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Postanesthesia Care Unit 

Postanesthesia Care Unit
Chapter:
Postanesthesia Care Unit
Author(s):

Sean M. Quinn

and Keith A. Candiotti

DOI:
10.1093/med/9780199377275.003.0012
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date: 08 April 2020

Altered Mental Status

Definition

A clinical spectrum that includes inappropriate or unexpected behaviors, ranging from emergence delirium through delayed awakening.

Presentation

  • Somnolence, disorientation, and mental sluggishness are common immediately after emergence.

  • Emergence excitation may result in a highly agitated state that includes combativeness, confusion, and disorientation that is resistant to treatment.

  • Delayed awakening occurs when a patient fails to respond to stimulation within 30 minutes following anesthesia with no obvious underlying cause.

Pathophysiology

Changes in mental status after surgery are generally not the result of organic brain disease. Pain may cause agitation, confusion, and aggressive behavior during emergence. Endotracheal tubes, drains, and catheters, as well as gastric and urinary distention cause discomfort and may lead to agitation or combativeness. Confusion and delirium also may be caused by metabolic and electrolyte derangements, hypoglycemia, hypothermia, and poor analgesia.

Differential Diagnosis

  • Hypoxia

  • Hypocarbia or hypercarbia

  • Hypotension

  • Electrolyte derangement (i.e., hyponatremia, hypercalcemia)

  • Hypoglycemia

  • Hypothermia

  • Acidemia

  • Stroke

  • Seizure

  • Infection

  • Central cholinergic syndrome

Immediate Management

  • Increase FiO2 to maintain oxygen saturation.

  • Ensure that the patient has an adequate respiratory rate and tidal volume.

  • Consider drawing an arterial blood gas to measure PaO2 and PaCO2.

  • Assess the patient’s blood pressure and heart rate.

  • Verbally reassure and reorient the patient.

  • Provide adequate analgesia and anxiolysis if indicated.

  • Consider administration of physostigmine 0.5 mg IV if cholinergic syndrome is suspected.

  • Restrain patient only if patient or staff safety is at risk.

Diagnostic Studies

  • Arterial blood gas analysis

  • Fingerstick for blood glucose level

  • Laboratory studies: Plasma electrolyte measurements and toxicology screen

  • Computed tomography (CT) of brain (if symptoms persist, to rule out acute bleed, stroke)

  • If indicated, administer incremental doses of naloxone (40 mcg IV bolus) and/or flumazenil (0.1 mg IV bolus)

  • Ensure adequate reversal of neuromuscular blocking agents.

Subsequent Management

  • Reassure the agitated or combative patient.

  • Correct all metabolic causes and ensure normothermia.

  • Consider administration of a butyrophenone (e.g., haldol 2.5 mg IV) to treat agitation without an obvious underlying cause.

  • Consider further neurologic consultation and workup (CT scan, magnetic resonance imaging [MRI], electroencephalograph [EEG]) if mental status does not improve.

Risk Factors

  • Hypoxia

  • Age (children and elderly)

  • Organic brain dysfunction

  • Mental retardation

  • History of substance intoxication or withdrawal

Prevention

Ensure adequate pain control in the postoperative period. Maintain hemodynamic and metabolic stability throughout the anesthetic and into the postoperative period. There is no clear strategy for preventing postoperative excitation and delirium in a susceptible patient. Some studies suggest that the use of dexmedetomidine or antipsychotics can prevent or reduce the incidence of postoperative delirium.

Special Considerations

  • Up to 30%–50% of elderly patients may experience some degree of postoperative confusion, delirium, or cognitive decline. General anesthesia combined with the stress of surgery and pre-existing cognitive abnormalities may all exacerbate this problem. Postoperative cognitive dysfunction may occur immediately in the postanesthesia care unit (PACU) or as late as several days after surgery.

Further Reading

Chang YL, Tsai YF, Lin PJ, et al. Factors for postoperative delirium in a cardiovascular intensive care unit. Am J Crit Care. 2008; 17(6): 567–575.Find this resource:

Neufeld KJ, Leoutsakos JS, Sieber FE, et al. Outcomes of early delirium diagnosis after general anesthesia in the elderly. Anesth Analg. 2013; 117(2): 471–478.Find this resource:

Chest Pain

Definition

Pain that may be of cardiac, respiratory, or musculoskeletal etiology. It is frequently described as heavy or pressing, substernal with possible radiation, and is rarely localized. Intensity may vary with respiration.

Presentation

  • Acute presentation of substernal chest pain or pressure, with frequent radiation to arm or jaw, described as squeezing pressure.

  • Blood pressure changes also may be noted (decreased or elevated).

  • May be associated with tachypnea, shortness of breath, dyspnea, cyanosis, or diaphoresis.

Pathophysiology

Postoperative chest pain is common and has a varied etiology. Classic symptoms of chest pain and tightness may be due to myocardial ischemia or infarction. Cardiac chest pain may also radiate to the arms, epigastric area, back, shoulders, neck, or jaw, and may follow skin dermatomes. Gastroesophageal reflux also may be reported as chest pressure or burning pain. Pulmonary thromboembolism may produce sharp, pleuritic pain that varies with respiration.

