The pediatric postanesthesia care unit (PACU) is a unique setting in which physicians and nurses must be prepared to deal with children in various stages of anesthetic emergence after surgery or therapeutic/diagnostic procedures. Pediatric patients may arrive in the PACU fully anesthetized (e.g., after deep extubation in the operating room [OR]), at an intermediate stage of early or late emergence, or fully awake. They may arrive endotracheally intubated, with a laryngeal mask airway (LMA) in place, extubated with an oral airway, or with a natural airway.

Transport of the patient from the OR to the PACU must be performed by an experienced team that includes an expertly trained pediatric anesthesiologist. Focus should be directed at cardiopulmonary stability while maintaining a patent airway. Children may be transported in the lateral position to decrease risk of airway obstruction by the tongue and to maximize oropharyngeal volume. An oral airway placed in the OR and left for transport may also be helpful in maintaining a patent airway. Supplemental oxygen via mask or nasal cannula should be initiated prior to leaving the OR. Utilization of continuous pulse oximetry and a precordial stethoscope is recommended.

The patient should be in stable condition before leaving the OR. All monitors used for the procedure (pulse oximetry, blood pressure cuff, electrocardiograph [ECG] leads, etc.) should remain in place during transport, and the specific face mask and oral airway used during the case should always accompany each pediatric patient to the PACU. A transport pack containing laryngoscopes, endotracheal (ET) tubes, and resuscitation/intubation medications should be present for transport of potentially unstable and/or intubated patients.

The goal of the anesthesiologist is to facilitate safe and seamless transition of care to the PACU staff upon arrival in the recovery unit. The patient should not be stimulated during this time unless absolutely necessary. Monitors are left in place from the OR so as to be reconnected quickly and unobtrusively in the PACU and to minimize stimulation of the patient. Initial attention should focus on airway patency, adequacy of ventilation, oxygen saturation, heart rate (HR), blood pressure, and temperature. Supplemental oxygen should be continued if needed.

The handoff to the PACU staff by the anesthesiologist should include verification of patient identity and a standardized report detailing the patient’s age, weight, allergies to medication, past medical history, medications, operative procedure, intraoperative issues, anesthetic technique and agents, intraoperative medications, intravenous (IV) access, estimated blood loss, fluid replacement, and urine output. Specific circumstances, such as family
dynamics, the child’s emotional status, developmental delay, or language barrier, should also be discussed.

Monitoring of vital signs and patient status should be continued throughout the patient’s stay in the PACU. Vital signs should be measured and recorded at least every 15 minutes after arrival until the patient is discharged. Parents or caregivers should be allowed into the recovery room as soon as the child is settled and determined to be stable with regard to cardiovascular and respiratory status. Adequate lighting should be provided to ensure the ability to assess the child’s condition from the doorway.

The anesthesiologist on staff in the PACU should be alerted immediately if any issue arises with the patient. The following section will discuss common problems and situations pertinent to the care of infants and children in the PACU.

Hypoxemia in children may result from causes similar to those in adult patients and may be broadly categorized as hypoxemia secondary to low inspired fraction of oxygen (FiO₂), hypoventilation, cardiac shunt, ventilation-perfusion mismatch, and diffusion hypoxia. In the pediatric patient, hypoxia occurs more rapidly than in adults, secondary to increased oxygen consumption, decreased functional residual capacity (FRC), increased airway resistance, increased chest wall compliance (resulting in poor maintenance of negative intrathoracic pressure, thus leading to functional airway closure), and increased work of breathing.

Hypoventilation and airway obstruction are the most common causes of hypoxemia for pediatric patients in the PACU.

In review, minute ventilation (MV) equals tidal volume (TV) multiplied by respiratory rate (RR). A decrease in TV or RR will result in decreased MV and subsequent hypoventilation. Causes of hypoventilation include a decrease in ventilatory drive, insufficient muscle strength, or other mechanical reasons.

