Postoperative Care

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Postoperative Care

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.

THE EARLY RECOVERY PERIOD

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.

Systems Affected

Staff, Equipment and Monitoring

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).

A wide range of drugs should be stored in the recovery area for the treatment of common complications and also emergency events (Table 40.1).

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 patient should not be discharged to the surgical ward until the following criteria have been met.

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.

CENTRAL NERVOUS SYSTEM

Conscious Level

Many patients are unconscious on arrival in the recovery ward because of residual effects of anaesthetic drugs. The duration of impaired consciousness depends on:

Undue prolongation of unconsciousness should not be attributed to these factors alone. Other causes should be considered, as their early recognition may prevent serious sequelae. These are:

Cerebral Pathology

Consciousness may be impaired by functional or structural cerebral damage. Possible causes include:

image episodes of cerebral ischaemia (e.g. carotid artery surgery, profound hypotension) or cerebral hypoxia during anaesthesia

image intracranial haemorrhage, thrombosis or infarction – these may occur coincidentally or may have been associated with intraoperative hypertension, hypotension or arrhythmias

image pre-existing cerebral lesions, e.g. tumour, trauma – anaesthetic techniques which increase intracranial pressure are likely to impair cerebral function

image epilepsy – convulsions may have been masked by anaesthesia or neuromuscular blocking drugs

image air embolism

image 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.

Confusion and Agitation

These occur occasionally during emergence from an otherwise uncomplicated anaesthetic.

Various drugs are associated with postoperative confusion, including:

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.

Pain

This subject is discussed fully in Chapter 41. The effects of pain should be differentiated from those of hypercapnia and hypovolaemia (Table 40.2).

RESPIRATORY SYSTEM

Hypoventilation

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:

TABLE 40.3

Causes of Postoperative Hypoventilation

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
 Oedema Hypothermia  Electrolyte abnormalities
 Foreign body Recent hyperventilation (PaCO2 low) Pain
 Tumour Abdominal distension
 Bronchospasm Obesity
Tight dressings
Pneumo-/haemothorax

CNS, central nervous system; PaCO2, arterial carbon dioxide tension.

Airway Obstruction

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.

Laryngeal Spasm

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.

Rarely, laryngeal obstruction occurs after thyroid surgery if both recurrent laryngeal nerves have been traumatized.

Ventilatory Drive

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.

Peripheral Factors

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.

TABLE 40.4

Clinical Assessment of the Adequacy of Antagonism of Neuromuscular Block

Subjective

Grip strength

Adequate cough

Objective

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.

Artificial ventilation of the lungs must be maintained or resumed in any patient who has inadequate neuromuscular function. Anaesthesia should be provided to prevent awareness.

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.

Hypoxaemia

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.

TABLE 40.5

Functional Classification of the Causes of Hypoxaemia in the Postoperative Period

Reduced inspired oxygen concentration

Ventilation–perfusion abnormalities

Shunting

Hypoventilation

Diffusion deficits

Diffusion hypoxia after nitrous oxide anaesthesia

Ventilation–Perfusion Abnormalities

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 (image) ratios is increased. Areas of lung with increased ratios constitute physiological dead space. Areas of lung with low imageratios increase venous admixture which results in hypoxaemia unless the inspired oxygen concentration is increased.

Hypoventilation

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.

Diffusion Hypoxia

Nitrous oxide is 40 times more soluble than nitrogen in blood. When administration of nitrous oxide is discontinued at the end of anaesthesia, nitrous oxide diffuses out of blood into the alveoli in larger volumes than nitrogen diffuses in the opposite direction. Consequently, the alveolar concentrations of other gases are diluted. PaO2 is reduced and arterial oxygenation impaired if the patient breathes air; PaCO2 decreases as a result of effective alveolar hyperventilation. SaO2 is reduced to values as low as 90% for several minutes in normal individuals after breathing 50% nitrous oxide in oxygen. Arterial desaturation is greater in elderly patients, if higher concentrations of nitrous oxide have been used, or if PaCO2 is initially low because of hyperventilation during anaesthesia.

Diffusion hypoxia is avoided by the administration of oxygen for 10 min after discontinuation of nitrous oxide anaesthesia.

Pulmonary Changes after Abdominal Surgery

Patients with previously normal lungs suffer impairment of oxygenation for at least 48 h after abdominal surgery. The extent of this impairment is related to the site of operation. It is less marked after lower abdominal surgery, more severe if there has been a large incision in the upper abdomen and worst after thoracoabdominal procedures. In these circumstances, the differences between pre- and postoperative PaO2 may be as much as 4 kPa.

Impairment of oxygenation in the postoperative period is related to a reduction in FRC. After induction of anaesthesia, there is an abrupt decrease in FRC. The magnitude of the decrease is similar for anaesthetic techniques in which the patient breathes spontaneously and those in which IPPV is employed. Postoperatively, this decrease is maintained by wound pain, which causes spasm of the expiratory muscles, and abdominal distension, which leads to diaphragmatic splinting. This is also influenced by the site of surgical incision; the greatest reduction follows thoracic or upper abdominal surgery. The supine position also reduces FRC.