Differential Diagnosis

  • Myocardial ischemia or infarction (MI)

  • Cardiac arrhythmia

  • Pericarditis

  • Pericardial tamponade

  • Pneumothorax

  • Pulmonary embolism (PE)

  • Pneumoperitoneum

  • Gastroesophageal reflux disease

  • Esophageal spasm or rupture

  • Thoracic aneurysm

  • Anxiety

Immediate Management

  • Increase FiO2 to maintain adequate oxygenation.

  • Aggressively treat hypotension or hypertension.

  • Provide analgesics (morphine) for relief of pain.

  • Consider nitroglycerin, either sublingual or as IV infusion (start at 0.5 mcg/kg/min).

  • Obtain an electrocardiogram and chest X-ray.

  • Initiate a review of surgical and anesthetic procedures.

Diagnostic Studies

  • 12-lead electrocardiogram

  • Chest X-ray

  • Cardiac enzymes

Subsequent Management

  • Electrocardiogram (ECG) interpretation should take into account the quality of chest pain, patient cardiac history, baseline ECG, and risk index.

  • If a PE is suspected, obtain a high-resolution computed tomography or refer for angiography. Consider duplex ultrasonography of lower extremities to identify the source of a thrombus. Any decision to begin anticoagulation (e.g., a heparin infusion) should be made in conjunction with the surgical service and take into account the risk of bleeding.

  • Treat a significant pneumothorax: Needle thoracostomy for life-threatening pneumothorax or request a surgical consultation for insertion of a chest tube if time permits.

  • If pericardial tamponade, request an emergency surgical consultation for a pericardiocentesis.

  • Consider administering a beta-blocker for control of tachycardia and hypertension (labetalol 5 mg IV or metoprolol 1–2 mg IV).

  • Treat hypotension with fluids and/or vasopressors (ephedrine 5 mg IV bolus or phenylephrine 100 mcg IV bolus).

  • Consider administering aspirin and/or sublingual nitroglycerin if an MI is suspected.

  • If an MI is suspected (especially ST segment elevation MI), obtain a cardiology consultation for possible intervention and revascularization.

Risk Factors

  • A cardiac etiology is more likely in the presence of coronary artery disease, peripheral vascular disease, advanced age, male sex, hyperlipidemia, obesity, and diabetes.

  • Pulmonary embolism diagnosis is supported in patients with known deep venous thrombosis (DVT), hypercoagulable states, malignancy, advanced age, high risk (e.g., orthopedic) or long procedures and prolonged bed rest.

  • A pneumothorax may occur in almost any setting, but should especially be considered after central line placement and surgical procedures involving the chest, neck, and upper abdomen. Also suspect a pneumothorax in any patient with recent trauma.

Prevention

Appropriate preoperative evaluation, cardiac risk stratification, and medical optimization can identify patients at risk for cardiac events. Appropriate DVT prophylaxis (e.g., unfractionated or low-molecular weight heparin) and early ambulation reduces the incidence of deep vein thrombosis and PE. The use of ultrasound may decrease the risk of pneumothorax caused by insertion of a central line.

Special Considerations

  • The initial evaluation of chest pain should always first rule out life-threatening conditions, including myocardial ischemia, pneumothorax, and pulmonary thromboembolism. Once those causes have been considered and ruled out, other etiologies (e.g., gastroesophageal reflux) may be considered. Abdominal laparoscopic procedures that induce a pneumoperitoneum can often cause referred pain into the chest, and esophageal pathology may also mimic cardiac pain.

Further Reading

Landesberg G, Beattie WS, Mosseri M, et al. Perioperative myocardial infarction. Circulation. 2009; 119(22): 2936–2944.Find this resource:

Hypoxia

Definition

Decreased arterial oxygen content in blood as measured by pulse oximetry or arterial blood gas analysis, usually transient as a result of atelectasis and/or alveolar hypoventilation in the early postoperative period.

Presentation

  • SpO2 <90% or pO2 <60 mm Hg

  • Patient is frequently lethargic and may be uncooperative or agitated.

  • Tachycardia and hypertension may be associated with hypoxia.

  • Tissue cyanosis may be seen in severe cases.

Pathophysiology

Hypoxia has many potential etiologies that may be related to comorbidity, the surgical procedure, and anesthesia. Even patients with normal lungs are susceptible to a variety of factors that can cause hypoxia. Factors include respiratory depression from residual anesthesia or neuromuscular blockade, atelectasis, and a ventilation/perfusion mismatch. Potent volatile anesthetics blunt the normal response to hypoxemia.

Differential Diagnosis

  • Hypoventilation due to residual anesthetics

  • Hypercarbia

  • Atelectasis

  • Impaired diffusion (pulmonary edema, pulmonary fibrosis, aspiration)

  • Increased oxygen consumption (shivering)

  • Pulmonary embolus

  • Pneumothorax

  • Transfusion-related lung injury

  • Acute respiratory distress syndrome

  • Mainstem bronchial or esophageal intubation

  • Carboxyhemoglobin or methemoglobin (normal PaO2 but impaired carrying capacity)

  • Inadequate FiO2

  • Obstructive sleep apnea

Immediate Management

  • Provide supplemental O2 via nasal cannula or face mask to maintain adequate oxygenation.

  • Insert an artificial airway if airway obstruction is present.

  • Obtain a serial arterial blood gas analyses to follow PaO2 and PaCO2.

  • If the patient is severely hypoxemic or respiratory failure is imminent, intubate the trachea and initiate mechanical ventilation.

