Respiratory failure is one of the commonest reasons for which patients are admitted to the intensive care unit. It may be the primary reason for admission to intensive care (for example, in a patient suffering an exacerbation of chronic obstructive pulmonary disease or acute pneumonia). Alternatively, it may be a feature of a non-respiratory pathological process, for example severe sepsis from an intra-abdominal source, though it is often the respiratory failure rather than the intra-abdominal sepsis which triggers intensive care admission. Respiratory failure is conventionally classified either as ‘type 1’ or ‘type 2’ based on blood gas findings.

The interpretation of blood gases is fundamental to the management of patients requiring intensive care, not just those with respiratory failure. When drawing an arterial blood sample into a heparinized syringe, ensure that any liquid heparin is completely expelled from the syringe before use, as this will contaminate the sample and influence the results. Arterial blood is obtained either by direct puncture of an artery or from an indwelling arterial line. (See Practical procedures: Arterial cannulation, p. 372.)

Most ICUs now have a blood gas analyser for ‘point of care testing’ (POCT). These are expensive to maintain and repair. You will be unpopular if you damage it by, for example, blocking the sample channels with clotted blood. If you do not know how to use it, ask for help. Normal blood gas values are as shown in Table 5.1.

TABLE 5.1 ‘Normal’ blood gas values

Interpreting blood gas results will eventually become second nature. To begin with, it is helpful to follow a system, for example:

Look at the PaO₂. Is the patient hypoxaemic?

Note the inspired oxygen concentration (FiO₂). The higher the FiO₂ required to achieve any given PaO₂ the more significant the problem (see below).

Look at the PaCO₂. Is it low, normal or high?

Look at the pH. Is the patient acidotic (pH < 7.34) or alkalotic (pH > 7.45)?

If the patient has a disturbance of acid–base balance, then it is necessary to examine the blood gas further to determine the cause.

Look again at the PaCO₂. Is the PaCO₂ consistent with the change in pH, i.e. if the patient is acidotic, is the PaCO₂ raised? If the patient is alkalotic, is the PaCO₂ low? If so the primary abnormality is likely to be respiratory.

If the PaCO₂ is normal or does not explain the abnormality in pH, look at the base deficit / base excess.

The base deficit / base excess is a calculation of how much base (e.g. bicarbonate) would need to be added to or taken away (by titration) to normalize the pH of the sample. For example, in a metabolic acidosis, bicarbonate would need to be added to correct the pH because there is insufficient buffering capacity present, i.e. there is a base deficit. In metabolic alkalosis, bicarbonate would need to be taken away to correct the pH, because there is too much base (or insufficient hydrogen ions) present, i.e. there is a base excess.

If the base deficit / base excess is consistent with the abnormality in pH then the primary abnormality is metabolic.

If both the PaCO₂ and the base excess/base deficit are both altered in a way that is consistent with the abnormality in pH then a mixed picture is present.

If the PaCO₂ and base excess / deficit are both altered in such a way that one is consistent with the change in pH and the other is not, then it is likely that a compensated acidosis / alkalosis is present (see descriptions below).

This simple scheme for the interpretation of blood gases is practical and will suffice for most situations. More complex systems, such as that described by Stewart, which take account of other plasma constituents, are beyond the scope of this book, but for which good up-to-date reviews are readily available. If in doubt always seek senior help.

A number of patterns of disturbance of acid–base balance are recognized.

Respiratory failure occurs when pulmonary gas exchange becomes impaired such that normal arterial blood gas tensions are no longer maintained, and hypoxaemia is present with or without hypercapnia. Two patterns are described: types 1 and 2.

Common causes of respiratory failure are listed in Table 5.3.

TABLE 5.3 Common causes of respiratory failure

Blood gases are only one indicator of respiratory function. The primary assessment of a patient with respiratory failure is clinical:

Look at the patient.

Is the patient conscious? Is he or she able to talk and is lucid?

Is the patient using accessory muscles of respiration and making adequate respiratory effort, or exhausted with minimal respiratory effort? Is there an adequate cough?

If possible, take a history. If the patient is too short of breath to talk, the history may be obtained from the notes, staff or relatives. Try to obtain some idea of the patient’s normal respiratory reserve. How far can the patient walk? Are they oxygen dependent? Can they leave the house?