The reduction in FRC may lead to closing capacity impinging upon the tidal breathing range. This results in small airways closure during normal tidal ventilation. Gas trapping occurs in the affected airways and subsequent absorption of air may lead to the development of small, discrete areas of atelectasis which are not visible on chest X-ray. This occurs mainly in the dependent parts of the lung and may be demonstrated by CT scan very soon after induction of anaesthesia. The result is an increase in the number of areas of low imageratio within the lungs. The relationship between changes in FRC and PaO2 postoperatively is shown in Figure 40.3.

In most patients, these abnormalities return towards normal by the fifth or sixth postoperative day. However, if the changes have been marked, the areas of low imageratio may become a focus for infection, particularly in the presence of retained secretions. The following factors contribute to retention of secretions after surgery.

A combination of these factors may result in retention of secretions, leading to areas of visible pulmonary collapse on chest X-ray and an increase in the work of breathing. Ultimately, oxygenation of the blood may become inadequate despite oxygen therapy, or carbon dioxide retention may occur. The sequence of events that culminate in ventilatory failure is shown in Figure 40.4.

Clinical Findings

Treatment

If a pulmonary complication is suspected, a sputum sample should be sent to the laboratory for bacteriological analysis. Appropriate antibiotic therapy may then be started. Intensive physiotherapy should be prescribed in an attempt to remove secretions and re-expand atelectatic areas of the lung.

Patients with pulmonary collapse are usually hypoxaemic, but PaCO2 remains normal or may be low as a result of tachypnoea, at least in the early stages. Usually, oxygen in moderate concentrations (30–40%) is sufficient to correct hypoxaemia, but this should be confirmed by blood gas analysis; CPAP given via a tightly fitting face mask is effective in re-expanding the collapsed alveoli and improving the mechanics of breathing. If the patient fails to respond to these measures, signs of respiratory distress develop. The patient becomes drowsy and ventilation is laboured, with rapid shallow breathing involving the accessory muscles. PaCO2 increases and arterial oxygenation deteriorates despite oxygen therapy. The presence of continued deterioration in blood gases is an indication for ventilatory support.

Reducing Pulmonary Complications

Preoperative

Measures to reduce pulmonary complications should begin preoperatively. Ideally, patients should be free from ongoing upper or lower respiratory tract infections but this may not always be possible, for instance in young children, adults with recurrent infective complications (such as COPD or bronchiectasis) or patients presenting for urgent or emergency surgery.

Pre-existing chronic respiratory disorders should be treated so that the patient is in optimal condition before surgery. Spirometry may be useful to monitor the effects of such treatment, but arterial blood gas analysis is the only assessment which has been demonstrated to correlate well with the need for postoperative ventilatory support. Smoking should be discouraged and weight loss encouraged where indicated. In patients with increased risk factors, heavy premedication should be avoided to ensure minimal ventilatory depression at the end of the procedure.

Oxygen Therapy

Hypoxaemia may occur to some degree in any patient during the early recovery period as a result of one or more of the mechanisms described above. Consequently, all patients should receive additional oxygen for the first 10 min after general anaesthesia has been discontinued. Oxygen therapy should be continued for a longer period in the presence of any of the conditions listed in Table 40.6.

TABLE 40.6

Conditions in Which Prolonged Oxygen Therapy is Required After Operation

Hypotension

Ischaemic heart disease

Reduced cardiac output

Anaemia

Obesity

Shivering

Hypothermia

Hyperthermia

Pulmonary oedema

Airway obstruction

After major surgery

Oxygen therapy is particularly beneficial in treating hypoxaemia caused by hypoventilation; PaO2 is substantially increased by a modest increase in FiO2. In contrast, higher concentrations are required in the presence of a shunt fraction in excess of 0.1–0.15 (Fig. 40.5). Known concentrations of oxygen may be administered by a tightly fitting mask supplied with metered flows of air and oxygen via either an anaesthetic breathing system or a CPAP system. In small children, an oxygen tent or headbox may be used. However, oxygen is usually administered by less cumbersome disposable equipment.

Oxygen Therapy Devices

The characteristics of oxygen face masks depend predominantly on their volume, the flow rate of gas supplied and the presence of holes in the side of the mask. If no gas is supplied, face masks act as increased dead space and result in hypercapnia unless minute volume is increased; the increase in dead space is proportional to the volume of the mask. If the mask contains holes, air is entrained readily during inspiration.

