Airway obstruction

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

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.

Subglottic edema

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.

Bronchospasm

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.

Aspiration

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

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.

Hypoxemia

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

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.

Pulmonary edema

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

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.

Pulmonary embolism

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.

Dysrhythmias

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.

Bradycardia

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.

Tachycardia

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

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.

FIG. 29-1 Causes of hypotension.

(From Litwack K: Postanesthesia care nursing, ed 2, St. Louis, 1995, Mosby.)

Hypertension

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

Acute myocardial infarction

The patient with a history of preexisting coronary artery disease, diabetes, and significant dysrhythmias is at risk for perioperative cardiac events (see Box 29-2). The pathology of perioperative myocardial infarction is shown in Fig. 29-2.⁹

FIG. 29-2 Pathology of perioperative myocardial infarction.

(From Kertai MD, et al: Predicting perioperative cardiac risk, Progress Cardiovasc Dis 47(4):240–257, 2005.)

When a patient has chest pain in the PACU, the cause needs to be evaluated, with the first consideration for the source as cardiac in origin (Box 29-3). The signs and symptoms of myocardial infarction include chest pain, tachypnea, tachycardia or other dysrhythmias, hypotension or hypertension, pallor, diaphoresis, cool extremities, nausea, vomiting, and generalized weakness. New Q waves or increasing prominence of existing ones, ST segment elevations, and T wave inversions may be seen on electrocardiogram (ECG) results. Initial treatment is aimed at relieving chest pain, reducing cardiac workload, stabilizing cardiac rhythm, limiting infarct size, preventing further damage, and detecting and treating complications. The first response is to order a 12-lead ECG; initiate supplemental oxygen to maintain arterial oxygen saturation (SaO₂) above 90%¹⁰; administer morphine, nitrates, and antiplatelet or anticoagulant agents; and continuously monitor the ECG. Laboratory blood studies are obtained, including troponin-I, troponin-T, MB fraction of creatine kinase (CK-MB), and CK-MB isoforms. The patient is evaluated and transferred to a critical care unit as indicated by diagnosis for continued monitoring and possible interventional procedures and management.

Hypothermia

Hypothermia is defined as a core temperature of less than 36° C.¹¹ Signs and symptoms of hypothermia include shivering, restlessness, discomfort, and cold pale cyanotic extremities and distal appendages from peripheral vasoconstriction. This state can lead to delayed drug clearance, myocardial ischemia, unexplained hypertension, and residual paralysis from neuromuscular blocking agents. The American Society of PeriAnesthesia Nurses Evidence-Based Clinical Practice Guideline for the Promotion of Perioperative Normothermia offers the perianesthesia nurse guidance for assessment and management of the patient who is hypothermic during the perianesthesia period.¹¹ Recommendations for treatment of the patient include active rewarming, supplemental oxygen administration, and ventilatory support if necessary.

Hyperthermia

Hyperthermia is defined as a core temperature of more than 38° C.¹¹ Temperature elevations may be the result of blood transfusion reactions, warm environment, drug-induced fever, use of anticholinergic drugs, overcorrected hypothermia, endocrine disorder, hypothalamic injury, or malignant hyperthermia (MH). Signs and symptoms include fever, tachycardia, and warm flushed skin and other sign and symptoms depending on the cause of the hyperthermia (shaking, chills or rigors, agitation). The cause should be identified and corrected when possible. Cooling blankets or pads may be used, and an antipyretic agent may be given.

Malignant hyperthermia

MH is a drug-induced hypermetabolic state of genetic origin (autosomal dominant inheritance) that can be triggered by succinylcholine or the volatile anesthetics. It can occur on induction, during emergence, or up to 24 hours after anesthesia. The exact incidence rate is unknown but is thought to be approximately 1:15,000 in children and less common in adults older than 30 years. Patients with central core disease and other muscle diseases may be at added risk for developing MH.

