Complications During Anaesthesia
Complications are unexpected and unwanted events. They occur in approximately 10% of anaesthetics. Only the minority of these complications cause lasting harm to the patient. Death complicates five anaesthetics per million given in the UK (0.0005%). Every complication has the potential to cause lasting harm to the patient. Therefore, deviations from the norm must be recognized and managed promptly and appropriately.
The most frequent complications during anaesthesia are arrhythmia, hypotension, adverse drug effects and inadequate ventilation of the lungs. Inadequate ventilation may be caused by poorly managed or difficult tracheal intubation, pulmonary aspiration of gastric contents, breathing system disconnections or gas supply failure. These complications are also the major causes of anaesthetic mortality, preventable intraoperative cardiac arrest and permanent neurological damage. In particular, hypotension and hypoxaemia are implicated consistently in studies of adverse outcome from anaesthesia.
Human error is a common contributor to anaesthetic complications, often in association with poor monitoring, equipment malfunction and organizational failure. Human error is commonly associated with poor training, fatigue, inadequate experience and poor preparation of the patient, the environment and the equipment. These conditions are, generally, avoidable, and good organization should usually prevent such circumstances. When complications do occur, effective monitoring and vigilance allow a greater period for action before the complication grows in severity. During this ‘window’, when the complication is apparent but has not yet damaged the patient, the anaesthetist must act with precision. Such precision of action may be obtained through the use of ‘action plans’ or ‘drills’ that have been rehearsed previously.
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.
Equipment failure may result in significant risk to the patient. In particular, failures of breathing systems, airway devices and gas supplies have resulted in several deaths in recent years. In addition, malfunction of mechanical infusion pumps and infusion pressurizing devices have caused injury and death in several cases. Meticulous checking of equipment before use is mandatory. The anaesthetist must not only ensure the correct functioning of items of equipment that may be life-saving or of critical importance but must also ensure that alternative devices are available should the primary device fail.
Some complications stem from the deterioration of the patient’s medical condition, which may have existed before the anaesthetist’s involvement. While such deterioration may be coincidental, it must be recognized that anaesthesia and surgery frequently introduce altered conditions into a patient’s finely balanced combination of pathology and compensatory physiology. This may be sufficient to generate instability in the patient’s condition and result in sudden worsening of an apparently stable pathology. Typical examples include diabetes mellitus, angina, hypertension and asthma.
There exists a subgroup of complications which may be classed as ‘inevitable’. Despite excellent surgical and anaesthetic practice, the patient may still experience a complication that brings morbidity or even death. While we must, at all times, make stringent efforts to save our patients from harm, it is also important to recognize that it is not always necessary to place the blame for a complication on a healthcare provider.
The most effective steps in preventing harm from complications are implemented before the complication occurs. Thorough preparation should prevent the majority of complications. This preparation includes:
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.
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.
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 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.
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.
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, 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.
A minority of complications result in a formal complaint, but litigation by patients who feel that they have been wronged by the healthcare system is becoming increasingly common. Defensive practice is consequently becoming widespread. Such practice aims to reduce the potential culpability of the anaesthetist should complications arise. In some situations, this may lead to overinvestigation of patients and even to the provision of care which is not necessarily optimal for the patient. The ‘culture of blame’ in which we now practise dictates that anaesthetists must protect themselves as well as their patients. Meticulous record-keeping, preoperative information and consent, and frank discussion of risks with the patient are vital.
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.
The presentation, causes and management of the most common and most dangerous complications which occur during anaesthesia are described below. Complications are classified, where possible, according to the body system involved. Some complications (such as hypothermia) do not fit easily into this classification and are described separately. This list of complications is not exhaustive and the reader is encouraged to consult the texts listed at the end of the chapter.
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.
Management: Any significant airway obstruction should be treated by gentle, manual ventilation of the patient’s lungs with oxygen. Location of the site of obstruction should be sought urgently. In the absence of a laryngeal mask airway (LMA) or tracheal tube, apposition of the tongue and pharyngeal soft tissue is a common cause of upper airway obstruction. This may be overcome by a jaw lift or neck extension. It may require the use of an oro- or nasopharyngeal airway, although these devices may themselves provoke laryngospasm or pharyngeal abrasion. Absolute obstruction suggests an equipment problem. Easy passage of a suction catheter through the tracheal tube confirms its patency. If obstruction persists and no obvious cause is identified, then the tracheal tube or laryngeal mask may be the site of obstruction and should be replaced.
Suction removes accumulated secretions in the pharynx, but may cause laryngospasm during light anaesthesia. The presence of symmetrical chest movements and breath sounds should be confirmed. Other causes of obstruction such as laryngospasm, bronchospasm, aspiration and pneumothorax should be excluded.
