Handbook of Clinical Anesthesia

Chapter 55

Post Anesthesia Recovery

Each patient recovering from an anesthetic has circumstances that require an individualized problem-oriented approach (Fowler MA, Spiess BD: Postoperative recovery. In Clinical Anesthesia. Edited by Barash PG, Cullen BF, Stoelting RK, Cahalan MK, Stock MC. Philadelphia: Lippincott Williams & Wilkins, 2009, pp 1419–1443). Dissemination of anesthesia services beyond the perisurgical arena has brought changes and greater demands on recovery units.

  1. Value and Economics of the Postanesthesia Care Unit (PACU)

PACU resources are efficiently utilized by having trained staff that routinely care for postsurgical patients, thereby recognizing and preventing complications and by having physicians institute appropriate and timely therapies. Routine testing and therapies may unnecessarily add to staffing resources required per patient without widespread demonstrated benefit to patient care.

  1. Communication is perhaps the least expensive tool in medicine and the one that is most universally proven to be involved in human error events.
  2. Having patients bypass the PACU creates a savings opportunity only if paid nursing hours are reduced or if more surgical cases are covered with the same hours.
  3. Levels of Postoperative and Postanesthesia Care
  4. Using a less intensive postanesthesia setting for selected patients may reduce costs for a surgical procedure and allow the facility to divert scarce PACU resources to patients with greater needs.

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  1. Creation of separate PACUs for inpatients, ambulatory patients, or offsite patients is one possible way to streamline PACU care for appropriately triaged patients. Phase I recovery would be reserved for more intense recovery and would require more one-on-one care for patients. Phase II recovery would be less intensive and would be appropriate for patients after less invasive procedures requiring less nursing attention while recovering.

III. Postanesthetic Triage

Postanesthetic Triage should be based on clinical condition, length and type of procedure and anesthetic, and the potential for complications that require intervention.

  1. An individual patient undergoing a specific procedure or anesthetic should receive the same appropriate level of postoperative care whether the procedure is performed in a hospital operating room, ambulatory surgical center, endoscopy room, invasive radiology suite, or outpatient office.
  2. After superficial procedures using local infiltration, minor blocks, or sedation, patients can almost always recover with less intensive monitoring and coverage (bypass phase I recovery to phase II).
  3. Safety in the Postanesthesia Care Unit
  4. The PACU medical director must ensure that the PACU environment is as safe as possible for both patients and staff.
  5. Observance of procedures for hand washing, sterility, and infection control should be strictly enforced.
  6. Compulsive documentation and clear delineation of responsibility protect staff against unnecessary medicolegal exposure.
  7. Admission to the Postanesthesia Care Unit
  8. Every patient admitted to a PACU should have their heart rate, rhythm, systemic blood pressure, airway patency, peripheral oxygen saturation, ventilatory rate and character, and level of pain recorded and

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periodically monitored. Assessment with periodic recording every 5 minutes for the first 15 minutes and every 15 minutes thereafter is a minimum.

  1. Documenting temperature, level of consciousness, mental status, neuromuscular function, hydration status, and degree of nausea on admission and discharge and more frequently if appropriate are also minimum standards of care.
  2. Every patient should be continuously monitored with a pulse oximeter and at least a single-lead electrocardiogram. Capnography is necessary for patients receiving mechanical ventilation and those at risk for compromised ventilatory function.
  3. Anesthesiology personnel should manage the patient until a PACU nurse secures admission vital signs and attaches appropriate monitors. Care should be transferred with a complete report to the nursing staff (Table 55-1).
  4. Postoperative Pain Management

Relief of surgical pain with minimal side effects is a major goal during PACU care and is a top priority for patients.

  1. In addition to improving comfort, analgesia reduces sympathetic nervous system response, avoiding hypertension, tachycardia, and dysrhythmias. In hypovolemic patients, the sympathetic nervous system activity may well mask relative hypovolemia.
  2. Administration of analgesics may precipitate hypotension in an apparently stable patient, especially if direct or histamine-induced vasodilation occurs. Before giving analgesics that might precipitate or accentuate hypotension, it is important to carefully assess a tachycardic patient with low or normal blood pressure who complains of pain.
  3. The best measure of analgesia is the patient's perception. Heart rate, respiratory rate and depth, sweating, and nausea and vomiting may be signs of pain, but their absence or presence is not in itself reliable as a measure of the presence of pain.
  4. Surgical pain can be effectively treated with intravenous (IV) opioids as part of a planned analgesic continuum that begins before the induction of surgical anesthesia and continues throughout the postoperative course.