The signs and symptoms of MH include the earliest sign of an unanticipated doubling or tripling of end-tidal CO₂ in the anesthetized patient. This sign may be followed by unexpected tachycardia, tachypnea, and jaw muscle rigidity. Respiratory acidosis and, after severe temperature increase, metabolic acidosis are present. Body rigidity is a specific sign of MH syndrome. Fever, when it develops, is a late sign of MH; the temperature may rise at a rate of 1° C every 3 to 5 minutes. The urine may become dark and cola colored from the breakdown of myoglobin.

Early recognition of MH is essential; additional help needs to be summoned. If it occurs in the operating suite, discontinue all volatile anesthetics, hyperventilate the patient’s lungs with 100% oxygen with a new circuit, and end the operative procedure as soon as safely possible. Dantrolene sodium (Dantrium should be available in sufficient quantities [36 vials recommended in all locations where volatile anesthetics or succinylcholine are administered]) as should diluent. Dosing begins at 2.5 mg/kg of dantrolene sodium, up to 10 mg/kg. Laboratory blood studies including coagulation profile, creatine, electrolytes, arterial blood gas, and creatinine kinase should be obtained. Acidosis not reversed with dantrolene sodium can be treated with sodium bicarbonate. The patient’s body temperature should be monitored, and cooling measures should be initiated if the temperature is more than 38.5° C. Dysrhythmias can be treated with standard antiarrhythmics, but calcium channel blockers should be avoided. Elevated potassium levels are treated with intravenous (IV) insulin, glucose, and calcium. Hydration and diuretics ensure urine output of at least 2 mL/kg/h.

After the MH crisis is treated and the patient’s condition is stabilized, the patient should be transferred to a critical care unit for continued monitoring, including temperature, for at least 24 hours because recrudescence can occur and does in approximately 25% of MH cases.

Patients who have had an MH episode during a previous surgery or have a family history of MH are treated as MH susceptible; triggering agents are avoided. Dantrolene sodium prophylaxis is not recommended for these patients. The patient who undergoes an uneventful anesthetic and is scheduled as an outpatient may be discharged home on the day of surgery; this patient should be monitored in the phase I PACU for a minimum of 1 hour and in the phase II PACU for an additional 1.5 hours.

Diagnosis of MH susceptibility involves a skeletal muscle biopsy specimen from the thigh. Only eight medical centers in the United States and Canada perform the test on fresh muscle. Genetic testing is available, but not all the genes responsible for MH have been identified; therefore risk may still exist for the patient whose test results are negative and who has unidentified genes.

When an MH crisis occurs, consultation is available from the MH Hotline at 1-800-MH-HYPER (1-800-644-9737) in the United States or 1-315-464-7079 outside the United States. Additional information and resources can be found at www.mhaus.org.

Awareness under anesthesia

One to two per thousand patients at low risk has an ability to recall some aspect of the surgical experience. The effects of awareness with anesthesia vary from pleasant recall to terror that leads to posttraumatic stress disorder. Difficulty in diagnosis of awareness adds to the challenge of this event. Patient recall can include events such as conversations, pain, or anxiety related to perception of an inability to breathe. Risk factors include a history of drug or alcohol abuse, extreme anxiety, or a previous episode of awareness. Patients undergoing cardiac, major trauma, and obstetric procedures are at greatest risk of awareness. Patients who are defined as sicker by the American Society of Anesthesiologists status appear to be at higher risk for awareness under anesthesia.

When patients arrive in the postanesthesia care unit, nurses tell the patients that surgery is over, they are in the PACU or wake-up room, they are doing well, and the nurses are going to take care of them while they are awakening. This reassurance can minimize fears of waking up while still in the operating suite. Frequent reminders to the patients of status and safety help reduce anxiety related to awareness or awakening. If a patient indicates recall of events from the operating suite, the perianesthesia nurse should contact the anesthesia care provider to come to the bedside and interview the patient. Telling the patient an event did not occur or was a dream is inappropriate. If an awareness event is suspected, the nurse should sympathize and apologize to the patient, explain and answer questions as appropriate, and notify the anesthesia care provider, surgeon, and risk management department.

