Clinical issues encountered in the postoperative patient may range from very common events, such as inadequate analgesia, to less frequently experienced clinical problems such as negative pressure pulmonary edema. This section reviews the more commonly occurring postoperative clinical events. For detailed discussion of less frequently encountered issues, please see Chapter 71.
Postoperative Nausea and Vomiting
Postoperative nausea and vomiting (PONV) is one of the most common complications of general anesthesia, and although less frequent, PONV can also occur after regional anesthesia techniques.10 Patients are commonly stratified preoperatively (see Chapter 6) with regard to their risk for PONV, with the incidence of PONV higher in women, nonsmokers, and patients with a history of PONV or motion sickness.11,12 Additional risk factors involve the administration of narcotics, nitrous oxide, volatile anesthetics, and neostigmine as components of the anesthetic.13 Certain types of surgery such as abdominal; breast; ear, nose, and throat; neurosurgery; and correction of strabismus may also increase the risk for PONV. Prolonged surgeries are associated with an increased incidence of PONV. A more careful implementation of the guidelines would improve the patients' outcomes.14 Apfel et al15 showed that a general anesthetic composed of a volatile anesthetic, nitrous oxide, and fentanyl without giving prophylactic antiemetics has an incidence of PONV as high as 59% in contrast with an anesthetic technique using propofol and avoiding nitrous oxide in combination with remifentanil, ondansetron, dexamethasone, and droperidol, in which the incidence for PONV was 17%. The same group showed that the overall incidence of PONV is about 34%, with a reduction of postoperative risk by 26% with administration of ondansetron, dexamethasone, or droperidol. Prevention of PONV is more effective than treatment after symptoms occur because the later options are much more limited.16,17
If PONV occurs in a patient who did not receive prophylaxis, therapy should be initiated with a serotonin antagonist and supplemented, if necessary, with other classes of drugs. In patients who received prophylaxis, subsequent therapy should consist of drugs from classes other than those already administered.18,19 Administration of drugs from the same class within the first 6 hours after the surgery is not effective in the treatment of PONV (Table 70-3). Tramèr20 suggests that treatment of nausea and vomiting may be more cost effective than prophylaxis. This view is, in part, based on the poor results associated with prophylaxis using a single agent.21 Common agents for the treatment of PONV include:
Table 70-3 Antiemetic Treatment for Patients with Postoperative Nausea and Vomitinga ||Download (.pdf)
Table 70-3 Antiemetic Treatment for Patients with Postoperative Nausea and Vomitinga
|Initial Therapy||Failed Prophylaxis|
No prophylaxis or dexamethasone
Small dose of a serotonin antagonist
Small dose of a serotonin antagonist plus a second agent
Use a drug from a different class
Triple therapy with serotonin antagonist plus two other agents when PONV occurs <6 h after surgery (V)
Do not repeat initial therapy
Use drug from different class or propofol, 20 mg as needed, in the PACU (adults)
Triple therapy with serotonin antagonist plus two other agents when PONV occurs > 6 h after surgery (V)
Repeat serotonin antagonist and droperidol (not dexamethasone or transdermal scopolamine)
Use drug from a different class (V)
Serotonin antagonists are effective as prophylactic antiemetics when administered before the use of narcotics or before the completion of surgery. About one quarter of the dose used for prophylaxis can be used for rescue therapy.
Phenothiazines (eg, Compazine) have been used both for prevention and treatment of PONV. This class of antiemetics can be associated with significant sedation.
Dexamethasone is most effective for prophylaxis if administered before the induction of anesthesia. It can also be used as a rescue drug.
Transdermal scopolamine, often used in the ambulatory care setting, is effective in prophylaxis when applied at least 4 hours before the end of surgery. Potential side effects include changes in vision, dry mucous membranes, and sedation.