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Table 55-1 Components of a Postanesthesia Care Unit Admission Report

Preoperative History and Procedures Medication allergies or reactions
Pertinent earlier surgical procedures
Underlying medical illness
Chronic medications
Acute problems (ischemia, acid–base status, dehydration)
Premedications (antibiotics and time given, beta-adrenergic blockers, antiemetics)
Preoperative pain control (nerve blocks, adjunct medications, narcotics)
Preoperative pain assessment (chronic and acute pain scores)
NPO status
Intraoperative Factors
Surgical procedure
Type of anesthetic
Type and difficulty of airway management
Relaxant and reversal status
Time and amount of opioids administered
Type and amount of IV fluids administered
Estimated blood loss
Urine output
Unexpected surgical or anesthetic events
Intraoperative vital sign ranges
Intraoperative laboratory findings
Drugs given (steroids, diuretics, antibiotics, vasoactive medications, antiemetics)
Assessment and Report of Current Status
Airway patency
Ventilatory adequacy
Level of consciousness
Level of pain
Heart rate and heart rhythm
Endotracheal tube position
Systemic pressure
Intravascular volume status
Function of invasive monitors
Size and location of intravenous catheters
Anesthetic equipment (epidural catheters, peripheral nerve catheters)
Overall impression
Postoperative Instructions
Expected airway and ventilatory status
Acceptable vital sign ranges
Acceptable urine output and blood loss
Surgical instructions (positioning, wound care)
Anticipated cardiovascular problems
Orders for therapeutic interventions
Diagnostic tests to be secured
Therapeutic goals and end points before discharge
Location of responsible physician

IV = intravenous.

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  1. Short-acting opioids are useful to expedite discharge and minimize nausea in ambulatory settings, although the duration of analgesia can be a problem. Other analgesic modalities provide pain relief in and beyond the PACU.
  2. IV opioid loading in the PACU is important for smooth transition to IV patient-controlled analgesia.
  3. Injection of opioids into the epidural or subarachnoid space during anesthesia or in the PACU yields prolonged postoperative analgesia in selected patients. Nausea and pruritus are troubling side effects, and immediate or delayed ventilatory depression may occur related to vascular uptake and cephalad spread in cerebrospinal fluid. Nausea should resolve with antiemetics, and pruritus and ventilatory depression often respond to naloxone infusion.
  4. Placement of long-acting regional analgesic blocks reduces pain, controls sympathetic nervous system activity, and often improves ventilation.
  5. After shoulder procedures, interscalene block yields almost complete pain relief with only moderate inconvenience from motor impairment. Paralysis of the ipsilateral diaphragm may impair postoperative ventilation in patients with marginal reserve, although the impact is small in most patients.
  6. Suprascapular nerve block might be an alternative to avoid this potentially serious side effect.
  7. Caudal analgesia is effective in children after inguinal or genital procedures. Infiltration of local anesthetic into joints, soft tissues, or incisions decreases the intensity of pain.

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VII. Discharge Criteria

(Table 55-2)

Table 55-2 The Two Most Commonly Used Postanesthesia Care Unit Discharge Criteria Systems

Modified Aldrete Scoring System

Postanesthetic Discharge Scoring System

Respiration

Vital Signs

2 = Able to take deep breath and cough

2 = BP and pulse within 20% of preoperative baseline

1 = Dyspnea or shallow breathing

1 = BP and pulse within 20%–40% of preoperative baseline

0 = Apnea

0 = BP and pulse >40% of preoperative baseline

O2 Saturation

Activity

2 = Maintains Spo2 >92% on room air

2 = Steady gait, no dizziness, or meets preoperative level

1 = Needs O2 inhalation to maintain O2 saturation >90%

1 = Requires assistance

0 = O2 saturation <90% even with supplemental O2

0 = Unable to ambulate

Consciousness

Nausea and Vomiting

2 = Fully awake

2 = Minimal; treated with PO medication

1 = Arousable on calling

1 = Moderate; treated with parenteral medication

0 = Not responding

0 = Severe; continues despite treatment

Circulation

Pain

2 = BP ± 20 mm Hg preoperative

Controlled with oral analgesics and acceptable to patient:

1 = BP ± 20–50 mm Hg preoperative

2 = Yes

0 = BP ± 50 mm Hg pre

1 = No

Activity

Surgical Bleeding

2 = Able to move four extremities voluntarily or on command

2 = Minimal or no dressing changes

1 = Able to move two extremities

1 = Moderate or ≤2 dressing changes required

0 = Unable to move extremities

0 = Severe or >3 dressing changes required

Score ≥ 9 for discharge

Score ≥ 9 for discharge

BP = blood pressure; PO = per os.