When oxygen is supplied, the inspired oxygen concentration increases, but to an extent which depends upon the relationship between the oxygen flow rate and the ventilatory pattern. If there is a pause between expiration and inspiration, the mask fills with oxygen and a high concentration is available at the start of inspiration; during inspiration, the inspired oxygen is diluted by air drawn in through the holes when the inspiratory flow rate exceeds the flow rate of oxygen. During normal tidal ventilation, the peak inspiratory flow rate (PIFR) is 20–30 L min−1, but is considerably higher during deep inspiration or in the hyperventilating patient. If there is no expiratory pause, alveolar gas may be rebreathed from the mask at the start of inspiration; this occurs especially when the oxygen flow rate is low or when no holes are present in the mask. A predictable and constant inspired oxygen concentration may be achieved only if the total gas flow to the mask exceeds the patient’s peak inspiratory flow rate (PIFR).

Fixed-Performance Devices: These masks, also termed high air flow oxygen enrichment (HAFOE) devices, provide a constant and predictable inspired oxygen concentration irrespective of the patient’s ventilatory pattern. This is achieved by supplying the mask with oxygen and air at a high total flow rate. Oxygen is passed through a jet which entrains air (Fig. 40.6). The mask is designed in such a way that the total flow rate of gas to the mask exceeds the expected PIFR of most patients who require oxygen therapy. For example, if a jet designed to supply 28% oxygen is supplied with an oxygen flow rate of 4 L min−1, approximately 41 L min−1 of air is entrained and a total flow of 45 L min−1 passes to the patient’s face.

Various types of HAFOE device are available; an example is shown in Figure 40.7. Ventimasks are the most accurate, but a different mask is required for each of the range of oxygen concentrations available. Some manufacturers produce masks in which the jet device can be changed by the user, so that the oxygen concentration may be adjusted as appropriate.

The air-entraining jets of HAFOE devices provide a relatively constant oxygen concentration irrespective of the flow rate of oxygen. The recommended oxygen flow rates are larger when jets providing a high concentration are used (e.g. 8 L min−1 for 40%, 15 L min−1 for 60%) so that the total flow rate supplied to the mask remains adequate despite the smaller proportion of air entrained. The total flow rates through masks which deliver more than 28% oxygen are between 20 and 30 L min−1 when the recommended oxygen flow rates are provided; higher flow rates of oxygen may be used in patients who are thought to have an increased PIFR.

Because of the high fresh gas flow rate, expired gas is rapidly flushed from the mask. Thus, rebreathing does not occur, i.e. fixed-performance devices do not act as an additional dead space.

Variable-Performance Devices: All other disposable oxygen masks and nasal cannulae provide an oxygen concentration which varies with the oxygen flow rate and the patient’s ventilatory pattern. Although there is no increase in dead space when nasal cannulae are used, all variable-performance disposable face masks add dead space, the magnitude of which depends on the patient’s pattern of ventilation. Table 40.7 gives an indication of the range of oxygen concentrations achieved with a number of commonly used variable-performance devices; an example is shown in Figure 40.8.

TABLE 40.7

Oxygen Masks, Flow Rates and Approximate Oxygen Concentration Delivered

Type of mask Oxygen flow (L min−1) Oxygen concentration (%)
Edinburgh  1 24–29
 2 29–36
 4 33–39
Nasal cannulae  1 25–29
 2 29–35
 4 32–39
Hudson  2 24–38
 4 35–45
 6 51–61
 8 57–67
10 61–73
MC  2 28–50
 4 41–70
 6 53–74
 8 60–77
10 67–81

Oxygen Therapy in the Recovery Ward

The large majority of patients recovering after anaesthesia require only a modest increase in FiO2 to overcome the combined effects of mild hypoventilation, diffusion hypoxia and some degree of increased imagescatter. Usually, an inspired concentration of 30% is adequate and this may be achieved in most instances by supplying an oxygen flow rate of 4 L min−1 to any of the variable-performance devices (see Table 40.7). However, in a small proportion of patients, it is necessary to control the FiO2 more strictly.

Controlled Oxygen Therapy: This is required in two categories of patient:

image Some patients with chronic bronchitis develop chronic hypercapnia, and ventilatory drive is produced largely by hypoxaemia. If PaO2 increases above the level which stimulates breathing, ventilatory depression may occur. However, these patients may become dangerously hypoxaemic after anaesthesia, and oxygen therapy is required so that adequate oxygenation of the tissues is maintained. The aim of oxygen therapy in these circumstances is to increase arterial oxygen content without an excessive increase in PaO2. This is achieved by a modest increase in FiO2. In the hypoxaemic patient, the relationship between arterial oxygen tension and saturation (and therefore oxygen content) is represented by the steep portion of the oxyhaemoglobin dissociation curve, and a small increase in oxygen tension results in significant increases in saturation and oxygen content (Fig. 40.9). The use of a variable-performance device in these patients is unsatisfactory, as an unacceptably high FiO2 may be delivered. A fixed-performance device delivering 24% oxygen should be used initially, and the response assessed. If the patient remains clinically well, and the PaCO2 does not increase by more than 1–1.5 kPa, 28% oxygen – and subsequently higher concentrations – may be administered if further increases in PaO2 are desirable. The aim is not to achieve ‘normal’ PaO2 or SaO2 but to provide acceptable oxygenation for that patient. Patients whose normal SaO2 is in the low 90s do not need postoperative SaO2 in the high 90s. Most patients with chronic bronchitis do not depend on hypoxaemia for respiratory drive and should not be denied adequate inspired concentrations of oxygen.

