Effect of induction on the airway

The induction of general anaesthesia or sedation tends to result in hypoxia because of:

1. Airway obstruction. Maintenance of a patent upper airway is a complex physiological mechanism. Even minor depression of consciousness can result in obstruction.

2. Respiratory depression.

3. Decreased cardiac output.

Mechanism of airway obstruction

It is a usual practice to induce anaesthesia with the patient supine and nearly horizontal, which is the least favourable position for airway patency, but the most convenient for intervention. Relaxation of the musculature of the pharynx, face and neck allows the soft palate, tongue and glottic opening to approach the posterior nasopharyngeal wall. The greatest contribution to obstruction is believed to be at glottic and velo-palatine level.

Signs of airway obstruction

1. An obstructed upper airway results in increases in negative intrathoracic pressure during inspiration. This causes tracheal ‘tug’, intercostal and supra-clavicular recession and paradoxical or ‘seesaw’ breathing (if the airway is obstructed the chest sinks in and the abdomen rises – the opposite of normal).

2. Turbulent flow may occur in the upper airway, resulting in noise. The noise is worse on inspiration. The characteristic timbre of snoring (palatal, tongue and peri-glottic level obstruction) and stridor (glottic and tracheal level) are readily recognized with experience. Absence of noise does not mean that the airway is not critically narrowed and a completely obstructed airway is silent. Auscultation of the neck to assess airway patency is a valuable examination.

3. Secretions or foreign bodies in the airway may cause obstruction. The noise of secretions is characteristic. Foreign bodies in anaesthetic circuits (introduced by accident or malicious design) have resulted in tragedies. If airway obstruction occurs, the anaesthetist must ensure that the circuit and any artificial airway is patent.

Thoracic surgical operations require the anaesthetist to be able to cease ventilation and allow deflation of the operative lung, to protect the lower lung from contamination with blood, tumour or infective material and to continue ventilation of the non-operative, dependent lung. Without the ability to separate and independently ventilate the lungs, thoracic surgery is hazardous. The first planned pulmonary resection by Block on a young female relative in 1883 was a disaster. She died on the operating table and Block committed suicide. A major component of safe thoracic anaesthesia is the appropriate use of endobronchial tubes, double-lumen tubes (DLTs) and bronchial blockers. Indications for their use are not restricted to pulmonary surgery and there are other clinical indications for lung separation (Table 14.1).

Endobronchial tubes

The First attempts at selective lung ventilation were with endobronchial tubes. These long, single-lumen tubes were placed in the bronchus of the dependent, non-operative lung. The classical technique, devised by Magill, was to load the tube onto a rigid intubating bronchoscope and place the tube under direct bronchoscopic view. It was possible to ventilate both lungs at the end of surgery by withdrawing the endobronchial tube into the trachea. The technique of one-lung ventilation by endobronchial placement of a single-lumen tube is still in practice in specialized circumstances, usually with blind or fibreoptic positioning into the appropriate bronchus. The next development was of a combined tracheal tube and bronchial blocker (Macintosh–Leatherdale). This tube consisted of a standard tracheal tube and a cuffed blocker limb which entered the bronchus of the operative lung. Both lungs could be ventilated when the blocker cuff was deflated, and subsequent inflation of the cuff would isolate the operative lung.

Serious problems with airway management are rare, but situations that have the potential to have a bad outcome are not uncommon. Most anaesthetists are exposed to a ‘just barely in control’ airway situation from time to time, and there is an element of becoming ‘sadder and wiser’ in many anaesthetic careers. Anaesthetists are increasingly exposed to legal action in the event of an unfavourable outcome. They are therefore inclined to adopt procedures that will be supported by a substantial majority of their peers, however because of the infrequency of serious airway problems it is difficult to compare one technique with another in a rigorous way and be certain of a ‘best buy’. Most techniques work in most situations. All will fail sometimes. We have no solid ‘evidence base’ to guide us. For instance, accepted canons of management such as the ‘rapid sequence induction’ (RSI) with cricoid pressure have never been subjected to a trial.

Most techniques require training and practice. It is hard both to obtain and provide training – and getting harder. Ethical constraints loom larger and larger and the trainee's time is increasingly at a premium. The advent of the laryngeal mask airway (LMA) has revolutionized anaesthesia, but it cannot be denied that most of us get less practice in mask anaesthesia and tracheal intubation than before its introduction.

Tracheal intubation is an essential skill in the care of the unconscious, anaesthetized or critically ill patient. Tracheal intubation can be difficult and may result in complications, the most serious being hypoxaemic brain damage and death. Soft tissue damage, sometimes fatal, can be caused by traumatic attempts at intubation. Maintenance of oxygenation must take precedence over all other considerations when difficulty with intubation is experienced and intubation attempts should be deferred until oxygenation is restored.