Examine the patient, particularly the cardiovascular and respiratory systems, bearing in mind the causes of respiratory failure. Note:

Pulse, BP, JVP, heart sounds, peripheral oedema. Is there any evidence of cardiac failure or of dehydration?

Increased or decreased respiratory rate, tracheal shift, percussion, bilateral air entry. Presence of crackles or wheeze. Is there any evidence of obstruction (stridor), collapse or consolidation, bronchospasm, pleural effusion?

If there is wheeze, peak flow measurement may help to document severity but is often unrecordable in the critically ill.

Look at the CXR, blood gases and other available investigations.

Management is based around correction of hypoxia, ventilatory support if required, and treatment of the underlying condition.

Hypoxaemia

Hypoxaemia is the primary concern and should be corrected:

If there is evidence of chronic CO₂ retention, (raised bicarbonate on blood gas) give controlled oxygen therapy 24–28%, via a Venturi system. While it may be appropriate to give higher oxygen concentrations this should only be done in a controlled environment where advanced respiratory support and close observation are available (see COPD, p. 152).

In all other cases, give high flow oxygen via a face mask, preferably via a humidified system. Higher inspired oxygen can be achieved with a reservoir mask (plastic bag attached to mask acts as an oxygen reservoir)

Consider facial CPAP or non-invasive ventilation (see Non-invasive ventilation, p. 122).

Hypercapnia

Exhausted patients with minimal respiratory effort will require immediate intubation and ventilation. In those patients that are not in extremis, non-invasive ventilation together with treatment of the underlying condition may lead to improvement (see Non-invasive ventilation, p. 122).

Oxygen, antibiotics, nebulizers, physiotherapy and non-invasive ventilation may prove highly effective. Continually reassess the response to treatment.

Treatment of the underlying condition

Bronchodilators. If there is wheeze, nebulized salbutamol may help. In more severe cases consider intravenous bronchodilators and steroids (see Asthma, p. 149).

Physiotherapy may help clear secretions and re-expand areas of collapse. If possible sit patients upright or in a chair.

Antibiotic therapy is best directed on the basis of Gram stains of sputum and on subsequent culture results. Seek microbiological advice. In the first instance broad-spectrum cover, e.g. with a cephalosporin is reasonable. A macrolide antibiotic such as clarithromycin should be added if there is a possibility of an atypical chest infection (see Pneumonia, p. 141).

Diuretics. If there is evidence of congestive cardiac failure and pulmonary oedema, then diuretics may help. Frusemide (furosemide) 40 mg or bumetanide 1–2 mg i.v.

Intravenous or nebulized steroids, nebulized adrenaline and helium oxygen mix may be of value in upper airway obstruction.

Continually reassess response to treatment. If there is no improvement or if the patient’s condition worsens, tracheal intubation and assisted ventilation may become necessary. Possible indications for intervention are shown in Box 5.1.

Box 5.1 Indications for ventilatory support in respiratory failure

Reduced conscious level

Exhaustion

Tachycardia / bradycardia

Hypotension

Increasing respiratory rate

Falling PaO₂ despite oxygen therapy

Rising PaCO₂ despite therapy

Worsening acidosis

Continuous positive airway pressure (CPAP) is a system for spontaneously breathing patients which is analogous to PEEP in ventilated patients (see p. 126). It may be provided either through a tight-fitting face mask or via connection to an endotracheal / tracheostomy tube. Newly developed full hood systems are useful for the claustrophobic / confused patient. A high gas flow (which must be greater than the patient’s peak inspiratory flow rate) is generated in the breathing system. A valve on the expiratory port ensures that pressure in the system, and the patient’s airways, never falls below the set level. This is usually +5 to +10 cm H₂O (Fig. 5.1).

Fig. 5.1 Typical CPAP system.

The application of CPAP has a number of effects:

Airways are splinted open, reducing alveolar collapse.

Alveolar recruitment leads to improved oxygenation.

Increased functional residual capacity (FRC) allows the lung to function on a more favourable part of the compliance curve and may therefore reduce the work of breathing.

CPAP is well tolerated by most patients even via a tight fitting face mask, although where it is required for a prolonged period there is a risk of skin necrosis over the bridge of the nose and this may be another indication for the use of a CPAP ‘hood’ rather than a face mask. Relative disadvantages of CPAP include noise, difficulties with humidification, distension of the stomach and increased risks of reflux and aspiration.