Anesthesia care providers, when interviewing patients after procedures, may use a structured interview tool, such as the Brice questionnaire (Box 29-4).¹² This interview may dispel concerns and identify awareness events with greater frequency.

Emergence excitement

Most patients emerge from general anesthesia in a calm tranquil manner. Some patients, however, emerge in a state of excitement, a condition characterized by restlessness, disorientation, crying, moaning, irrational talking, and inappropriate behavior. In the extreme form of excitement, which is also called emergence delirium (Fig. 29-3) or agitation, the patient screams, shouts, and wildly thrashes. Postoperative delirium or emergence excitement is defined as responsive or unresponsive agitation.

FIG. 29-3 Emergence delirium in the postanesthesia care unit: contributing factors and treatment.

(From Nagelhout JJ, Plaus KL: Nurse anesthesia, ed 4, St. Louis, 2010, Saunders.)

The incidence rate of emergence excitement is higher among children, the elderly, and those with a history of drug dependency or psychiatric disorders. Medications administered before or during surgery, including ketamine, droperidol, opioids, benzodiazepines, large doses of metoclopramide, and atropine or scopolamine, may precipitate delirium. Patients who are emotional or anxious before induction of anesthesia or who awaken restrained are at increased risk of emergence excitement or delirium.

The PACU nurse should assess the patient’s status if emergence excitement is encountered. The patient’s cardiopulmonary function, airway patency, and oxygen saturation should be checked first because restlessness and agitation are well-known manifestations of hypoxemia. Other causes include bladder distention, cramped or sore muscles and joints from prolonged abnormal positioning on the operating table, the presence of pain, incomplete reversal of neuromuscular blockade, withdrawal from alcohol and other drugs, central anticholinergic syndrome, acid-base disturbances, and electrolyte abnormalities.

The restless patient needs constant careful observation. Gentle physical restraint may be necessary for prevention of injury. Several nurses or attendants may be needed to provide safety for the patient, and for the caregivers too. Treatment is symptomatic. If hypoxia, pain, and full bladder are ruled out, a change in position may have a quieting effect. Physostigmine can be used to reverse central anticholinergic drug effects. Anxiolytics, such as midazolam, usually calm the patient. If sedative treatment is instituted, the patient should be monitored for respiratory depression. Nurses should be alert to increased agitation after benzodiazepine administration. These agents may contribute to restlessness rather than decreasing it; a paradoxical reaction to benzodiazepines can occur.

Anticholinergic syndrome (ACS), or central anticholinergic syndrome, is rare but occurs most frequently with atropine and scopolamine. Other agents that cause ACS are glycopyrrolate, antihistamines, and antipsychotics. This syndrome or response to anticholinergic agents may present as emergence excitement in the PACU. It is produced by the inhibition of cholinergic neurotransmission at muscarinic receptor sites. It can manifest before surgery or in the PACU when patients are given atropine or have applied transdermal scopolamine patches. Signs and symptoms include sinus tachycardia, agitation, flushing, dry skin and mucous membranes, mydriasis with loss of accommodation, altered mental status, fever, decreased bowel sounds, functional ileus, urinary retention, hypertension, tremulousness, and myoclonic jerking. Patients with central ACS may have ataxia, disorientation, short-term memory loss, confusion, hallucinations (visual, auditory), psychosis, agitated delirium, seizures (rare), coma, respiratory failure, and cardiovascular collapse. Supportive care, removal of scopolamine patches, and administration of IV physostigmine constitute initial treatment of ACS.