image Patients with increased shunt, e.g. those with acute respiratory distress syndrome (ARDS), pulmonary oedema or pulmonary consolidation, may require a high inspired oxygen concentration (see Fig. 40.5), which cannot be guaranteed if a variable-performance device is used. In addition, serial blood gas analysis is normally used to assess improvement or deterioration in their condition. Changes in PaO2 and the degree of shunt may be interpreted accurately only if the FiO2 is known. Thus, controlled oxygen therapy should be employed, using a fixed-performance device which delivers 40% oxygen or more.

CARDIOVASCULAR SYSTEM

Hypotension

Residual Effects of Anaesthetic Drugs

Hypotension may result from the residual vasodilator effect of i.v. or inhalational anaesthetic drugs, particularly in patients who are experiencing little pain. Subarachnoid or epidural nerve block may also cause hypotension which persists into the postoperative period. Heart rate is seldom elevated, and the peripheries are warm if anaesthetic drugs or regional anaesthesia are the cause of hypotension. Up to 20% decrease in the mean arterial pressure is tolerated well except by the elderly or patients with myocardial disease. No treatment is required in most patients. Elevation of the legs often increases arterial pressure by increasing venous return. Intravenous infusion of 7–10 mL kg−1 of colloid solution is usually effective in restoring normotension if there is concern; infusion should be undertaken cautiously in elderly patients and in those with cardiovascular disease.

Other causes of hypotension in the recovery period are more sinister and must be excluded before it may be assumed that residual anaesthesia is responsible.

Hypovolaemia

This may result from inadequate or inappropriate replacement of preoperative or intraoperative fluid and blood losses, or from postoperative haemorrhage. Surgical bleeding may be obvious from inspection of wounds and drains, but may be concealed, particularly in the abdomen, retroperitoneal space or thorax, even when drains are present.

Inadequate surgical haemostasis is the usual cause of postoperative bleeding, but coagulation disorders may be present in the following circumstances:

A coagulation disorder is frequently associated with prolonged bleeding after venepuncture, oozing from the wound and the development of petechiae or bruises. The investigation and management of coagulation disorders are discussed in Chapter 13.

Hypotension caused by hypovolaemia may be accompanied by signs of poor peripheral perfusion, e.g. cold, clammy extremities and pallor. Tachycardia may be present but is masked, not infrequently, by the effects of drugs (e.g. anticholinesterases, β-blockers). Central venous pressure is a poor guide to volaemic status. Urine output is reduced (< 30 mL h−1). The effects of hypovolaemia on arterial pressure are more pronounced in the presence of vasodilatation or reduced myocardial contractility resulting from the effects of residual anaesthetic drugs, or antihypertensive, calcium channel or β-blocker therapy. In patients who have undergone prolonged surgery, and particularly if the core temperature is below normal, vasoconstriction may be profound and hypovolaemia may be unmasked at a relatively late stage, as normal vasomotor tone returns with rewarming.

Treatment comprises elevation of the legs and administration of appropriate crystalloid or colloid solutions; in elderly or high-risk patients, or if hypovolaemia is profound, administration of fluids should be monitored with the assistance of invasive arterial blood pressure and often some form of cardiac output monitoring. Red cells, clotting factors or platelets should be administered if appropriate, and surgical bleeding treated by re-operation if necessary.

Ventricular Failure

Left or right ventricular failure may cause hypotension. Right ventricular failure is uncommon in the postoperative period and is secondary usually to acute pulmonary disease, e.g. ARDS.

Left ventricular failure in the postoperative period is associated most commonly with perioperative myocardial infarction or ischaemia, or sometimes with fluid overload. The peripheral circulation is poor. Usually, tachycardia is present and there is clinical and radiological evidence of pulmonary oedema. Jugular venous pulse and CVP are usually elevated, but they may remain normal despite a substantial increase in left atrial pressure, particularly if right ventricular hypertrophy is present. Thus, left ventricular failure may be misdiagnosed as hypovolaemia in some patients, and in some instances the two conditions coexist. If there is doubt about the diagnosis, a small intravenous fluid bolus may be administered (no more than 200 mL) and the response of arterial pressure and CVP monitored; if the diagnosis remains uncertain, more involved testing may include echocardiography or rarely the insertion of a pulmonary artery catheter.

Treatment comprises administration of oxygen, fluid restriction, diuretics and, if necessary, inotropic support or vasodilator therapy. ECG, arterial pressure and CVP should be monitored. The possibility of myocardial infarction should be investigated.