Over recent years, there has been increased use of non-invasive ventilation to manage acute respiratory failure. It may avoid the need for endotracheal intubation and conventional ventilation, so avoiding many of the associated complications. Patients with acute exacerbations of COPD have been demonstrated to have a better outcome where non-invasive positive pressure ventilation (NIPPV) has been used in place of conventional ventilation. Non-invasive ventilation techniques are also increasingly being used in the management of pulmonary oedema in congestive cardiac failure and to aid weaning from conventional ventilation (see COPD, p. 152, and Weaning from artificial ventilation, p. 135).

Most intensive care ventilators are now highly sophisticated, computer-controlled machines with complicated interfaces, a large number of different ventilatory modes, and inbuilt monitoring and alarm systems. Detailed descriptions and discussion are beyond the scope of this book.

One problem is that there is no uniformly agreed terminology in relation to ventilator modes and different manufacturers use different terms for similar functions. The following terms and modes are in common use but are by no means universal. Before using a ventilator you should familiarize yourself with it. If you have any difficulties seek advice.

Volume controlled ventilation

The simplest form of volume controlled ventilation is controlled mandatory ventilation (CMV) (Fig. 5.2).

Fig. 5.2 Controlled mandatory ventilation.

The patient is ventilated at a preset tidal volume and rate (for example, tidal volume 500 mL and rate 12 breaths/min). The tidal volume delivered is therefore predetermined and the peak pressure required to deliver this volume varies depending upon other ventilator settings and the patient’s pulmonary compliance. One disadvantage, therefore, of volume controlled modes of ventilation is that high peak airway pressures may result and this can lead to lung damage or barotrauma.

This is suitable for patients who are heavily sedated and/or paralysed and who are making no respiratory effort. It is not suitable for patients who are attempting spontaneous breaths. There is no pressure support for spontaneous breaths and ventilator valves may be closed during attempted inspiration or expiration. The ventilator may also deliver a breath immediately after the patient’s own inspiration, or as the patient tries to breathe out. This is uncomfortable and distressing, and may result in trauma to the lungs (see below).

Pressure controlled ventilation

To overcome some of the disadvantages of volume controlled ventilation, pressure controlled modes of ventilation are preferred in patients with poor pulmonary compliance. Instead of setting a predetermined tidal volume, a peak inspiratory pressure is set. The tidal volume delivered is a function of the peak pressure, the inspiratory time and the patient’s compliance. By using lower peak pressures and slightly longer inspiratory times the risks of barotrauma can be reduced. As the patient’s condition improves and lung compliance increases, the tidal volume achieved for the same settings will increase and the inspiratory pressure can therefore be reduced (see Acute lung injury p. 154).

It is important when using pressure controlled ventilation to understand the relationship between rate, inspiratory time and the I:E ratio (ratio of inspiratory time to expiratory time). Rate determines the total time period for each breath (60 s divided by rate = duration in seconds for each breath). The I:E ratio then determines how this time is apportioned between inspiration and expiration.

For example:

If respiratory rate is 10/min, total time for breath 60/10 s = 6 s.

If I:E ratio 1:2, then inspiratory time = 2 s and expiratory time = 4 s.

If the rate is reduced while the I:E ratio is fixed, inspiratory time becomes progressively longer, effectively holding the patient in sustained inspiration. To avoid this, the inspiratory time should be fixed whenever pressure controlled ventilation is used (e.g. 1.5–2 s), so that, as the respiratory rate is changed, it is only the length of expiration that alters.

Synchronized intermittent mandatory ventilation (SIMV)

Although historically a volume controlled mode of ventilation, the equivalent of SIMV is now available in both volume controlled and pressure controlled modes (Fig. 5.3). Immediately before each breath there is a small time window during which the ventilator can recognize a spontaneous breath and respond by delivering the set (SIMV) breath early.

Fig. 5.3 Synchronized intermittent mandatory ventilation.

SIMV modes improve patient synchrony with the ventilator and reduce the problems described with CMV above. SIMV modes are therefore potentially more comfortable for the patient.

