oxygen and nebulized mist treatment with racemic epinephrine. Further treatment may include inhalation of a helium-oxygen mixture, administration of dexamethasone, and calming with analgesics and parental or caregiver presence. Ambulatory surgery patients with subglottic edema treated with racemic epinephrine may be considered for overnight admission because of the risk of rebound edema. Extended observation for up to 8 hours may be sufficient if the parents are comfortable and emergency resources are readily available.
Sudden constriction of the smooth muscles in the walls of the bronchioles results in bronchospasm. Bronchospasm may be the result of preexisting asthma, allergy or anaphylaxis, chronic diseases of the lung (chronic bronchitis, emphysema), histamine release, mucus plugging, aspiration, pulmonary edema, wheezing with acute heart failure but without any other acute pulmonary pathology (cardiogenic asthma), or foreign body aspiration. Signs and symptoms include cough, expiratory wheezing, dyspnea, use of accessory muscles, and tachypnea. Treatment of the patient includes removal of the identified cause, oxygen administration, inhaled bronchodilators, and epinephrine. Depending on cause, an antihistamine or dexamethasone may be appropriate. Secretions should be suctioned. If the condition results from foreign body aspiration, such as a tooth, emergent bronchoscopy is needed. Ventilatory support may be necessary, and the patient may need reintubation for maintenance of oxygenation and ventilation.
Identified as a high-risk, low-frequency occurrence, aspiration may be observed in the postanesthesia setting. The patient with a nasal or oropharyngeal airway in place and returning gag reflexes may become nauseated and vomit. In a nonresponsive state and supine position, the patient is at greater risk for aspiration. Types of aspirates include large particle, clear acidic or nonacidic fluid, foodstuff or small particle, and contaminated material. In addition, foreign bodies such as teeth or blood may be aspirated. Symptoms include unexplained tachypnea and tachycardia, cough, bronchospasm, hypoxemia, atelectasis, interstitial edema, hemorrhage, and acute respiratory distress syndrome. The aspiration can trigger laryngospasm, infection, and pulmonary edema.
Prevention of aspiration is preferred. Patients at risk should be identified before surgery and premedicated. Patients at risk are patients with emergent procedures, known full stomachs, or history of gastroesophageal reflux disease; those older than age 65 years; patients who are obese; and women in labor. Premedications include histamine blockers, nonparticulate antacids, and anticholinergic agents. During surgery, rapid sequence induction and nasogastric tube placement may help to minimize aspiration in the highest risk patients. However, preemptive use of a nasogastric tube may contribute to increased vomiting and subsequent aspiration; use should be limited to patients with known or suspected obstruction or ileus.2,3 After surgery, maintenance of the endotracheal tube until airway reflexes have returned and positioning of the patient with the head to the side or in a left lateral decubitus position can aid in decreasing the risk of aspiration. If aspiration occurs, hypoxemia should be corrected and hemodynamic stability maintained. The patient may need reintubation, suctioning, and mechanical ventilation. Arterial blood gases assist in planning respiratory management of the patient. A chest radiograph can be obtained, but findings may be inconclusive initially; radiographic findings may lag behind clinical signs by 24 hours after the suspected aspiration event. Prophylactic antibiotics or steroids are not recommended. Tracheal secretions should be cultured; if results are positive, antibiotics can be prescribed.
Hypoventilation may be the result of residual anesthetic agents; opioids; neuromuscular blocking agents; inadequate reversal of opioids, sedatives, or neuromuscular blocking agents; thoracic or abdominal incisions and procedures and subsequent splinting of incisions; or neuromuscular diseases. Additional discussion on opioid induced sedation and respiratory depression can be found in Chapter 31.
Signs and symptoms include decreased respiratory rate, shallow respirations, increased end-tidal carbon dioxide (ETCO2), and increased Paco2 (>45 mm Hg [hypercarbia]). Treatment includes identification and management of the cause of the hypoventilation, supplemental oxygen administration, verbal and tactile stimulation, deep breathing exercises, repositioning, and cautious use of opioid analgesics or sedatives. Oxygen saturation monitoring is necessary, and capnographic monitoring may be appropriate for patients at risk.
Unidentified hypoxemia in the postanesthesia patient is not as common since the advent of noninvasive oxygen saturation monitoring with pulse oximetry. Hypoxemia may be the result of a low inspired concentration of oxygen, hypoventilation, ventilation–perfusion inequality, increased intrapulmonary right to left shunt, or pneumothorax. It can also be caused by diffuse airway collapse, pulmonary edema, and pulmonary embolism. Treatment includes identification and correction of the cause, stimulation of the patient, supplemental oxygen administration, and noninvasive respiratory support (e.g., high-flow nasal oxygen [HFNO], continuous positive airway pressure [CPAP], or bilevel positive airway pressure [BiPAP]).4 Patients who cannot maintain oxygen levels may need tracheal intubation and mechanical ventilation and positive end-expiratory pressure (PEEP) support.