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VIII. Standards for Postanesthesia Care

The American Society of Anesthesiologists (ASA) House of Delegates approved Standards for Postanesthesia Care on October 12, 1988, and last amended them on October 27, 2004.

  1. Cardiovascular Complications
  2. The first sign of myocardial ischemia may well be hypotension, and the most common sign of myocardial ischemia is tachycardia. Early intervention with nitrates, opioids, beta-blockers, and even anticoagulants may save lives. Cardiology should be involved to gain immediate and timely access to the cardiac catheterization laboratory or for anxiolytic drug therapy.
  3. Congestive heart failure is epidemic in our ever-aging population. Echocardiography allows rapid viewing of myocardial contractility, regional wall motion, volume status, and valvular dysfunction.
  4. Postoperative Pulmonary Dysfunction
  5. Inadequate postoperative ventilationshould be suspected when (1) respiratory acidemia occurs coincident with tachypnea, anxiety, dyspnea, labored ventilation, or increased sympathetic nervous system activity; (2) hypercarbia reduces the arterial pH below 7.30; or (3) PaCO2 progressively increases with a progressive decrease in arterial pH.
  6. Inadequate Respiratory Drive
  7. During early recovery from anesthesia, residual effects of IV and inhalational anesthetics blunt the ventilatory responses to both hypercarbia and hypoxemia. Sedatives augment depression from opioids or anesthetics and reduce the conscious desire to ventilate.
  8. Hypoventilation and hypercarbia may evolve insidiously during transfer and admission to the PACU. Although the effects of intraoperative medications are usually waning, the peak depressant effect of IV opioid given just before transfer occurs in the PACU.
  9. Patients may communicate lucidly and even complain of pain while experiencing significant opioid-induced

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hypoventilation. A balance must be struck between an acceptable level of postoperative ventilatory depression and a tolerable level of pain or agitation.

  1. Patients with abnormal CO2/pH responses from morbid obesity, chronic airway obstruction, or sleep apnea are more sensitive to respiratory depressants.
  2. The abrupt diminution of a noxious stimulus (tracheal extubation, placement of a postoperative block) may promote hypoventilation or airway obstruction by altering the balance between arousal from discomfort and depression from medication.
  3. Increased airway resistanceincreases the work of breathing and CO2 production.
  4. In postoperative patients, increased upper airway resistance is caused by obstruction in the pharynx, larynx (laryngospasm, laryngeal edema), or large airways (extrinsic compression from hematoma).
  5. Weakness from residual neuromuscular relaxation may contribute but is seldom the primary cause of airway compromise.
  6. Laryngospasm can usually be overcome by providing gentle positive pressure (10–20 mm Hg continuous) in the oropharynx by mask with 100% oxygen. Prolonged laryngospasm is relieved with a small dose of succinylcholine (0.1 mg/kg) or deepening sedation with propofol.
  7. Decreased complianceaccentuates the work of breathing. Obesity affects pulmonary compliance, especially when adipose tissue compresses the thoracic cage or increases intra-abdominal pressure in the supine or lateral positions. Allowing patients to recover in a semi-sitting (semi-Fowler's) position reduces the work of breathing.
  8. Neuromuscular and Skeletal Problems
  9. Postoperative airway obstruction and hypoventilation are accentuated by incomplete reversal of neuromuscular relaxation. Residual paralysis compromises airway patency, the ability to overcome airway resistance, airway protection, and the ability to clear secretions.
  10. PACU staff should be aware of patients who have received nondepolarizing muscle relaxants but have not received reversal agents because these patients often exhibit low levels of residual paralysis, and in the presence of severe kyphosis or scoliosis may cause postoperative ventilatory insufficiency.