Pressure support / assisted spontaneous breathing (ASB)

Breathing through a ventilator can be difficult because respiratory muscles may be weak and ventilator circuits and tracheal tubes provide significant resistance to breathing. These problems can be minimized by the provision of pressure support. The ventilator senses a spontaneous breath and augments it by addition of positive pressure. This reduces the patient’s work of breathing and helps to augment the tidal volume. Pressure support modes are available on all modern ventilators and can be used in conjunction with both volume and pressure controlled modes of ventilation.

Pressure support is usually set at 15–20 cm H₂O in the first instance and can be reduced as the patient’s condition improves. It is best not to remove pressure support completely, however, because of the resistance of the ventilator. (See Weaning from artificial ventilation, p. 135.)

Positive end expiratory pressure (PEEP)

Intubation, artificial ventilation and the effects of lung disease leads to a reduction in the functional residual capacity (FRC) of the lung. This results in the collapse of small airways, particularly in dependent lung zones, increasing ventilation–perfusion mismatch and worsening blood gases. To prevent this +5 to +10 cm H₂O of PEEP can be used to help maintain FRC and alveolar recruitment. Disadvantages of PEEP include reduced venous return to the heart and a subsequent reduction in CO and blood pressure. Unnecessarily high levels of PEEP are therefore best avoided.

Patients with severe expiratory airflow limitation, e.g. due to asthma or obstruction, may develop high levels of intrinsic PEEP, with the risk of progressive air trapping. Most modern ventilators include functions for displaying dynamic compliance curves and calculating intrinsic PEEP. If you are unsure how to use or interpret these functions, seek advice.

If a patient has high levels of intrinsic PEEP, evidence suggests that applying external PEEP up to, but not exceeding, the level of intrinsic PEEP, causes little cardiovascular compromise, does not increase air trapping and may improve gas exchange by facilitating recruitment in non-flow limited parts of the lung. Increasing external PEEP above the level of intrinsic PEEP may worsen hyperinflation and should be avoided. Seek advice.

PEEP is relatively contraindicated in asthmatics and in chronic emphysema. Although some patients benefit, there are also risks: seek senior help.

Triggering

Both SIMV and pressure support modes of ventilation require the ventilator to be able to detect the patient’s own respiratory effort in order to trigger the appropriate ventilator response. Historically triggering was achieved by detection of pressure changes in the circuit. There was no gas flow in the breathing circuit between ventilator delivered breaths and the patient’s inspiratory effort was detected as a drop in pressure in the breathing circuit. This was an inefficient method of triggering which was uncomfortable and exhausting for patients. Modern ventilators rely on flow triggering. There is a constant low level of gas flow in the circuit at all times. Flow sensors detect small changes in flow in the circuit in response to spontaneous respiratory effort by the patient, triggering the appropriate ventilator response. This is a more efficient and comfortable method of triggering.

In patients with low pulmonary compliance, conventional IPPV can result in high airway pressures, barotrauma and haemodynamic disturbance. High frequency ventilation has been tried as a means of reducing transpulmonary pressure, while providing adequate gas exchange. In most cases the tidal volume generated is less than anatomical dead space, and the exact mechanisms by which gas exchange is maintained are poorly understood. If you are considering these alternative modes of ventilation seek senior advice.

High frequency oscillation

A piston oscillates a diaphragm across the open airway resulting in a sinusoidal flow pattern with I:E ratio 1:1 (variable). This is unique in that both inspiration and expiration are active. Airway pressure oscillates around a slightly increased mean but the peak airway pressure is reduced. Increasing the mean airway pressure recruits more alveoli and improves oxygenation. CO₂ clearance is controlled by altering the rate and amplitude of oscillation. Clearance of secretions is improved. This type of ventilation is well established in neonatal and paediatric intensive care. Oscillators capable of use in adults have recently become available and are becoming more established in adult practice. A typical approach to establishing high frequency oscillation is shown in Table 5.8. Always seek senior advice.

TABLE 5.8 Approach to establishing high frequency oscillation ventilation

Mean airway pressure	3–5 cm H2O above mean airway pressure on conventional ventilation
Amplitude	Increase sufficiently to generate visible and effective chest ‘wobble’
Frequency	6–8 Hz
Inspiratory time	33%
FiO2	1.0

Once established, HFOV is highly effective in alveolar recruitment leading to improved oxygenation. As recruitment continues lung compliance improves and the lung can become overdistended with potential for volume trauma. Perform regular chest X-rays and reduce mean airway pressure as the patient’s condition improves.