Hypertension

Arterial hypertension is a common complication in the early postoperative period. The causes include the following:

A combination of these causes may be present. Hypertension results in increased cardiac work and myocardial oxygen consumption, and may result in myocardial ischaemia or infarction, left ventricular failure or cerebral haemorrhage. The cause should be elicited rapidly and treated if possible. Oxygen should be administered. If no remediable cause is found and the hypertension is felt to be a risk to the patient, careful antihypertensive treatment can be started using vasodilators such as hydralazine (i.v.), nifedipine (sublingual) or glyceryl trinitrate (sublingual or i.v.), or beta-blockade (labetalol has combined α- and β-antagonism, esmolol is short-acting). Such treatment may unmask hypovolaemia (see above) and additional i.v. fluids may be required.

Arrhythmias

These are common during and immediately after anaesthesia (see also Ch 8). The majority are benign and require no treatment. However, the cause should be sought and its effect on the circulation assessed. Common causes include the following:

Sinus tachycardia is common and may be a reflex response to hypovolaemia or hypotension. It also occurs in the presence of hypercapnia, anaemia or hypoxaemia, and if the metabolic rate is elevated by fever, shivering, restlessness or malignant hyperthermia. The commonest cause is pain. Tachycardia increases myocardial oxygen consumption and decreases coronary artery perfusion by reducing diastolic time. The combination of arterial hypertension and tachycardia is dangerous in the presence of ischaemic heart disease and should not be allowed to persist, as it may result in myocardial infarction. Sinus tachycardia should be treated specifically only if it persists after therapy for underlying causes has been given; a small i.v. dose of a short-acting β-blocker (esmolol) should be administered, followed by a continuous intravenous infusion. The ECG must be monitored.

Sinus bradycardia may result from inadequate antagonism by glycopyrronium of vagal stimulation by neostigmine, pharyngeal stimulation during suction or the residual effects of volatile anaesthetic agents. Other causes include hypoxaemia (especially in neonates and infants), raised intracranial pressure, myocardial infarction and some cardiac drugs, e.g. β-blockers, digoxin. Oxygen should be administered. Intravenous atropine or glycopyrronium is usually effective if there is associated hypotension or evidence of inadequate cardiac output. In the presence of severe bradycardia, external cardiac massage is necessary to increase cardiac output.

Bradycardia may also occur as a result of complete heart block; this may require electrical pacing.

Bradycardia may also be normal for certain individuals in which case treatment is likely to cause more problems than it solves.

Supraventricular arrhythmias, including atrial fibrillation, flutter or supraventricular tachycardia, are treated as in other circumstances. Rapid arrhythmias are best treated by cardioversion, but may require pharmacological therapy to prevent recurrence. Nodal rhythm with a normal heart rate is common in the perioperative period, particularly when volatile anaesthetic agents have been used. Supraventricular arrhythmias may cause moderate hypotension because of the loss of synchronization between atrial and ventricular contractions.

Ventricular arrhythmias. Ectopic beats usually require no treatment. Ventricular tachycardia should be treated according to current Resuscitation Council (or equivalent) guidelines.

Acute Coronary Syndrome

Myocardial infarction (MI) occurs in 1–2% of unselected patients over 40 years of age undergoing major non-cardiac surgery. Pre-existing coronary artery disease and, in particular, evidence of a previous MI, result in a higher risk. Mortality in patients who suffer a perioperative MI used to be as high as 60% but is somewhat lower now. Perioperative MI occurs most commonly on the second or third postoperative day, but may happen at any time during or after surgery. Acute coronary syndromes in the perioperative period are most commonly caused by atheromatous plaque rupture, in the same way as non-operative events. Non-thrombotic acute coronary syndrome (ACS) may also occur when myocardial oxygen delivery is insufficient for demand.

Several factors which may be detected during preoperative assessment are known to increase the likelihood of perioperative MI (see Ch 17). The most important of these is the time interval between surgery and a previous MI. One extensive study of risk factors which might predict major cardiac complications (including, but not exclusively, MI) showed that preoperative evidence of cardiac failure, arrhythmias (of any type) or aortic stenosis, and age were also associated with a high risk. In addition, there is evidence that pre-existing uncontrolled hypertension is associated with increased risk. These problems are discussed more fully in Chapter 18.

The incidence of perioperative MI is related also to intraoperative and postoperative factors. The magnitude and type of surgery are important determinants; in patients with a history of previous MI, the incidence of perioperative reinfarction associated with major vascular surgery is considerably higher than when surgery is performed outside the thorax and abdomen. In patients with ischaemic heart disease, postoperative MI is more likely if there is evidence of ischaemic changes on ECG during operation. Such changes are associated most commonly with episodes of intraoperative hypotension, hypertension or tachycardia; the last two occur most frequently in response to noxious stimuli, e.g. tracheal intubation, surgical incision. The drugs used and the manner in which they are employed by the anaesthetist influence the incidences of both intraoperative ischaemia and perioperative MI. There is ongoing debate as to whether regional anaesthesia reduces risk when major surgery is undertaken.