Droperidol is no longer used as a first-line drug for the prevention and treatment of PONV. A "black box" warning issued in 2001 by the Food and Drug Administration associated droperidol with QT segment prolongation and producing torsades de pointes in some patients. Documentation of a normal QT segment before droperidol administration and continuous ECG monitoring for 2 to 3 hours after administration are currently recommended. Droperidol can be used for the treatment of PONV that has been refractory to other drugs. Charbit et al22 demonstrated that patients with PONV have a high incidence of a prolonged QTc interval because of a variety of factors associated with anesthesia even before the administration of an antiemetic such as low-dose droperidol or ondansetron. And both classes of agents may increase the QTc interval after administration for treatment of PONV. Given this concern for producing cardiac arrhythmias, clinicians have sought alternatives to droperidol and have given haloperidol at low doses. In a recent meta-analysis, Büttner et al23 demonstrated that low-dose IV haloperidol is an effective drug for PONV with minimal side effects.
A generalized approach to the perioperative evaluation, prophylaxis, and treatment of PONV is provided in Figure 70-1.
Algorithm for the treatment of postoperative nausea and vomiting (PONV). The algorithm is a suggested approach for the prophylaxis of patients at moderate to high risk for PONV. Prophylaxis of patients at minimal risk for PONV appears relatively ineffective. However, in the setting of patients undergoing procedures in which the potential risk for damage caused by postoperative emesis is unacceptable, prophylaxis should be initiated. The characters IA to V noted in the boxes of the diagram reflect the strength of evidence supporting the therapeutic intervention as explained by Sessler.63
Respiratory and Airway Complications
Most surgical patients arrive in the PACU after extubation in the OR with supplemental oxygen provided. Supplemental oxygen is delivered by nasal cannula or a face mask during transport of the patient from the OR and is generally well tolerated by the patient. Most patients wean from the supplementary oxygen soon after arrival in the PACU. However, some patients may have a continued requirement for supplemental oxygen in the PACU or may require escalation of therapy such as a high-flow mask, noninvasive mechanical ventilation, or reintubation. For hypoxia not responsive to oxygen therapy and management of intubated patients, please refer to Chapters 71 and 79.
Respiratory and airway complications are some of the most common perioperative problems occurring in the immediate postoperative period. Risk factors for postoperative pulmonary complications include preexisting patient conditions such as chronic obstructive pulmonary disease (COPD), obstructive sleep apnea (OSA), extreme age, tobacco use, high ASA status, and malnutrition as well as surgical factors such as the proximity of the surgical site to the diaphragm. Thoracic; neurosurgical; upper abdominal; peripheral vascular surgery; and ear, nose, and throat procedures as well as emergency surgery all increase the risk for postoperative pulmonary complications.24 The predominant issues include inadequate oxygenation or ventilation, upper airway obstruction, laryngospasm, and aspiration.25
General anesthesia is associated with inhibition of hypoxic and hypercapnic ventilatory drive and a reduction of functional residual capacity (FRC). These changes may persist for a variable period of time postoperatively and predispose the patient to hypoventilation and hypoxemia. In the immediate postoperative period, hypoxia is commonly caused by the presence of residual anesthetic agents. After sufficient time for recovery from anesthetic depressant effects, hypoxia may be attributable to the side effects of other medications prescribed for the patient. Analgesia and the degree of respiratory depression can differ based on the route of administration. The effects may range from a slight decrease in oxygen saturation (Spo2) requiring supplemental oxygen to severe hypoventilation requiring administration of the opioid antagonist naloxone to reverse the respiratory depression.26 The present standard of care suggests that all patients should receive supplemental oxygen in the immediate postoperative period.4 Although supplemental oxygen may mask and delay the detection of hypoventilation by pulse oximetry,27 evidence suggests that the use of supplemental oxygen in the immediate postoperative period may be associated with a reduced rate of wound infection.28-30 Therefore, the decision to administer supplemental oxygen should be individualized for each patient. Clinical signs of hypoxemia include dyspnea, cyanosis, altered mental status, agitation, obtundation, tachycardia, hypertension, and arrhythmias. Causes of hypoxemia include the following:
Atelectasis, with increased intrapulmonary shunting, is a predictable effect of a decreased FRC caused by general anesthesia. An additional reduction in the FRC that occurs in obese patients and after thoracic or upper abdominal procedures can further potentiate the impact of atelectasis in postoperative patients. Patients undergoing procedures with epidural anesthesia without general anesthesia usually have little or no atelectasis.31 Deep breathing and incentive spirometry are equally effective in reexpanding small areas of alveolar collapse. Noninvasive ventilation can reinflate atelectasis and improve oxygenation in postoperative patients. Occasionally, hypoxemia may persist and a chest radiograph may reveal a segmental or lobar collapse. Chest physiotherapy or fiberoptic bronchoscopy may facilitate the inflation of atelectatic segments.