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  1. Simple tests help assess the patient's mechanical ability to ventilate. The ability to sustain head elevation in a supine position, a forced vital capacity of 10 to 12 mL/kg, an inspiratory pressure that is lower than -25 cm H2O, and tactile train-of-four assessment imply that the strength of ventilatory muscles is adequate to sustain ventilation and to take a large enough breath to cough. However, none of these clinical end points reliably predicts the recovery of airway protective reflexes, and failure on these tests does not necessarily indicate the need for assisted ventilation.
  2. Inadequate Postoperative Oxygenation
  3. Systemic arterial partial pressure of oxygen (PaO2) is the best indicator of pulmonary oxygen transfer from alveolar gas to pulmonary capillary blood.
  4. Arterial hemoglobin saturation monitored by pulse oximetry yields less information on alveolar–arterial gradients and is not helpful in assessing the impact of hemoglobin dissociation curve shifts or carboxyhemoglobin.
  5. In postoperative patients, the acceptable lower limit for PaO2varies with individual patient characteristics. Maintaining PaO2 between 80 and 100 mm Hg (saturation, 93% to 97%) ensures adequate oxygen availability. Little benefit is derived from elevating PaO2 above 110 mm Hg because hemoglobin is saturated, and the amount of additional oxygen dissolved in plasma is negligible.
  6. During mechanical ventilation, a PaO2above 80 mm Hg with 0.4 fraction of inspired oxygen (FIO2) and 5 cm H2O positive end-expiratory pressure (PEEP), continuous positive airway pressure (CPAP), or a spontaneous breathing trial usually predicts sustained adequate oxygenation after tracheal extubation.
  7. Obstructive sleep apnea(OSA) is a syndrome in which patients exhibit a period of partial or complete obstruction of the upper airway (Table 55-3).
  8. In May 2003, the ASA Task Force on Perioperative Management of Patients with Obstructive Sleep Apnea issued guidelines for patients with OSA.
  9. The perioperative management of a patient with OSA must start preoperatively with a well-planned anesthetic, taking into account the type, location, and recovery of surgery.

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Table 55-3 Manifestations of Obstructive Sleep Apnea

Daytime hypersomnolence
Decreased ability to concentrate
Increased irritability
Episodic oxygen desaturation
Hypercarbia

  1. Postoperative management concerns include analgesia, oxygenation, patient positioning, and monitoring.
  2. Regional anesthesia with minimal sedation (rather than increased use of opioids) is best for recovery.
  3. Patients who use CPAP or noninvasive positive-pressure ventilation should continue to use these therapies.
  4. Pulse oximetry should be used until the patient's oxygen saturation remains above 90% on room air while sleeping.
  5. Anemia
  6. Patients with vascular disease are at increased risk of vital organ ischemia as hematocrit decreases.
  7. It is now well accepted that patients who are stable, not bleeding, and euvolemic can tolerate a hemoglobin level of 6.0 g/dL. Transfusion may be of some benefit between 6 and 8 g/dL but is rarely of use above 10 g/dL.
  8. Supplemental Oxygen
  9. Clinical observation and assessment of cognitive function do not accurately screen for hypoxemia, so monitoring with oximetry is essential throughout the PACU admission.
  10. One cannot predict which patients will develop hypoxemia or when hypoxemia will occur. However, patients with lung disease or obesity, those recovering from thoracic or upper abdominal procedures, and those with preoperative hypoxemia are at increased risk.
  11. Supplemental oxygen does not address the underlying causes of hypoxemia in postoperative patients, its use does not guarantee that hypoxemia will not occur, and it is likely to mask hypoventilation.

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  1. Perioperative Aspiration.During anesthesia, depression of airway reflexes places patients at risk for intraoperative pulmonary aspiration that may manifest in the PACU or for aspiration during recovery.
  2. Aspiration of acidic gastric contents during vomiting or regurgitation causes chemical pneumonitis initially characterized by diffuse bronchospasm, hypoxemia, and atelectasis.
  3. The incidence of serious aspiration is relatively low in PACU patients, but the risk is still significant. Hypotension, hypoxemia, or acidemia cause both emesis and obtundation, increasing the risk of aspiration.
  4. Suspicion that aspiration has occurred mandates 24 to 48 hours of monitoring for development of aspiration pneumonitis. If the likelihood of aspiration is small in an ambulatory patient, outpatient follow-up can be done, assuming hypoxemia, cough, wheezing, and radiographic abnormalities do not appear within 4 to 6 hours. The patient should receive explicit instructions to contact a medical facility at the first appearance of malaise, fever, cough, chest pain, or other symptoms of pneumonitis. If likelihood of aspiration is high, the patient should be admitted to the hospital.
  5. Postoperative Renal Complications
  6. The ability to voidshould be assessed because opioids and autonomic side effects of regional anesthesia interfere with sphincter relaxation and promote urine retention. An ultrasonic bladder scan helps assess bladder volume before discharge.
  7. Oliguria(≤0.5 mL/kg/hr) occurs frequently during recovery and usually reflects an appropriate renal response to hypovolemia. The stress response of surgery also increases antidiuretic hormone (ADH), which may lead to decreased urine output. Decreased urine output may also indicate abnormal renal function. Systemic blood pressure must be adequate for renal perfusion based on preoperative pressures.
  8. After urine is sent for electrolyte and osmolarity determinations, a 300- to 500-mL IV crystalloid bolus helps assess whether oliguria represents a renal response to hypovolemia. If output does not