High frequency jet ventilation

This appears at present to be an increasingly obsolete mode of ventilation in critical care units. Pulses of gas are delivered at high pressure either through an attachment to the endotracheal tube or via a special endotracheal tube. The driving pressure and frequency can be varied. The jet of gas produced entrains air / oxygen from an open circuit (e.g. T-piece) and the tidal volume generated is generally of the order of 70–170 mL. Expiration is passive. Gas trapping may occur. The technique can be noisy and cumbersome. Humidification can be problematic. Typical settings are shown in Table 5.9.

TABLE 5.9 Typical settings for jet ventilator

Driving pressure	1.5–2.5 atmospheres (150–250 kPa)
Frequency	60–200/min
I:E ratio	1:1–1:1.5

There are two possible roles for jet ventilation:

Management of bronchopleural fistula. During conventional ventilation most of the tidal volume may be lost through the fistula, making effective ventilation of the patient impossible. Jet ventilation has been claimed to reduce transpulmonary pressures, thus reducing the leak. The evidence for this, however, is not strong; the main determinant seems to be the mean airway pressure, regardless of ventilator used.

As an aid to weaning. Patients can comfortably breathe over jet ventilation. As the patient’s condition improves, driving pressure is reduced and frequency increased. The use of non-invasive ventilation as an aid to weaning has reduced the use of jet ventilation for this indication.

As the patient’s condition improves, artificial ventilation can gradually be reduced until the patient is able to breathe unassisted. The decision to start weaning is largely one of clinical judgement, based on improving respiratory function and resolving underlying pathology. Studies have shown, however, that weaning is often delayed unnecessarily and there is evidence that the use of weaning protocols may reduce the time to extubation and reduce ICU stay. Typical criteria for successful weaning are shown in Table 5.10.

TABLE 5.10 Typical criteria for successful weaning

Some patients, particularly postoperative elective surgical cases, will tolerate weaning well and can be rapidly extubated. Others, particularly those who have been ventilated for some time, or who have significant lung damage or muscle wasting, may take longer and benefit from tracheostomy. There is no widely agreed policy on the best way to wean patients from ventilation. A typical approach is described below:

Ensure the patient’s general condition is optimal.

Reduce / stop sedative drugs.

Ensure adequate but not excessive analgesia for surgical wounds, etc.

Where possible, sit the patient up or out in a chair, and mobilize as much as possible.

Gradually reduce the ventilator rate to allow the patient to take more breaths. Ensure adequate pressure support and PEEP to reduce the work of breathing.

When the patient is taking an adequate number of breaths with a good and sustained respiratory pattern, switch to CPAP with pressure support.

If the patient manages well, gradually reduce the level of pressure support further. When the pressure support is down to 10 cm H₂O do not reduce it any further.

Either extubate directly from CPAP and pressure support if the patient is likely to manage or switch to separate flow generator CPAP system and extubate later when it is anticipated that the patient will manage without any support (see Extubation, p. 403).

Different patients will progress through weaning at different rates depending on their underlying problems. Some patients may be so agitated that there is no choice but to rapidly wean and extubate. Others may manage only brief periods of CPAP and pressure support before getting tired, as indicated by sweating, increasing pulse and respiratory rate (rapid shallow breaths). These patients will need rest periods on the ventilator between periods of CPAP and pressure support and weaning is often protracted.

Following weaning some patients will extubate without difficulty, others will rapidly deteriorate. This is often due to inability to clear secretions. These patients will require reintubation, ventilation and another period of optimization. Consider tracheostomy to aid clearance of secretions and weaning. (See Percutaneous tracheostomy, p. 404.)

Airway obstruction is common in the immediate postoperative period while patients are in the recovery room and the effects of anaesthetic drugs wear off. Occasionally airway obstruction may persist or may be a potential risk following a particular surgical procedure. These patients will frequently be admitted to the ICU. (See Postoperative complications, p. 355.) Causes of airway obstruction are shown in Box 5.2.