  • Cardiovascular support may be necessary in extreme cases of arterial hypoxia.

Diagnostic Studies

  • Chest X-ray

  • Arterial blood gas

  • Arterial co-oximetry

Subsequent Management

  • Continue supplemental O2.

  • Consider intubation and mechanical ventilation for significant hypoxia or hypercarbia.

  • Consider naloxone (40 mcg IV bolus), flumazenil (0.1 mg IV bolus), or additional neostigmine and glycopyrrolate to reverse narcotics, benzodiazepines, or neuromuscular blocking agents.

  • Provide analgesia if splinting is the cause of hypoventilation.

  • Insert a chest tube to decompress a pneumothorax.

  • Administer diuretics (furosemide 20 mg IV) to treat volume overload causing pulmonary edema.

  • Consider initiating an anticoagulant (e.g., heparin) if PE is suspected. Consult the surgical team before administering anticoagulants.

Risk Factors

  • Advanced age

  • Obesity

  • Pre-existing pulmonary disease (emphysema, fibrosis, pulmonary hypertension)

  • Congestive heart failure

  • Increased production of carbon dioxide (i.e., malignant hyperthermia, shivering)

Prevention

Prevention of postoperative hypoxia is largely based on appropriate administration of supplemental oxygen in the immediate postoperative period. Appropriate levels of positive end-expiratory pressure and recruitment maneuvers may help to decrease atelectasis and right-to-left shunt. Hypoxia may also be prevented by appropriate postoperative respiratory care to prevent and treat atelectasis.

Special Considerations

Diffusion hypoxia can contribute to postoperative hypoxia after a nitrous oxide anesthetic, and may persist for up to approximately 10 minutes, emphasizing the need for supplemental oxygen immediately after emergence and during patient transport.

Further Reading

Neligan PJ. Postoperative noninvasive ventilation. Anesthesiol Clin. 2012; 30(3): 495–511.Find this resource:

Myocardial Ischemia

Definition

Myocardial oxygen supply insufficient to meet metabolic requirements. Ischemia can be caused by decreased regional perfusion or increased oxygen demand.

Presentation

  • Chest pain or pressure reported by an awake patient

  • ST-segment elevation or depression on ECG

  • Possible tachycardia and hypertension or profound hypotension

  • Arrhythmias, congestive heart failure, acute mitral regurgitation

  • Hypoxia, dyspnea

  • Dizziness or syncope

  • Timing may occur hours to days after surgery.

Pathophysiology

Etiologies include platelet aggregation, vasoconstriction, and thrombus formation at the site of a plaque in a coronary artery that decreases or interrupts blood flow. In patients with ischemic coronary artery disease, a sudden increase in myocardial oxygen demand (tachycardia) or decrease in oxygen supply (hypotension, hypoxia) can precipitate acute myocardial ischemia and/or infarction.

Immediate Management

  • Increase FiO2 to maintain adequate oxygenation.

  • Ensure adequate ventilation.

  • Treat pain with narcotics (morphine intravenously [IV]).

  • Aggressive fluid resuscitation and/or vasporessors for hypotension.

  • Initiate beta-blockers (metoprolol 1–2 mg IV q 5 min or esmolol IV infusion 50 mcg/kg/min to a max of 300 mcg/kg/min) for treatment of tachycardia and hypertension. Titrate to a target heart rate of approximately 60 beats per minute if possible.

  • Administer aspirin after consulting with surgeon to determine risk of bleeding.

  • Request a cardiology consultation for a possible interventional procedure.

Differential Diagnosis

  • Coronary vasospasm

  • Pericarditis

  • Aortic dissection

  • Pulmonary embolus

  • Anxiety

Diagnostic Studies

  • 12-Lead electrocardiogram

  • Cardiac enzymes (troponin, CPK, CPK-MB)

  • Complete blood count, metabolic profile

  • Arterial blood gas

  • Chest X-ray

Subsequent Management

  • Continuous monitoring and serial ECGs and cardiac enzymes to assess for ST segment changes, new Q waves, or conduction defects.

  • Echocardiography for new wall motion defects, ejection fraction, valvular dysfunction, or thrombus.

  • Administer beta-blockers (e.g., labetalol 5 mg IV or metoprolol 1 mg IV bolus or an esmolol infusion) to control heart rate and blood pressure.

  • Consider a nitroglycerin infusion (start at 0.5 mcg/kg/min) for coronary vasodilatation.

  • Request a cardiology consultation for possible emergency coronary artery stenting and initiation of anticoagulation and antiplatelet therapy.

Risk Factors

  • Known history of coronary artery disease (CAD), previous myocardial infarction, or significant risk factors of CAD

  • Major abdominal, thoracic, vascular, or emergency surgeries carry the highest risk of postoperative myocardial infarction.

Prevention

Preoperative optimization of the patient with known or suspected coronary artery disease is essential for prevention of postoperative complications. Maintaining stable hemodynamics helps to ensure adequate myocardial oxygen supply and minimize myocardial demand throughout the perioperative period. With the possible exception of angiotensin converting enzyme (ACE) inhibitors, angiotensin II receptor blockers (ARB) and diuretics, all cardiac medications should generally be continued on the day of surgery.

