In modern anaesthetic practice, the patient is monitored and supervised closely and continuously during induction and throughout the operative procedure. However, many problems associated with anaesthesia and surgery may occur in the immediate postoperative period, and it is essential that supervision by adequately trained and experienced personnel is continued during the recovery period. In addition, some major and minor complications of anaesthesia and surgery may occur at any time in the first few days after operation.
Most hospitals have a recovery ward (or postanaesthesia care unit, PACU) within, or in close proximity to, the operating theatre suite (see Ch 20). The Association of Anaesthetists of Great Britain and Ireland (AAGBI) recommends that fully staffed recovery facilities must be available at all times in hospitals with an emergency surgical service. Some locations where anaesthesia is provided (e.g. the X-ray department) may not have a recovery ward. This section describes common problems which occur in the immediate postoperative period and refers specifically to their management in a recovery ward; however, the same principles are applicable to recovery in other locations.
The recovery period starts as soon as the patient leaves the operating table and the direct supervision of the anaesthetist. All the complications described below may occur at any time, including the period of transfer from operating theatre to recovery ward; in some operating theatre suites, the transfer to the recovery ward may last for several minutes, and it is essential that the standard of observation does not diminish during the journey. The patient must be supervised and monitored closely at all times.
Consciousness may not return for several minutes after the end of general anaesthesia and may be impaired for a longer period of time. During this period, a patent airway must be maintained. There is a risk of aspiration into the lungs of any material, e.g. gastric content or blood, which is present in the pharynx. Consciousness may also be depressed in patients who have received sedation to facilitate endoscopy or regional anaesthesia.
Peripheral vascular resistance and cardiac output may be reduced because of residual effects of anaesthetic drugs in the absence of surgical stimulation. Hypovolaemia may be present because of inadequate fluid replacement during surgery, continued bleeding postoperatively or expansion of capacitance of the vascular system as a result of rewarming. Cardiac output may also be reduced as a result of arrhythmias or pre-existing disease. Hypertension may occur as a result of increased sympathoadrenal activity after restoration of consciousness, especially if analgesia is inadequate.
Hypoventilation occurs commonly, usually as a result of residual effects of anaesthetic drugs or incomplete antagonism of neuromuscular blocking drugs. Hypoxaemia may result from hypoventilation, ventilation/perfusion imbalance or increased oxygen consumption produced by restlessness or shivering.
The recovery ward should be staffed by trained and experienced nurses. One nurse must remain with each patient at all times until consciousness and airway reflexes return. The responsibility for the patient’s welfare remains with the anaesthetist. Ideally, an anaesthetist should be available immediately to treat complications detected by the nursing staff in the recovery ward.
The patient is nursed in a bed if available or if a prolonged stay is anticipated, but sometimes on a trolley (Fig. 40.1). All beds and trolleys must have the facility to be tipped head-down. Suction apparatus, including catheters, an oxygen supply with appropriate face mask, a self-inflating resuscitation bag and anaesthetic mask, a pulse oximeter and an automated non-invasive blood pressure monitor must be available for each patient. In addition, there should be a complete range of resuscitation equipment within the recovery area; this includes an anaesthetic machine, a range of laryngoscopes, tracheal tubes, bougies, intravenous (i.v.) cannulae, fluids, emergency drugs, electrocardiogram (ECG) monitor and defibrillator. Facilities for emergency airway management including surgical airways should also be available (see Ch 22).
FIGURE 40.1 Part of a recovery ward. Many patients are nursed on a trolley, but a bed is used if available, and particularly for those who have undergone major surgery and those who need to stay for several hours.
On arrival in the recovery ward, the anaesthetist should give the nurse full details of pre-existing medical problems, surgical procedure, anaesthetic technique, drugs, regional blocks, fluids, blood loss/replacement, any untoward events and any anticipated problems during recovery. All patients should be monitored by measurement of pulse rate, arterial pressure, arterial oxygen saturation and respiratory rate, and by assessment of level of consciousness, peripheral circulation and adequacy of ventilation. Depending on the nature of work undertaken in the theatre suite, a proportion of bed stations should have the facility for monitoring ECG, systemic and pulmonary arterial pressures and central venous pressure (CVP) continuously; this may be required in high-risk patients or those who have undergone major surgery. Capnography should be available for use in patients who require tracheal intubation. At least one mechanical ventilator should be available, although more may be required depending on the workload. Urine output should be measured routinely in patients who have undergone major surgery. Wounds and surgical drains should be inspected regularly for signs of bleeding.