It is crucial to recognize actual or impending airway obstruction before the patient suffers a hypoxic episode. In the spontaneously breathing patient, airway obstruction produces obvious respiratory distress. Use of accessory muscles of respiration, tracheal tug, intercostal recession (mostly in children) and paradoxical respiratory movements all suggest significant obstruction. Stridor is typical, but indicates at least some airflow; the silent patient may be in much greater danger.

Management

The management of any patient with airway obstruction is essentially the same, i.e. secure the airway by endotracheal intubation or tracheostomy as soon and as safely as possible. There are, however, a few points to bear in mind, depending on the situation and your own experience:

Do not leave the patient unattended.

Do not delay management of the problem by sending the patient for investigations.

Give high flow oxygen by face mask.

Nebulized adrenaline may reduce obstruction caused by airway oedema

Support ventilation with a bag and mask if necessary and practicable.

Simple manoeuvres such as extending the neck, jaw thrust and suctioning of the airway may improve the situation particularly in the obtunded patient.

Seek help from senior anaesthetist and ENT surgeon as appropriate. In these circumstances intubation / reintubation can often be difficult.

Helium–oxygen mix is less dense than air and may reduce the work of breathing in patients with airway obstruction. Heliox® is a commercially available mixture containing 79% helium / 21% oxygen. The low fractional inspired oxygen limits its usefulness.

Seek urgent senior help. Do not delay getting help because of apparently good oxygenation. Hypoxia on the pulse oximeter / arterial blood gases is likely to be a very late sign.

The definitive management is to secure the airway by tracheal intubation or tracheostomy. If time allows, this should be performed in theatre with surgeons scrubbed and prepared for emergency tracheostomy. Awake fibreoptic intubation, awake tracheostomy or gaseous anaesthetic induction with the patient breathing spontaneously may be appropriate, depending on the circumstances. It is beyond the scope of this text to cover these in detail. The usual problem at intubation is gross swelling and distortion of the tissues, which makes the laryngeal inlet difficult to visualize. Often the endotracheal tube has to be passed blindly through swollen tissues into the larynx. Occasionally obstruction proves to be lower down the airway and ventilation may be impossible even when the trachea is intubated.

Once the airway is secured the management is that of the underlying condition. Allow time for swelling to subside. Steroids may be of value. Elevate the head of the bed, and reassess over time.

Airway obstruction in the intubated patient

This is common in the ICU and may be due to kinking of the endotracheal or tracheostomy tube or the effects of thick secretions, blood clot or even occasionally a foreign body. Adequate humidification, regular suctioning and careful fixation of endotracheal tubes avoid most problems, but these may still arise, particularly in children where the endotracheal tube is smaller in diameter and blocks more easily.

It is important to recognize and act on these problems immediately. Typical clues are increased airway pressure, inability to inflate the chest manually with a bag, falling SaO₂ and absent ETCO₂ trace.

Ventilate with 100% oxygen if possible. If not, remove the endotracheal tube and manually ventilate the patient with a bag and mask before reintubation.

If able to ventilate satisfactorily, suction the endotracheal tube. Use 10–20 mL saline instilled down the endotracheal tube to loosen secretions.

Bronchoscopy may be helpful.

In‘ball valve’ obstruction the chest can be inflated but exhaled gas is trapped by a plug of mucus or blood impinging on the end of the tracheal tube. Apply suction directly to the endotracheal or tracheostomy tube. If the obstructing plug does not come up the tube, remove the tube while maintaining suction hopefully dragging the plug out at the same time. (A similar effect can be achieved by pulling plugs out on the end of a bronchoscope.) Ventilate the patient by bag and mask before reintubation.

Post-extubation stridor

Airway obstruction and stridor may occur following extubation. This may be as a result of underlying pathology but frequently results from laryngeal oedema, particularly in children whose airways are narrower. This may occasionally require reintubation. Two or three doses of dexamethasone (4 mg) given prior to extubation may reduce laryngeal swelling. Nebulized adrenaline and use of CPAP may be helpful. Where these measures prove ineffective, reintubation should not be delayed. A range of (small) endotracheal tubes and other emergency airway adjunct should be available. Seek senior help.

Pneumonia is defined as infection occurring in terminal respiratory airways. The pattern of illness and pathogens responsible depend on whether the infection was acquired in the community or in hospital, and on the patient’s immune status. Community acquired pneumonias can be divided into those of ‘typical’ and ‘atypical’ presentation.

