Communication Failure

Failure of communication is frequently implicated in the generation of complications in the perioperative period. Poor working relationships, varying levels of training amongst staff and poor working conditions make such failure more likely. Team training and simulation-based training are effective in reducing the incidence of this type of error.

 preoperative assessment, investigation and counselling of the patient

 preoperative checking of equipment and the assurance of backup equipment

 the availability of an appropriately trained assistant

 preoperative consultation with more experienced personnel, where necessary, regarding the most appropriate anaesthetic technique

 the use of appropriate monitoring techniques.

Experience

Complications occur more commonly in inexperienced hands. Clearly, finite resources exist, and appropriately experienced personnel are not always allocated to appropriate patients and procedures. It is the individual anaesthetist’s responsibility to ensure that he or she has adequate training for the task presented. If the anaesthetist does not have the necessary experience, then senior assistance must be sought.

Record-Keeping

The maintenance of accurate records of a patient’s treatment and vital signs is of paramount importance in preventing complications. It allows the observation of trends in vital signs, often providing valuable clues to a gradual deviation from a stable physiological state and allowing early intervention before a harmful condition arises. Accurate record-keeping also allows safer sharing of care between anaesthetists, facilitating handover of care during long operations and allowing better teamwork in complex cases in which two anaesthetists are required. It also allows after-the-event investigation and learning – an important system-level mechanism for reducing the impact and incidence of complications.

Redundant Systems

The use of redundant systems helps prevent complications. The availability of at least two working laryngoscopes illustrates this. Should one system fail, another may be put in its place. Other examples include the insertion of two or more intravenous cannulae if significant blood loss is expected, and monitoring of expired volatile agent concentration in addition to depth of anaesthesia monitors to minimize the risk of awareness.

Monitoring

Monitoring systems have been designed to detect and prevent complications during anaesthesia. Aspects of the patient should be monitored that are likely to deviate from the norm, or that are dangerous if they deviate from the norm. The Association of Anaesthetists of Great Britain and Ireland (AAGBI) has produced guidelines stipulating the acceptable minimum level of intraoperative monitoring (see Ch 16).

Modern monitoring systems have automatically activated alarms, and the anaesthetist chooses the values at which these alarms sound. The default values are not always the optimal choices. Thought should be applied to the values at which the anaesthetist gains useful insight into the patient’s deviation from the healthy status quo, without generating unnecessary visual and auditory pollution which may detract from the anaesthetist’s concentration and reduce the effectiveness of the monitor. In general, alarms should sound before the value in question reaches a potentially damaging level, but should not sound at values that would be considered within the patient’s expected range. Clearly, this is different for each patient, whose coexisting disease, age, anaesthesia and surgical procedure vary greatly. The repeated sounding of an alarm should not trigger reflex silencing of the alarm but should cause the anaesthetist to consider if treatment of the patient is required or if the alarm limit should be altered.

Generic Management of Complications

The majority of complications that result in serious harm to the patient compromise the delivery of oxygen to tissues. Organs which are damaged most rapidly by a deficiency in oxygen supply include the brain and heart. The liver and the kidneys are less fragile, but potentially at risk from even short interruptions of oxygen supply. Cessation of perfusion results in more rapid damage to organs than low levels of oxygenation while perfusion is maintained. Treatment must be provided rapidly when organ perfusion is threatened or when arterial oxygenation is impaired. The management of virtually any significant complication should include the provision of a high inspired oxygen fraction and the assurance of an adequate cardiac output.

In general, complications should be dealt with through a sequence of:

The Evolving Problem

The early recognition of an evolving problem allows the anaesthetist time to manage a complication before it damages the patient. Appropriate selection of monitoring alarm limits and the anaesthetist’s vigilance should allow more time for pre-emptive treatment can be provided to reduce the impact of the complication.

The first response to an emerging complication should be to minimize the potential harm to the patient. Such harm may be produced by the anaesthetist’s treatment or by a pathological source. It is important to ensure that an abnormal reading from a monitor is not an artefact; inaccurate information may be displayed if, for example, a pulse oximeter probe is poorly positioned or if an ECG electrode becomes displaced and the anaesthetist should ensure, through rapid clinical assessment of the patient, that the values shown on the monitor screen are consistent with the patient’s clinical appearance and the context. For example, a sudden reading of arterial oxygen saturation of 70% when the values have been greater than 96% throughout the procedure should prompt a rapid examination of the patient; if the patient is not cyanosed and ventilation appears to continue uninterrupted, then the position of the pulse oximeter probe should be checked, particularly if the plethysmograph trace is poor.

In most situations in which complications become apparent, the diagnosis is simple and treatment may progress in a linear fashion. Such linear treatment of complications is detailed later in this chapter. However, the causes of some complications, such as hypoxaemia, are not always immediately clear, and several potential aetiologies may exist. Where the differential diagnoses relating to a problem appear equally likely, the anaesthetist should treat the problem that threatens the most harm to the patient. During the management of problems during anaesthesia, the anaesthetist must constantly be reconsidering the list of differential diagnoses, re-arranging them mentally in order of likelihood and treating the most likely and most dangerous possibilities first.

Record-Keeping

Record-keeping, while useful in preventing complications, is also important during complications. Trends in a patient’s physiological data may become apparent only when charted, and new differential diagnoses may be generated through examination of the recorded data. Review of critical incidents and complications is vitally important in preventing future repetitions of the incident and in providing continuing education to individual practitioners and to Departments of Anaesthesia. Thorough record-keeping is vital in allowing informed review of these cases. Finally, some complications result in harm to the patient and it is very important for the practitioner and the patient that detailed records are available for later review. In a minority of such cases, legal action may result and detailed, legible records are vital in defending the actions of the staff and in providing an adequate explanation to the patient (and possibly to the court) of what happened in the operating theatre.

Management of the Medicolegal Aspects of Complications

Complications must be recognized promptly and treated efficiently, with the patient’s best outcome the aim of treatment. Record-keeping must continue to be meticulous, even during the occurrence of problems during an anaesthetic. Help should be sought early if there is any doubt about the anaesthetist’s ability or experience.

Complaints by patients should be dealt with promptly and professionally. The complaint and the anaesthetist’s response must be recorded clearly in the patient’s records. The anaesthetist should express regret and sympathy that the complication has occurred, and explain why. A frank discussion of the difficulties that occurred during an anaesthetic may provide the patient with sufficient information. If human error has occurred, then the anaesthetist should apologize, and assure the patient that further information will be provided when it becomes available. If the anaesthetist is a trainee, then it is prudent to enlist the assistance of a consultant to attend discussions with the patient. The clinical director should be informed of all discussions with the patient. It may be prudent that the clinical director accompanies the anaesthetist during their dealings with the patient. The results and content of all such discussions must be recorded in the patient’s medical records.

Any complaint that goes further than an informal conversation should be referred to the hospital’s complaints department and the anaesthetist’s defence organization should be informed. The defence organization will provide advice on subsequent action. It must be emphasized that throughout this often distressing process, meticulous and professional record-keeping may make the difference between exoneration and condemnation, irrespective of the true source of fault.

Respiratory Obstruction

Table 43.1 details the common causes of respiratory obstruction during anaesthesia. Obstruction may occur at any point from the gas delivery system through the patient’s airway and bronchi to the expiratory parts of the breathing system and the scavenging tubing. It is common and potentially very dangerous. The commonest sites for obstruction are the larynx (e.g. laryngospasm), the tracheal tube (e.g. biting or secretions) and the bronchi (e.g. bronchospasm). Respiratory obstruction causes inadequate ventilation and impaired gas exchange. This causes hypercapnia, hypoxaemia and reduced uptake of volatile anaesthetic agent. Respiratory obstruction prevents the mass inflow of ambient gas which occurs during apnoea and thus produces hypoxaemia more rapidly than does apnoea with an open airway.