Physostigmine is a reversible acetylcholinesterase inhibitor that directly antagonizes the central nervous system manifestations of anticholinergic toxicity. Increased acetylcholine allows for stimulation at muscarinic and nicotinic receptors. The drug crosses the blood-brain barrier and reverses the central effects of coma, seizures, severe dyskinesias, hallucinations, agitation, and respiratory depression. Adverse effects include vomiting, diarrhea, abdominal cramps, diaphoresis, and rare bradyasystole in the presence of prolonged PR or QRS intervals on the ECG.

Delayed emergence (awakening)

Occasionally patients awaken from anesthesia more slowly than expected. Causes include prolonged action of anesthetic and other drugs; metabolic problems such as hypoglycemia, hypocalcemia, hyponatremia, and hypermagnesemia; hypovolemia; hypothermia; and neurologic injury. Respiratory inadequacy with resultant hypercarbia and hypoxemia can result from opioids, sedatives, other anesthetic agents and adjuncts, or neurologic causes. The most common cause of delayed awakening is prolonged drug effects (Fig. 29-4).

FIG. 29-4 Delayed emergence (awakening).

(From Litwack K: Postanesthesia care nursing, ed 2, St. Louis, 1995, Mosby.)

Treatment consists of thorough assessment and identification of the cause or causes of the delayed arousal. Oxygenation and ventilation along with adequate cardiac output must be maintained. Residual anesthetic agents may be treated with maintenance of ventilation. Residual opioids, sedatives, neuromuscular blocking agents, and anticholinergic drugs can be reversed with the appropriate antagonists. Metabolic disturbances should be corrected. If hypothermia is the suggested cause, warming measures are instituted with appropriate temperature monitoring. Neurologic evaluation may be needed if other causes of delayed arousal have been excluded.

Evaluation of the patient for possible cerebrovascular accident (stroke) should be included in the immediate assessment of the postanesthesia patient. Observe facial symmetry assessing for droop, evaluate speech assessing for slurring of words and abnormal speech, and assess arm drift. In addition, neurologic assessment including level of orientation, pupillary response, movement, and muscle strength can assist in determining variations and need for intervention to avoid further neurologic deterioration.

Nausea and vomiting

A common problem for the postanesthesia patient is postoperative nausea and vomiting (PONV). The incidence rate of nausea and vomiting has remained between 20% and 30% of all patients undergoing anesthesia and rises up to 80% in patients at high risk. PONV contributes to postoperative complications, increases the costs of care, and delays patient recovery and return to work. PONV is a major source of patient discomfort and fear.

Incidence of postoperative nausea and vomiting

Primary risk factors for postoperative nausea and vomiting fall into three categories: patient-specific, anesthetic-related, and surgery-related.¹³ Patient-specific risk factors include female gender, nonsmoking status, history of PONV, and history of motion sickness. Use of volatile anesthetics, nitrous oxide, and postoperative opioids are the anesthetic-related factors. Duration of surgery and anesthesia and the type of surgery are the surgery-related factors.

Simplified risk factor assessment tools are used to identify patients at greatest risk for development of PONV. Risk can be predicted depending on the number of factors that are present. The factors in these tools include female gender, nonsmoking status, history of PONV or motion sickness, postoperative opioid use, or duration of surgery greater than 60 minutes.

The presence of each additional factor predicts increased risk of development of PONV and guides antiemetic prophylaxis for the prevention of PONV. Patients with zero to one factor have a low level risk of PONV; those with two are at moderate risk, with an approximately 40% chance of PONV. With three or more factors, patients have a 60% chance of development of PONV. Very severe risk, a more than 80% risk of PONV, can be found in patients with four to five risk factors. See Fig. 29-5 for recommendations for preoperative antiemetic prophylaxis from the American Society of PeriAnesthesia Nurses Evidence-Based Clinical Practice Guideline for the Prevention and/or Management of PONV/PDNV.¹⁴

FIG. 29-5 Preoperative patient management.