Typical pneumonia

The features of a ‘typical’ pneumonia include the following:

sudden onset of fever with rigors

cough productive of mucopurulent sputum

shortness of breath

pleuritic chest pain.

Chest X-rays show the appearances of consolidation, which may affect a single lobe, a whole lung or both lungs. The diagnosis is confirmed by raised WCC (predominantly neutrophils) and CRP, and by results of sputum and blood culture. The common causative organisms are shown in Table 5.11.

TABLE 5.11 Common causes of typical community-acquired pneumonia

Lobar pneumonia	Streptococcus pneumoniae
Bronchopneumonia	Strep. pneumoniae Haemophilus influenzae Staphylococcus aureus Enterobacteria (less common unless risk factors/comorbidity)

Atypical pneumonia

Atypical pneumonias are so called because their mode of presentation is different from that seen in classic pneumonia. In particular the following presentations occur:

Present over a few days, compared to the 24–36 h of classic pneumonia.

Non-respiratory symptoms may predominate. Fever, malaise, myalgia and arthralgia are common. Some may be associated with severe systemic illness.

Cough may only appear after a few days and is often non-productive. Sputum that is produced is clear and often negative on Gram stain and culture.

There may be disparity between the clinical signs on chest examination and the CXR with minimal signs on examination of the chest, whereas CXR shows widespread patchy consolidation with interstitial and alveolar infiltrates.

WCC may be normal or mildly elevated.

Causes of atypical community-acquired pneumonia are shown in Table 5.12.

TABLE 5.12 Cont’d

Viral	Influenza A, B Parainfluenza Respiratory syncytial virus
Bacterial	Legionella pneumophila Coxiella burnetii Mycobacterium tuberculosis
Chlamydia	Chlamydia psittaci
Mycoplasma	Mycoplasma pneumoniae

While the list of causes is not exhaustive it gives an indication of the range of pathogens that may be responsible. The difficulty is often in making the diagnosis. You should seek advice from local microbiologists regarding investigations and treatment. The features of some atypical pneumonias are described below.

Mycoplasma pneumonia

Mycoplasma pneumoniae is a community-acquired infection that tends to affect young adults. It may progress to a multisystem disease with the following features:

haemolytic anaemia, thrombocytopenia

pericarditis, myocarditis, rarely endocarditis

meningitis, encephalitis, peripheral and central nerve palsies

vomiting and diarrhoea, hepatitis

rashes, myalgia and arthralgia.

The diagnosis is confirmed by rising antibody titre. Cold agglutinins occur in up to 50% of patients, although this is non-specific and can occur in other atypical pneumonias, notably Legionella.

Legionella pneumonia

Legionella pneumoniae infection may occur in outbreaks associated with infected showers and water-cooling systems, but also occurs sporadically, particularly among older patients. Typical features are:

prodromal flu-like illness

dry cough

fever up to 40°C associated with rigors

mental confusion

nausea, vomiting, diarrhoea, abdominal pain, and jaundice

haematuria and renal failure may develop

multi-lobar shadowing and small pleural effusions on CXR.

The diagnosis is confirmed by rising antibody titre. Legionella may be identified by immunofluorescence on sputum, bronchial washings and urine.

There is ongoing concern regarding the potential for future pandemic influenza affecting large subsets of the population with the risk of acute medical services becoming rapidly overwhelmed with patients in respiratory and multiple organ failure. There are national and local contingency plans for dealing with this (and other contagious outbreaks). See DOH guidance and local policies.

Hospital-acquired pneumonias are a common cause of morbidity in hospitalized patients. Up to 20% of all mechanically ventilated patients develop ventilator-associated pneumonia and the incidence is higher in the immunocompromised patient. Gram-negative organisms and Staphylococcus aureus are particularly common. A number of factors may increase the risk of pneumonia in critically ill patients, by impairing host defence mechanisms and increasing colonization of the upper airway. These are summarized in Table 5.13.

TABLE 5.13 Factors predisposing to nosocomial pneumonia

Since little can be done to improve host defence mechanisms in the critically ill ventilated patient, the best approach to reducing the incidence of nosocomial infection is to prevent contamination of the airway with pathogenic bacteria, in particular by reducing the incidence of colonization of the upper airway.