Partial obstruction is indicated by noisy breathing or stridor, while complete obstruction is silent. In spontaneously breathing patients, tracheal tug, paradoxical chest and abdominal movement (‘see-saw’ ventilation) and reduced movement of the breathing system’s reservoir bag are other signs. The generation of a large negative intrathoracic pressure during powerful attempts to inhale may cause pulmonary oedema in some patients, particularly young adults. In patients whose lungs are mechanically ventilated, respiratory obstruction may be associated with increased inflation pressure, a prolonged expiratory phase, hypercapnia and alteration of the end-tidal carbon dioxide waveform.

Laryngospasm

Laryngospasm is a reflex, prolonged closure of the vocal cords. It occurs usually in response to a trigger, and this is often laryngeal stimulation by airway devices, secretions or gastric contents during light anaesthesia. Laryngospasm is most common during induction and emergence. It may also be produced by surgical and visceral stimuli such as skin incision, peritoneal traction and anal or cervical dilatation. Children are particularly prone to laryngospasm. The use of thiopental inhibits laryngeal reflexes to a lesser extent than propofol and increases the risk of laryngospasm. Poor management of laryngospasm may lead to inadequate ventilation with hypoxaemia, hypercapnia and reduced depth of anaesthesia. Crowing inspiratory noises with signs of respiratory obstruction suggest laryngospasm. Complete obstruction caused by severe laryngospasm is silent.

Bronchospasm

General anaesthesia may alter airway resistance by influencing bronchomotor tone, lung volumes and bronchial secretions. Patients with increased airway reactivity from recent respiratory infection, asthma, atopy or smoking are more susceptible to bronchospasm during anaesthesia. Bronchospasm may be precipitated by the rapid introduction of a pungent volatile anaesthetic agent (e.g. isoflurane, desflurane), the insertion of an artificial airway during light anaesthesia, stimulation of the carina or bronchi by a tracheal tube or by drugs causing β-blockade or release of histamine. Drug hypersensitivity, pulmonary aspiration and a foreign body in the lower airway may also present as bronchospasm. Bronchospasm causes expiratory wheeze, a prolonged expiratory phase (evident from the upwardly sloping end-tidal carbon dioxide plateau) and increased ventilator inflation pressures. Wheezing may occur in association with other causes of respiratory obstruction, such as pneumothorax, and these should be excluded. If bronchospasm is very severe, ventilation may be quiet and wheeze may not be apparent.

Difficult Intubation

Some difficulty is experienced during tracheal intubation in about one in ten patients (10%). Approximately one in ten of these patients (1%) presents significant difficulty in intubation. Intubation is impossible in about one in ten of these patients (0.1%), and both intubation and ventilation are impossible in about one in ten of these (0.01%). In most instances, the cause of difficulty with the airway is difficulty in attaining an adequate view of the laryngeal inlet at laryngoscopy.

Poor management of difficult intubation is a significant cause of morbidity and mortality during anaesthesia. Sequelae include dental and airway trauma, pulmonary aspiration, hypoxaemia, brain damage and death. Table 43.2 shows the commonest causes of difficulty in intubation. The single most important cause is an inexperienced or inadequately prepared anaesthetist and the difficulty is often compounded by equipment malfunction. The anatomical features associated with difficult laryngoscopy are listed in Table 43.3. Of these, the atlanto-occipital distance is the best predictor of difficulty but requires a lateral cervical X-ray. Many of these factors are normal anatomical variations, but extreme abnormalities do occur. A cluster of normal variations in an apparently healthy patient may be sufficient to cause major difficulties in laryngoscopy.

Inhalational Induction

Premedication with an antisialagogue is desirable. Depth of anaesthesia is increased carefully by spontaneous ventilation of increasing concentrations of a volatile anaesthetic agent in 100% oxygen until laryngoscopy may be performed safely. Sevoflurane currently provides the best conditions for this purpose. If the larynx is viewed easily, intubation may be performed with or without a muscle relaxant. If the view is limited, a suitable bougie may be inserted to assist passage of the tracheal tube through the larynx. Correct insertion of the bougie in the trachea may be confirmed by detecting the palpable bumps of the tracheal rings or resistance when the carina is encountered. The tracheal tube is then passed over the bougie into the trachea. This manoeuvre is facilitated by rotating the tracheal tube 90° as it passes through the glottis. If intubation during direct laryngoscopy is unsuccessful, anaesthesia may be maintained and the use of fibreoptic laryngoscopy, blind nasal intubation or a retrograde technique considered.

Awake Intubation

Fibreoptic laryngoscopy and intubation require special equipment, skill and time. The procedure may be performed by the nasal or oral route after topical anaesthesia has been achieved by spraying the nasal and oropharyngeal mucosa or gargling viscous preparations of local anaesthetic. The injection of 3–5 mL of 2% lidocaine through the cricothyroid membrane induces coughing and anaesthetizes the tracheal and laryngeal mucosa.

Conventional laryngoscopy can also be performed in conscious patients under local anaesthesia. After cricothyroid injection of lidocaine, laryngoscopy is performed in stages. The oropharynx is progressively anaesthetized with lidocaine spray until the patient tolerates deep insertion of the laryngoscope, enabling the larynx to be viewed.

Failed Intubation

The total incidence of failed tracheal intubation is approximately 1 in 1000 (0.1%), but about 1 in 300 (0.3%) in obstetric patients. However, failed intubation in obstetric patients is now a rare event because of the high percentage of obstetric surgical patients operated on under regional anaesthesia.

Most failed intubations result from the anaesthetist failing to insert the tube, but occasionally the tube may be misplaced, most commonly in the oesophagus. This complication has resulted in many deaths since the advent of tracheal intubation. It should be suspected whenever difficulty has been experienced in inserting a tracheal tube, particularly when direct visual confirmation of the passage of the tube into the larynx has not been possible. Auscultation of the chest is recommended, although inflation of the stomach may occasionally mimic breath sounds. Auscultation over the stomach usually detects a bubbling sound if the oesophagus has been intubated.

Observation of a normal capnogram usually provides assurance of tracheal placement of the tube, but cases have been described of patients who have ‘expired’ carbon dioxide briefly despite oesophageal intubation, having ingested carbonated drinks or bicarbonate antacids shortly before anaesthesia. A normal and persistent expiratory capnogram should be sought as confirmation of tracheal tube placement.

Fibreoptic bronchoscopy provides an excellent method of assuring the location of the tube, but is not usually available in every operating theatre. The ‘Wee’ oesophageal intubation detector tests for the free aspiration of air via the tracheal tube into a rubber bulb. The device is cheap, easy to use and accurate, but total reliance should not be placed on this device. The capnogram is the ‘gold standard’ for confirming correct tracheal intubation.

Poor management of failed intubation is a significant cause of serious morbidity and mortality. The aims of management are to maintain oxygenation and prevent aspiration of gastric contents. The ‘failed intubation drill’ is now established as an important skill for safe anaesthetic practice. An early decision to use a failed intubation protocol and to call for assistance is essential, because continued attempts at tracheal intubation may result in trauma to the airway, pulmonary aspiration or hypoxaemia (see Ch 22). The obstetric patient is a special case and is considered in Chapter 35.