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improve, a larger bolus or a diagnostic trial of furosemide (5 mg IV) should be considered.

  1. The persistence of oliguria despite hydration, adequate perfusion pressure, and a furosemide challenge increases the likelihood of acute tubular necrosis, ureteral obstruction, renal artery or vein occlusion, and inappropriate ADH secretion. Consultation with a nephrologist is prudent.

XII. Metabolic Complications

  1. Postoperative Acid–Base Disorders.Categorization of postoperative acid–base abnormalities into primary and compensatory disorders is difficult because rapidly changing pathophysiology can often generate multiple primary disorders.
  2. Respiratory acidemiais frequently encountered in PACU patients because anesthetics, opioids, and sedatives promote hypoventilation by depressing central nervous system (CNS) sensitivity to pH and PaCO2.
  3. Symptoms of respiratory acidemia include agitation, confusion, and tachypnea. Sympathetic nervous system response to low pH causes hypertension, tachycardia, and dysrhythmias.
  4. Treatment consists of correcting the imbalance between CO2production and alveolar ventilation. Increasing the level of consciousness by the judicious reversal of opioids or benzodiazepines improves ventilatory drive. It is important to ensure that the patient does not have increased airway resistance or residual neuromuscular blockade. If spontaneous ventilation cannot maintain CO2 excretion, tracheal intubation and mechanical ventilation are necessary.
  5. Metabolic Acidemia(Table 55-4)
  6. Large volumes of saline infusions during surgery can generate a mild hyperchloremic, metabolic acidemia, but use of lactated Ringer's solution avoids this problem.
  7. Postoperative metabolic acidemia almost always represents lactic acidemia secondary to insufficient delivery or utilization of oxygen in peripheral tissues. Peripheral hypoperfusion is often caused by low cardiac output (hypovolemia, cardiac failure, dysrhythmia) or peripheral vasodilation (sepsis, catecholamine depletion, sympathectomy).

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Table 55-4 Causes of Acidemia

Normal Anion Gap Acidosis
GI loss of bicarbonate
   Diarrhea
   Urinary diversion
   GI fistulas or drains
Renal loss of bicarbonate
   Renal tubular acidosis
   Renal insufficiency
   Recovery phase of ketoacidosis
Increased Anion Gap Acidosis
Ketoacidosis (diabetic, alcoholic, severe cachexia)
Lactic acidosis (seizures, neuroleptic malignant syndrome, MH, severe asthma, pheochromocytoma, cardiogenic shock, hypovolemia, severe anemia, regional ischemia, sepsis, hypoglycemia)
Respiratory Acidosis

GI = gastrointestinal; MH = malignant hyperthermia.

  1. A spontaneously breathing patient will increase minute ventilation in response to metabolic acidemia and quickly generate a respiratory alkalosis to compensate for metabolic acidemia (general anesthetics and analgesics suppress this ventilatory response).
  2. Respiratory Alkalemia
  3. Pain or anxiety during emergence causes hyperventilation and acute respiratory alkalemia. Excessive mechanical ventilation also generates respiratory alkalemia, especially if hypothermia or paralysis has decreased CO2production.
  4. Acute respiratory alkalemia may lead to confusion, dizziness, atrial dysrhythmias, and abnormal cardiac conduction. Alkalemia decreases cerebral blood flow. If the alkalemia is severe, reduced serum ionized calcium concentration precipitates muscle fasciculation or hypocalcemic tetany.
  5. Metabolic compensation for acute respiratory alkalemia is limited because time constants for bicarbonate excretion are large.
  6. Treatment necessitates reducing alveolar ventilation, usually by administering analgesics and sedatives for pain and anxiety. Rebreathing of CO2has little application in the PACU.