It is important that the handover from anaesthetist to recovery nurse is systematic and undertaken in an unhurried way when both anaesthetist and nurse can concentrate on the handover. In general this will be after essential monitoring, such as pulse oximetry and blood pressure, has been reapplied and checked. The anaesthetist should not leave the patient until he or she is satisfied that there are no immediate problems, particularly with regard to the airway, and respiratory and cardiovascular systems.
A record should be made of pulse rate, arterial pressure and arterial oxygen saturation, respiratory rate, level of consciousness, pain score, sensory level (if regional anaesthesia has been used), and any other relevant information (such as complications, and drug and fluid administration) obtained while the patient is in the recovery area. In most units, recordings of physiological measurements are made every 5 min until consciousness has returned and then at intervals of 10–15 min.
The cardiovascular system is stable with no unexplained cardiac irregularity or persistent bleeding. Consecutive measurements of pulse rate and arterial pressure should approximate to the patient’s normal preoperative values or be at an acceptable level commensurate with the planned postoperative care. Peripheral perfusion should be adequate.
High-risk patients or those who have undergone major surgery may stay in the recovery ward for up to 24 h. If this is not feasible, or if instability persists for longer than 24 h, the patient should be transferred to a high-dependency or intensive care unit. The level of monitoring and care during transfer should be the same as that in the recovery room.
Although the recovery room nurse undertakes the direct care of the patient, the responsibility for the patient remains with the anaesthetist. Patients must only be discharged to the ward with the anaesthetist’s consent.
The remainder of this chapter is devoted to the diagnosis and management of common problems which occur in the postoperative period. Some of these occur most frequently in the immediate recovery period, while others may occur at any time during the patient’s convalescence from surgery. Some surgical procedures are associated with specific complications.
The timing of drug use. Delayed recovery may occur if a long-acting i.v. anaesthetic or analgesic drug has been given towards the end of the procedure, or if the more soluble volatile agents have been continued until the end of surgery.
Pain. The presence of pain speeds recovery of consciousness. Recovery may be delayed after minor procedures or if potent analgesia has been provided by administration of opioids or by regional anaesthesia.
This occurs most commonly in diabetic patients treated with oral hypoglycaemic agents or insulin and an inadequate intake of glucose. The perioperative management of the diabetic patient is discussed in Chapter 18.
Hyperglycaemia in known diabetics may occur as a result of inadequate provision of insulin or injudicious infusion of glucose. However, coma is unusual in acute hyperglycaemia. Undiagnosed diabetics with hyperglycaemia and ketosis may present for surgery because of abdominal pain, and prolonged postoperative coma may occur unless the metabolic defect is diagnosed and treated.
intracranial spread of local anaesthetic solution after subarachnoid injection – introduction into the subarachnoid space may be accidental, e.g. during epidural block or, rarely, interscalene brachial plexus block; unconsciousness is almost always accompanied by apnoea.
Atropine crosses the blood–brain barrier and may result in the central anticholinergic syndrome, characterized by restlessness and confusion, together with obvious antimuscarinic effects. Glycopyrronium does not cross the blood–brain barrier and is preferable to atropine for antagonism of the muscarinic effects of neostigmine in elderly patients; in addition to its lack of central effects, it produces less tachycardia and antagonizes the effects of neostigmine for a longer period.
All the factors listed above as causes of prolonged coma may also result in confusion and agitation. Pain may also contribute, although it is seldom responsible alone. Emergence delirium is associated particularly with the use of ketamine and may occur after the administration of etomidate. Septicaemia may result in confusion, as may distension of the stomach or bladder.
A lightly sedated, conscious patient with inadequate antagonism of neuromuscular blocking drugs may appear to the inexperienced observer to be agitated and confused. Movements are uncoordinated. The condition is distressing to the patient and is an indication of a poor anaesthetic technique. It should never be allowed to develop.
Common causes of hypoventilation in the immediate postoperative period are listed in Table 40.3. Hypoventilation results in an increase in PaCO2 (Fig. 40.2) and a decrease in alveolar oxygen tension (PAO2), and thus hypoxaemia, which may be corrected by increasing the inspired concentration of oxygen. The risk factors for developing hypoventilation include:
|Factors Affecting Airway||Factors Affecting Ventilatory Drive||Peripheral Factors|
|Upper airway obstruction||Respiratory depressant drugs||Muscle weakness|
|Tongue||Preoperative CNS pathology||Residual neuromuscular block|
|Laryngospasm||Intra- or postoperative cerebrovascular accident||Preoperative neuromuscular disease|
|Foreign body||Recent hyperventilation (PaCO2 low)||Pain|
FIGURE 40.2 Gas exchange during hypoventilation. Note the relatively rapid increase in alveolar partial pressure of carbon dioxide (PCO2) compared with the slow decrease in arterial oxygen saturation. PO2, partial pressure of oxygen.