If the airway is obstructed and ventilation is inadequate during management of a failed intubation, then insertion of an LMA should be considered (see Figs 22.3–22.5). It has been used successfully to provide an airway and allow ventilation when attempts to intubate the trachea and ventilate the lungs by other means have failed. Alternatively, it may be possible to pass a small-diameter tracheal tube or a bougie through the LMA into the trachea; a variant of the LMA, the intubating LMA (ILMA) is designed specifically to facilitate tracheal intubation. The LMA should not be regarded as providing protection against pulmonary aspiration, although it is claimed that the ProSeal™ LMA, which has a rearward port for the downward passage of a gastric tube or the upward passage of gastric contents, is better in this regard. The oesophageal obturator airway and similar devices are alternatives in an emergency, but there are doubts about their efficacy and there have been reports of misplacement and oesophageal rupture associated with their use. A recent innovation is an ILMA which incorporates a video camera and LCD screen, allowing direct visualization of the introduction of a tracheal tube through the larynx.

When consciousness cannot be restored rapidly for pharmacological reasons, then transtracheal ventilation can be life-saving. A cannula or small-diameter tracheal tube may be passed via the cricothyroid membrane. Ventilation through a cannula requires high-pressure, ‘jet’ ventilation from a Sanders injector or the high-pressure oxygen outlet of the anaesthetic machine. More conventional ventilation is possible through a small-diameter tube placed via the cricothyroid membrane, but the procedure, which requires a transcutaneous scalpel incision, requires some practice and may result in haemorrhage. Both techniques allow adequate oxygenation for many minutes, and should provide time to allow the patient to awaken. Exhalation through a cricothyroid cannula may be inadequate, and if the laryngeal inlet is not patent then inadequate ventilation and barotrauma may result. In this situation, an additional cannula should be inserted to allow gas to escape.

If it is essential that surgery proceeds without the patient awakening then oxygenation and carbon dioxide elimination must be maintained while ensuring an adequate depth of anaesthesia. Any of the rescue techniques described above may be used, but usually the laryngeal mask or the fibreoptic bronchoscope prove most useful.

Unintentional Bronchial Intubation

Bronchial intubation results in the ventilation of one lung and denial of ventilation to the other. This causes hypoxaemia through the inevitably large pulmonary shunt caused by atelectasis and collapse of the unventilated lung. Intubation of the right main bronchus is more common because of its smaller angle with the trachea. This complication is avoided by cutting the tracheal tube to an appropriate length before intubation, observation of the passage of the tube through the vocal cords and adjusting the length of the tube at the patient’s incisors, and by confirmation of its position by auscultation after intubation and after changes in position of the patient on the operating table.

Aspiration of Gastric Contents

Regurgitation of gastric contents is common during anaesthesia. Frequently, regurgitation proceeds only as far as the mid-oesophagus, but occasionally gastric contents enter the oropharynx. This is particularly likely in patients with a hiatus hernia or a full stomach. The latter may result from recent eating or drinking or may be the result of gastric outlet or bowel obstruction, pain, stress or drugs which delay gastric emptying, such as morphine and alcohol. Once gastric contents enter the oropharynx, there exists the potential for aspiration into the lungs. This is uncommon, but remains an important cause of morbidity and mortality associated with anaesthesia. Aspiration of oropharyngeal contents is more likely if those contents are allowed to remain in the oropharynx for a significant time, and if laryngeal reflexes are depressed. Aspiration may occur also in the sedated patient, whose laryngeal reflexes are diminished. Aspiration is more common during difficult intubation, emergency cases and in obese or pregnant patients.

Mortality is high after aspiration of large quantities of gastric contents and the aspiration of solids, in particular, is associated with a poor prognosis. The acidity of gastric contents is also important in determining the degree of severity of the pulmonary reaction to aspiration, with highly acid material being particularly inflammatory. Bronchospasm may be the first sign of pulmonary aspiration during general anaesthesia. If a large quantity of gastric material is aspirated, respiratory obstruction, ventilation–perfusion mismatch and intrapulmonary shunting may produce severe hypoxaemia, with later development of chemical pneumonitis and/or infection.

Hiccups

Regular and repeated spasmodic diaphragmatic movements may occur after i.v. induction of anaesthesia and in association with vagal stimulation during light anaesthesia. Anticholinergic premedication reduces the incidence of hiccups. Although difficult to treat, hiccups are of little consequence unless surgery, or rarely oxygenation, is compromised. Persistent hiccups may be abolished by deepening anaesthesia, stimulating the nasopharynx with a suction catheter or administering metoclopramide. Profound muscle relaxation may be justified to stop all diaphragmatic movement if hiccups are causing surgical difficulty.

Hypoxaemia

Hypoxaemia is an inadequate partial pressure of oxygen in arterial blood. Hypoxia is oxygen deficiency at the tissue level. A practical classification of the causes of hypoxaemia is shown in Table 43.5. Hypoxaemia threatens tissues globally and, if allowed to persist, risks permanent damage to those organs most delicately dependent upon continued oxygen supply. The first organs to be damaged, most commonly, are the brain and heart, and any pathological impairment of their blood supply increases the risk of early and permanent damage. There is no categorically safe or unsafe level of arterial oxygen tension (PaO₂). The risk presented by a level of hypoxaemia is dependent upon the patient’s haemoglobin concentration, cardiac output, state of hydration, concurrent disease processes (especially vasculopathic diseases) and the duration of exposure to the lowered PaO₂. In general, few patients are harmed by arterial oxyhaemoglobin saturations of greater than 80%, but clearly, this low level provides very little margin for safety should any other complication occur. Most anaesthetists choose to set the arterial oxygen saturation alarm limits on the pulse oximeter at 92–94%.

Severe hypoxaemia produces tachycardia, sweating, hypertension and arrhythmias, although bradycardia is the commoner response in children. Tachypnoea occurs in spontaneously breathing patients. There may also be clinical signs associated with the cause. As arterial desaturation progresses, bradycardia and hypotension (caused by myocardial depression) develop. Eventually, cardiac arrest occurs, usually in asystole. By this stage, the heart, brain, kidneys and liver may have incurred irreversible ischaemic damage.

Hypoventilation is very common during anaesthesia, but in the presence of an adequate inspired oxygen concentration (i.e. over 30%) must be very severe to cause hypoxaemia. Reduction of the ventilatory minute volume from a normal value of 5 L min⁻¹ to 2 L min⁻¹ in the presence of an inspired oxygen concentration of 30% causes arterial oxygen saturation to decrease to only around 90% in an otherwise healthy patient. This represents severe hypoventilation, and produces an arterial carbon dioxide tension of approximately 13 kPa. The pulmonary shunting and atelectasis that can occur during anaesthesia are much more likely to cause hypoxaemia than is hypoventilation.

Apnoea

Apnoea occurs during most anaesthetics. It is eminently treatable, and usually results in no harm to the patient. The occurrence of hypoxaemia, hypercapnia and acidaemia are predictable consequences of prolonged apnoea. The development of hypoxaemia after induction of anaesthesia is often delayed by preoxygenation of the patient’s lungs. However, when hypoxaemia becomes evident, it progresses swiftly and inexorably unless oxygenation of the lungs is restored. Rapid progression of hypoxaemia occurs in the presence of airway obstruction, high oxygen consumption and small FRC. Such factors may appear in combination in small children, pregnancy and obesity. Carbon dioxide is retained during apnoea, and PaCO₂ increases by 0.4–0.8 kPa min⁻¹, while arterial pH decreases by approximately 1.5 h⁻¹ or 0.025 min⁻¹. Atelectasis develops quickly during apnoea under anaesthesia, particularly in obese patients.