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  1. Metabolic alkalemiais rare in PACU patients unless vomiting, gastric suctioning, dehydration, alkaline ingestion, or potassium-wasting diuretics have caused an alkalemia that existed before surgery. Respiratory compensation through retention of CO2 is rapid but limited because hypoventilation eventually causes hypoxemia. Hydration and correction of hypochloremia and hypokalemia allow the kidney to excrete excess bicarbonate.

XIII. Glucose Disorders and Control

Tight glucose control has been recommended to reduce morbidity in a variety of postsurgical patients. The potential for hypoglycemia and coma should not be discounted.

  1. Hyperglycemia.Glucose infusions and stress responses commonly elevate serum glucose levels after surgery. For most patients, glucose should not be included in maintenance IV solutions during anesthesia.
  2. Moderate postoperative hyperglycemia (150–250 mg/dL) resolves spontaneously and has little adverse effect in nondiabetic patients.
  3. Higher glucose levels cause glycosuria with osmotic diuresis and interfere with serum electrolyte determinations. Severe hyperglycemia increases serum osmolality to a point that cerebral disequilibrium and hyperosmolar coma occur.
  4. Hypoglycemiain the PACU is rare and easily treated with IV 50% dextrose followed by glucose infusion. Either sedation or excessive sympathetic nervous system activity masks the signs and symptoms of hypoglycemia after anesthesia. Diabetic patients and especially patients who have received insulin therapy intraoperatively must have serum glucose levels measured to avoid the serious problems related to hypoglycemia.

XIV. Electrolyte Disorders

  1. Hyponatremia.Postoperative hyponatremia occurs if free water is infused IV during surgery or if sodium-free irrigating solution is absorbed during transurethral prostatic resection or hysteroscopy.
  2. Symptoms of moderate hyponatremia include agitation, disorientation, visual disturbances, and

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nausea. Severe hyponatremia causes unconsciousness, impaired airway reflexes, and CNS irritability that progress to grand mal seizures.

  1. Therapy includes IV normal saline and IV furosemide to promote free water excretion.
  2. Hypokalemia
  3. A potassium deficit caused by chronic diuretic therapy, nasogastric suctioning, or vomiting often underlies hypokalemia.
  4. Potassium is an intracellular ion, and a plasma potassium deficit is indicative of a far greater intracellular deficit. The intracellular to extracellular ratio may well be important, and rapid changes may contribute to as many dysrhythmias as can mild hypokalemia alone.
  5. Hyperkalemia
  6. A high serum potassium level raises the suspicion of spurious hyperkalemia from a hemolyzed specimen

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or from sampling near an IV catheter containing potassium or banked blood. Acute acidemia exacerbates hyperkalemia.

Table 55-5 Miscellaneous Complications in the Postanesthesia Care Unit

Incidental trauma (should be documented and the physician notified)
Ocular injuries and visual changes (corneal abrasion caused by dry or inadvertent eye contact)
Hearing impairment (after dural puncture for spinal anesthesia)
Oral, pharyngeal, and laryngeal injuries (dental injury, sore throat, hoarseness)
Nerve injuries (malpositioning, compression, postspinal anesthesia, idiopathic)
Soft tissue and joint injuries
Skeletal muscle pain (succinylcholine, immobility)
Hypothermia and shivering (complicates and prolongs care in the PACU)
Persistent sedation (approximately 90% of patients regain consciousness within 15 minutes of admission to the PACU; unconsciousness persisting for a greater period is considered prolonged, and pharmacologic reversal should be considered; if the condition is persistent, a neurologist should be consulted)
Altered mental status (combativeness, disorientation)
Emergence reactions (evaluate oxygenation and ventilation)
Delirium and cognitive decline (especially elderly patients)

PACU = postanesthesia care unit.

  1. Treatment with IV insulin and glucose acutely lowers potassium, and treatment with IV calcium counters myocardial effects.
  2. Miscellaneous Complications

(Table 55-5)

Editors: Barash, Paul G.; Cullen, Bruce F.; Stoelting, Robert K.; Cahalan, Michael K.; Stock, M. Christine

Title: Handbook of Clinical Anesthesia, 6th Edition

Copyright ©2009 Lippincott Williams & Wilkins

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