(From American Society of PeriAnesthesia Nurses: Evidence-based clinical practice guideline for the prevention and/or management of PONV/PDNV, J Perianesth Nurs 21:230–250, 2006.)

Pharmacologic interventions

If the previous intervention does not relieve the nausea and vomiting, a pharmacologic intervention is needed (Fig. 29-6; Table 29-1). As previously discussed, the following receptors are in the CTZ: serotonin (5-HT₃), dopamine (D₂), histamine, and muscarinic. Drugs that block serotonin (5-HT₃) receptors are ondansetron (Zofran), dolasetron (Anzemet), granisetron (Kytril), or palonosetron (Aloxi) and the drugs that block the dopamine (D₂) receptors are droperidol (Inapsine), prochlorperazine (Compazine), or metoclopramide (Reglan). For the histamine receptors, promethazine (Phenergan) or diphenhydramine (Benadryl) can be given. For the muscarinic receptors, atropine, glycopyrrolate (Robinul), or scopolamine patches can be used. Dexamethasone (Decadron) is often administered in combination with a serotonin (5-HT₃)–blocking drug and dopamine (D₂)–blocking agent. Another neurotransmitter of interest is substance P, which belongs to the tachykinin family of neurotransmitters, known as neurokinins. Substance P has the greatest affinity for neurokinin 1 (NK-1) receptors, which are found centrally in the brainstem vomiting center and peripherally in the gastrointestinal tract. Currently, the only available medication that targets these neurokinin 1 receptors is aprepitant (Emend), available orally for prophylaxis of PONV.

FIG. 29-6 Postoperative management of postanesthesia nausea and vomiting (PONV): PACU Phase I and Phase II.

(From American Society of PeriAnesthesia Nurses: Evidence-based clinical practice guideline for the prevention and/or management of PONV/PDNV, J Perianesth Nurs 21:230–250, 2006.)

Table 29-1 Pharmacologic Interventions

Evidence-Based Practice

The use of steroids in the perianesthesia period has been linked to reduced pain and nausea after ambulatory surgery. It was unknown whether the use of steroids would influence the quality of recovery after surgery. The researchers in this study hypothesized that perioperative dexamethasone would enhance the quality of recovery in patients who had undergone laparoscopic cholecystectomy. The 120 patients were randomized to receive either a placebo or 8 mg of dexamethasone. Nausea, vomiting, fatigue, and pain scores were collected. Global quality of recovery scores were higher in the treatment group compared with the placebo group. Nausea, fatigue, pain scores, and analgesic requirements were reduced in the dexamethasone group during hospitalization. Total length of stay in the hospital was also reduced.

Implications for practice

The use of preoperative steroids in patients who have had laparoscopic cholecystectomy surgery improved quality-of-recovery scores in all areas, including pain, fatigue, and nausea. More research needs to be conducted in this area to determine whether the use of steroids affects quality of recovery in other patient populations.

Source: Glenn S, et al: Preoperative dexamethasone enhances quality of recovery after laparoscopic cholecystectomy, Anesthesiology 114:882–890, 2011.

Postdischarge nausea and vomiting

After discharge, up to 30% to 50% of patients undergoing outpatient surgery have postdischarge nausea and vomiting (PDNV).¹⁷ PDNV affects the quality of recovery, increases the potential for patient morbidity and hospitalization of patients at high risk, and decreases patient satisfaction. PDNV is defined as nausea and vomiting that occurs up to 24 hours after the patient is discharged from the facility. See Fig. 29-7 for rescue and treatment recommendations. More research is needed to establish the scope of the PDNV problem and the effectiveness of these recommendations.

FIG. 29-7 Management of postdischarge nausea and vomiting (PDNV).

(From American Society of PeriAnesthesia Nurses: Evidence-based clinical practice guideline for the prevention and/or management of PONV/PDNV, J Perianesth Nurs 21:230–250, 2006.)