Pneumothorax, an accumulation of air or gas in the pleural space, can occur during the perianesthesia period. It may be the result of percutaneous internal jugular and subclavian vein cannulation, hemodynamic monitoring line placement, certain upper extremity blocks (supraclavicular and infraclavicular approaches to the brachial plexus), or operative procedures of the chest. The patient may have sharp ipsilateral chest pain and dyspnea. Assessment findings include decreased breath sounds and hyper-resonance on the affected side of the chest. Treatment includes supplemental oxygen administration and obtaining a chest radiograph. If a less than 20% pneumothorax is diagnosed based on the chest radiograph, the treating physician may opt to observe the patient for an extended time period until the pneumothorax either resolves or increases. If the pneumothorax is greater than 20% or the patient has cardiovascular compromise, a chest tube may be needed.
Fluid overload, congestive heart failure, or acute pulmonary injury can result in pulmonary edema. Signs and symptoms include hypoxemia, crackles (rales), and decreased pulmonary compliance. Pulmonary infiltrates are seen on chest radiograph results.
Identification and treatment of the cause of the pulmonary edema is the first step in treatment. In addition, diuretics and fluid restriction to decrease afterload and supplemental oxygen administration may be ordered. Patients with an inability to maintain oxygenation or adequate ventilation may undergo intubation and mechanical ventilation and PEEP.
Noncardiogenic pulmonary edema, also known as negative pressure pulmonary edema, may be the result of upper airway obstruction, laryngospasm, bolus dosing with naloxone, incomplete reversal of neuromuscular blockade, or a significant period of hypoxia. When the cause is obstructive in origin, two types of postobstructive pulmonary edema (POPE) have been identified: type I and type II.5 Both present with acute respiratory distress. Type I usually occurs within 60 minutes of a precipitating event, but onset can be delayed up to 6 hours. Type I POPE may follow postextubation laryngospasm, epiglottitis, croup, choking or foreign body, strangulation, hanging, endotracheal tube obstruction, laryngeal tumor, goiter, mononucleosis, postoperative vocal cord paralysis, migration of the urinary catheter balloon used for tamponade epistaxis, near drowning, and intraoperative direct suctioning of an endotracheal tube adapter. Type II POPE develops soon after relief of chronic upper airway obstruction such as after tonsillectomy or adenoidectomy, removal of upper airway tumor, choanal stenosis, and hypertrophic redundant uvula.
Signs and symptoms include hypoxemia, cough, failure to maintain oxygen saturation levels, tachypnea, and frothy sputum. Treatment includes supplemental oxygen administration and maintenance of a patent upper airway. Noninvasive pressure ventilation (e.g., CPAP) may be used. Patients with an inability to maintain a patent airway may need intubation and mechanical ventilation with PEEP. For patients with significant compromise, hemodynamic support and continued observation in an intensive care unit may be needed. Patients with noncardiogenic pulmonary edema typically recover rapidly after the intense initial phase and leave the critical care unit within approximately 24 to 48 hours and without permanent sequelae from the event.
Patients predisposed to development of pulmonary emboli include patients who are obese or immobile, are undergoing pelvic or long bone procedures, or have a history of congestive heart failure, congenital heart disease, or malignant disease.6 Signs and symptoms can include tachypnea, pleuritic chest pain, hemoptysis, breathlessness, and a sense of impending doom. Treatment is supportive for correction of hypoxemia and hemodynamic instability. Intravenous heparin and morphine sulfate may be given to help stabilize the pulmonary capillary membrane. Prevention of venous thromboembolism and subsequent pulmonary emboli development includes pharmacologic prophylaxis (e.g., subcutaneous unfractionated heparin, low–molecular-weight heparins) or intermittent or sequential pneumatic compression devices.
Cardiovascular complications that occur in the PACU range from relatively benign ectopic beats to hemodynamic collapse from an acute myocardial infarction. The perianesthesia nurse monitors the patient continuously in phase I, observing rate, rhythm, and blood pressure, and noting any signs or symptoms of hemodynamic compromise. The following section briefly discusses the more common cardiovascular complications seen in the perianesthesia setting.