Reduction of Risk

The incidence of perioperative MI may be reduced by the following.

image Identification of patients at risk. Elective surgery should be postponed if possible until at least 3 months after a previous MI.

image Treatment of risk factors. Cardiac failure, hypertension and arrhythmias should be controlled before surgery. If necessary, the operation should be postponed until control is achieved. Coronary artery bypass grafting or aortic valve replacement may be required in patients with severe coronary artery disease or aortic stenosis, respectively, before other major abdominal or thoracic surgery is undertaken.

image Avoidance of ischaemia. The anaesthetic technique and postoperative management should ensure adequate oxygenation of the myocardium and should minimize myocardial oxygen demand (see Ch 18).

image Monitoring. ECG must be monitored throughout anaesthesia, including induction, in all patients at risk; the CM5 electrode configuration (see Fig. 16.2) is suitable for detection of ischaemic changes. Arterial pressure should be monitored regularly, and continuously in patients undergoing major surgery.

OTHER MAJOR POSTOPERATIVE COMPLICATIONS

Deep Venous Thrombosis

The main factors postulated by Virchow as contributing to the formation of venous thrombi are:

However, the exact trigger mechanism which initiates venous thromboembolic disease in some patients but not others remains unknown. Most DVTs are subclinical and peak occurrence is around 7 days after surgery. The degree of association between subclinical distal (calf) DVT and fatal pulmonary embolism (PE) is unclear. There remains a degree of controversy over the optimal approach to management.

Risk Factors

A higher incidence of deep venous thrombosis (DVT) has been reported in patients with:

DVT is commoner after hip, pelvic and abdominal surgery than after other types of surgery; regional anaesthetic techniques, with general anaesthesia or in isolation, may reduce the risk. There is a well-established association between spontaneous DVT and oestrogen, and DVT may occur in women who take some types of oral contraceptive pill. The number of women who develop this complication is small. However, the incidence increases if surgery is performed while the patient is currently taking the drug. The risk is reduced but not abolished if a low-oestrogen (50 μg or less) preparation is used. Women who take hormone replacement therapy are also at increased risk.

Prophylaxis

As with most complications, appropriate assessment is a key step in reduction of events. Prophylactic measures to minimize the risk of DVT and PE are detailed in Chapter 13.

Elimination of Stasis: Early ambulation after operation is widely promoted as a method to reduce the incidence of DVT, although the degree of benefit is not clear. Attempts directed at preventing stasis, including physiotherapy, elastic stockings and elevation of the feet, may reduce the incidence of DVT but have not been shown to influence the incidence of pulmonary embolism.

Two methods are currently used for increasing venous return from the lower limbs during surgery.

image Pneumatic compression of the calves. The legs are encased in an envelope of plastic material, which is inflated and deflated rhythmically, thus squeezing the calves intermittently. These devices mimic the effect of the calf muscle pump, promoting venous return, and also stimulate fibrinolytic activity. This technique may be continued postoperatively.

image Anti-embolism stockings. It is important that these are fitted properly because ill-fitting stockings are at best useless and at worst may cause injury due to local constrictions. There is no good evidence that thigh-length stockings confer benefit over knee-length stockings. They are contraindicated in patients with:

Although the incidence of DVT is reduced substantially by these techniques, there is no reduction in the incidence of, or mortality from, PE. However, there is no increased risk of bleeding, and if fitted appropriately, few complications.

Alteration of Blood Coagulability

Pulmonary Embolism

This term covers a range of events from sudden circulatory collapse and death, through minor episodes of pleurisy and haemoptysis, to the long-standing disability of patients with chronic thromboembolic pulmonary hypertension. The acute forms of pulmonary embolism are encountered after anaesthesia and surgery. In the elderly, multiple small pulmonary emboli may be misdiagnosed as bronchopneumonia.

The common sites of origin for thrombi which result in pulmonary embolus are the veins of the pelvis and lower extremities. The most common time for presentation of a postoperative pulmonary embolism is during the second week. In some patients, predisposing factors may have existed preoperatively for some time, and the whole time-scale of events may be shifted; the embolus may occur at the time of, or shortly after, surgery.

Investigations

image ECG (Fig. 40.10). This reflects acute right ventricular strain, with features that often include right axis deviation, T-wave inversion in leads V1–V4 and sometimes right bundle branch block. The classic S1–Q3–T3 pattern is less common.

image Chest X-ray. This is often unremarkable but may show areas of oligaemia reflecting pulmonary vascular obstruction.

image Arterial blood gases. There is usually hypoxaemia because of ventilation–perfusion imbalance, and hypocapnia resulting from hyperventilation.

image Pulmonary angiography. This provides a definitive diagnosis of major obstruction in the pulmonary circulation, and is now performed usually by CT scan. This investigation is particularly useful if the patient is critically ill and the diagnosis is in doubt, and is essential if pulmonary embolectomy is planned. However, it requires transfer of the patient to the X-ray department.