Special Considerations

Interpretation of ECG changes, including ST segment elevation or depression, must be interpreted taking into account a patient’s history and cardiac risk. ST segment depression and chest pain in a low-risk patient rarely indicates myocardial ischemia, but rather a more benign etiology such as anxiety, hyperventilation, and hypokalemia, and generally only requires observation in the PACU. High-risk patients with ST segment changes should undergo an immediate evaluation for myocardial ischemia or infarction. Although monitoring of leads II and V5 detects 80% of ischemic events, a 12-lead ECG should always be performed for verification and evaluation.

Further Reading

Biccard BM. Detection and management of perioperative myocardial ischemia. Curr Opin Anaesthesiol. 2014; 27: 336–343.Find this resource:

Feringa HH, Bax JJ, Poldermans D. Perioperative medical management of ischemic heart disease in patients undergoing noncardiac surgery. Curr Opin Anaesthesiol. 2007; 20(3): 254–260.Find this resource:

Oliguria/Acute Renal Failure

Definition

Urine output <0.5 mL/kg/h that may signify loss of kidney function due to prerenal, renal, or postrenal etiologies.

Presentation

  • Urine output <0.5 mL/kg/h.

  • Often associated with a pre-existing renal insufficiency that is exacerbated by an intraoperative event.

  • May be associated with electrolyte abnormalities (hyperkalemia), acidosis, and rising blood urea nitrogen and creatinine.

Pathophysiology

Prerenal causes of oliguria include hypovolemia due to bleeding, third-space fluid loss, and inadequate fluid replacement. Preoperative or intraoperative insults, such as radiographic contrast dye, hypotension, sepsis, or exposure to nephrotoxic medications may cause acute tubular necrosis, particularly in a patient with baseline renal insufficiency. Postrenal causes of oliguria include obstruction of the ureters, surgical injury to the ureter, and obstruction of a urinary catheter.

Differential Diagnosis

  • Hypovolemia

  • Low cardiac output

  • Abdominal hypertension or compartment syndrome

  • Acute tubular necrosis

  • Nephrotoxic agent exposure

  • Ureter obstruction

  • Mechanical catheter obstruction.

Immediate Management

  • Insert a urinary catheter and evaluate for patency.

  • Administer a fluid challenge (10–20 mL/kg crystalloid).

  • Discontinue administration of nephrotoxic agents.

  • Consider diagnostic administration of a diuretic (furosemide 10–40 mg IV) after ruling out hypovolemia.

Diagnostic Studies

  • Basic metabolic panel

  • Arterial blood gas

  • Chest X-ray

  • Urine electrolytes and creatinine

Subsequent Management

  • Consider inserting a central venous catheter or noninvasive cardiac output monitor if volume status is unclear.

  • Consider starting a vasopressor (norepinephrine 2-4 mcg/min IV or dopamine 2–5 mcg/kg/min IV infusion) for vasodilated states or an inotrope (dobutamine 2–5 mcg/kg/min IV infusion) for low cardiac output to treat hypotension and ensure adequate renal perfusion.

  • Treat severe metabolic acidosis and hyperkalemia if present (see pages [link], [link]).

  • Initiate hemodialysis for worsening renal failure and volume overload refractory to treatment.

Risk Factors

  • Chronic renal insufficiency

  • Left ventricular dysfunction

  • Advanced age

  • Significant intraoperative blood loss

  • Intraoperative hypotension

Prevention

Careful perioperative fluid balance is important in patients with baseline renal insufficiency. Avoidance of nephrotoxic agents and maintenance of adequate renal perfusion may also be useful in preventing postoperative renal failure.

Special Considerations

  • Aortic cross-clamping, severe hypotension, massive transfusion, possible ureteral injury, and other intraoperative events may predispose to postoperative renal failure. Aggressive early rehydration and maintaining an adequate systemic blood pressure are useful in preventing further renal insult.

Further Reading

Josephs SA, Thakar CV. Perioperative risk assessment, prevention, and treatment of acute kidney injury. Int Anesthesiol Clin. 2009; 47(4): 89–105.Find this resource:

Noor S, Usmani A. Postoperative renal failure. Clin Geriatr Med. 2008; 24(4): 721–729.Find this resource:

Postoperative Hypertension

Definition

Elevated systemic blood pressure, frequently seen with tachycardia.

Presentation

Elevated systolic and/or diastolic blood pressure in postoperative patients. Pain is one of the most common precipitating factors of hypertension commonly associated with tachycardia.

Pathophysiology

Patients with a history of pre-existing hypertension have an exaggerated blood pressure response that is caused by noncompliant vasculature, elevated peripheral vascular tone, and increased endogenous sympathetic nervous system activity. Peripheral arterial and venous constriction is mediated by alpha-adrenergic stimulation causing increased systemic vascular resistance and venous return. Increased contractility and heart rate results from an increase in beta-1 receptor stimulation.

Immediate Management

  • Ensure adequate oxygenation and ventilation.

  • Administer analgesics (morphine 1–2 mg IV) or anxiolytics (midazolam 1–2 mg) to control pain and anxiety.

  • Treat acidosis if present.

  • Ensure ability to void or insert a bladder catheter to rule out bladder distention.

  • If hypertension persists, consider treatment with intravenous labetalol (5-mg IV bolus), esmolol (10-mg IV bolus or 0.1 mg/kg/min), hydralazine (5-mg IV bolus) or nicardipine (infusion starting at 5 mg/h).