Airway obstruction caused by the tongue, by indrawing of the pharyngeal muscles or by blood or secretions in the pharynx may be ameliorated by placing the patient in the lateral or recovery position (see Fig. 21.7). This position should be used for all unconscious patients who have undergone oral or ear, nose and throat surgery, and for patients at risk of gastric aspiration.
Partial obstruction of the airway is characterized by noisy ventilation. As the obstruction increases, tracheal tug and indrawing of the supraclavicular area occur during inspiration. Total obstruction is signalled by absent sounds of breathing and paradoxical movement of the chest wall and abdomen.
In many patients, a clear airway is maintained only by displacing the mandible anteriorly and extending the head. In some, it is necessary also to insert an oropharyngeal airway, although this may stimulate coughing, gagging and laryngospasm during recovery of consciousness. A nasopharyngeal airway is often tolerated better, but there is a risk of causing haemorrhage from the nasopharyngeal mucosa. Occasionally, insertion of a laryngeal mask airway is necessary to maintain the airway until consciousness has returned fully; very occasionally, tracheal intubation is required.
Blood, oral secretions or regurgitated gastric fluid which have accumulated in the pharynx should be aspirated and the patient placed in the recovery position to allow any further fluid to drain anteriorly.
Foreign bodies, such as dentures (particularly partial dentures) or throat packs, may cause airway obstruction. It may be difficult to maintain a patent airway in an unconscious patient with an oral, pharyngeal or laryngeal tumour.
Obstruction of the upper airway occurs intermittently after recovery from anaesthesia. Obstructive sleep apnoea is common in the postoperative period and may result in decreases of arterial oxyhaemoglobin saturation (SaO2) to less than 75%. Episodes occur with the greatest frequency in the first 4 h after anaesthesia and are more common and severe in patients who receive opioids for postoperative analgesia than in those in whom analgesia is provided by a regional technique. However, the use of regional techniques does not reduce the risk to zero.
Airway obstruction may result from haemorrhage after surgery to the neck, including thyroid, carotid and spinal surgery; the wound should be opened urgently and the haematoma drained. This may not relieve the obstruction if venous engorgement or tissue oedema are marked. Occasionally, tracheal collapse occurs after thyroidectomy in patients who have developed chondromalacia of the cartilaginous rings of the trachea caused by pressure from a large goitre. Inspiratory stridor may be present or there may be total obstruction during inspiration; the trachea must be reintubated immediately.
This complication is relatively common after general anaesthesia. In particular, children undergoing oropharyngeal surgery are more at risk. It may be partial or complete and is caused usually by direct stimulation of the cords by secretions or blood, or of the epiglottis by an oropharyngeal airway or laryngeal mask. It may follow extubation of the trachea in the semiconscious patient. It may be difficult to differentiate this condition from airway obstruction caused by the pharyngeal wall; if airway obstruction persists despite implementation of the measures described above, laryngoscopy should be undertaken.
Any obvious foreign material causing laryngospasm should be removed by aspiration, and oxygen 100% administered. If obstruction is complete, positive-pressure ventilation by mask may force some oxygen through the cords to maintain arterial oxygenation until the spasm has subsided; there is a significant risk of inflating the stomach with oxygen during this procedure. If attempts to oxygenate the lungs fail, a small dose of succinylcholine should be administered, and the lungs ventilated with oxygen when the spasm is relieved. When satisfactory oxygenation has been achieved, it may be advisable to intubate the trachea to reduce the risk of regurgitation of gastric contents, as the stomach may have been inflated with oxygen. Appropriate methods to avoid awareness should be instituted. When the effects of succinylcholine have terminated, oxygen 100% is administered and the trachea is extubated when the patient regains consciousness.
This occurs occasionally after tracheal intubation and may result in severe obstruction, particularly in a child. Treatment depends on the severity of the obstruction; immediate reintubation may be required if obstruction is complete, but partial obstruction may subside if the patient is treated with heated humidified gases. Dexamethasone may hasten resolution of the oedema.
This may result from stimulation of the airway by inhaled material. It is commoner in asthmatic or bronchitic patients and in smokers. It may result directly from intrinsic asthma or may be part of an anaphylactic reaction. Several drugs used in anaesthetic practice may precipitate bronchospasm either by a direct effect on bronchial muscle or by releasing histamine; these include barbiturates, morphine, mivacurium and atracurium. Treatment comprises the removal of any predisposing factor and the administration of oxygen and bronchodilators.