As a consequence of its water solubility, very little carbon dioxide enters the lungs during apnoea and the net flow of ambient gas through an open airway and into the alveoli is very nearly equal to the rate of oxygen consumption (i.e. 250 mL min⁻¹). Consequently, adequate oxygenation may be assured for many minutes by the provision of 100% oxygen to the open airway during apnoea. If the airway is obstructed then this mass flow cannot occur and hypoxaemia develops much more quickly. In addition, the intrathoracic pressure may become significantly hypobaric if the airway is obstructed, and this further reduces the alveolar and arterial oxygen tensions.

Hypercapnia

Hypercapnia is an abnormally high partial pressure of carbon dioxide in arterial blood (PaCO₂). Typically, this is indicated by a PaCO₂ greater than 6 kPa. Hypercapnia is caused by either inadequate carbon dioxide removal (e.g. caused by hypoventilation or increased pulmonary dead space) or excessive carbon dioxide production. During anaesthesia, hypercapnia may also result from an inadequate fresh gas flow rate into a semiclosed anaesthetic breathing system, or by exhausted carbon dioxide absorbent in a circle system, resulting in rebreathing of carbon dioxide.

Carbon dioxide production increases during pyrexia, malignant hyperthermia and shivering. Inadvertent or excessive carbon dioxide delivery from the anaesthetic machine and absorption of carbon dioxide during laparoscopic procedures are other causes of hypercapnia.

Hypercapnia stimulates activity of the sympathetic nervous system and causes tachycardia, sweating and arrhythmias (usually ectopics or tachyarrhythmias), increased cerebral blood flow, increased intracranial pressure, tachypnoea and alterations in arterial pressure. As anaesthetic drugs suppress autonomic responses, these signs may not occur during anaesthesia until PaCO₂ is markedly increased. Acute respiratory acidosis produces an increase in serum potassium concentration.

Hypocapnia

Hypocapnia is an abnormally low PaCO₂ (less than 4.5 kPa). The most common cause is mechanical hyperventilation. Decreased carbon dioxide production may occasionally be responsible if the patient is cold or deeply anaesthetized. Hypocapnia produces respiratory alkalosis with a decrease in serum potassium concentration. There is generalized vasoconstriction and reductions in cerebral blood flow, cardiac output and tissue oxygen delivery. Patients with critical cerebrovascular stenosis may risk cerebral ischaemia, but otherwise hypocapnia tends not to produce significant morbidity. There may be a delay in onset of spontaneous ventilation at the conclusion of anaesthesia in which mechanical ventilation has been used while PaCO₂ increases to levels which stimulate ventilation.

Pneumothorax

The causes of pneumothorax include trauma, central venous cannulation especially via the subclavian route, brachial plexus blockade, cervical and thoracic surgery, and barotrauma. Occasionally, pneumothorax may develop spontaneously in patients with asthma, chronic obstructive pulmonary disease, congenital cystic pulmonary disease or Marfan’s syndrome. During anaesthesia, very high mechanically generated peak inspiratory airway pressures greatly increase the risk of pulmonary barotrauma and pneumothorax. Patients with recent chest trauma, asthma or chronic lung disease (particularly with bullae) are most at risk. Pneumothorax significantly reduces ventilation of the affected lung with resultant carbon dioxide retention. Simultaneously, pulmonary shunting often occurs, with resultant hypoxaemia.

Nitrous oxide diffuses into air-filled spaces more rapidly than nitrogen diffuses out, and causes pneumothoraces to expand. Mechanical ventilation forces gas into the pleural space if the lung has been punctured, with a rapid increase in the size of the pneumothorax. Increasing mismatch and hypoxaemia follow. If the pneumothorax is under tension, hypoxaemia, mediastinal shift, reduced venous return and impairment of cardiac output may be life-threatening. A pneumothorax should be excluded during anaesthesia if unexplained tachycardia, hypotension, hypoxaemia, hypoventilation (in the spontaneously breathing patient) or high inflation pressures (in the ventilated patient) occur intraoperatively. Examination may reveal unequal air entry, asymmetrical chest movement, wheeze, surgical emphysema, elevated jugular or central venous pressure, or mediastinal shift. Chest X-ray examination provides a definitive diagnosis, but treatment should not be delayed for this investigation if severe hypoxaemia or hypotension exist and a pneumothorax is suspected.

Atelectasis

The reduction in functional residual capacity and the tendency to hypoventilation which occur during general anaesthesia make alveolar collapse, or atelectasis, common. Atelectasis causes impairment of gas exchange and increases the risk of postoperative chest infection. Risk factors for its development include pre-existing lung disease, lengthy anaesthesia, spontaneous ventilation, high abdominal pressures, high inspired oxygen fractions and the head-down position. Extended exposure of the open airway to atmospheric pressure adds significantly to the risk of alveolar collapse. In particular, prolonged apnoea during anaesthesia (e.g. while awaiting the onset of spontaneous ventilation) causes atelectasis.

Hypertension

Intraoperative hypertension may be defined as an arterial pressure (systolic, mean or diastolic) 25% greater than the patient’s preoperative value. Systolic hypertension increases myocardial work by increasing afterload and left ventricular wall tension. It is often associated with tachycardia, which places additional metabolic demands on the myocardium. Patients with ischaemic heart disease or left ventricular hypertrophy may be placed at risk of myocardial ischaemia or infarction. Chronic hypertension is associated with impaired organ perfusion through atherosclerosis. Acute intraoperative hypertension increases the risks of ischaemia, infarction and haemorrhage in other organs, and in particular, the brain.

Table 43.6 shows the commonest causes of hypertension during anaesthesia. In the absence of pre-existing hypertension, the majority of instances of intraoperative hypertension are related to increased activity of the sympathetic nervous system. This may be associated with tachycardia and arrhythmias. The commonest causes of hypertension are inadequate analgesia, light anaesthesia, surgical stimulation and airway manipulation. Drug administration errors are probably under-recognised underlying causes. However, all instances of intraoperative hypertension must prompt exclusion of awareness and malignant hyperthermia as the cause.

Hypotension

During anaesthesia, hypotension is usefully defined as a mean arterial pressure 25% less than the patient’s usual, resting value. Hypotension may impair perfusion and, consequently, oxygenation of vital organs. During anaesthesia, myocardial and cerebral metabolic rates are reduced significantly, and intraoperative hypotension is less likely to cause permanent damage to these organs than would be the case in the conscious state. However, pathological processes (e.g. atherosclerosis) commonly compromise the arterial supply to organs, and hypotension during anaesthesia occasionally results in critical loss of flow to vital organs. Left ventricular coronary artery flow occurs predominantly in diastole, and diastolic arterial pressure is particularly important in determining myocardial viability in patients with ischaemic heart disease.

Hypotension is caused by decreases in cardiac output or systemic vascular resistance. Table 43.7 shows the common causes of intraoperative hypotension. Most anaesthetic agents cause vasodilatation and have a negative inotropic effect, and moderate hypotension is very common during anaesthesia, particularly before the start of surgery when there is no physical stimulation to counteract the effects of anaesthetic drugs. Concurrent hypovolaemia caused by preoperative fluid restriction, in combination with haemorrhage or concurrent antihypertensive drugs, may result in decreases in mean arterial pressure during anaesthesia and surgery. A mean arterial pressure of 50 mmHg or less is potentially damaging, even in healthy individuals, and should not be allowed to persist. The patients most at risk from the effects of hypotension are, unfortunately, often the patients most likely to develop it because of concurrent medications, poor myocardial reserve and atherosclerosis. Elderly or hypertensive patients should, therefore, be observed carefully for the development of hypotension, and it should be treated promptly.