Treatment

Postoperative Renal Dysfunction

The kidney is vulnerable to a wide range of drugs (see Ch 10), chemicals and pathological insults. It is particularly susceptible to toxic substances for the following reasons:

Acute kidney injury (AKI) following surgery is relatively common; almost 25% of elderly patients who died following emergency surgery were found to have evidence of acute kidney injury on admission. There is no single diagnostic criterion for defining acute kidney injury, but a consensus clinical tool is the ‘RIFLE’ criteria (Table 40.8).

Unfortunately, the RIFLE criteria essentially give information about what has happened already, rather than providing information about current injury at a time when preventative action may be possible. There is ongoing research into biomarkers of early/ongoing renal injury but there is no reliable and practical test available yet.

Acute kidney injury in the surgical patient is often multifactorial. Key factors are:

Outcome following illness and surgery is worse when complicated by AKI, with increased length of stay and increased mortality.

Postoperative care should therefore focus on:

Effects of Anaesthesia

All anaesthetic techniques depress renal blood flow and, secondary to this, interfere with renal function. Provided that prolonged hypotension is avoided, the effects are temporary. However, there is the potential for some anaesthetic agents to produce permanent renal damage.

The administration of the volatile anaesthetic agent methoxyflurane was associated with a relatively high incidence of renal dysfunction. Clinically, the defect was characterized by failure of the concentrating ability of the kidney. In certain instances, this progressed to high-output renal failure. The nephrotoxicity of methoxyflurane was dose-dependent and was caused by inorganic fluoride ions produced during its metabolism. Administration of methoxyflurane in combination with other nephrotoxic drugs, e.g. aminoglycosides, was particularly hazardous.

Large quantities of fluoride ion are also produced during metabolism of enflurane and sevoflurane, although a much smaller proportion of these drugs (2–3%) is metabolized in comparison with methoxyflurane (45%). Concentrations of fluoride ion in blood following administration of sevoflurane may exceed the value associated with renal impairment after anaesthesia with methoxyflurane. However, there has been no evidence to suggest that either enflurane or sevoflurane is associated with renal impairment related to the production of fluoride ions. The reason is probably related to the fact that the very soluble methoxyflurane continues to be metabolized for some days, resulting in prolonged production of fluoride ions, whereas the peak concentrations associated with the use of enflurane and sevoflurane are of short duration because of their relative insolubility in tissues.

Postoperative Hepatic Dysfunction

There are many causes of postoperative hepatic dysfunction (Table 40.9). Most patients show no evidence of hepatic damage after anaesthesia and surgery. If it occurs, it is usually attributable to one of the causes shown in Table 40.9. However, if other causes are excluded, consideration should be given to the possibility of hepatotoxicity from anaesthetic drugs.

TABLE 40.9

Causes of Postoperative Hepatic Dysfunction

Increased Bilirubin Load Hepatocellular Damage Extrahepatic Biliary Obstruction
Blood transfusion
Haemolysis and haemolytic disease
Abnormalities of bilirubin metabolism		 Pre-existing liver disease
Viral hepatitis
Sepsis
Hypotension/hypoxia
Drug-induced hepatitis
Congestive heart failure		 Gallstones
Ascending cholangitis
Pancreatitis
Surgical misadventure

Chloroform was the first anaesthetic agent to be suspected of causing hepatic damage. In large doses, chloroform is a direct hepatotoxin, and after anaesthesia a hepatitis-like syndrome, with histological evidence of centrilobular hepatic necrosis, occurred occasionally. Methoxyflurane was also associated with hepatic damage, causing a syndrome clinically similar to viral hepatitis. Two of the volatile agents in current use have been implicated in cases of postoperative hepatic dysfunction.

Halothane

Attention was first focused on halothane-associated hepatitis in the early 1960s. Numerous case reports prompted institution in 1969 of the largest retrospective anaesthetic study ever undertaken (United States National Halothane Study). The incidence and causes of fatal hepatic necrosis occurring within 6 days of anaesthesia were reviewed. The overall incidence was 1 in 10  000; that associated with halothane was 1 in 35  000 and was no greater than the incidence associated with other anaesthetic agents. However, it is believed at present that there is a small number of patients who develop postanaesthetic jaundice in which halothane is the aetiological agent.

There are two categories of halothane hepatotoxicity. Type 1 is common and self-limiting. It is characterized by modest increases in liver transaminases and changes in drug metabolism. There is no jaundice and there are no signs of liver disease. It appears to be essentially halothane-specific and is probably due to reductive rather than oxidative metabolism of halothane. Type 2 is associated with centrilobular necrosis and acute liver failure. It is clinically similar to viral hepatitis with fever, jaundice and markedly elevated transaminases. The exact mechanism of liver damage is not known. At present, there are two main hypotheses.