The most common airway complication is partial respiratory obstruction during spontaneous ventilation or during assisted manual ventilation in the absence of a formal (equipment) airway. A gentle jaw thrust, head tilt and chin lift usually clear a partially obstructed airway, and insertion of an oropharyngeal or nasopharyngeal airway resolves almost all of the remainder. In the rare situation of complete inability to ventilate the patient’s lungs manually, and after equipment failure has been excluded, the insertion of a laryngeal mask airway or tracheal tube may be necessary. Allowing the patient to awaken is prudent if there is no urgency to proceed with the operation. If it is necessary to continue the operation or if the patient cannot be wakened, and insertion of a laryngeal mask airway and tracheal tube have proved impossible, then it becomes necessary to establish a surgical airway. This may take the form of a cricothyroid cannula, a surgical cricothyrotomy or an emergency tracheostomy. These procedures must be learned and practised before the occurrence of the incident. They are technically demanding and are themselves potentially life-threatening to the patient if performed inexpertly (see Ch 22).
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.
Management: Where possible, airway and surgical stimulation should be avoided during light anaesthesia and the lateral position should be used for control of secretions during extubation and transfer. Surgical stimuli should be anticipated and anaesthetic depth should be adjusted accordingly. The anaesthetist should remove the stimulus to laryngospasm, administer 100% oxygen and provide a clear airway. Gentle pharyngeal suction should be applied. Where appropriate, anaesthetic depth may be increased by administration of an intravenous anaesthetic agent and the lungs ventilated manually, applying continuous positive airway pressure (CPAP). Most episodes of laryngospasm respond to this treatment. If laryngospasm persists and hypoxaemia ensues, a small dose of succinylcholine (e.g. 25 mg in adults) relaxes the vocal cords and allows manual ventilation and oxygenation. A full dose of succinylcholine may be given if tracheal intubation is indicated, but this is usually unnecessary. Doxapram, an analeptic and respiratory stimulant, has also been used successfully in the treatment of laryngospasm.
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.
Management: Bronchospasm during anaesthesia results in hypercapnia, hypoxaemia and pulmonary gas trapping, which may cause hypotension (through reduction in left ventricular preload). Management is aimed at preventing hypoxaemia, and resolving the bronchospasm. Initially, 100% oxygen should be given, anaesthesia deepened if appropriate and any aggravating factors removed (e.g. the tracheal tube should be repositioned and surgery stopped). If further treatment is necessary, a bronchodilator should be given in increments according to the response. Recommended drugs include intravenous aminophylline (up to 6 mg kg−1) or salbutamol (up to 3 μg kg−1). Volatile anaesthetic agents and ketamine are also effective bronchodilators. Adrenaline is indicated in life-threatening situations and may be given via the tracheal tube. Steroids and H1-receptor antagonists have no immediate effect but may be indicated in the later management of severe cases of bronchospasm.
If hypoxaemia develops in the spontaneously breathing patient, then tracheal intubation and artificial ventilation should be considered. Mechanical ventilation should incorporate a long expiratory phase to prevent the development of high end-expiratory alveolar pressures, which may cause hypotension, alveolar barotrauma and further hypoventilation. Severe gas trapping (intrinsic PEEP) may result in thoracic hyperexpansion, poor ventilation and pulmonary barotrauma. A very long expiratory phase or disconnection from the ventilator for up to 30 s may be necessary to allow thoracic depressurization. Positive end-expiratory pressure (PEEP) and high ventilatory rates should be avoided if bronchospasm is present because these favour the development of gas trapping. Hypercapnia may have to be tolerated in order to avoid gas trapping and barotrauma.
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.
Short, wide, muscular neck
High, arched palate
Receding lower jaw
Poor mobility of the mandible
Increased anterior depth of mandible
Increased posterior depth of mandible (reduces jaw opening, requires X-ray)
Decreased atlanto-occipital distance (reduces neck extension, requires X-ray)
Management: Preoperative examination of the airway (Table 43.4) is essential. Identification of patients with a potentially difficult airway (see Tables 43.2 and 43.3) before anaesthesia allows time to plan an appropriate anaesthetic technique. The Mallampati test is a widely used and simple classification of the pharyngeal view obtained during maximal mouth opening and tongue protrusion (see pp. 455–456). In practice, this test suggests a higher likelihood of difficult laryngoscopy if the posterior pharyngeal wall is not seen. The predictive value of this test may be strengthened if the thyromental distance (the distance between the thyroid cartilage prominence and the bony point of the chin during full head extension) is less than 6.5 cm.
General appearance of the neck, face, maxilla and mandible
Head extension and neck movement
Teeth and oropharynx
Soft tissues of the neck
Recent chest and cervical spine X-rays
Previous anaesthetic records
Premedication with an antisialagogue reduces airway secretions. This is advantageous before inhalational induction and essential for awake fibreoptic laryngoscopy to maximize the effectiveness of topical local anaesthesia. An anxiolytic may also be given (but is contraindicated in patients with airway obstruction, e.g. caused by burns, trauma, tumour or infection affecting the larynx or pharynx). The presence of a trained assistant is essential and the availability of an experienced anaesthetist and a ‘difficult intubation’ trolley with a range of equipment such as bougies, a variety of laryngoscopes and tracheal tubes, and cricothyrotomy needles is desirable (see Ch 22).
A variety of options exists for the patient in whom a difficult laryngoscopy is anticipated. If the procedure can be carried out under local or regional anaesthesia, then this technique should be used as the first choice (see Ch 24). However, the patient, anaesthetist and equipment must be prepared for general anaesthesia in case a complication arises.
If general anaesthesia is necessary for the procedure, or if the patient refuses local or regional anaesthesia despite a frank discussion of the risks, then steps must be taken to secure the airway safely. Unless tracheal intubation is essential for airway protection or to enable muscle relaxation and ventilation, the use of an artificial airway such as the laryngeal mask with spontaneous ventilation is usually a safe technique. If intubation is essential, the appropriate anaesthetic technique depends on the anticipated degree of difficulty, the presence or absence of airway obstruction and the risk of regurgitation of gastric fluid. The management of the patient in whom difficulties with airway management are anticipated is detailed in Ch 22.
There is no place for the use of a long-acting muscle relaxant to facilitate tracheal intubation if difficulty is anticipated. Correct positioning of the head and neck is essential and the lungs should be denitrogenated after establishing intravenous access and appropriate monitoring.
1. Patients with an increased risk of regurgitation and aspiration (e.g. full stomach, intra-abdominal pathology, pregnancy). An inhalational induction is inappropriate in these patients. Regional anaesthesia is preferable in the parturient (see Ch 35). Preoxygenation and a rapid sequence induction with succinylcholine can be used if there is little anticipated difficulty. If intubation is unsuccessful, no further doses of neuromuscular blocking drug should be used, the patient allowed to wake and further assistance sought. If there is a high degree of anticipated difficulty, an awake technique is recommended (see below).
2. Patients with little anticipated difficulty and no airway obstruction (e.g. mild reduction of jaw or neck movement). After a sleep dose of intravenous induction agent and confirmation of the ability to ventilate the lungs manually by mask, succinylcholine may be given to provide the best conditions for tracheal intubation. If difficulty is encountered, the patient is allowed to wake up and the procedure replanned. Where appropriate, anaesthesia is deepened by spontaneous ventilation using a volatile agent and alternative techniques to facilitate tracheal intubation used (see Ch 22).
3. Patients with severe anticipated difficulty and no airway obstruction (e.g. severe reduction of jaw or neck movement). Appropriate techniques include inhalational induction with sevoflurane or the use of fibreoptic laryngoscopy either in the awake patient or after inhalational induction. Neuromuscular blocking drugs must not be used until the ability to ventilate the lungs manually and view the vocal cords is confirmed.
4. Patients with airway obstruction (e.g. burns, infection, trauma). An inhalational induction may be used; otherwise an awake technique should be considered. Neuromuscular blocking drugs should not be used until tracheal intubation is confirmed.
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.
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.
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.
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.
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.
Management: At-risk patients should be managed actively to prevent the aspiration of gastric contents. The volume and acidity of the gastric contents should be reduced as far as possible. Preoperative fasting, histamine H2-receptor blockers and a gastric prokinetic drug (e.g. metoclopramide) are recommended. If general anaesthesia is essential, then the trachea must be intubated. Most commonly, this is achieved using a rapid-sequence induction with cricoid pressure (see Ch 37), but awake intubation is advisable if difficulty in intubation is predicted. During emergence, the tracheal tube should not be removed until protective airway reflexes are regained when the patient is awake.
If aspiration occurs during anaesthesia, further regurgitation should be prevented by immediate application of cricoid pressure, and the patient should be placed in a head-down position. The left lateral position should also be considered to encourage the drainage of gastric contents out of the mouth. In all but the mildest cases, the trachea should be intubated to facilitate removal of the aspirated material by suction before the use of positive-pressure ventilation. However, ventilation should not be delayed if significant hypoxaemia is present. Bronchodilator therapy may be required and the inspired oxygen concentration should be increased. Positive end-expiratory pressure may be used if hypoxaemia is refractory to increasing inspired oxygen fraction. Non-emergency surgery should be abandoned if significant morbidity develops. Flexible bronchoscopy permits the removal of liquids, although rigid bronchoscopy may be necessary for the removal of solid matter. Intravenous steroids and pulmonary lavage with saline via a flexible bronchoscope may reduce the post-aspiration inflammatory response. A chest X-ray and arterial blood gas measurement help in the assessment of the severity of injury. The patient should be transferred to a critical care unit for further monitoring and respiratory care.
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 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.
Management: Hypoxaemia occurring during anaesthesia is almost invariably treatable and its complications are preventable. Cyanosis should seldom be witnessed by the vigilant anaesthetist because the routine use of pulse oximetry allows early detection and treatment of hypoxaemia. If hypoxaemia is detected, the following drill should be instituted.