Hypovolaemia

Hypovolaemia is a common intraoperative cause of hypotension. Its common aetiologies are listed in Table 43.8. The additive effects of anaesthesia, positive-pressure ventilation and hypovolaemia may cause sudden and severe hypotension, which may be life-threatening. All patients who are undergoing surgery, and in particular patients who require emergency surgery, should be assessed preoperatively with regard to intravascular fluid volume and fluid balance. Signs of hypovolaemia include thirst, dryness of mucous membranes, cool peripheries, oliguria (urine output < 0.5 mL kg⁻¹ h⁻¹), reduced tissue turgor, tachycardia and postural hypotension. Patients treated with a β-blocking drug may not develop a compensatory tachycardia despite being hypovolaemic. Fluid deficit and replacement are easily underestimated, especially in patients with intestinal obstruction or concealed haemorrhage. Surgery, unless immediately life-saving, should be delayed to allow adequate fluid resuscitation and restoration of intravascular volume. The response of central venous pressure (CVP) to fluid challenges is a useful guide when assessing and treating patients with significant hypovolaemia. Hypokalaemia and other electrolyte abnormalities are often associated with fluid deficits, particularly when there have been gastrointestinal losses.

In the presence of hypovolaemia, hypotension after induction of anaesthesia is often exaggerated in the elderly and in patients with decreased cardiac reserve or pre-existing hypertension. It is made less likely by fluid preloading and by titration of the induction agent to effect. Etomidate and ketamine produce less cardiovascular depression than do other induction agents.

Blood loss during surgery may be concealed. The anaesthetist must note carefully the total loss in suction jars, swabs and spillage. Body water is lost during anaesthesia and surgery in urine, sweat and exhaled breath. Adequate intraoperative fluid replacement must account for all of these losses. During abdominal surgery, up to 5 mL kg⁻¹ h⁻¹ may be required to replace evaporative and third-space losses in addition to maintenance requirements and replacement of blood loss.

Haemorrhage

Haemorrhage is the loss of blood and is inevitable during most forms of surgery. Loss of a significant proportion of the total intravascular volume threatens the patient’s well-being. Hypovolaemia causes reduced tissue perfusion, while loss of red cell mass causes reduced oxygen carriage in arterial blood. There is no safe degree of haemorrhage, in that patients differ in their ability to tolerate blood loss. Anaemic or hypovolaemic patients are less able to compensate for haemorrhage than healthy patients. Patients with pre-existing compromise of vital organ perfusion (e.g. patients with diabetes mellitus or hypertension) suffer deleterious consequences of haemorrhage sooner than healthy patients. In general, adults who have lost 15% of circulating blood volume may require red blood cell transfusion to maintain oxygen-carrying capacity.

Blood loss can be estimated by weighing swabs, measuring the volume of blood in suction bottles and assessing the clinical response to fluid therapy. Estimation is often difficult if large volumes of irrigation fluid have been used, e.g. during transurethral resection of the prostate. Intraoperative measurement of haemoglobin concentration aids estimation of blood loss and guides therapy. With severe or ongoing haemorrhage, maintenance of intravascular volume is essential. When the cardiac output is preserved, very severe anaemia is often well tolerated for short periods, but low tissue blood flow in the presence of anaemia may produce rapid and irreversible organ damage.

Massive blood loss may require the administration of stored blood, fresh frozen plasma, clotting factors and electrolytes. The problems of massive transfusion are discussed in Chapter 13.

Disturbances of Heart Rate

Myocardial Ischaemia

The heart has the highest oxygen consumption per tissue mass of almost all the organs (second only to the carotid body). Resting coronary blood flow is 250 mL min⁻¹ and represents 5% of the cardiac output. The oxygen extraction ratio of the myocardium is 70–80%, compared with an average of 25% for other tissues. Increased oxygen consumption must be matched by an increase in coronary blood flow. Ischaemia results when the oxygen demand outstrips supply. Even very brief reductions in supply result in ischaemia, which may lead rapidly to infarction and permanent loss of muscle function in the affected area.

Myocardial oxygen delivery is the product of arterial oxygen content and coronary artery blood flow. The diastolic pressure time index (DPTI) reflects coronary blood supply. It is the product of the coronary perfusion pressure (predominantly diastolic arterial pressure) and diastolic time. Oxygen demand is represented by the tension time index (TTI), the product of systolic pressure and systolic time.

The ratio of DPTI/TTI is the endocardial viability ratio (EVR) and represents the myocardial oxygen supply–demand balance. The EVR is usually greater than one. A value of less than 0.7 is associated with subendocardial ischaemia. Such a value may be reached in a patient with the data shown in Table 43.10.

It is clear from the above that tachycardia is particularly dangerous in generating myocardial ischaemia, while systolic hypertension and diastolic hypotension may also contribute. Patients with coronary artery disease are most at risk. Intraoperative myocardial ischaemia may manifest clinically as arrhythmia, hypotension or pulmonary oedema. It is diagnosed by ECG ST-segment changes (usually depression), although these are not always detected reliably without computer-assisted analysis. The use of the V5 electrode is recommended for ECG monitoring in susceptible patients (e.g. the CM5 configuration; see Ch 16) because it is the most sensitive ECG lead for the detection of left ventricular ischaemia. When used alone, it may detect up to 85% of the ST abnormalities on a standard 12-lead ECG.

Transoesophageal echocardiography may detect abnormal myocardial wall motion, which is a sensitive indicator of ischaemia and is associated with increased perioperative morbidity. Regional wall dysfunction often persists into the postoperative period without clinical signs. Increased myocardial work during this period (e.g. from pain) may precipitate further ischaemia or infarction in susceptible patients. While the risk of infarction in the general surgical population is low, the overall mortality rate following perioperative myocardial infarction approaches 50%.

Thromboembolus

Embolization of thrombus occurs usually from the deep veins of the legs or pelvis. It is uncommon during anaesthesia. It is often preceded by a period of immobilization, so that patients whose hospital stay is extended or who have suffered major trauma are at highest risk. Other risk factors include malignancy, smoking, pelvic and limb surgery, the oral contraceptive or hormone replacement therapy, and a past history of venous thromboembolism. Venous stasis caused by venous compression, hypovolaemia, hypotension, hypothermia or the use of tourniquets also increases the risk of deep venous thrombosis. Veins may sustain trauma during positioning and surgery, and increased blood coagulability, with a consequent increase in the risk of venous thrombosis, is a consequence of the stress response to surgery.

During anaesthesia, pulmonary thromboembolism may present with tachycardia, hypoxaemia, arrhythmia, hypotension, bronchospasm, an acute decrease in the end-tidal carbon dioxide concentration or cardiovascular collapse.

Gas Embolus

Gas usually enters the circulation through a surgical wound. A subatmospheric venous pressure greatly encourages the entrainment of air into the venous system. Therefore, positions that place the operative site above the right atrium carry an increased risk of air embolism. Such positions include sitting, park bench, knee-chest and head-up. Vascular catheters are another potential route for air entry, particularly during their insertion. Gas embolism (usually carbon dioxide) may also occur during laparoscopy and thoracoscopy.

Clinical presentation varies with the volume and rate of gas entry into the circulation. An entry rate of 0.5 mL kg⁻¹ min⁻¹ has been reported to produce clinical signs. If a significant volume of gas enters the right side of the heart, an airlock may develop, preventing ejection of blood and effectively halting cardiac output. A ‘millwheel murmur’ may be heard via a precordial or oesophageal stethoscope, although this is reported to be a late sign and only occurs with very large emboli. The sudden decrease in right ventricular output results in a rapid decrease in end-tidal carbon dioxide concentration. Hypoxaemia, tachycardia, ECG changes (especially arrhythmia) and an increase in pulmonary artery pressure follow.