Differential Diagnosis

  • Preoperative essential hypertension

  • Postoperative pain and agitation

  • Arterial hypoxemia

  • Hypercapnea

  • Hypervolemia

  • Gastric or bladder distention

  • Increased intracranial pressure

  • Emergence delirium

  • Inappropriately small blood pressure cuff or improperly calibrated arterial line

Diagnostic Studies

Initially, none indicated. Further workup should be based on clinical evidence of ruling out an underlying etiology (i.e., acidosis, hypercapnea).

Subsequent Management

  • Resume usual antihypertensive medication as soon as possible.

  • Persistent hypertension may require intermittent boluses of a beta-blocker (e.g., labetalol), continuous IV infusions (e.g., nicardipine), invasive blood pressure monitoring, and intensive care unit admission.

  • Potent vasodilators such as nitroprusside or nitroglycerine are reserved for refractory or life-threatening hypertension.

Risk Factors

  • Pre-existing essential hypertension.

  • Cessation of antihypertensive medications in the perioperative period.

  • Inadequate pain control, either during or after surgery.

  • Patients undergoing intracranial procedures.

Prevention

Antihypertensive medications should generally be continued throughout the perioperative period (ACE inhibitors, angiotensin receptor blockers, and diuretics are often held on the morning of surgery) since abrupt withdrawal may precipitate rebound hypertension. Pain should be treated with judicious use of narcotics, regional anesthetic techniques, or other forms of analgesia.

Special Considerations

Postoperative hemodynamic instability in the postanesthesia care unit (PACU) is relatively common, but postoperative systemic hypertension and tachycardia are more predictive of an adverse outcome than are hypotension and bradycardia. Although the exact etiology of hypertension cannot always be found, it is crucial to treat common postoperative causes (i.e., pain, hypoxia) rapidly, and then use pharmacotherapy to restore hemodynamic stability as quickly as possible.

Further Reading

Rodriguez MA, Kumar SK, De Caro M. Hypertensive crisis. Cardiol Rev. 2010; 18(2): 102–107.Find this resource:

Postoperative Hypotension

Definition

Decreased systemic blood pressure that may lead to tissue hypoperfusion and ischemia.

Presentation

  • Decreased systemic arterial blood pressure associated with either bradycardia or tachycardia.

  • Alteration in mental status.

  • Organ system failure may be seen after prolonged hypotension (e.g., myocardial infarction, acute renal failure, hepatic ischemia).

Pathophysiology

Systemic hypotension can be categorized as either hypovolemic (decreased preload), cardiogenic (decreased contractility), or distributive (decreased afterload). Hypotension in the PACU is usually caused by decreased preload and ongoing fluid losses (e.g., blood loss). These factors lead to decreased ventricular filling and cardiac output, sympathetic-mediated tachycardia, increased systemic vascular resistance, and venoconstriction. Neuraxial anesthetic techniques may also lead to a loss of sympathetic tone causing hypotension.

Immediate Management

  • Ensure adequate oxygenation and ventilation.

  • Resuscitate with IV fluids (crystalloid or colloids). Many patients will often respond to a moderate fluid challenge (e.g., incremental boluses of lactated Ringer’s solution or normal saline 500 cc IV).

  • Support blood pressure with phenylephrine, ephedrine, or epinephrine boluses. Consider beginning an infusion of phenylephrine (0.5–1 mcg/kg/min) or epinephrine (0.03–0.05 mcg/kg/min) in the setting of refractory hypotension.

  • Consider placing patient in Trendelenberg position (benefits controversial).

Differential Diagnosis

  • Hypovolemia

  • Hemorrhage

  • Myocardial ischemia or infarction

  • Cardiac arrhythmia

  • Cardiac tamponade

  • Tension pneumothorax

  • Pulmonary embolus

  • Anaphylaxis

  • Spinal shock

  • Sepsis

  • Drug-induced (beta-blocker, calcium channel blocker)

Diagnostic Studies

  • Chest X-ray if clinical suspicion of pneumothorax.

  • Hemaglobin and hematocrit

  • Arterial blood gas analysis to determine hematocrit and acid-base status (hematocrit may be unreliable during acute blood loss).

  • 12-Lead ECG and/or echocardiogram may be useful if a cardiogenic origin is suspected.

Subsequent Management

Continue supportive care with fluids, blood products, and vasopressors as necessary. Monitor hemodynamics (arterial, central venous pressure) to guide infusion of fluids and drugs. Determine and treat the primary etiology (i.e., myocardial ischemia or pneumothorax).

Risk Factors

  • Inadequate replacement of fluids from ongoing fluid losses, including bowel preparation, gastrointestinal losses, or significant bleeding.

  • Pre-existing hypertension and cardiac disease.

  • Neuraxial anesthetic techniques are often associated with hypotension.

Prevention

Postoperative hypotension is most often prevented by careful intraoperative volume replacement. Blood and fluid losses are often underestimated in many surgical procedures. A fluid load prior to initiating neuraxial anesthesia may help to prevent hypotension. Critically ill patients rely on increased sympathetic tone to maintain normotension and may be more sensitive to anesthetic agents. Administration of ketamine to a catecholamine-depleted patient may cause significant hypotension.

Special Considerations

  • Although relative hypovolemia is usually the reason for systemic hypotension, shock resulting from more catastrophic causes must be considered. Significant hemorrhage can develop rapidly in the PACU, often without obvious signs, and must be suspected in any patient with unexplained hypotension. Tension pneumothorax, pulmonary embolus, or pericardial tamponade may occur suddenly and may be lethal if not immediately diagnosed and treated. Anaphylaxis always should be considered as a cause of refractory hypotension.