Hypoventilation is characterized by a low minute ventilation and causes hypoxemia by promoting alveolar collapse despite increasing the CO2 partial pressure in arterial blood. When severe, hypoventilation produces hypoxemia, CO2 narcosis, and ultimately apnea. Supplemental oxygen may mask the early detection of hypoventilation by preventing desaturation. A decline in oxygen saturation, as a sign of hypoventilation, has been found to be accurate only in patients breathing room air.27 Therefore, monitoring the ventilatory status of postoperative patients should not rely entirely on pulse oximetry. Etiologies of postoperative hypoventilation may be divided into two groups. Decreased ventilatory drive, resulting from medications and agents administered during the intraoperative course, is normally short lived and resolves shortly after the patient's arrival in the PACU. Pulmonary and respiratory muscle insufficiency or compromise caused by conditions such as COPD, obesity, or surgical manipulation can limit the patient's ventilatory capability in the postoperative setting. Additionally, the effects of residual neuromuscular blockade can markedly impair the patient's respiratory efforts in the immediate postoperative setting.
Upper airway obstruction is most often caused by inadequate recovery of airway reflexes and muscle tone. Principal signs are the lack of adequate air movement, intercostal and suprasternal retractions, and discoordinate abdominal and chest wall motion during inspiration. Whereas complete upper airway obstruction is silent, partial obstruction is often accompanied by snoring (if the obstruction is above the larynx) or inspiratory stridor (if perilaryngeal). Obstruction is commonly seen in patients with OSA, obesity, or nasal obstruction caused by tonsillar or adenoidal hypertrophy.32 To treat this, 100% oxygen is delivered by mask, and rapid airway management is required. A chin lift, with or without a jaw thrust, often reduces the obstruction, but some patients (eg, patients with OSA) may benefit from applying continuous positive airway pressure (CPAP). This is especially true in patients using CPAP at home. Additional conditions with the potential to impact respiratory function in the postoperative patient include laryngospasm, bronchospasm, pulmonary edema, and aspiration of gastric contents. For a detailed discussion of postoperative respiratory complications, please refer to Chapter 71.
The differential diagnosis of hypotension is aided by a review of the patient's history and intraoperative management. Preoperative dehydration in the setting of a bowel preparation or inadequate intraoperative fluid resuscitation is a common cause of hypotension in the immediate postoperative patient. Review of the patient's intraoperative course by a review of the anesthetic record and a discussion with the intraoperative team often yield insights to the nature of postoperative hypotension. Common causes of postoperative hypotension include:
Hypovolemia is the most common cause of hypotension in the PACU, and bleeding must be considered to be the proximate cause until proven otherwise. Inadequate fluid replacement, osmotic polyuria, and fluid sequestration (intestinal obstruction, ascites) are other common causes of hypovolemia in the postoperative patient. Nonspecific signs of hypovolemia include hypotension, tachycardia, decreased skin turgor, dry mucous membranes, oliguria, and thirst. An IV volume challenge (250-1000 mL of crystalloid or an equivalent volume of a colloidal solution) should be considered in the setting of a patient suspected of hypovolemia after surgery. Persistent hypotension after adequate volume replacement mandates further assessment, including placement of a urinary bladder catheter and, if necessary, invasive monitoring.
Impaired venous return can occur when mechanical forces decrease venous return to the heart. Common causes include positive-pressure ventilation and an increased intra-abdominal compartment pressure caused by edema or a fluid collection. Signs of obstruction to venous return may be differentiated from true hypovolemia by the presence or absence of jugular vein distension. Volume administration is the mainstay of symptomatic therapy, but treatment of the cause is the ultimate intervention.