There are several possible causes of reduced ventilatory drive during recovery from anaesthesia (see Table 40.3). The presence of intracranial pathology, e.g. tumour, trauma or haemorrhage, may affect ventilatory drive in the postoperative period. Ventilation is reduced in the presence of hypothermia, although it is usually appropriate for the metabolic needs of the body. Hypoventilation occurs in the hypocapnic patient, e.g. after a period of hyperventilation until PaCO2 is restored to normal, and in the presence of primary metabolic alkalosis.
The most important cause of reduced ventilatory drive during recovery is the effect of drugs administered by the anaesthetist in the perioperative period. All the volatile and i.v. anaesthetic agents – with the exception of ketamine – depress the respiratory centre; significant concentrations of these drugs remain in the brainstem during the early postoperative period.
All opioid analgesics depress ventilation. With most opioids, the effect is dose-dependent, although the agonist-antagonist agents are claimed to have a ceiling effect. In the majority of patients, opioids do not produce apnoea, but result in decreased ventilatory drive and an increase in PaCO2, which plateaus at an elevated value. The elderly are particularly sensitive to drug-induced ventilatory depression. The treatment of postoperative pain begins in the recovery area, often by administration of i.v. opioids by the medical or nursing staff, and ventilation must be monitored carefully after each dose.
Spinal (intrathecal or epidural) opioids, particularly lipid-insoluble agents such as morphine, may produce ventilatory depression some hours after administration. Patients who have received subarachnoid or epidural opioids should be cared for in areas where protocols and training programmes for surgical ward nurses have been implemented.
Reduced ventilatory drive is easy to diagnose if the ventilatory rate or tidal volume is clearly reduced. However, lesser degrees of hypoventilation may be difficult to detect, and the signs of moderate hypercapnia, e.g. hypertension and tachycardia, may be masked by the residual effects of anaesthetic agents, or misdiagnosed as pain-induced (see Table 40.2).
Mild hypoventilation is acceptable provided that oxygenation remains adequate; this may easily be achieved by a modest increase in the inspired fractional concentration of oxygen (FiO2; see below). If ventilatory drive is reduced excessively by opioids, resulting in an increasing PaCO2 or delayed recovery of consciousness, naloxone in increments of 1.5–3 μg kg−1 should be administered every 2–3 min until improvement occurs. Administration of excessive doses of naloxone reverses the analgesia induced by systemic (but not to the same extent by spinal) opioids; large doses may cause severe hypertension and have been associated with cardiac arrest on rare occasions. The effects of i.v. naloxone last only for 20–30 min; in order to prevent recurrence of reduced ventilation after long-acting opioids, an additional dose (50% of the effective i.v. dose) may be administered intramuscularly or an i.v. infusion commenced.
The commonest peripheral factor associated with hypoventilation is residual neuromuscular blockade. This may be exaggerated by disease of the neuromuscular junction, e.g. myasthenia gravis, or by electrolyte disturbances. Inadequate reversal of neuromuscular blockade is usually associated with uncoordinated, jerky movements, although these may occur occasionally during recovery of consciousness in patients with normal neuromuscular function. Measurement of tidal volume is not a reliable guide to adequacy of reversal of neuromuscular blockade; a normal tidal volume may be achieved with only 20% return of diaphragmatic power, but the ability to cough remains severely impaired. Traditional clinical signs of adequacy of reversal of neuromuscular blockade (such as if the patient is able to lift the head from the trolley for 5 s or maintain a good hand grip) correlate poorly with objective signs of neuromuscular function. Some more objective means of assessment are listed in Table 40.4, but these require the cooperation of the patient. In the unconscious or uncooperative patient, nerve stimulation (see Ch 6) provides the best means of assessing neuromuscular function, although there are differences among the non-depolarizing relaxants in the relationship between their actions in the forearm and diaphragm.
Ability to sustain head lift for at least 5 s
Ability to produce vital capacity of at least 10 mL kg−1
If residual non-depolarizing blockade is confirmed, further doses of neostigmine may be administered (with glycopyrronium) up to a total of 5 mg; in higher doses, neostigmine can worsen neuromuscular function. Patients who have received rocuronium or vecuronium can be given sugammadex (2 mg kg −1 if there are signs of reversal of neuromuscular blockade; or 4 mg kg− 1 if there are no twitches present using train-of-four stimulation). If the block persists, artificial ventilation must be maintained while the cause is sought.