Further Reading

Cohn SL, Harte B. Postoperative hypertension/hypotension. In: Perioperative medicine. London: Springer; 2011:421–430.Find this resource:

Postoperative Nausea and Vomiting

Definition

Significant nausea or vomiting experienced either in the PACU or after discharge is a common complication.

Presentation

  • Range of symptoms from mild nausea to retching and vomiting in the postoperative period.

  • Severe vomiting increases intra-abdominal pressure and may disrupt abdominal or inguinal suture lines.

  • Increased risk of gastric aspiration, especially when airway protective reflexes are not completely intact.

  • Increased sympathetic nervous system response, producing hypertension and tachycardia.

Pathophysiology

Postoperative nausea and vomiting (PONV) is the result of multiple of perioperative factors such as fasting, autonomic imbalance, pain, and anesthetic effects on chemotactic centers. The emetic centers are located in the lateral reticular formation of the medulla. Pharmacologic treatment aims to target specific receptors, including dopaminergic, histaminergic, cholinergic, substance P, and serotonergic.

Immediate Management

  • Increase FiO2 to ensure adequate oxygenation. Exclude potentially serious causes of PONV (i.e., impending shock, increased intracranial pressure).

  • Ensure adequate hydration with intravenous crystalloids.

  • Administer medication for rescue (i.e., ondansetron 4 mg IV). Do not repeat the same class of agents used for prophylaxis unless a prolonged benefit was previously noted (>6 hours).

Differential Diagnosis

  • Anesthetics (narcotic, inhalational agents)

  • Pain

  • Anxiety

  • Hypoxia

  • Hypotension

  • Hypoglycemia

  • Increased intracranial pressure

  • Gastric bleeding

  • Bowel obstruction

Diagnostic Studies

  • Clinical diagnosis

  • Request additional diagnostic studies as clinically indicated to rule out other more severe etiologies.

Subsequent Management

  • Continue to treat severe PONV with multimodal therapy.

  • Phenothiazines (promethazine 25 mg IV or prochlorperazine 10 mg IV) are good second-line agents.

  • Droperidol (0.625 mg IV) is highly effective but carries a black-box warning for QTc prolongation.

  • Propofol (10–20 mg) may be also be beneficial for refractory nausea.

Risk Factors

  • Female sex

  • Nonsmoking status

  • Prior history of motion sickness or PONV

  • Laparoscopic surgery

  • Strabismus and middle ear surgery

  • Opioid-based and nitrous oxide anesthetic

  • Without prophylaxis, 10%–80% of patients may experience postoperative nausea and vomiting (PONV) after a volatile anesthetic technique.

Prevention

Prophylaxis of PONV is often more effective than rescue therapy. Patients who have a higher risk of developing PONV should receive double- or triple-agent prophylaxis. Prophylaxis in patients at very low risk may not be indicated.

Special Considerations

Patients with a history of protracted PONV, despite adequate prophylactic therapy, may benefit from an alteration in anesthetic technique in addition to the usual prophylactic treatment. Regional anesthesia techniques reduce the incidence of PONV significantly. When a general anesthetic is required, limited use of narcotics, volatile anesthetics, and nitrous oxide may be possible with a total intravenous anesthetic technique.

Further Reading

Gan TJ, Diemunsch P, Hib AS, et al. Consensus guidelines for the management of postoperative nausea and vomiting. Anesth Analg. 2014; 118(1): 85–113.Find this resource:

Prolonged Neurologic Impairment after Regional Anesthesia

Definition

Prolonged neurological impairment after regional anesthesia that may include prolonged paralysis or sensory deficit after a neuraxial anesthesia technique. The deficit may be caused by the anesthetic, its contaminants, surgical procedure, positioning, or exacerbation of a pre-existing condition.

Presentation

  • Prolonged motor and sensory blockade that is denser or longer in duration than expected.

  • Sensory deficits such as numbness and paresthesias.

Pathophysiology

The most serious neurologic complication of neuraxial anesthesia is paraplegia due to ischemia, infection, or drug toxicity. Spinal cord ischemia or infarction may be due to arterial hypotension or compression of the cord by an expanding epidural hematoma or abscess. Neurotoxicity can also occur as a result of either intrathecal local anesthetics or preservatives.

Differential Diagnosis

  • Spinal/epidural hematoma

  • Spinal/epidural abscess (not acute)

  • Neuropathy due to positioning (i.e., lithotomy position)

  • Toxicity of anesthetic or additive introduced into the intrathecal space

  • Cauda equina syndrome

  • Longer than expected effect of anesthetic agents

Immediate Management

  • Neurologic examination to evaluate extent of residual effect.

  • Schedule an emergency MRI of the spinal cord to evaluate for hematoma or other pathology.

  • Request an emergency neurosurgical consultation.

Diagnostic Studies

Emergency MRI of spinal cord after an intrathecal or epidural block.

Subsequent Management

  • Emergency surgical decompression if evidence of hematoma or abscess.

  • Other than surgical decompression, further treatment of significant neurologic injury is largely supportive.

  • Most transient paresthesias resolve over about 6 months.