Vasodilation. Neuraxial anesthesia, residual inhalation agents, rewarming after hypothermia, transfusion reactions, adrenal insufficiency, anaphylaxis, systemic inflammation, sepsis, liver failure, and the administration of vasodilators can induce vasodilation, resulting in hypotension. Hypovolemia accentuates the hypotension secondary to vasodilation, and volume replacement alone may not fully restore the systemic blood pressure. Pharmacologic treatment may include α-adrenergic receptor agonists such as phenylephrine or norepinephrine. The use of such agents mandates close monitoring of blood pressure. Diagnosis and treatment of the specific etiology must be concurrent with such symptomatic treatment.
Additional causes of hypotension can be the result of cardiac dysfunction, sepsis, and chronic antihypertensive therapy. For a detailed discussion of the causes of postoperative hypotension, please refer to Chapter 71.
Increased sympathetic outflow, hypoxemia, hypercarbia, electrolyte and acid–base imbalance, myocardial ischemia, increased intracranial pressure (ICP), drug toxicity, thyrotoxicosis, pericardial irritation, and malignant hyperthermia (MH) are possible causes of perioperative dysrhythmias. Premature atrial contractions and unifocal premature ventricular contractions (PVCs) generally do not require treatment.33 Assessment and definitive therapies are presented in Chapters 9 and 71.
Commonly occurring cardiac dysrhythmias seen in the immediate postoperative setting include:
Sinus tachycardia may be secondary to pain, agitation, hypovolemia, fever, hyperthermia, hypoxemia, hypercarbia, congestive heart failure, or pulmonary embolism. The symptomatic treatment of tachycardia with β-blockers should be instituted only after the underlying etiology is sought. However, a high risk for myocardial ischemia may dictate early drug intervention.
Sinus bradycardia may result from a high neuraxial anesthetic block, opioid administration (with the exception of meperidine), vagal stimulation, α-adrenergic blockade, and increased ICP. Symptomatic treatment with anticholinergic muscarinic agents is indicated when hypotension is present or for severe bradycardia compromising cardiac output.
Stable ventricular dysrhythmias. Patients with PVCs and stable nonsustained ventricular tachycardia do not routinely require intervention. However, reversible causes, such as hypoxemia, myocardial ischemia, acidosis, hypokalemia, and hypomagnesemia, should be treated. PVCs resulting from ventricular irritation in the setting of a central venous catheter generally resolve after withdrawal of the catheter.
For further discussion and therapy, refer to Chapters 9, 71, and 76
Other Cardiac-Related Events
Postoperative pain, respiratory distress, hypovolemia, and anemia are common clinical conditions that may result in excess stress on the cardiovascular system and can result in myocardial ischemia or infarction in the PACU. Changes in the ECG may provide the earliest indication of cardiac compromise. Common abnormal findings on the ECG include:
T-wave changes (inversion, flattening, pseudonormalization) may be associated with myocardial ischemia and infarction, electrolyte imbalance, hypothermia, surgical manipulation of the mediastinum, or incorrect lead placement. Isolated T-wave changes must be considered within the clinical context of the individual patient because these changes may be benign in the postoperative setting. It is essential that postoperative changes in the ECG be compared with preoperative ECGs.34
ST-segment elevation or depressions are generally indicative of myocardial infarction (MI) and ischemia, respectively. ST-segment elevation can be a normal variant or may occur in other conditions such as left ventricular hypertrophy, left bundle-branch block, pericarditis, or hyperkalemia.35 Unlike MIs in the nonsurgical setting, in the postoperative period, most MIs are associated with ST-segment depression and have a non–Q-wave pattern. While initiating standard therapy for myocardial ischemia, including supplemental oxygen, narcotics for pain, and heart rate and blood pressure control, potential precipitating factors for the ST-segment changes must be sought and corrected.