Surgical and patient characteristics predict risk for a major adverse cardiac event (MACE) including death or myocardial infarction.7,8 Examples of low-risk procedures (risk of MACE <1%) include noncardiac procedures without significant fluid shifts and stress such as cataract extraction or simpler plastic surgery procedures. Typically, patients at low risk of perioperative MACE do not require further testing before procedures. Noncardiac procedures for which elevated risk for MACE is ≥1% include operations for peripheral vascular disease as well as emergent procedures and others during which stress and fluid shifts may be significant. Patient risk factors are associated with coronary artery disease, recent myocardial infarction <60 days, cerebrovascular disease, heart failure, cardiomyopathies, valvular heart disease, arrhythmias and conduction disorders including patients with cardiovascular implantable electronic devices (CIEDs), pulmonary hypertension, and adult congenital heart disease. Additionally, the risk of cardiovascular complications is increased in patients with reduced functional status (i.e., limited exercise capacity or ability to perform activities of daily living and age ≥55 years).
Dysrhythmias can occur as the result of hypoxia, hypercarbia, electrolyte abnormalities, acid-base alterations, myocardial ischemia, medication effects, pain, hypovolemia, bladder distention, and hypothermia. Occasional ectopic beats may be seen in healthy patients. Significant dysrhythmias necessitate immediate identification and treatment; these include premature ventricular contractions (more than five per minute, coupled [more than two together], or multifocal), ventricular tachycardia, ventricular fibrillation, asystole, heart block, pulseless electric activity, and new-onset atrial fibrillation. Treatment includes identification and treatment of the cause, supplemental oxygen administration, ventilatory and hemodynamic support, and pharmacologic therapy. Advanced cardiac life support (ACLS) or pediatric advanced life support (PALS) protocols are initiated when appropriate.
Sinus bradycardia can occur as the result of vagal responses, hypoxia, medication effects, increased intracranial pressure (ICP), or distended bladder. Treatment is dependent on the cause and can include anticholinergic agents (e.g., atropine), supplemental oxygen administration, and stimulation. If the condition is the result of elevated ICP, hyperventilation and pharmacologic therapy may be indicated.
Sinus tachycardia occurs commonly in the postanesthesia setting. Causes include hypoxia, hypercarbia, hypovolemia, sepsis, hyperthermia, heart failure, pain, medications, and psychological stress. Treatment includes administration of supplemental oxygen, ventilation support, and evaluation of fluid and cardiac status. If the condition results from pain, medication with analgesics is the treatment. Sedatives may be needed if the condition is from anxiety or stress. If the patient is hyperthermic, the patient’s core temperature is lowered with recommended cooling devices. Tachycardia in patients with coronary artery disease can increase the risk of myocardial ischemia.
Hypotension is defined as blood pressure less than 20% to 30% of the baseline blood pressure.9 Causes range from use of an inappropriately sized cuff to hypovolemia, myocardial dysfunction, and a decrease in systemic vascular resistance (Fig. 29.2). Management and treatment of hypotension in the PACU include use of a cuff of the appropriate size, administration of supplemental oxygen, initiation of fluid resuscitation, stoppage of medication infusions if causative, and passive leg raising for an evaluation of fluid responsiveness.10 Inotropic agents or vasopressor or vasoconstrictive agents may be ordered.
Hypertension is defined as persistent elevation of systolic blood pressure greater than 140 mm Hg and a diastolic blood pressure greater than 90 mm Hg.11 Too small or narrow of a cuff can result in abnormally elevated blood pressures. Pain; stress; hypoventilation; hypoxemia; hypercarbia; fluid overload; delirium; medications; bladder, bowel, or stomach distention; or hypothermia can cause hypertension. Many of the patients in the PACU in whom hypertension develops have preexisting hypertension. The elevation in blood pressure is usually benign and short lived; however, the hypertension can precipitate myocardial ischemia in the patient with coronary artery disease because of stimulation of the sympathetic nervous system. Treatment for hypertension includes use of an appropriately sized cuff and identification and management of the underlying cause first. This condition may necessitate ventilatory support and oxygen administration, analgesics or sedatives, bladder decompression, and antihypertensive medications.
Patients who have had a cervical or thoracic spinal cord injury (above T6) are at risk for developing autonomic dysreflexia, which is a massive uninhibited sympathetic cardiovascular response to noxious stimuli (e.g., bowel or bladder overdistention) characterized by paroxysmal hypertension, severe headache, flushing above the level of injury, diaphoresis, temporal or neck vessel engorgement, nasal congestion, blurred vision, piloerection, bradycardia, cardiac arrhythmias, and atrial fibrillation.12,13 Treatment includes elimination of the precipitating stimuli if known and elevation of the head of the bed. Pharmacologic treatment may be needed to reduce the blood pressure if the blood pressure remains elevated after these measures. Medications for the treatment of hypertension include nifedipine.
The patient with a history of preexisting coronary artery disease, diabetes, and significant dysrhythmias is at risk for perioperative cardiac events.7 The pathology of perioperative myocardial infarction is shown in Box 29.2.14