Transoesophageal echocardiography and precordial Doppler ultrasound are the most sensitive monitors for gas embolus. Clinical and ECG signs have a low sensitivity for detection of gas embolism. As the foramen ovale is potentially patent in more than 25% of the population, an increase in right heart pressure may open the foramen in these patients. Paradoxical gas embolism via this route or across the pulmonary capillary bed to the coronary or cerebral circulations may cause myocardial or cerebral ischaemia and infarction.

Other Emboli

Fat dislodged from long bone fractures may embolize to the lungs. Patients typically develop sudden mental disturbance, shortness of breath, hypoxaemia, and axillary and subconjunctival petechiae. Onset is usually 2–48 h after the injury. Fat globules may be seen in the urine and sputum, or in the retinal vessels during fundoscopy. There should be a high index of suspicion if unexpected haemodynamic events or hypoxaemia occur in patients undergoing surgery for pelvic or lower limb fractures. Treatment is with intravenous fluids, steroids and ventilatory support as necessary. The use of intravenous albumin to bind free fat is controversial.

Other material which may embolize includes tumour fragments, amniotic fluid and orthopaedic cement. Air or clot may embolize via arterial cannulae and produce distal ischaemia.

Awareness

Recall of intraoperative events occurs in 0.03–0.3% of anaesthetics. Such recall may be spontaneous, or may be provoked by postoperative events or questioning. Awareness during anaesthesia may be a very distressing event for a patient, particularly if it is accompanied by awareness of the painful nature of an operation or the presence of paralysis. However, the majority of recalled events are not painful, and 80–90% of patients recalling intraoperative events have not experienced pain. Awareness may have psychological sequelae including insomnia, depression and post-traumatic stress disorder (PTSD) with distressing flashbacks.

The risk of awareness correlates with depth of anaesthesia. Light anaesthesia, particularly when the patient is paralysed by muscle relaxants, is associated with the highest risk of awareness. Awareness is associated frequently with poor anaesthetic technique. Errors include the omission or late commencement of volatile agent, inadequate dosing or failure to recognize the signs of awareness. Underdosing of anaesthetic agent may occur during hypotensive episodes, when anaesthetic is withheld in an attempt to maintain arterial pressure. Breathing system malfunctions, misconnections and disconnections have been associated with awareness.

The signs of awareness in a paralysed patient arise from activation of the sympathetic nervous system (sweating, tachycardia, hypertension, tear formation), and dilatation and reactivity to light of the pupils. Unparalysed patients experiencing noxious stimulation may move or grimace. Depth of anaesthesia may be assessed through clinical examination, monitoring of the patient’s expired volatile agent concentration or using specialized monitoring equipment. Such equipment includes processed electroencephalography such as the bispectral index and auditory evoked potential monitoring systems. If the end-tidal concentrations of inhaled anaesthetic agents summate to a total of greater than about 0.8–0.9 MAC, it is exceptionally unlikely that a patient experiences intraoperative awareness.

Awareness is more likely to occur during emergency and obstetric surgery, during neuromuscular paralysis, during periods of hypotension and in patients treated with a β-blocker (which prevents tachycardia and hypertension). The use of intravenous drugs for maintenance of anaesthesia (e.g. propofol target-controlled infusion) may be associated with an increased risk of awareness compared with the use of inhaled anaesthetic agents. It is not possible currently to monitor, in real time, the concentration of intravenous agents in blood, while it is possible to monitor exhaled volatile agents. Additionally, the scatter about the mean of the minimum inhibitory concentration (MIC) for intravenous agents is greater than the equivalent for inhaled agents (MAC).

Ischaemia of the Central Nervous System

Transient disruptions of central nervous system (CNS) perfusion and oxygenation are common during anaesthesia. However, prolonged reduction in oxygenation of the CNS may result in ischaemia or infarction. Ischaemic injury varies from minimal, focal dysfunction to stroke or death. The mechanism is related usually to hypoxaemia and/or hypotension. The risk of ischaemic brain damage related to hypotension is increased in patients with atherosclerosis, and, in particular, cerebrovascular disease. A history of previous transient ischaemic attacks or stroke makes CNS injury much more likely during anaesthesia. Rarely, intracerebral haemorrhage may occur during anaesthesia, with consequent local compression and downstream ischaemic injury. Although the risk is increased if arterial pressure has been very high, there have been reports of intracerebral haemorrhage during anaesthesia without episodes of hypertension. It is likely that previously undetected vascular abnormalities were present in these cases.

The cervical spinal cord may be damaged during tracheal intubation and positioning in patients with cervical spine instability from fractures, rheumatoid arthritis or congenital conditions such as Down’s syndrome. Extreme rotation, flexion or extension of the neck may cause cerebral ischaemia because of vertebrobasilar insufficiency in susceptible patients. Ischaemic spinal cord injury may also occur during major vascular and spinal surgery, when the local arterial supply may be compromised.

Peripheral Nerve Injury

Peripheral nerves may be injured through hypotension and hypoxaemia, but they are far more resistant than is the CNS. Peripheral injuries occur more commonly because of poor positioning or direct injury during nerve blockade or vascular catheter placement. This topic is dealt with in more detail later in this chapter.

Hypothermia

Body temperature very commonly decreases during anaesthesia. A decrease to a core temperature below 36 °C represents hypothermia. Hypothermia causes physiological derangement and increases perioperative morbidity (see also Ch 11).

Heat production is decreased during anaesthesia. Anaesthetic agents alter hypothalamic function, reduce metabolic rate, abolish behavioural responses to heat loss and abolish shivering. Heat loss increases during anaesthesia and surgery because of heat redistribution to the peripheries by vasodilatation and increased radiation by the exposure of large, moist surfaces. Evaporative heat loss is increased by ventilation of the lungs with cold dry gas, the use of wet packs and operations on open body cavities. Heat loss is exacerbated by low ambient temperature, and high air flow in the operating theatre promotes convective and evaporative loss. Irrigation and intravenous infusion of cold fluids are also associated with increased heat loss. The risks of hypothermia are greatest in neonates and infants, patients with a low metabolic rate (such as the elderly) and patients with burns.

The effects of hypothermia are dependent upon the change in core temperature. Metabolic rate reduces by approximately 10% for each 1 °C reduction in core temperature. Cardiac output decreases and the affinity of haemoglobin for oxygen is increased, causing a reduction in tissue oxygenation. Significant hypothermia is associated with metabolic (lactic) acidosis, oliguria, altered platelet and clotting function, and reduced hepatic blood flow with slower drug metabolism. The MAC of volatile agents is reduced (also by approximately 10% for each 1 °C decrease) and muscle relaxants have a longer and more variable duration of effect. Postoperative shivering increases oxygen consumption and myocardial work. Peripheral vasoconstriction increases afterload, further increasing the risk of myocardial ischaemia. Hypothermia also increases the risk of postoperative infections because of suppression of function of the immune system.

Hyperthermia

Hyperthermia during anaesthesia may be defined as a core body temperature greater than 37.5 °C and is usually caused by an increase in heat production. Common causes include sepsis and infection, drug reactions (anaphylaxis, incompatible blood transfusion), excessive catecholamine activity (phaeochromocytoma, thyroid storm) and malignant hyperthermia. Elevated metabolic rate may lead to acidosis. Without treatment, sweating and vasodilatation produce hypovolaemia and tissue hypoxia. Seizures and CNS damage may ensue.