Common causes of myocardial ischemia in the immediate postoperative period include hypoxemia, anemia, tachycardia, hypotension, and hypertension. Cardiac enzymes should be monitored in patients with persistent ECG changes. If clinically appropriate, aspirin, β-blockade, and IV nitroglycerin should be considered, particularly in the setting of patients with ST-segment elevation. Consultation with the cardiology service is indicated in the setting of hemodynamic instability and transfer to a cardiac intensive care unit (ICU) may be required. Ongoing ischemia mandates the institution of invasive monitoring or specialized treatment (eg, thrombolysis, percutaneous angioplasty).
In patients at high risk for cardiac events (patients with ischemic heart disease, cerebrovascular disease, renal insufficiency, diabetes mellitus and patients undergoing intrathoracic, intraperitoneal, or suprainguinal vascular procedures), β-blockade has been found to decrease the risk of perioperative cardiac events.36-38 An institutional perioperative β-blockade protocol may be useful to standardize care. For patients receiving vasoactive agents for hemodynamic support, the use of β-blockade should be initiated on an individual basis. The patient with a permanent pacemaker (PPM) or an implantable cardioverter defibrillator (ICD) requires special consideration in the perioperative setting.38 Information regarding the patient's pacemaker dependency state and the features of the device (model, manufacturer) must be obtained from the OR team. Continuous ECG monitoring is essential with particular attention to the patient's rhythm, rate, and hemodynamic status. Electrocautery used during surgery can electrically reset pacemakers, with older models likely more susceptible. Placement of a magnet over the PPM or ICD during surgery can temporarily or permanently deactivate or reset it, depending on the age and specifics of the device. Newer pacemakers may have rate-adaptive capabilities, requiring intervention by the pacemaker service before surgery. Given the potential for inadvertent program modification in the perioperative setting, interrogation of the device and communication with the electrophysiology service before and after the surgery is generally recommended. Although the ASA recommends that all patients with ICDs should have their devices interrogated in the PACU, this practice appears to be controversial because many cardiologists and manufacturers support follow-up after discharge for many patients. Interrogation of the ICDs before discharge is recommended in situations in which diathermy was used within 15 cm of the device or its leads or if there were perioperative problems with the device.39 For a detailed discussion of patients with cardiac pacemakers and ICDs, please refer to Chapter 9.
Postoperative hypertension is commonly observed in patients not receiving scheduled antihypertensives preoperatively in patients having undergone vascular, head and neck, thoracic, or neurosurgical procedures. Additional postoperative causes of hypertension include pain, bladder distension, fluid overload, hypoxemia, hypercarbia, hypothermia, increased ICP, and overzealous administration of vasoconstrictors. Hypertension is usually asymptomatic but may present as a headache, visual disturbances, dyspnea, restlessness, or chest pain. The initial assessment should include a review of the patient's history and operative course and verification of the accuracy of the blood pressure measurement. The management of hypertension is targeted to restoring blood pressure to within 20% of the patient's baseline. When appropriate, resumption of the patient's chronic antihypertensive oral therapy is ideal. If necessary, this can be supplemented or substituted with parenteral medication. Commonly used medications include:
β-Adrenergic antagonists. Labetalol (an α- and a β-blocker), metoprolol, esmolol, and propranolol are effective in controlling heart rate and blood pressure.
Calcium channel blockers. Verapamil or diltiazem can be used as a bolus or an infusion, and nicardipine can be administered enterally. Sublingual nifedipine is no longer recommended because it can be associated with rapid and severe hypotension, resulting in myocardial ischemia. Clevidipine, a novel third-generation dihydropyridine calcium channel blocker, is a very short-acting agent approved for use in the management of acute perioperative hypertension. Acting primarily as an arterial vasodilator, its half-life of only 2 minutes combined with metabolism by esterases in the blood and extravascular tissues makes it an appealing drug for use in the perioperative period.40
Hydralazine is a potent vasodilator that may induce reflex tachycardia.
Nitrates. Nitroglycerin is preferentially a venodilator that is particularly useful in patients with known myocardial ischemia. Sodium nitroprusside is a potent arterial and venodilator and requires invasive blood pressure monitoring.
Fenoldopam, a selective peripheral dopaminergic receptor agonist, may be administered as an IV infusion. Side effects include tachycardia, headache, and increased intraocular pressure.
Enalaprilat, a parenterally administered angiotensin-converting enzyme (ACE) inhibitor, is of particular value in patients routinely treated with ACE inhibitors or angiotensin receptor blockers in a setting where enteral medications are not clinically appropriate.
Neurologic complications include:
Residual paralysis after general anesthesia, described as residual neuromuscular blockade or residual curarization, has a prevalence between 4% and 50%.41 This phenomenon is most often observed in the PACU, making it an important consideration in the postoperative recovery period. Residual paralysis usually results in mild muscle weakness, but it can also result in serious complications such as hypoxia, pulmonary collapse, and acute respiratory failure. Supportive therapy and reversal of neuromuscular blockade with an acetylcholinesterase inhibitor may be indicated in the immediate postoperative period. The selective binding relaxant sugammadex, a γ-cyclodextrin, which binds rocuronium and to a lesser extent vecuronium and pancuronium, may soon be available for rapid reversal of residual blockade.42
Delayed awakening is most often the result of persistent cerebral depression by anesthetic and analgesic agents.43 Metabolic causes of delayed awakening include hypothermia, sepsis, preexisting encephalopathies, hypoglycemia, and electrolyte or acid–base derangements. Additional causes of delayed awakening include decreased cerebral perfusion during or after surgery that may cause diffuse or localized injury to the brain. In patients with cerebrovascular disease, short periods of hypotension may cause a critical reduction of cerebral perfusion and stroke. If such an event is suspected, immediate consultation with a neurologist should be obtained together with radiologic imaging (eg, computed tomography, magnetic resonance imaging, or angiography). If a seizure is suspected as the cause of delayed awakening, then treatment should be started immediately (see Chapter 51). Neurologic damage may range in severity and be as benign as diplopia after cataract surgery or as severe peripheral nerve injury or may be caused by a stroke.44 Strokes have an incidence of 0.08% to 2.9%, even as high as 5.2%, depending on patient risk factors and the type of surgery and may be ischemic or hemorrhagic.45,46 Early diagnosis of a stroke may be difficult because symptoms such as slurred speech, visual changes, dizziness, agitation, confusion, psychosis, numbness, muscular weakness, or paralysis may overlap with residual anesthetic effects.
Ischemic strokes are more common in patients with cerebrovascular disease, hypercoagulable states, or atrial fibrillation and may be associated with intraoperative hypotension. Fat emboli secondary to long bone fractures can also produce strokes.
Hemorrhagic strokes are more common in patients with coagulopathies, uncontrolled hypertension, and cerebral aneurysms or arteriovenous malformations and head trauma. Hemorrhagic strokes are more frequent after intracranial surgery, carotid endarterectomy, cardiac surgery, or multiple traumas. Neurologic consultation in conjunction with appropriate imaging techniques is mandatory to guide the possible choice of immediate and possibly lifesaving treatment options.
Emergence delirium is characterized by excitement alternating with lethargy, disorientation, and inappropriate behavior. Delirium can vary from hyperactive delirium, characterized by a state of agitation, hyperarousal, or hyperalertness, or hypoactive delirium, in which patients present with a flat affect and are poorly responsive or lethargic. Delirium may occur in any patient but more frequently occurs in elderly patients and in those with a history of drug dependency, dementia, or other psychiatric disorders. Many perioperative agents, such as ketamine, opioids, benzodiazepines, metoclopramide, anticholinergics (atropine or scopolamine), and droperidol, may precipitate delirium. Delirium may be symptomatic of a wide variety of clinical abnormalities, including hypoxemia, acidemia, hyponatremia, hypoglycemia, intracranial injury, sepsis, severe pain, and alcohol withdrawal and as such mandates investigation to exclude these causes.47 The mainstay of treatment of patients with postoperative delirium is reassurance and reorientation while identifying and reversing treatable causes. Antipsychotic medications such as haloperidol can be used for management of agitation in patients with hyperactive delirium. Physostigmine may reverse delirium caused by anticholinergic agents. Other strategies used with some success are using different classes of medication in smaller doses, such as mood stabilizers (Depakote or Tegretol) with benzodiazepines and antipsychotics and even the use of dexmedetomidine.