Antibodies to halothane have been demonstrated in patients who have suffered hepatic damage after administration of the drug. At present, this is the most promising method for evaluating the aetiology of a condition which has been a source of great controversy.

The following groups of patients are believed to be at the greatest risk of developing hepatic dysfunction after halothane anaesthesia:

Pre-existing liver disease is not a risk factor for developing hepatotoxicity. Type 2 hepatotoxicity has been reported rarely with other volatile anaesthetics and appears to be related to the degree of hepatic metabolism.

OTHER COMPLICATIONS (TABLE 40.10)

Serious complications are described in detail in Chapter 43.

TABLE 40.10

Minor Morbidity Resulting from Anaesthesia

Nausea and vomiting (see Chapter 42)

 Related to nature of operation
 Females > males

Sore throat

 Around 12% of all general anaesthesia
 Around 45% of those with tracheal tubes

Hoarseness
Around 50%

Laryngeal granulomata

Headache

 Up to 60% of patients

Backache

Discomfort from catheters, drains, nasogastric tubes

Anxiety

Muscle pains

 Up to 100% of those who receive succinylcholine

Shivering

Drowsiness

Anorexia

Disorientation

Thrombophlebitis at injection site

Oral trauma
Around 5%

Dental injury
Around 1%; 0.02% require surgical treatment

Corneal abrasions
Around 0.05–0.1%

Sore Throat

Around 12% of patients complain of sore throat after anaesthesia and surgery. Some of the common causes include the following.

image Trauma during tracheal intubation. Damage to the pharynx and tonsillar fauces may be caused by the laryngoscope blade.

image Trauma to the larynx. This is more likely if the tube has been forced through the vocal cords. A poorly stabilized tube causes more frictional damage to the larynx than one which is securely stabilized.

image Trauma to the pharynx. This may occur during passage of a nasogastric tube or insertion of an oropharyngeal or laryngeal mask airway, and is particularly common when a throat pack has been used. Occasionally, the pharynx or upper oesophagus may be perforated during insertion of a nasogastric tube, or during difficult tracheal intubation, and severe pain in the throat is often the first symptom. Sore throat is likely if a nasogastric tube remains in situ during the postoperative period.

image Other factors. The mucous membranes of the mouth, pharynx and upper airway are sensitive to the effects of unhumidified gases; the drying effect of anaesthetic gases may cause postoperative sore throat. The antisialagogue effect of anticholinergic drugs may also contribute to this symptom.

The use of topical local anaesthetics does not reduce the incidence of sore throat. Lubrication of the tracheal tube is effective in reducing the incidence, although there is no difference in this respect between plain or local anaesthetic jellies. Sore throat is less common, but not completely avoided, when a face mask or supraglottic airway is used for airway management.

In the absence of a nasogastric tube, postoperative sore throat is usually of short duration; most patients are symptom-free within 48 h.

Muscles

Problems associated with inadequate reversal of neuromuscular blocking drugs are discussed above. The detection and treatment of malignant hyperthermia are described on page 879; it is important to appreciate that this condition may present during recovery.

Shivering

This is a common complication in the recovery room. It may occur in patients who are hypothermic as a result of prolonged surgery, or during injection of local anaesthetic solution into the epidural space. However, in most patients, the onset of shivering is not related to body temperature, and there is evidence from electromyography that the characteristics of postoperative (or postanaesthetic) shivering differ from those of thermoregulatory shivering. The incidence and severity of shivering are increased in patients who have received an anticholinergic premedication, and women are more likely to shiver in the luteal than in the follicular phase of the menstrual cycle.

Shivering increases oxygen consumption and carbon dioxide production and may result in hypoxaemia and hypercapnia if the response of the respiratory centre to carbon dioxide is impaired by drugs. Oxygen should be administered. A small dose of pethidine (20 mg i.v.) is frequently effective in aborting postoperative shivering.

Succinylcholine Pains

Muscle pains after succinylcholine are very common, occurring in at least 50% of patients who receive the drug. The muscles involved most frequently are those of the shoulder girdle, neck and thorax. The pain is similar in nature to that caused by viral-related myositis. The incidence is influenced by the following factors.

The exact cause of muscle pains after succinylcholine is unknown, although it is thought that fasciculations produced by depolarization of the motor nerve end-plate are involved in the pathogenesis. However, the visible extent of fasciculations does not correlate with the severity of subsequent pain. Myoglobinuria occurs after administration of succinylcholine, demonstrating that muscle cell injury does occur.

After minor surgery, the patient may be disturbed by the muscle pains to a greater extent than the discomfort caused by the operative procedure. Analgesics such as paracetamol or NSAIDs may be required for 2–3 days to relieve the pain.

It is possible to reduce, but not to eliminate, the incidence of succinylcholine pains by pretreatment with one of the following agents:

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