Malignant Hyperthermia

Malignant hyperthermia (MH) is an inherited disorder of muscle. The incidence varies geographically from 0.02% to 0.002% (1 in 5000 to 1 in 50 000). MH had a mortality rate of 75% at the time it was identified in 1960. Treatment consisted of cooling the patient and treating complications as they arose. The cause was then unknown, and could not be treated. Currently, mortality is approximately 5%. Increased awareness amongst anaesthetists has resulted in earlier diagnosis and treatment. Since 1979, dantrolene has been available for the treatment of MH and has resulted in the dramatic decline in death and disability from the condition.

Malignant hyperthermia is an inherited disorder. Mutations in the human ryanodine receptor in skeletal muscle (a calcium-release channel with a role in excitation-contraction coupling) are apparent in some families. Predisposition to MH has been identified in only three rare clinical myopathies. Abnormal calcium release and re-uptake by the sarcoplasmic reticulum lead to myofibrillar contraction, depletion of high-energy muscle phosphate stores, accelerated metabolic rate, increased carbon dioxide and heat production, increased oxygen consumption and metabolic acidosis. The usual triggering agents are succinylcholine or any volatile anaesthetic agent.

The MH syndrome may present at any time during the perioperative period. The clinical features and their severity vary considerably. The most consistent and early signs are unexplained tachycardia and an increase in the end-tidal PCO₂. Spontaneously breathing patients may present with tachypnoea. MH should be considered in any anaesthetized patient if core temperature increases during anaesthesia. Core temperature increases typically by 2 °C h⁻¹ and may exceed 40 °C. Muscle rigidity is common and usually involves the limbs and jaw. Without treatment, the full MH syndrome may develop, with sweating, cyanosis, mottled skin, hypoxaemia, ventricular arrhythmias and severe metabolic and respiratory acidosis. Muscle injury causes significant potassium release, with ECG signs of hyperkalaemia. Coagulopathy hypocalcaemia, oliguria, myoglobinuria and acute renal failure are other sequelae.

Masseter muscle rigidity (MMR) occasionally complicates anaesthesia, particularly following administration of succinylcholine. This progresses to MH in approximately 10% of cases.

Anaesthesia for the MH-Susceptible Patient

A ‘clean’ anaesthetic machine is used, and this may be prepared by flushing the machine for 12 h with 100% oxygen and by using a new breathing system. Contact with volatile agents and succinylcholine is absolutely contraindicated. Regional anaesthesia should be used if possible. If general anaesthesia is unavoidable, then total intravenous anaesthesia with propofol is recommended. Dantrolene is not usually used as a premedicant, but should be immediately available throughout the perioperative period. Monitoring of end-tidal carbon dioxide concentration, ECG, arterial pressure, oxygen saturation and core temperature is mandatory.

Hypersensitivity

Susceptible patients may display an enhanced immunological reaction to a trigger, which may be a drug or an environmental agent. These hypersensitivity reactions may be anaphylactic or anaphylactoid. Some drugs produce histamine release directly, without an immunological basis.

The incidence of anaphylaxis varies according to the antigen involved. Of the intravenous drugs, reactions are most commonly to muscle relaxants (1 in 5000 to 1 in 10 000). Succinylcholine is the most immunogenic, although reactions to all non-depolarizing relaxants have also been reported. The majority of reactions are IgE-mediated. There is significant cross-reactivity between muscle relaxants and other drugs which contain a quaternary ammonium group. Pancuronium appears to be the least likely muscle relaxant to cause anaphylaxis.

Reactions to intravenous induction agents are far less common (1 in 15 000 to 1 in 50 000). Hypersensitivity to benzodiazepines and etomidate is rare and these drugs do not cause direct histamine release.

Hypersensitivity to local anaesthetics is very rare. Reactions are more likely to be the result of dose-related toxicity, sensitivity to the effects of added vasoconstrictor or a reaction to preservatives such as paraben, sulphites and benzoates. Amide local anaesthetic agents are less allergenic than esters.

Antibiotics are frequently implicated in allergic reactions. Penicillins are most often to blame, and there is cross-reactivity with cephalosporin antibiotics in 10% of penicillin-allergic patients.

Latex is emerging as one of the more important causes of anaphylaxis during anaesthesia and surgery. Reactions usually begin 30–60 min following exposure, and may be very severe. Previous frequent exposure to latex (e.g. spina bifida) is a strong risk factor for latex allergy. There is often a history of intolerance to some foods, including banana and avocado. Many medical devices contain latex (e.g. arterial pressure cuffs, surgical gloves), and it is important that all such products are eliminated from the care of latex-susceptible patients.

Anaphylaxis also occurs in response to radiocontrast media, blood products, colloid solutions, protamine, streptokinase, aprotinin, atropine, bone cement and opioids. Allergic reactions to volatile agents are exceptionally uncommon.

Anaphylaxis (type 1 hypersensitivity) is an IgE-mediated reaction to an antigen. Antibodies bind to mast cells, which degranulate, releasing the chemical mediators of anaphylaxis. These include histamine, prostaglandins, platelet-activating factor (PAF) and leukotrienes. The signs produced by the actions of these mediators of anaphylaxis include urticaria, cutaneous flushing, bronchospasm, hypotension, arrhythmia and cardiac arrest. Only one of these signs may be present, and it is important to have a high index of suspicion. Anaphylaxis has been reported in patients without apparent previous exposure to the specific antigen, probably because of immunological cross-reactivity. This is true particularly of reactions to muscle relaxants; cosmetics and some foods contain structurally similar compounds.

Anaphylactoid reactions are not IgE-mediated, although the clinical presentation is identical to anaphylaxis. The precise immunological mechanism is not always evident, although many reactions involve complement, kinin and coagulation pathway activation.

Non-immunological histamine release is caused by the direct action of a drug on mast cells. The clinical response depends on both the drug dose and the rate of delivery but is usually benign and confined to the skin. Anaesthetic drugs which release histamine directly include d-tubocurarine, atracurium, doxacurium, mivacurium (all of similar chemical derivation), morphine and pethidine. Clinical evidence of histamine release, usually cutaneous, occurs in up to 30% of patients during anaesthesia. However, some very serious reactions have been reported in association with administration of atracurium and mivacurium.

Hypersensitivity reaction should be considered in the differential diagnosis of any major cardiorespiratory problem during anaesthesia. Reactions are more common in women, and in patients with a history of allergy, atopy or previous exposure to anaesthetic agents. Over 90% of reactions occur immediately after induction of anaesthesia. There is a clinical spectrum of severity from the mildest urticaria to immediate cardiac arrest. Coughing, skin erythema, difficulty with ventilation and loss of a palpable pulse are common early signs. Reactions often involve a single, major physiological system (e.g. bradycardia and profound hypotension without bronchospasm). This may make diagnosis confusing, but every instance of bronchospasm, unexpected hypotension, arrhythmia or urticaria should be considered to be due to anaphylaxis until proved otherwise. Erythema of the skin may be short-lived or absent because cyanosis from poor tissue perfusion and hypoxaemia may occur rapidly and be profound. The conscious patient may experience a sense of impending doom, dyspnoea, dizziness, palpitations and nausea. The differential diagnosis includes anaesthetic drug overdose and other causes of bronchospasm, hypotension or hypoxaemia.

Anaesthesia in the Susceptible Patient

Unless the patient is allergic to local anaesthetics, regional anaesthesia should be used if possible. If the patient requires general anaesthesia, the preoperative use of corticosteroids and histamine H₁– and H₂-receptor antagonists should be considered as prophylaxis. The anaesthetic technique chosen should avoid re-exposure to implicated agents. Drugs should be chosen that have a low potential for hypersensitivity and direct histamine release. Typically safe drugs include volatile agents, etomidate, fentanyl, pancuronium and benzodiazepines. All drugs should be given slowly in diluted form, and resuscitation facilities must be immediately available.