Peripheral nerve injury may result from improper intraoperative positioning, direct surgical damage, or as a complication of regional anesthetic techniques. In the ASA closed claim analysis, ulnar nerve injury accounted for approximately one-third of the cases of nerve injury followed by damage to the brachial plexus and the common peroneal nerve.48 Risk factors for nerve injury after surgery include a slender body habitus, a previous history of neuropathy, smoking, and diabetes. Additional information on perioperative nerve injury is discussed in Chapter 49.
Intraoperative awareness and recall are rare complications of general anesthesia (0.13% in a large multicenter trial) that may initially be detected in the PACU.49,50 Awareness and recall are most commonly associated with trauma, cardiac, and obstetric surgery.51 Risk factors include young age, history of substance abuse, ASA physical status III to V, a history of recall, light anesthesia, and the use of muscle relaxants.52 The modified Brice Questionnaire (Box 70-1) may be used as a screening tool in the PACU to identify patients at risk for recall. Patients with evidence of recall should receive reassurance, sympathetic care, and referral for psychologic counseling as required.53
Box 70-1 ||Download (.pdf)
Brice Questionnaire for Awarenessa
What is the last thing you remember before going to sleep for the operation?
What is the first thing you remember on waking after the operation?
Do you remember anything between going to sleep and waking up?
Did you have any dreams?
What was the most unpleasant thing you remember from the operation and anesthesia?
aThe Brice questionnaire can be used in the immediate postoperative period to determine any issues that may suggest the possibility of intraoperative awareness. Although the first indications that intraoperative recall may have occurred can be noted in the PACU, it is important to ensure that the patient has recovered adequately from the effects of anesthesia to be able to appropriately cooperate with the examination.
Principles of Pain Management
Adequate analgesia begins in the OR and continues in the PACU.54 In the postoperative period, incisional pain is the most common discomfort experienced by patients.55,56 A detailed discussion of the management of postoperative pain is presented in Chapter 72. A general overview of some common therapeutic modalities is described below:
Opioids (IV or epidural) are the mainstay of postoperative analgesia. Fentanyl, a potent synthetic opioid with a rapid onset of action, is commonly limited to the intraoperative setting. However, small parenteral doses can be titrated postoperatively to establish rapid analgesia. Morphine, hydromorphone, and meperidine are effective longer acting analgesic agents.
Meperidine must be avoided in patients taking monoamine oxidase inhibitors.
Nonsteroidal anti-inflammatory drugs (NSAIDs) and acetaminophen are used in combination with other analgesics to provide more effective analgesia compared with either drug alone.57 Ketorolac is a potent IV NSAID commonly given for postoperative analgesia. Potential toxicities of all NSAIDs include decreased platelet aggregation, gastrointestinal bleeding, and nephrotoxicity.58 Additional adjuvant analgesics include spasmolytics (cyclobenzaprine) and small doses of benzodiazepines.
IV patient-controlled analgesia has been shown to be superior in patient satisfaction compared with intermittent analgesia administered by the medical staff. Continuous epidural analgesia, when appropriate, should be continued postoperatively or promptly initiated in the PACU if not used in the OR.59
Neuraxial and regional sensory blocks, discussed in Chapter 47, are attractive alternatives for postoperative analgesia, especially for patients in whom opioids may be contraindicated.60 Although the use of ultrasonography for placement is widespread because it seems to be associated with an increased success rate of regional blocks, any role for acupuncture or transcutaneous electrical nerve stimulation for postoperative pain control is uncertain.61
Hypothermia is a common occurrence in the PACU, resulting from the cold environment in the OR combined with anesthesia-induced impairment of effective thermoregulation. Even mild hypothermia (a body temperature between 34°C and 36°C) can be perceived as uncomfortable by a conscious patient. Additional side effects associated with hypothermia include shivering,62 increased duration of residual paralysis, coagulopathy, cardiac dysrhythmias, surgical site infections, and an increased duration of postanesthetic recovery.63 Treatment with warm blankets or with forced-air warming systems is generally effective.64 If fluid administration or transfusion is required, fluid warming should be used to avoid further cooling of the patient.