  • Numerous case reports show unexplained prolonged block with no known nerve damage (i.e., clonidine patch prolonging blockade).

Risk Factors for a Hematoma

  • Leukemia, blood dyscrasias, thrombocytopenia

  • Antiplatelet therapy or anticoagulation

  • Traumatic or difficult needle placement

Prevention

Although it is impossible to prevent all neurologic complications of spinal and epidural anesthetics, proper patient selection is important in limiting the potential of catastrophic complications. Avoid regional anesthesia in patients who are treated with antiplatelet agents (aspirin alone is usually acceptable) and therapeutic anticoagulation. Regional anesthesia should also be avoided in patients who have an ongoing significant infection or who are severely immunocompromised.

Special Considerations

An association between paresthesias and radiating pain on injection of local anesthetics has been suggested. Although redirecting the needle may be safe if a paresthesia develops during placement, consider stopping the procedure or relocating the needle if a paresthesia occurs during local anesthetic injection.

Further Reading

Horlocker TT. Regional anaesthesia in the patient receiving antithrombotic and antiplatelet therapy. Br J Anaesthes. 2011; 107(Suppl 1): i96–i106.Find this resource:

Respiratory Depression or Failure

Definition

Impaired ventilation or oxygenation or loss of airway patency due to a variety of mechanical, hemodynamic, and pharmacologic factors.

Presentation

  • Airway obstruction and loss of pharyngeal muscle tone

  • Decreased minute ventilation and possible hypoxia

  • Excessive sedation and somnolence

  • Residual neuromuscular blockade with muscle weakness

Pathophysiology

The residual effects of intravenous and inhalational anesthetics blunt the normal responses to both hypercarbia and hypoxemia. Benzodiazepines and narcotics act synergistically to further decrease respiratory drive, and can cause upper airway obstruction. Residual neuromuscular blockade may cause further compromise of the upper airway. Pharyngeal muscles normally contract with the diaphragm to open the airway during inspiration, but this function is often impaired in the sedated patient, causing airway obstruction and respiratory depression.

Differential Diagnosis

  • Residual anesthetics (benzodiazepines, opioids, volatile anesthetics)

  • Residual neuromuscular blockers

  • Upper airway obstruction, edema, or hematoma

  • Laryngospasm

  • Bronchospasm

  • Pulmonary edema

  • Pulmonary embolus

  • Pneumothorax

  • Obstructive sleep apnea

Immediate Management

  • Increase FiO2 to maintain adequate oxygenation.

  • Perform a jaw thrust or insert an oral, nasal, or laryngeal mask airway.

  • Intubate the trachea for respiratory failure or for significant airway obstruction that does not immediately resolve with the preceding interventions.

Diagnostic Studies

  • Chest X-ray

  • Arterial blood gas

  • Assess the patient for the presence of residual neuromuscular blockade.

Subsequent Management

  • Reverse residual opioids or benzodiazepines with incremental doses of the appropriate antagonist (i.e., naloxone 40 mcg IV or flumazenil 0.1 mg IV).

  • Reverse residual neuromuscular blocking agents.

  • Administer beta-2 agonists for treatment of bronchospasm or reactive airway disease.

  • Initiate continuous positive airway pressure (CPAP).

  • Intubate the trachea and initiate mechanical ventilation.

Risk Factors

  • Advanced age

  • Obesity

  • Chronic obstructive pulmonary disease

  • Severe asthma

  • Obstructive sleep apnea

Prevention

The synergistic effects of respiratory depressants (e.g., residual anesthetic agents, opioids) are a common cause of hypoventilation. Titrate sedatives and opioids carefully, especially in patients who are prone to postoperative respiratory failure.

Special Considerations

  • Hypoventilation and airway obstruction may be seen after discontinuing noxious stimuli (i.e., extubation or infiltration of a wound with local anesthetic solution). Slow titration of naloxone (40 mcg IV incremental doses) can reverse opioid-induced respiratory depression without affecting analgesia. An overdose of naloxone causes severe pain, tachycardia, hypertension, and possibly myocardial ischemia. Consider the possibility of a hematoma obstructing the airway in a patient who has just undergone neck surgery.

Further Reading

Murphy GS, Szokol JW, Marymont JH, Greenberg SB, Avram MJ, Vender JS. Residual neuromuscular blockade and critical respiratory events in the postanesthesia care unit. Anesthes Analges. 2008; 107(1): 130–137.Find this resource:

Severe Postoperative Pain

Definition

Postoperative pain is a complex physiological response to tissue trauma, visceral distention, and ongoing disease processes. The goal of postoperative pain management is to provide subjective comfort while inhibiting trauma-induced nociceptive signals in order to blunt autonomic and somatic reflex responses to pain.

Presentation

  • Constant pain near the surgical site, burning or aching in nature.

  • Frequent acute exacerbation of pain with normal postoperative activities such as coughing, ambulating, and dressing changes.

  • Hypertension, tachycardia, myocardial ischemia, increased oxygen consumption, and increased sympathetic tone may be present.

Pathophysiology

Nociception involves the recognition and transmission of noxious stimuli via afferent sensory nerves through the dorsal horn of the spinal cord to the contralateral cortex via the thalamus. Modulation of this signal may occur at any level of the pathway with medications such as opioids, NSAIDs, cyclooxygenase-2 inhibitors (COX-2), and local anesthetics.