Other Drug Reactions

An idiosyncratic drug reaction is a qualitatively abnormal and harmful drug effect which occurs in a small number of individuals and is precipitated usually by small drug doses. There is often an associated genetic defect and the reaction may be severe or even fatal.

Succinylcholine sensitivity, malignant hyperthermia (see above) and acute intermittent porphyria are important examples of drug idiosyncrasy in anaesthetic practice.

Central Techniques

Epidural and subarachnoid anaesthesia are often chosen to reduce the patient’s perioperative risk. However, these techniques may pose independent risks.

Local Anaesthetic Toxicity

Local anaesthetic drugs may cause toxic side-effects when excessive serum concentrations are achieved. This is most commonly caused by accidental intravenous injection, excessively rapid absorption or absolute overdosage. Some sites of injection display a much more rapid uptake into the systemic circulation, usually because of local vascularity. Intercostal nerve blocks result in higher serum concentrations than subcutaneous infiltration, which produces higher serum concentrations than plexus blocks.

Cerebral symptoms occur first. Dizziness, drowsiness, confusion, tinnitus, circumoral tingling, anxiety and a metallic taste are common signs of toxicity. Patients should be asked about the presence of these symptoms. In severe toxicity, tonic-clonic convulsions occur. Cardiovascular symptoms include bradycardia with hypotension, although solutions which contain adrenaline may produce tachycardia and hypertension. Cardiovascular collapse occurs usually at 4–6 times the serum concentration at which convulsions occur. Local anaesthetics directly depress the myocardium and cause systemic vasodilatation. Cardiovascular collapse occurs earlier with bupivacaine than with lidocaine because of myocardial binding. Severe and intractable arrhythmias may occur with accidental intravenous injection. The toxicity of local anaesthetics is increased by a rapid rate of increase of serum concentration. Thus, a rapid intravenous injection of a small dose has the potential to cause toxicity.

Cutaneous and Muscular Injury

Skin is damaged easily by poor or prolonged positioning, the use of highly adhesive tape and incautious movement of the patient. In particular, elderly patients and patients who have been treated with steroids for a prolonged period may have very fragile skin, and this must be protected. These patients also tend to heal very slowly, and an apparently minor skin injury may produce many months of suffering postoperatively. Pressure sores which originate during the intra-operative period are increasingly recognised. Muscle injury is produced most commonly by poor positioning, but tourniquets may also cause direct muscle damage.

Peripheral Nerve Injury

Peripheral nerves may be injured directly, through peripheral nerve blockade or vascular catheter insertion or surgery, indirectly, by poor positioning during anaesthesia, or through ischaemia during severe hypoxaemia or hypotension. Peripheral nerve injury occurs during 0.1% of anaesthetics. The position of the patient during general anaesthesia is the commonest cause of injury. The brachial plexus and superficial nerves of the limbs (ulnar, radial and common peroneal) are the most frequently affected nerves. The usual mechanism of injury to superficial nerves is ischaemia from compression of the vasa vasorum by surgical retractors, leg stirrups or contact with other equipment. Nerve injury may occur as part of a compartment syndrome after ischaemia from poor positioning, particularly when the legs are placed in Lloyd-Davies supports and the patient is positioned head-down. Ischaemic injury is more likely to occur during periods of poor peripheral perfusion associated with hypotension or hypothermia. Nerves may also be injured by traction (e.g. the brachial plexus during excessive shoulder abduction).

Meticulous care is necessary when positioning the patient. Padding should be used beneath tourniquets and to protect pressure points. Extreme joint positions should be avoided. Close surveillance of tourniquet ischaemia times is essential. Although many injuries recover within several months, all patients with a peripheral nerve injury must be referred to a neurologist for assessment and continuing care. Many ulnar nerve palsies occur in patients with an anatomical predisposition, and this may be deduced from a history of numbness after sleep or as a result of posture at work. In these patients, the elbows should not be placed in flexion during surgery.

Injury During Airway Management

Dental damage is the most frequently reported anaesthetic injury and is usually sustained during laryngoscopy. Damage to teeth is much more likely if laryngoscopy is difficult. Most dental injuries result from a rotational force applied to the laryngoscope during attempts to lever the tip of the laryngoscope blade upwards using the upper incisors as a fulcrum. The correct, and much safer, practice is to apply a force upwards and away from the anaesthetist without any leverage on the incisors. Injuries vary from chipped teeth to complete avulsion. The upper incisors are most commonly involved. Preoperative assessment and documentation of dentition are essential. Patients with poor dentition, or in whom a difficult laryngoscopy is anticipated, should be warned of the possibility of dental injury. If a tooth is accidentally avulsed, it should be reimplanted in its socket with minimal interference and a dental surgeon consulted at the earliest opportunity.

Mucosal damage is common during airway management, and mucosal abrasion may be very painful postoperatively. Overinflation of the cuff of a tube in the larynx or trachea may produce local ischaemia, with consequent scarring and stenosis; cuff pressure should be checked regularly, particularly during prolonged surgery and when nitrous oxide is used. Other reported injuries include dislocated arytenoid cartilages (intubation), recurrent laryngeal nerve damage (laryngoscopy), uvular ischaemia (Guedel airway), epistaxis and nasal turbinate fracture (nasal intubation).

Ophthalmic Injury

Retinal ischaemic injury may follow prolonged pressure on the orbit from equipment or the use of the prone position. Permanent blindness may result. Corneal abrasions are associated with inadequate eye protection, especially during transfer or use of the prone position. The use of adhesive tape to close the eyelids is also a risk factor. Lubricated dressings such as sterile paraffin gauze may be a preferable method of securing the eyelids.

Thermal and Electrical Injury

The high-density electrical current of surgical diathermy is a potential source of injury. If the return current path is interrupted by incorrect application of the diathermy pad, then the ECG electrodes or other points of contact between skin and metal may provide an alternative electrical path, producing serious burns. Failure of thermostatic control on warming devices is a potential source of thermal injury. Warming devices should always be used in accordance with the manufacturer’s guidelines. In particular, hot air hoses used to inflate convective warming blankets must never be used alone to blow hot air under the patient’s blankets, as serious thermal injury may result. Ignition of alcohol-based surgical preparation solutions is possible, especially if they are not allowed to evaporate fully and if diathermy is used. Airway fires have occurred during laser surgery to the larynx; it is advisable to use a low inspired oxygen fraction and omit nitrous oxide in this situation.

Fires should be extinguished immediately and the area should be soaked in cool saline or covered with saline-soaked swabs. If the burned area is significant, the opinion of a burns surgeon should be sought.

Vascular Injury and Tourniquets

Arterial catheters may produce significant arterial injury, resulting in ischaemia and, potentially, loss of the distal limb. Arterial tourniquets reduce surgical bleeding but also rob the distal tissue of its perfusion. An absolute maximum duration of 2 h should be observed, and inflation pressures should be just high enough to occlude arterial flow. Typically, a pressure of 200–250 mmHg is adequate for the upper limb, and 250–300 mmHg for the lower limb. Vascular occlusion (e.g. during tourniquet use, aortic cross-clamping) risks distal ischaemia and infarction. Assurance of an adequate arterial pressure and oxygen saturation is important in facilitating distal oxygenation via collateral flow. Parts distal to an arterial occlusion should never be warmed, because this raises local metabolic rate and causes the onset of ischaemia to be more rapid.