Spinal epidural hematoma

Particular attention should be paid to patients who have undergone spinal or epidural anesthesia who are seen in the PACU with severe back pain and symptoms of cord compression. The severe pain is a cardinal symptom of an emergent situation: spinal epidural hematoma. Typically, a rapid onset of sensory and motor deficits progresses to paralysis if not identified and promptly treated. Rapid action is needed to prevent permanent neurologic sequelae.

Patients at greatest risk for developing this serious complication are female and older, may have had a traumatic needle or catheter placement, and have indwelling epidural catheters. Also at risk are patients who received low-molecular-weight heparin therapy near the time of the epidural placement. In addition, concomitant dosing with anticoagulants or antiplatelet agents contributes to risk.

If the patient has severe back pain during recovery and has received epidural or spinal anesthesia, the nurse should immediately notify the anesthesia care provider to evaluate the patient. Definitive diagnosis of an epidural hematoma is with magnetic resonance imaging. When the condition is determined to be a hematoma, emergency laminectomy and hematoma evacuation needs to occur quickly, ideally within 6 to 8 hours, to minimize the risk of permanent neurologic damage from the cord compression.

Plasma cholinesterase deficiency

Plasma cholinesterase deficiency is an uncommon genetic disorder that creates unusual sensitivity to succinylcholine and ester local anesthetic agents. The typical response to succinylcholine is skeletal muscle paralysis that lasts approximately 5 to 10 minutes. The patient with abnormal or deficient plasma cholinesterase may remain apneic and paralyzed for 2 hours or more. The deficiency renders the patient unable to hydrolyze the ester bonds in succinylcholine, which leads to the prolonged skeletal muscle paralysis.

Questioning the patient regarding a blood relative’s history of any anesthetic events may help to identify the patient at risk. The deficiency in plasma cholinesterase may also be acquired as the result of liver disease, malignant disease, pregnancy, collagen vascular disease, malnutrition, hypothyroidism, chronic infections (tuberculosis), extensive burn injuries, organophosphate pesticide poisoning, or uremia. Neonates and older patients are at risk. Other causes of lower plasma cholinesterase activity include plasmapheresis and medications such as anticholinesterase inhibitors, contraceptives, echothiophate eye drops, esmolol, glucocorticoids, metoclopramide, monoamine oxidase inhibitors, and pancuronium.

Care is supportive, with mechanical ventilation until the patient regains spontaneous respiratory effort, because succinylcholine is not reversible. After recovery, the patient should be counseled to carry identification that indicates plasma cholinesterase deficiency and to alert blood relatives that they may also have this genetic variant.

Testing for plasma cholinesterase deficiency can be accomplished with dibucaine, an amide local anesthetic agent, combined with the patient’s blood, which reflects the ability of plasma cholinesterase to metabolize succinylcholine. This test does not measure levels of the enzyme in the plasma. Also available is a simplified screening test of plasma cholinesterase enzyme activity that can be performed with specialized test paper (i.e., Acholest Test Paper).

Postdural puncture headache

Postdural puncture headache typically develops 24 to 48 hours after lumbar puncture from spinal needle placement or inadvertent dural puncture during epidural placement. Patients may either contact the facility reporting severe headache relieved by lying down or respond on follow-up by the perianesthesia nurse that they have a severe headache. The headache is caused by leakage of cerebrospinal fluid. The incidence rate of postdural puncture headache is greater in younger patients and women, especially during pregnancy.

Treatment is initially conservative; recommendations include mild analgesics, bed rest, caffeinated beverages, and increased fluid intake. Caffeine may also be given IV. If the symptoms continue, definitive treatment is an epidural blood patch, in which fresh autologous blood is injected into the epidural space until the headache resolves or fullness or pain is felt. Epidural blood patches are effective in greater than 95% of symptomatic patients.

Perforated viscus

Internal organs may be perforated during the operative procedure. Commonly caused by various types of endoscopic procedures (e.g., laparoscopy, gastroscopy), perforations can appear as pain out of proportion to the procedure; a distended, firm abdomen; hypotension, or bleeding. The esophagus, stomach, bladder, uterus, or bowel may be damaged and not noticed until after the patient arrives in the PACU and becomes symptomatic. The nurse should call the surgeon immediately, provide hemodynamic support as ordered (fluid resuscitation, blood component therapy, vasoactive medications, positioning, additional line placement), and analgesia or sedation if appropriate. The nurse may need to prepare for emergent transfer to the operative suite for repair of the perforation.

Hemorrhage

Bleeding after operative procedures should be minimal. Dressings remain dry with minimal bloody drainage. However, hemorrhage can and does occur in the PACU and requires the attentive nurse to respond promptly to avert potential serious events. Any operative site may bleed if hemostasis is inadequate. Some sites may be more prone to bleeding, such as the tonsillar beds, nasopharynx resulting in epistaxis, the cervix after conization, and the uterus after dilatation and curettage vaginal/cervical. Signs and symptoms of overt or hidden hemorrhage include bright red bleeding; saturation of more than one pad per hour after uterine, cervical, or vaginal procedures, hypotension, tachycardia, restlessness, hematoma formation, and pain. Initial treatment for minor bleeding may be the application of ice or reinforcement of dressings or binders. More severe bleeding requires immediate action by the nurse. Pressure is applied depending on the location of the bleeding, the surgeon is called, fluid resuscitation is initiated, and preparations are made to return the patient to the operative suite for ligation of bleeding veins or arteries, hematoma evacuation, or other necessary surgical interventions to stop the bleeding.

Dilutional hyponatremia

Referred to as TURP syndrome when primarily seen in men undergoing prostate resections, dilutional hyponatremia can also occur in women undergoing hysteroscopic procedures. The usual cause is absorption of irrigating solutions through open blood vessels or perforation of the uterine or bladder wall that leads to circulatory overload from water intoxication. Signs and symptoms include hyponatremia, hypertension, bradycardia, agitation, nausea, central nervous system aberrations, muscle twitching, visual disturbances, excessive sedation, obtundation, increased ICP, seizures, coma, cardiovascular compromise including hemodynamic instability, pulmonary edema, and cardiovascular collapse. Patients may behave in a confused manner, have difficulty seeing, or be difficult to arouse. Treatment includes diuresis with loop diuretics and IV normal saline solution administration. If the serum Na⁺ level is less than 120 mEq/L, 3% to 5% saline solution should be given and hemodynamic support should be provided. Visual disturbances generally resolve with prompt treatment. Permanent blindness can occur if the severe hyponatremia is left untreated.

Allergic reactions or anaphylaxis

Although allergic reactions to anesthetics are rare, they can occur. Patients also react to antibiotics, latex products, analgesics, and other agents while in the perianesthesia setting. The target organs in an allergic response are the cutaneous, gastrointestinal, respiratory, and cardiovascular.

Cutaneous responses include erythema, flushing, and pruritus, especially of the palms, soles, and groin. Nausea, cramping, abdominal pain, vomiting, and diarrhea are the gastrointestinal responses. The respiratory responses involve laryngeal edema with hoarseness, dysphonia or a “lump in throat,” chest tightness, shortness of breath, coughing, and wheezing. Cardiovascular responses may be most significant with hypotension, tachycardia, lightheadedness, faintness, syncope, myocardial infarction, dysrhythmias, and cardiovascular collapse experiences. Other symptoms may include nasal, ocular, and palatal pruritus, sneezing, diaphoresis, disorientation, and incontinence.