Immediate Management

  • Evaluate the quality and level of pain using a visual analog scale or similar method.

  • If the pain is severe and refractory to appropriate management, re-evaluate the patient and notify the surgical team.

  • For severe postoperative pain, opioids are the mainstay of therapy.

  • Administer incremental doses of opioids (e.g., morphine 1–2 mg IV or hydromorphone 0.2 mg IV) until patient appears comfortable. A pain score of 3–4 is usually acceptable.

  • Consider administering acetaminophen 1 g IV as an adjuvant to opioids for improved analgesia.

  • Provide supplemental O2 to ensure adequate oxygenation in case opioids cause hypoventilation.

Differential Diagnosis

  • Inadequate analgesic regimen (inadequate or infrequent dosing)

  • Wound complications (infection, hematoma, nerve injury)

  • Chronic pain disorder

  • Drug-seeking behavior

Diagnostic Studies

Clinical diagnosis

Subsequent Management

  • Intrathecal or epidural administration of local anesthetics and opioids may provide superior pain relief in many abdominal or lower-extremity orthopedic procedures.

  • Nonsteroidal anti-inflammatory drugs and COX-2 inhibitors have no hemodynamic effects and do not cause respiratory depression, but decrease levels of inflammatory mediators at the site of tissue injury. Cyclooxygenase-2 agents do not affect platelet function.

  • Consider switching opioids if pain control is inadequate (i.e., morphine to hydromorphone or meperidine).

  • Consider patient-controlled analgesia (PCA) once pain is at an acceptable level and the patient is comfortable.

  • Transition pain medications to oral route as soon as feasible.

Risk Factors

  • Male sex

  • Preoperative pain

  • Prior history of poor pain management

  • Coexisting medical conditions (substance abuse, withdrawal, anxiety)

  • Opioid addiction

Prevention

Pre-emptive analgesic therapy may significantly help in controlling postoperative pain in many patients. Local and regional anesthetic techniques can be used to decrease the intensity and duration of postoperative pain.

Special Considerations

  • In addition to patient comfort, adequate control of pain may have a further benefit in improving clinical outcome by preventing myocardial ischemia or infarction, impaired wound healing, atelectasis, and thromboembolic events. Postoperative pain is usually a self-limiting condition with progressive improvement over a relatively short period of time. The severity of postoperative pain has been shown to predict chronic pain.

Further Reading

Apfelbaum JL, Ashburn MA, Connis RT, et al. Practice guidelines for acute pain management in the perioperative setting: an updated report by the American Society of Anesthesiologists Task Force on Acute Pain Management. Anesthesiology 2012; 116(2): 248.Find this resource:

Stroke

Definition

Development of a new acute focal neurological deficit due to either an ischemic or embolic event in the brain, diagnosed either immediately after emergence or early in the postoperative period.

Presentation

  • Weakness or paralysis in one or more extremities

  • Cranial nerve deficits and/or dysarthria

  • Severe confusion and altered mental status

  • Blurred vision or diplopia

Pathophysiology

A stroke may occur as the result of an occlusion of a cerebral artery and subsequent infarct of brain tissue due to profound hypotension, a thrombotic event, or an embolism (e.g., air or fat). Embolic strokes may be of cardiac origin. Hemorrhagic strokes due to aneurysm or arteriovenous malformation are also possible, but far less common in the perioperative setting.

Differential Diagnosis

  • Thrombo-embolic stroke

  • Ischemic stroke

  • Hemorrhagic stroke

  • Intracerebral hemorrhage

  • Gas embolism (through a patent foreman ovale)

  • Seizure

Immediate Management

  • Ensure adequate oxygenation and ventilation.

  • Ensure hemodynamic stability, using vasoactive drug infusions as needed to maintain an adequate systemic arterial blood pressure (systolic blood pressure of 120–140 mm Hg is adequate for most patients).

  • Request an emergency CT of brain without contrast.

  • Request an emergency neurology consultation and call a “stroke code.”

Diagnostic Studies

  • Clinical diagnosis

  • Brain CT to rule out bleeding

  • Possible MRI of brain

Subsequent Management

  • Consider inserting an arterial catheter to facilitate continuous hemodynamic monitoring.

  • Consider initiating tissue plasmogen activator (t-PA) or antiplatelet therapy if there is no surgical contraindication.

  • Request a neurosurgical or neurology consultation for possible endovascular intervention.

Risk Factors

  • Recent stroke

  • Transient ischemic attack (TIA) or amaurosis fugax

  • Cardiac, carotid, or neurosurgical procedure

  • Atrial fibrillation

  • Significant hypotension

Prevention

Preoperative screening for significant carotid disease or risk of cardiogenic embolus may be of benefit. Careful surgical technique during cardiac and carotid surgery is also crucial to prevent embolism of arterial plaques, thrombus, or air entry. Avoidance of hypotension in at-risk patients is also important to reduce the risk of stroke due to hypoperfusion and ischemia.

Special Considerations

  • Many patients exhibit slurred speech or behavior that under other circumstances might indicate a primary neurologic event while emerging from a potent volatile anesthetic. Close observation is necessary to assure that patients return to their expected level of functioning prior to discharge from the PACU.

Further Reading

Macellari F, Paciaroni M, Agnelli G, Caso V. Perioperative stroke risk in nonvascular surgery. Cerebrovasc Dis. 2012; 34(3): 175–181.Find this resource: