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Complications are undesirable events arising from anaesthesia. 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 recognised, and managed promptly and appropriately.
Certain complications of anaesthesia manifest as emergencies during the intraoperative phase of surgery, such as arrhythmias, hypotension, adverse drug effects and inadequate ventilation of the lungs. These are commonly termed ‘critical incidents’ because without rapid correction they lead directly to anaesthetic mortality preventable intraoperative cardiac arrest or permanent organ injury. Such intraoperative events are described in detail in Chapter 27 . The focus of this chapter is on complications that occur as a result of anaesthesia but which manifest in the postoperative period.
Human error is a common contributor to anaesthetic complications, often in association with inadequate monitoring, equipment malfunction and organisational failure. Human error is commonly associated with insufficient training, fatigue, inadequate experience and poor preparation of the patient, environment or equipment. These circumstances are generally avoidable and should be preventable by good organisation. When complications do occur, effective monitoring and vigilance allow for 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. This may be facilitated through the use of action plans or drills that have been rehearsed previously.
Failure of communication is often implicated in the generation of complications in the perioperative period. Poor working relationships, varying levels of training amongst staff and challenging 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 pressurising devices have also been responsible for patient morbidity and mortality. Meticulous checking of equipment before use is mandatory (see Chapter 22 ).
Some complications stem from the deterioration of the patient's medical condition, which may have existed before the anaesthetist's involvement. Although such deterioration may be coincidental, it must be recognised that anaesthesia and surgery often introduce altered conditions into a patient's finely balanced combination of pathological condition and compensatory physiological characteristics. This may be sufficient to cause instability in the patient's condition and result in sudden worsening of an apparently stable condition. Typical examples include diabetes mellitus, ischaemic heart disease, hypertension and asthma.
There is a subgroup of complications that may be classed as inevitable. Despite excellent surgical and anaesthetic practice, the patient may still experience a complication that brings morbidity or even death. Although we must, at all times, make stringent efforts to save our patients from harm, it is also important to recognise that it is not always appropriate to assign causation of a complication to the healthcare provider.
The most effective steps in preventing harm from complications are implemented before the complication occurs. Thorough preparation will prevent most complications. Such preparation includes:
preoperative assessment, investigation and counselling of the patient;
preoperative checking of equipment and the assurance of backup equipment;
availability of an appropriately trained assistant;
preoperative consultation with more experienced personnel, where necessary, regarding the most appropriate anaesthetic technique; and
use of appropriate monitoring techniques.
Complications occur more commonly in inexperienced (or incautious) hands. Clearly, finite resources exist, and suitably experienced personnel cannot always be 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 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 minimise the risk of awareness.
The Association of Anaesthetists has produced guidelines stipulating the acceptable minimum level of intraoperative monitoring (see Chapter 22 ).
Modern monitoring systems have automatically activated alarms, and the anaesthetist selects the values at which these alarms sound. The default values are not always the optimal choices. Consideration should be given 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 that 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 may vary greatly. The repeated sounding of an alarm should not trigger reflex silencing of the alarm but should cause the anaesthetist to consider whether treatment of the patient is required or whether 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 that are damaged most rapidly by a deficiency in oxygen supply include the brain and heart. The liver and the kidneys are less fragile but are potentially at risk from even short interruptions in oxygen supply. Cessation of perfusion results in more rapid damage to an organ than hypoxaemia 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:
continual vigilance and monitoring;
recognition of the evolution of a problem;
creation of a list of differential diagnoses;
choice of a working diagnosis, which is either the most likely or the most dangerous possibility;
treatment of the working diagnosis ;
assessment of the response of the problem to the treatment administered;
refinement of the list of differential diagnoses, especially if the response has not been as expected;
confirmation or elimination of the choice of working diagnosis ; if the response to treatment has been unexpected, then replacement with a more likely working diagnosis is indicated; and
return to step 5 and repeat until the problem is resolved.
The early recognition of an evolving problem allows the anaesthetist time to manage the complication before it damages the patient. Appropriate selection of monitoring alarm limits and the anaesthetist's vigilance will allow more time for pre-emptive treatment to be provided to reduce the impact of the complication.
The first response to an emerging complication should be to minimise 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 S p o 2 reading 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 causes 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, rearranging 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. 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. 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 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 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 that is not necessarily optimal for the patient. The culture of blame in which we now practise mandates 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.
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 anaesthetic administration may provide the patient with sufficient information. If human error has occurred, then the anaesthetist should apologise and reassure the patient that further information will be provided when it becomes available. If the anaesthetist is a trainee, then it is sensible 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 organisation should be informed, who will provide advice on subsequent action. It must be emphasised 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 serious complications arising from anaesthesia are described next.
Postoperative pulmonary complications (PPCs) occur in 10% of patients undergoing non-thoracic surgery. Many respiratory complications can be prevented, or their severity mitigated, with adequate preoperative patient assessment, careful selection of anaesthetic technique and suitable postoperative monitoring and respiratory rehabilitation ( ). Risk factors for the development of PPCs are shown in Box 26.1 ( ) (see also Chapter 19 ). A carefully selected regional anaesthetic technique is likely to decrease the risk of respiratory complications in individual patients compared with general anaesthesia.
Age
Low preoperative oxygenation saturation
Respiratory infection in the month preceding surgery
Preoperative anaemia (haemoglobin concentration <100 gL –1 )
Upper abdominal or thoracic surgery
Duration of surgery >2 h
Emergency surgery
The most common postoperative respiratory complications are atelectasis, pneumonia and pulmonary thromboembolism.
The reduction in functional residual capacity and tendency for hypoventilation which occur during general anaesthesia make alveolar collapse, or atelectasis, common. Atelectasis causes impairment of gas exchange and increases the risk of postoperative pneumonia. The most common presentation is a gradual downward drift in arterial oxygen saturation or a gradual increase in peak inspiratory pressure during mechanical ventilation.
Risk factors for its development include:
pre-existing lung disease;
prolonged anaesthesia or spontaneous ventilation;
increased intra-abdominal pressure;
high inspired oxygen fraction;
head-down positioning;
extended exposure of the open airway to atmospheric pressure; and
prolonged apnoea during anaesthesia (e.g. while awaiting the onset of spontaneous ventilation).
Atelectasis may be reduced by the use of:
mechanical ventilation during lengthy operations;
head-up positioning where possible;
PEEP during mechanical ventilation; or
CPAP or pressure-support during spontaneous ventilation.
If intraoperative atelectasis is suspected, gentle hyperinflation of the lungs usually reinflates the collapsed alveoli and results in an increase in arterial oxygen saturation. Inflation for 20–30 s at an inspiratory pressure up to 40 cmH 2 O is often required. Such a recruitment manoeuvre is probably best performed using a mechanical ventilator and may usefully be achieved by adding substantial PEEP (e.g. 20–30 cmH 2 O) for 20–30 s. Prevention of recollapse is best achieved by adding and/or increasing PEEP.
If atelectasis becomes established during anaesthesia, then the patient is at increased risk of pulmonary dysfunction postoperatively. In this situation the provision of good analgesia (to encourage coughing and mobilisation), use of the sitting position and physiotherapy (including incentive spirometry and deep breathing exercises) may reduce postoperative morbidity.
Pneumonia is the third most common postoperative infection, after urinary tract and wound infection, with an incidence of 2%–20%. It is suggested by new cough, purulent sputum or dyspnoea, often more than 48 h after surgery. There may be systemic evidence of sepsis (tachycardia, pyrexia, hypotension) and hypoxaemia; these indicate severe infection. Chest radiography is likely to show new infiltrate(s), consolidation or effusion. Isolation of responsible organisms is possible from blood or sputum cultures but should not delay the commencement of antibiotic therapy to target likely community- and hospital-acquired organisms. Perioperative atelectasis and the aspiration of bacterially colonised subglottic secretions are thought to be responsible for pneumonia in many cases. Aspiration of gastric contents (see Chapter 27 ) resulting in a chemical pneumonitis predisposes the damaged lung parenchyma to subsequent bacterial infection. The prognosis for patients with postoperative pneumonia is poor, with 30-day mortality ten times higher than patients without pneumonia, and an overall mortality of approximately 10%.
Embolisation of thrombus occurs usually from the deep veins of the legs or pelvis. Venous emboli usually become lodged in the lung, where they impair gas exchange and cause a local inflammatory reaction. Risk factors include the following:
active cancer or cancer treatment;
age >60 years;
critical care admission;
known thrombophilia;
BMI >30 kg m –2 ;
one or more significant medical comorbidities (e.g. heart or respiratory disease, acute infections, inflammatory conditions);
personal history or first–degree relative with a history of venous thromboembolism (VTE);
use of hormone replacement therapy/oestrogen contraceptive therapy; and
varicose veins with phlebitis.
Venous stasis caused by venous compression, hypovolaemia, hypotension, hypothermia or the use of tourniquets also increase the risk of VTE. Pulmonary embolism (PE) may present with tachycardia, hypoxaemia, arrhythmia, hypotension and/or cardiovascular collapse. This is rare during anaesthesia and more common in the postoperative period.