Volatile anesthetics, opioids, benzodiazepines, and other sedating medications decrease the ventilatory drive in the pediatric patient. This effect is more profound in infants with apnea of prematurity, former preterm infants less than 55 weeks of age, children with central nervous system (CNS) injuries, morbidly obese children, and children with obstructive sleep apnea. If opioid overdose is suspected (slow RR, large TV), naloxone 0.5 to 1 µg/kg IV, administered in incremental doses, may reverse respiratory depression without precipitating pain or anxiety. Flumazenil 0.01 to 0.02 mg/kg IV may reverse benzodiazepine-induced respiratory depression.

Muscular weakness may result from inadequate reversal of neuromuscular-blocking agents or preexistent neuromuscular disease (muscular dystrophy, myasthenia gravis, etc.). Inability to lift extremities, perform a sustained head lift, paradoxic chest wall movement, or demonstration of residual neuromuscular blockade via peripheral nerve stimulator should be managed with administration of supplemental reversal agents. In children with preexisting neuromuscular disease, supplemental ventilatory support may need to be considered.

Mechanical causes of hypoventilation include airway obstruction, splinting secondary to pain, restriction from casts or bandages, or abdominal distention due to procedural insufflation or gastric air from positive-pressure ventilation (PPV) via mask airway.

The most common and serious pediatric respiratory problem in the PACU is airway obstruction. This is a broad classification of complications that encompass upper airway obstruction, laryngospasm, and bronchospasm. Inspiratory stridor, paradoxic chest wall motion, and intercostal and tracheal retractions are common findings in upper airway obstruction and laryngospasm. Retractions, expiratory wheezing, and prolonged expiratory period may be observed in bronchospasm. Children with current upper respiratory infections (URIs) or those recovering from URIs are more prone to desaturation secondary to laryngospasm or bronchospasm, likely as a result of airway hyperreactivity and increased secretions.

Infants and children are more susceptible than adults to upper airway obstruction because of several anatomic differences (Fig. 30.1). These differences include presence of enlarged tonsils, a larger tongue in proportion to the rest of the oral cavity, a more cephalad larynx, and smaller distance between the tongue and glottis, resulting in easier obstruction.

Initial interventions should include stimulation of the child, repositioning to improve airway patency, suctioning of secretions, and, if needed, insertion of an oral or nasal airway or application of jaw thrust. Care must be taken in placing a nasal airway because resultant intranasal bleeding can further aggravate obstruction. If the airway is not recovered with these interventions, tracheal intubation should be considered.

Laryngospasm is defined as glottic closure due to reflex contraction of the laryngeal muscles and may be categorized as complete (silent chest movement with no ventilation possible) or partial (chest movement accompanied by “crowing” stridor with marginal ventilation possible). It occurs because of an anesthetic-induced depression of CNS inhibition of the glottic reflexes accompanied by stimulation at an inadequate depth of anesthesia. The incidence of laryngospasm is 17/1,000 in children up to 9 years of age and increases to 96/1,000 in children with URIs within 6 weeks of the anesthetic.

Immediate treatment involves administration of 100% FiO₂, firm jaw thrust, and application of positive airway pressure (Fig. 30.2). If laryngospasm cannot be broken with these measures, pharmacologic treatment should be
considered early. Succinylcholine 1 to 2 mg/kg IV or 2 to 4 mg/kg IM along with atropine 0.02 mg/kg IV/IM, to prevent succinylcholine-induced bradycardia, is the gold standard for treatment of complete laryngospasm. Propofol has been used to treat partial laryngospasm but should not delay administration of succinylcholine if oxygenation worsens or if bradycardia develops. Intubation may be required to reoxygenate the child or if laryngospasm recurs after treatment. Post-laryngospasm, children should be observed for 2 to 3 hours to monitor for potential sequelae (e.g., negative-pressure pulmonary edema).

Postintubation croup or subglottic edema are complications that can arise in the PACU. These conditions are more common in children with a history of croup and previous prolonged intubation and are thought to develop secondary to edema from tight-fitting ET tubes, traumatic intubation, large volume shifts, and long surgical procedures. Treatment includes humidified
oxygen and nebulized racemic epinephrine (0.5 mL in 3 mL normal saline over 10 minutes). Dexamethasone 0.5 mg/kg IV should be administered if it was not already given intraoperatively. Heliox (70%:30% helium/oxygen) may offer improved ventilation because of decreased airway resistance. The definitive treatment for ongoing severe respiratory compromise secondary to subglottic edema is tracheal intubation with a smaller ET tube than what was originally used intraoperatively.