Factors responsible most commonly for difficulty in antagonism of neuromuscular block include overdosage with muscle relaxant, too short an interval between administration of the drug and the antagonist, hypokalaemia, respiratory or metabolic acidosis, administration of aminoglycoside antibiotics, local anaesthetic agents, diseases affecting neuromuscular transmission and muscle disease.
Delayed elimination of all of the non-depolarizing muscle relaxants (except atracurium and cisatracurium) has been reported, and causes prolonged neuromuscular block. Delayed elimination occurs most frequently in the presence of renal or hepatic insufficiency, or in dehydrated patients with low urine output. Muscle paralysis may recur 30–60 min after administration of neostigmine if elimination of the relaxant is inadequate, even if antagonism appears to be satisfactory initially. A similar phenomenon may occur if acidosis develops, or when patients who have been hypothermic are rewarmed.
Prolonged neuromuscular block after succinylcholine or mivacurium occurs in the presence of atypical plasma cholinesterase or a low concentration of normal plasma cholinesterase. Paralysis after succinylcholine may persist for up to 8 h, although in most instances recovery occurs within 20–120 min. Neostigmine should not be administered if prolonged neuromuscular block occurs after administration of succinylcholine.
Hypoventilation may be caused also by restriction of diaphragmatic movement resulting from abdominal distension, obesity, tight dressings or abdominal binders. Pain, particularly from thoracic or upper abdominal wounds, may cause reduced ventilation.
The presence of air or fluid in the pleural cavity may result in hypoventilation. Pneumothorax may occur during intermittent positive-pressure ventilation (IPPV). It is an occasional complication in healthy patients, but is a particular risk in those with chronic obstructive airways disease, especially if bullae are present, and after chest trauma. It may complicate brachial plexus nerve block, central venous cannulation or surgery involving the kidney or neck. Haemothorax may result from chest trauma or central venous cannulation. Hydrothorax may be caused by pleural effusions or inadvertent infusion of fluids through a misplaced central venous catheter. These rapidly remediable causes of hypoventilation are often overlooked.
This consists primarily of treatment of the cause. Mild or moderate hypoventilation resulting from residual effects of anaesthetic drugs may respond to a bolus dose or infusion of doxapram. Artificial ventilation should be started if severe hypercapnia is present or PaCO2 continues to increase, or if the clinical condition of the patient is deteriorating.
A functional classification of causes of hypoxaemia in the early recovery period is shown in Table 40.5. An inspired oxygen concentration of less than 21% should never occur, although PaO2 is decreased when air is breathed at high altitudes.
Reduced inspired oxygen concentration
Diffusion hypoxia after nitrous oxide anaesthesia
These are the commonest cause of hypoxaemia in the recovery room. Cardiac output and pulmonary arterial pressure may be reduced after general or regional anaesthesia, causing impaired perfusion of some areas of the lungs. Functional residual capacity (FRC) is reduced during and immediately after anaesthesia. Patients who are elderly, obese or those undergoing thoracic or upper abdominal surgery are particularly at risk. The closing capacity may encroach on the tidal breathing range, resulting in reduced ventilation of some lung units, particularly those in dependent alveoli. Thus, the scatter of ventilation/perfusion () ratios is increased. Areas of lung with increased ratios constitute physiological dead space. Areas of lung with low ratios increase venous admixture which results in hypoxaemia unless the inspired oxygen concentration is increased.
Physiological shunt may be increased in the immediate postoperative period if small airways closure has been extreme. Shunting may be present also in patients with pulmonary oedema of any aetiology, or if there is consolidation in the lung. Shunt may be increased in the later postoperative period as a result of retention of secretions and underventilation of the lung bases because of pain; these changes lead to alveolar consolidation and collapse.
This has been discussed in detail above. Moderate hypoventilation, with some elevation of PaCO2, leads to a modest reduction in PaO2 (Fig. 40.2). Obstructive sleep apnoea may produce profound transient but repeated decreases in arterial oxygenation. SaO2 may decrease to less than 75%, corresponding to a PaO2 of less than 5 kPa (40 mmHg). These repeated episodes of hypoxaemia cause temporary, and possibly permanent, defects in cognitive function in elderly patients and may contribute to perioperative myocardial infarction. Obstructive sleep apnoea is exacerbated by opioid analgesics, and patients who are known to suffer from this condition should be monitored carefully in the postoperative period, preferably in a high-dependency unit. Patients who normally use a continuous positive airways pressure (CPAP) mask to reduce obstructive sleep apnoeic episodes should use the mask at night throughout the postoperative period.