Hyperthermia is less common than hypothermia in the immediate postoperative period. Fever in the PACU may be associated with postoperative atelectasis or a normal inflammatory response related to surgery. However, the presence of an elevated temperature in the immediate postoperative patient can also be associated with conditions such as sepsis or reactions to medications and requires appropriate investigation. Fever should not be automatically assumed to be a sign of infection, and suppressing fever may be harmful in some patients.65 Although relatively uncommon, hypermetabolic states such as MH and thyrotoxicosis may present as a fever in the PACU. Hypothermia and hyperthermia are discussed in Chapter 87.
Fluid Administration and Hemorrhage
All patients in the PACU must be evaluated for the adequacy of the intraoperative fluid resuscitation. Parameters that may indicate that the patient requires additional fluid administration include hypotension, tachycardia, and low urine output. Hypovolemia is the most common cause of postoperative hypotension. And until proven otherwise, bleeding must be the primary concern in postoperative hypotension. Gan et al66 demonstrated that intraoperative goal-directed fluid administration can decrease postoperative complications and is associated with an earlier return of the gastrointestinal function and a shorter hospital stay. The approach to fluid resuscitation can vary according to the clinical situation and institutional protocol.
There is significant debate in the literature regarding the appropriate fluid for resuscitation of postoperative patients. Some clinicians advocate the use of colloid solutions for resuscitation because they may ensure a more rapid and effective expansion of the intravascular volume and do not cross capillary membranes into the interstitial space as readily as crystalloids. Investigators in the Saline Versus Albumin Fluid Evaluation (SAFE) trial demonstrated that albumin and saline are both safe and clinically equivalent, rendering the same 28-day outcome for resuscitation of critically ill patients in the ICU.67
Blood transfusion carries specific risks, including viral infections, bacterial contamination, parasites, prions, hemolytic transfusion reactions, alloimmunization, autoimmunization, immunosuppression, and transfusion-related lung injury. Hebert et al68 showed that critically ill patients who receive a restrictive approach to blood transfusion have a better outcome than patients who receive liberal blood transfusions, thereby motivating a trend to limit phlebotomies, decrease transfusion thresholds, and ultimately reduce the number of blood transfusions in critically ill patients. Ultimately, clinicians must consider the risks and benefits for the individual patient in developing a volume replacement strategy that may involve blood component therapy.69
Unrecognized or ongoing hemorrhage, although uncommon in the immediate postoperative patient, is an emergency requiring immediate treatment and can rapidly overwhelm PACU resources. Coordination with the blood bank, surgery and anesthesia team members, and the ORs is necessary in a timely manner. Personnel assigned to the PACU must have a plan established to address the requirements of rapidly hemorrhaging postoperative patients.
Hemorrhage may present in an obvious manner, such as the rapid saturation of a dressing or an increase in drainage or chest tube output. However, the presentation may be more subtle, with signs of hypovolemia such as hypotension or tachycardia, abdominal distension, a decrease in urine output, or a downward trend of hematocrit or hemoglobin values.
In laparoscopic procedures involving the abdomen and thorax, signs of bleeding may not be apparent in the OR and may only later be identified in the PACU.70 This bleeding of a delayed nature may be associated with procedures requiring the insertion of tracers.71
Patients receiving chronic anticoagulation therapy may be at greater risk for postoperative complications associated with bleeding. In a study of 600 surgical patients chronically anticoagulated with Coumadin when anticoagulation was either discontinued or reversed before surgery, Torn and Rosendaal72 demonstrated an increased incidence of hemorrhage-related complications. A detailed discussion regarding the management of fluid and blood component replacement therapy is presented in Chapters 71 and 83.