Lower airway diseases such as asthma, secondhand cigarette smoke exposure, and airway manipulation are associated with a higher risk of perioperative bronchospasm in the pediatric patient. First-line treatment in the PACU includes administration of 100% FiO₂, short-acting inhaled β-agonists (e.g., albuterol nebulizer 0.05 to 0.15 mg/kg/dose in infants and 2.5 mg/dose for older children), and inhaled anticholinergic agents. Epinephrine 5 to 10 µg/kg IV bolus followed by 0.1 to 0.5 µg/kg/minute continuous infusion may be initiated in severe bronchospasm. Methylprednisolone 0.5 to 1 mg/kg IV or hydrocortisone 2 to 4 mg/kg IV should be administered but will not help in the acute period. IV magnesium 50 mg/kg and/or reinduction of anesthesia with sevoflurane should be considered in severe refractory bronchospasm. Emergent intubation may be required in children at high risk for respiratory arrest.

As in the adult patient, the pediatric patient may also exhibit cardiac rhythm disturbances in the postoperative period. Most concerning in the pediatric PACU is bradycardia, which is significant because of the resultant decrease in cardiac output (CO). In review, CO is equal to HR multiplied by stroke volume (SV). As opposed to adults, small infants and children are unable to compensate for a decrease in CO by increasing SV because of their relatively stiff ventricles and diminished contractile ability. CO is therefore dependent on maintenance of an adequate HR (Table 30.1).

The most common cause of bradycardia in infants and children is hypoxemia until proven otherwise. Other secondary causes of bradycardia include medication effect, vagal stimulation, high neuraxial blockade, and increased intracranial pressure. Treatment should include immediate administration of 100% FiO₂, ensuring a patent airway, and assisting ventilation if necessary, followed by identifying and correcting the underlying problem. Atropine 0.02 mg/kg IV should be administered if oxygen supplementation does not correct the bradycardia. Epinephrine 2 to 10 µg/kg IV may also be needed. If there is no response, cardiopulmonary resuscitation (CPR), including chest
compressions for HR <60 beats/minute, should be initiated and is outlined in the following section.

Tachycardia in the pediatric patient may signify pain, anxiety, distended bladder, medication effect, or emergence delirium (ED), or may be an indicator of a more severe underlying process such as hypoxemia, hypercarbia, hypovolemia, developing sepsis, or previously unrecognized congenital heart disease or conduction abnormality.

Premature atrial or ventricular beats are uncommon in children and may warrant further investigation and cardiology consultation.

The normal blood pressure range for the pediatric patient depends on the age of the patient (Table 30.2).

The most common cause of hypotension in children is hypovolemia, usually as a result of inadequate intraoperative fluid resuscitation or ongoing blood loss. Other common signs of hypovolemia in children include dry mucus membranes, poor skin turgor, and urine output <0.5 mL/kg/hour. Hypovolemia should be initially treated with an isotonic crystalloid bolus of 10 to 20 mL/kg. Packed red blood cells (PRBCs) 4 mL/kg may be administered if anemia is suspected.

Other causes of hypotension in the pediatric patient may be categorized similarly to the adult patient as decreased preload (PPV, pneumothorax, cardiac tamponade, inferior vena cava compression), decreased afterload (vasodilation, medication effect, sepsis, sympathetic blockade from regional anesthesia), or pump failure (dysrhythmias, decreased inotropy, medication effect, sepsis, congestive heart failure, or hypothermia). Rare causes include anaphylaxis, transfusion reaction, severe liver failure, or adrenal insufficiency. Evaluation should include a full survey of infusion lines to assess for kinking or infiltration.

Hypertension is less common in the pediatric patient and is often caused by incorrect blood pressure measurement or pain. Other causes include hypervolemia, distended bladder, hypoxemia, hypercarbia, ED, increased intracranial pressure, medication effect, preexisting hypertension, or, rarely, malignant hyperthermia, undiagnosed coarctation, or pheochromocytoma. Treatment with antihypertensive agents is rarely required.