The risk of postoperative VTE can be reduced by two types of intervention.
Mechanical
Graduated compression stockings
Intermittent pneumatic compressive devices
Vena caval filters
Pharmacological
Low molecular weight heparin
Unfractionated heparin
Vitamin K antagonists (e.g. warfarin)
Newer direct oral anticoagulants (e.g. rivaroxaban).
The provision of good analgesia to facilitate early mobilisation and adequate hydration to optimise blood viscosity are also important to prevent PE. A high clinical index of suspicion and a low threshold for investigation and presumptive treatment are needed to allow effective management of PE in postoperative patients because the signs and symptoms of the condition overlap with many other respiratory and cardiovascular disease processes.
The most common causes of cardiac morbidity and mortality after anaesthesia are hypotension, myocardial ischaemia and arrhythmia, all of which can lead to cardiac failure. Together these account for a third of postoperative deaths.
Risk factors include:
age;
pre-existing cardiovascular, renal or metabolic disease;
recent stroke or myocardial ischaemia; and
intraoperative haemorrhage, hypotension, tachycardia or hypothermia.
The revised cardiac risk index is one model for the prediction of cardiovascular complications in patients undergoing non-cardiac surgery (see Chapter 19 ).
There is no agreed definition of intraoperative hypotension, although ≥20% reduction in MAP from the patient's usual resting value is commonly used. Hypotension may impair perfusion and consequently oxygen supply to vital organs. During anaesthesia, myocardial and cerebral metabolic rates are reduced, 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, heart rate and/or systemic vascular resistance. Most anaesthetic agents cause vasodilatation and have a mildly negative inotropic effect; moderate hypotension is very common during and immediately after anaesthesia. Spinal and epidural anaesthesia commonly result in hypotension through sympathetic pharmacodenervation. Concurrent hypovolaemia caused by preoperative fluid restriction, in combination with haemorrhage and/or concurrent antihypertensive drugs, may result in further decreases in MAP. The causes of perioperative hypovolaemia are listed in Box 26.2 .
Haemorrhage
Trauma
Obstetrics
Gastrointestinal
Major vessel rupture (e.g. aortic aneurysm)
Gastrointestinal
Vomiting
Obstruction
Fistulae
Diarrhoea
Other
Fasting
Diuretics
Fever
Burns
Haemorrhage
Insensible loss
Sweating
Expired water vapour
Third-space loss
Prolonged procedures/extensive surgery
Drainage of stomach, bowel, or ascites
A MAP ≤55 mmHg is potentially harmful, even in healthy individuals, and should not be allowed to persist; in patients with significant comorbidities, persistent hypotension (even if less severe) may be detrimental. 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. Older or hypertensive patients should, therefore, be observed carefully for the development of hypotension, and it should be treated promptly.
Treatment principles for hypotension in the perioperative period are to:
seek an underlying cause ( Table 26.1 );
Decreased stroke volume | Decreased heart rate | Decreased systemic vascular resistance |
---|---|---|
Reduced preload
Reduced myocardial contractility
|
|
|
optimise preload with i.v. fluid or blood resuscitation;
provide systemic vasoconstriction (usually with α-adrenergic agonists, e.g. metaraminol); and
increase myocardial contractility (using agents with some β-adrenergic effects, e.g. ephedrine).
The myocardium has the largest oxygen consumption per tissue mass of almost all the organs; the oxygen extraction ratio is 70%–80%, compared with an average of 25% for other tissues (see Chapter 9 ). Increased oxygen consumption must be matched by an increase in coronary blood flow. Ischaemia results when oxygen demand exceeds 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.
Perioperative myocardial ischaemia may manifest in the awake patient with chest pain, dyspnoea, nausea, arrhythmia, hypotension or pulmonary oedema. It is diagnosed by ECG ST-segment changes (typically depression), elevated cardiac biomarkers (usually troponin) and/or echocardiography to detect abnormal myocardial wall motion ( ).
Increased myocardial work during the perioperative period (e.g. tachycardia and increased afterload secondary to inadequate analgesia) may precipitate further myocardial ischaemia or infarction in susceptible patients. The therapeutic management of myocardial ischaemia depends on the underlying pathological process: acute coronary syndrome with plaque rupture (also known as type 1 perioperative myocardial infarction), or prolonged oxygen supply–demand imbalance without plaque rupture (type 2 perioperative myocardial infarction); these conditions are discussed in Chapter 29 . Although the risk of infarction in the general surgical population is low, the overall mortality rate is 4%–25%.
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