No technique of airway management is always successful. It is important to have a pre-formulated strategy to cope with unanticipated difficulties. Use of the Difficult Airway Society guidelines is recommended. Many alternative techniques can facilitate tracheal intubation under vision in patients in whom this is not possible with the standard Macintosh laryngoscope. Expertise in at least one alternative visual technique should be acquired and skills maintained; the necessary equipment should be available. Two types of rigid direct laryngoscope (Macintosh and straight) and one indirect rigid laryngoscope (Bullard) will be discussed in this chapter.

Anatomical basis of direct laryngoscopy for tracheal intubation

Successful direct laryngoscopy depends on achieving a line of sight (LOS) (Figure 8.1) from the maxillary teeth to the larynx; management of the base of the tongue and the epiglottis is particularly important (Figure 8.2). The best initial patient position is the ‘sniff’ position, achieved by flexion of the lower neck and extension of the head. Maximum head extension, which rotates the maxillary teeth out of the LOS, is probably the most important factor. Changes in position should be made as required to optimize the view. In particular, elevation of the shoulders of obese patients may facilitate head extension.

Introduction

Acute victims often require immediate tracheal intubation and when this is necessary there are a number of concurrent problems to consider. There may or may not be immediate airway obstruction caused by extensive disruption to normal airway anatomy from both blunt and penetrating injuries. Airway haematoma and oedema may be present and certain injury patterns are recognized as causing airway compromise including the ‘flail’ mandible, where loss of support for the tongue anteriorly encourages it to fall backwards. Additionally, there may be severe haemorrhage and other debris present in the airway, which can make fibre-optic techniques impractical. There is invariably a full stomach with the associated risk of aspiration and finally, one must always consider injuries to the cervical spine.

Cervical spine injury

Approximately, 5% of severe, blunt injuries to the head and neck have cervical spine damage. Up to 14% of these injuries may be unstable, and between 1% and 5% of these injuries are initially missed. Fractures most commonly occur at the level of C2 and dislocations at the C5/6/7 regions (Figure 18.1). All such injuries may predispose to further airway obstruction from haematoma formation and soft tissue oedema in the neck (Table 18.1). Sadly, about 5% of patients admitted to hospital with cervical spine trauma will suffer a neurological deterioration after admission. Some of these deteriorations occur for no discernible reason, but some are associated with general anaesthesia. It seems sensible, therefore, to assume that there is an un-quantified risk of neurological deterioration in patients undergoing general anaesthesia with cervical spine injuries.

Effects of aspiration

Aspiration is the process by which material is carried from the pharynx to the lower respiratory tract. The clinical outcome depends on the volume and nature of the aspirate, its distribution and the host defence mechanisms. The consequences can vary from relatively benign to fulminant acute respiratory failure and death. Aspiration of solids or semisolids may cause airway obstruction. Aspiration of acidic gastric contents can cause a pneumonitis with bronchospasm and pulmonary oedema (Mendelson's Syndrome). A ventilation–perfusion mismatch will occur. In some patients worsening hypoxaemia may develop and lead to the adult respiratory distress syndrome (ARDS). Of those patients that aspirate 64% have no respiratory sequelae, 20% require ventilation on an intensive therapy unit (ITU) for more than 6 h and 5% die. If no symptoms or signs are present 2 h after an episode of aspiration, respiratory sequelae are unlikely.

Diagnosis of aspiration

Symptoms: Most patients are unconscious and asymptomatic, but conscious patients will complain of breathing difficulty.

Signs: Dyspnoea and tachypnoea develop, often with a cough productive of pink frothy sputum. Tachycardia and hypotension are observed. The principal sign of aspiration is hypoxaemia. Even a few millilitres of saline instilled into the trachea will cause a temporary drop in oxygen saturation. Localized or diffuse wheeze and crackles may be heard on auscultation of the chest.

Investigations: Diffuse alveolar infiltrates usually in the lower lobes are apparent on the chest radiograph.

The risk of pulmonary aspiration

Aspiration occurs in 1 in 4000 anaesthetics for elective surgery and 1 in 900 for emergency surgery. If a tracheal tube is used then aspiration is just as likely after extubation as during induction.

Introduction

Intensive care units (ICUs) were originally developed more than 50 years ago to offer patients prolonged respiratory support. Of course, more recently there have been great advances in the support of other organs. Nevertheless, ventilation and its accompanying airway management techniques remain at the centre of intensive care practice.

Endotracheal intubation

Indications for intubation

Respiratory failure is the main indication for endotracheal intubation in the ICU. However, there are other indications, including: control of partial pressure of carbon dioxide (PaCO2) in head injury patients, airway protection (e.g. during endoscopy), to allow investigations (e.g. bronchoscopy, computed tomography or magnetic resonance imaging scan), for transfer to another hospital or for uncontrolled seizures. Haemodynamic instability due to septic or cardiogenic shock is also an under-recognized indication for intubation.

Decision to intubate in respiratory failure

The decision to intubate should be primarily made on clinical grounds and the figures in Table 25.1 should be used as a guideline only. As an example the patient with chronic neurological weakness managed with nocturnal bilevel positive airway pressure (BIPAP) may normally have a (PaCO2) of 8.0 kPa and would almost certainly not require intubation. However, a young asthmatic patient who is deteriorating rapidly despite aggressive treatment may require intubation with a (PaCO2) of only 7.0 kPa. In general terms consideration should be given to the underlying diagnosis, the possibility of improvement with intensification of treatment, the trend in the clinical picture and most importantly whether the patient is tiring.

Organizational factors such as the availability of skilled support and the time of day are also often important considerations. Respiratory function and the ability to observe changes in respiratory function are decreased at night.

Every anaesthetist will reach the end of his/her career with a collection of difficult airway experiences.There can be few more terrifying experiences in medical practice than the realization that a cyanosed patient is getting worse, not better, particularly when the patient was nice and pink before the anaesthetic began. Many seasoned anaesthetists recognize the change that comes over trainees after their first experience of serious difficulty with the airway. One of the editors remembers a conversation with a distinguished American paediatric anaesthetist about the difficulty of keeping up with bright young residents. Her observation that ‘a few deep paediatric desaturations sure does take the shine off'em’ was correct. All of us who have been around for some time have ‘been there’, and we know we could find ourselves in difficulty any time we give an anaesthetic.

Management of the airway of patients who are sedated, obtunded or anaesthetized is the responsibility of nursing and medical practitioners in anaesthesia, emergency medicine, intensive care medicine and other critical care areas. Anaesthetists do not own the airway and their right to be considered expert can be based only on good clinical practice, knowledge of relevant basic science and critical evaluation of every component of airway care.

There is an uneasy combination of science and art in airway management. We know a good deal about the physics and physiology, but are less certain about the safest way to manage the airway in many patients. Meetings of the Difficult Airway Society have often been lacking in consensus, sometimes confusing, but always educational. It is probably just that there really are several ways to pluck a chicken.

Anatomical and physiological differences

At birth the human larynx is well developed for the demands of life and the neonate is capable of breathing, limited phonation, and airway protection during feeding. The larynx lies opposite the third cervical vertebra and the epiglottis is long and curled, often in the classical ω shape and is in frequent contact with the soft palate during the first 6 months of age. This allows for feeding and breathing to occur simultaneously by interlocking of these structures, creating lateral channels for feeding and a central passage for breathing via the nasal airway. This situation lasts for 12–18 months. The tongue is large relative to the mandibular space and fills the oral cavity, allowing the tongue to protrude during feeding. Infants are preferential nasal breathers and the presence of nasal obstruction (e.g. choanal atresia) can cause significant airway problems.

The subglottic area in the term-baby is funnel shaped from the top down and the posterior lamina of the cricoid ring is tilted back and inferiorly making it particularly susceptible to trauma during endotracheal intubation. The smaller size of the paediatric airway means that a small decrease in diameter may cause significant airway obstruction. The cricoid ring is the narrowest part of the child's airway. The length of the trachea in the newborn is 5–6 cm and increases during the first year of life to about 8 cm. The epiglottis moves away from the soft palate at around 6 months and the tongue descends into the pharynx at about 1 year of age allowing greater phonation. The differences between the infant and the older child's skull can be seen in Figure 16.1.

Ethical constraints make the study of this all important topics very difficult. Simple questions, such as how long will an apnoeic patient survive? – cannot be answered with precision.

Classification of hypoxia

‘Cellular respiration’ occurs at the level of the mitochondria, when electrons are passed from an electron donor (reduced nicotinamide adenine dinucleotide (NADH)) via the mitochondrial respiratory cytochromes to ‘reduce’ molecular oxygen (O2). The energy from this redox reaction is used to phosphorylate adenosine diphosphate (ADP), thereby generating the universal energy source, adenosine triphosphate (ATP), which powers all biological processes. If molecular O2 cannot be reduced in this way, this bit of biochemistry fails and cellular hypoxia occurs. Based on Barcroft's original classification, four separate causes of cellular hypoxia can be considered. Three of these four factors affect O2 delivery to the tissues (D. O2), which is described mathematically by the equation in Box 2.1. Derangements of each of the terms on the right-hand side of this equation will reduce O2 delivery to tissues.

The fourth cause of cellular hypoxia in our classification is histotoxic hypoxia. An example of this is cyanide or carbon monoxide poisoning. In histotoxic hypoxia, there is not (or there need not be) any deficit in O2 delivery. Cellular and mitochondrial partial pressure of O2 (PO2) may be more than adequate, but the deficit lies in the reduction of molecular O2 due to a failure of electron transfer. In order to fully understand the classification of hypoxia, it is useful to consider the example of carbon monoxide poisoning.

What is the mechanism of death in severe carbon monoxide poisoning?

After an unsuccessful suicide attempt involving motor exhaust-gas inhalation, a patient is taken to hospital.