The nurse should respond immediately when a patient exhibits signs and symptoms of an allergic or potential anaphylactic reaction. The nurse should stop the administration of drugs, attempt to reduce the absorption of the offending agent, maintain the airway, and administer 100% oxygen. Intubation may need to be considered, particularly if significant respiratory distress or laryngeal swelling is present. Fluid bolus for volume expansion is initiated. Epinephrine should be administered. Start with 0.1 mL/kg of 1:1000 subcutaneously (subcut) or intramuscularly (IM) or 0.1 mL/kg of 1:10,000 IV (maximal dose, 5 mL) and titrate to effect on the basis of physician orders. Secondary treatment includes antihistamines, glucocorticoids, continuous catecholamine infusion, and sodium bicarbonate if acid-base status indicates the need. With supportive care, and especially if the patient is not intubated and symptoms continue, continually reevaluate the airway to ensure adequate oxygenation and ventilation.

Transfusion reactions

The exact incidence rate of transfusion reactions is unknown. Reports of the incidence rate vary from 0.2% to 10%, and some reactions are undoubtedly unrecognized and unreported.

Nurses in the PACU must be especially adept at assessing the patient receiving blood, because many of the signs and symptoms of an adverse reaction to blood may be difficult to separate from those caused by other variables, such as the patient’s illness, surgery, or medications (including anesthesia). In addition, the patient who is not fully conscious may not report symptoms. Blood transfusion reactions or complications may be either immediate or delayed.¹⁸ Immediate reactions include hemolytic, nonhemolytic febrile, and anaphylactic reactions. Other reactions include transmission of infectious disease (acquired disease), graft-versus-host disease, and transfusion-related acute lung injury.

Delayed reactions

Delayed reactions include the transmission of disease (hepatitis, cytomegalovirus, HIV, human T cell lymphotropic virus I and II), graft-versus-host disease, circulatory overload, citrate intoxication, cardiac dysrhythmias, and bleeding caused by depleted coagulation factors. Delayed hemolytic reactions commonly occur 4 to 8 days after blood transfusion, but can develop up to 1 month later. Symptoms are generally mild and can include a mild elevation in serum bilirubin or fever.

Circulatory overload results when fluid is infused into the circulatory system either too rapidly or in too great a quantity. Elderly patients and those with minimal cardiac reserve are particularly susceptible. The use of packed RBCs in these patients should be considered carefully. Symptoms of circulatory overload include cough, dyspnea, edema, tachycardia, hemoptysis, and frothy pink-tinged sputum. If the patient is conscious, the patient may have a pounding headache, a feeling of constriction around the chest, back pain, and chills. If these symptoms develop, the transfusion should be stopped and the physician should be notified.

When large amounts of banked blood are transfused, citrate intoxication may occur. If the blood is infused rapidly, the liver cannot metabolize the citrate ions, which combine with the calcium in the blood and cause calcium deficit symptoms such as tingling of the fingers, muscular cramps, and nervousness. If the calcium deficit is not corrected, cardiac dysrhythmias, including ventricular fibrillation, can occur. Treatment consists of slow IV administration of calcium gluconate, 1 g for every 1000 mL of blood the patient received. If calcium gluconate is unavailable, calcium chloride can be used, but this is more irritating to the veins.

The rapid infusion of cold blood can result in cardiac dysrhythmias or cardiac arrest. Blood should be warmed to room temperature or passed through a warming infuser, with care taken not to overheat it, which would cause hemolysis of the RBCs.

In cases of massive blood replacement, bleeding from dilution of coagulation factors and platelets can occur. If massive transfusions are necessary, several fresh blood infusions (<4 hours old) are suggested to be used along with banked blood.

Blood must be properly stored and refrigerated at 5° C, except for platelets. In most instances, blood should be stored in the blood bank until needed. If blood is to be kept in the PACU, proper storage requirements must be met. When units of blood prepared for a given recipient are not used, they should be promptly returned to the blood bank.

Following blood bank protocols for acquiring blood specimens, proper handling and storage of the blood products, checking patient identification with blood products before transfusion, and managing transfusion reactions are necessary for safe blood product administration.