29 Postanesthesia care complications
Awareness During Anesthesia: Occurs when a person is aware of some portion of the procedure (sometimes even pain) during general anesthesia; can cause long-term psychologic effects and symptoms of posttraumatic stress.
Dilutional Hyponatremia: Absorption 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.
Hemolytic Transfusion Reactions: An ABO-incompatible blood reaction that precipitates a hemolytic reaction that results 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.
Malignant Hyperthermia (MH): A pharmacogenetic (autosomal dominant inheritance) disorder of muscle metabolism involving hypermetabolism that can be triggered by succinylcholine or the volatile anesthetics.
Plasma Cholinesterase Deficiency: An 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.
Pulmonary Edema: Increase 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.
Spinal Epidural Hematoma: A 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.
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.
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.
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, 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
Data from Smetana GW, et al: Preoperative pulmonary risk stratification for noncardiothoracic surgery: systematic review for the American College of Physicians, Ann Intern Med 144:581–595, 2006.
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 is seen in the patient who has not fully recovered from anesthesia, who has received opioid or sedative drugs, or who has residual neuromuscular blocking agents on board. Other causes include swelling or edema of the airway, airway injury, bleeding (hemorrhage), or obstructive sleep apnea. Treatment includes verbal or tactile stimulation of the patient, airway repositioning with chin lift or jaw thrust, 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.
Laryngospasm is an involuntary partial or complete closure of the vocal cords, caused by secretions or 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 includes 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 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.
For the pediatric patient, obstruction may be caused by subglottic edema, usually 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 can 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 who are 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.
Narrowing of the bronchi and bronchioles from smooth muscle contraction results in bronchospasm. Bronchospasm may be the result of preexisting asthma; allergy or anaphylaxis; histamine release; mucous 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; and women in labor. Medications include histamine blockers, nonparticulate antacids, and anticholinergic agents. During surgery, rapid sequence induction and nasogastric tube placement may help to minimize the risk of aspiration. 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 and suctioning and mechanical ventilation. Arterial blood gases assist in planning respiratory management of the patient. A chest radiograph is 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; or neuromuscular diseases.
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 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 continuous positive airway pressure (CPAP), which can be used in the spontaneously breathing patient. 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 hyperresonance on the affected side of the chest. Treatment includes supplemental oxygen administration and ordering of a chest radiograph. If a less than 20% pneumothorax is diagnosed based on the chest radiograph, the treating physician may want to observe the patient for a period of time 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 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.2 Both are 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.3 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.3
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. 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 36 hours and without permanent sequelae from the event.
Patients predisposed to development of pulmonary emboli include patients who are obese or immobile, who are undergoing pelvic or long bone procedures, and who have a history of congestive heart failure or malignant disease.4 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 can be given to help stabilize the pulmonary capillary membrane. Prevention of venous thromboembolism and subsequent pulmonary emboli development includes subcutaneous unfractionated heparin, low–molecular-weight heparins, or intermittent or sequential 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 and 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.
Major cardiovascular perioperative risks are identified as myocardial infarction, heart failure, and death. Clinical predictors of increased perioperative cardiovascular complications are listed in Box 29-2.5
Data from Fleisher LA, et al: 2009 ACCF/AHA focused update on perioperative beta blockade incorporated into the ACC/AHA 2007 guidelines on perioperative cardiovascular evaluation and care for noncardiac surgery, J Am Coll Cardiol 54(22):e13–e118, 2009.
Dysrhythmias can occur as the result of hypoxia, hypercarbia, electrolyte abnormalities, acid-base alterations, myocardial ischemia, drug 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, drug 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, drugs, and psychologic 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 that is less than 20% to 30% of the baseline blood pressure.6 Causes range from use of an inappropriately sized cuff, to hypovolemia, myocardial dysfunction, and a decrease in systemic vascular resistance (Fig. 29-1). Management and treatment of hypotension in the PACU includes use of a cuff of the appropriate size, administration of supplemental oxygen, initiation of fluid resuscitation, stoppage of drug infusions if causative, and elevation of the legs. 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 or a diastolic blood pressure greater than 90 mm Hg or requires an antihypertensive treatment.”7 Too small or narrow of a cuff can result in abnormally elevated blood pressures. Pain, stress, hypoxemia, hypercarbia, fluid overload, delirium, drugs, bladder, bowel or stomach distention, or hypothermia can cause hypertension. Many of the patients in 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 as a result 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 agents.
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, pounding headache, facial flushing, sweating, temporal or neck vessel engorgement, nasal congestion, blurred vision, chill bumps, chills, nausea, and occasional bradycardia. Treatment includes elimination of the precipitating stimuli if known and elevation of the head of 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, nitrates, captopril, prazosin, phenoxybenzamine hydrochloride, prostaglandin E2, and sildenafil.8