(See also The immunocompromised patient, p. 226.)

Patients who are immunocompromised for any reason may present with pneumonia. In addition to the typical and atypical conditions already described, a number of other opportunistic pathogens typically infect these patients. These are shown in Box 5.3.

Pneumocystis carinii pneumonia (PCP)

Typical features are:

fever

dry cough

breathlessness and severe hypoxaemia

bilateral diffuse alveolar and interstitial shadowing.

Eighty per cent of PCP can be detected by immunofluorescence on bronchoalveolar lavage fluid (BAL). PCR tests are now also available. Occasionally transbronchial biopsy may be necessary.

Fungal pneumonia

Colonization of the pharynx, GIT, perineum, wounds and skin folds is common and rarely requires treatment. Significant fungal infections may occur after prolonged treatment with antibiotics and particularly in immunocompromised patients. Infection is suggested by significant growth in sputum, tracheal aspirates, BAL fluids and blood cultures. In addition there may be rising serum antibody titres to Candida or the presence of Aspergillus antigens. Fungal infection, particularly fungal septicaemia, is associated with a high mortality.

Cytomegalovirus (CMV)

CMV pneumonitis in immunocompromised patients is generally part of a disseminated infection in which there may be encephalitis, retinitis and involvement of the gastrointestinal tract. Cytology (BAL washings or biopsy) may show characteristic inclusion bodies. Diagnosis may be made by polymerase chain reaction (PCR), fluorescent antibody tests and tissue culture.

All patients with pneumonia requiring admission to intensive care should have full blood count, urea and electrolytes, liver function tests, C-reactive protein (CRP) and CXR performed. Possible microbiological investigations are summarized in Table 5.14. Not all patients require the full spectrum of investigations: these should be guided by severity, risk factors and response to treatment.

TABLE 5.14 Microbiological investigations for pneumonia

The treatment of any pneumonia is twofold:

Supportive therapy including humidified oxygen and ventilation as necessary. Regular physiotherapy and tracheal suction to aid clearance of secretions.

Antibiotic therapy. Choice will depend upon the clinical picture and the nature of the infecting organism. Wherever possible, microbiological specimens should be obtained prior to the commencement of antibiotics.

Flexible bronchoscopy may be helpful for obtaining specimens and removal of tenacious secretions. Where this is not available, blind (non-directed) bronchoalveolar lavage has been shown to be a very effective diagnostic aid (see BAL, p. 415).

Recommended empirical antibiotic therapy for severe community-acquired pneumonia is either a second-generation cephalosporin (e.g. cefuroxime) or a broad-spectrum lactamase stable antibiotic (e.g. coamoxiclav), plus a macrolide antibiotic (e.g. clarithromycin) to cover the common atypical agents. Where specific infective agents are identified or suspected, treatment should be based on microbiological advice.

The presence of effusion should be looked for on chest X-ray or ultrasound. Effusions can be tapped for diagnostic purposes. If the effusion is large, drainage increases lung volume and improves lung compliance. Empyema requires physical drainage to remove the source of infection. Occasional surgical intervention may be required, particularly in the case of complex multi-loculated collections. Surgical drainage and decortication by video-assisted thoracoscopic surgery may be the only solution in some cases.

Lung abscess are suggested by the presence of fluid levels and progressive cystic changes in the lungs. Abscesses may complicate a number of bacterial and other infections. The management is largely supported with postural drainage and appropriate antibiotics and other support. There is little place for thoracic surgical intervention in this context.

Hospital-acquired pneumonia

The management of hospital acquired pneumonia is similar to the management of any other pneumonia (see above). Ideally antibiotics should be used only for microbiologically proven infection. If, however, the patient’s condition dictates blind antibiotic therapy, ensure microbiological specimens are obtained before commencing treatment. Antibiotic therapy needs to be guided by the likely source of the pathogens and by the local pattern of microbial antibiotic resistance. Seek microbiological advice. (See Empirical antibiotic therapy, p. 336, MRSA, p. 336 and VRE, p. 336.)

Pneumonia in immunocompromised patients

This group of patients provides a great clinical challenge, as there may be diagnostic difficulty distinguishing the radiological and clinical features of pneumonia from those of some other interstitial process. For example, lymphomatous infiltrates in the lung may resemble the picture of an immunocompromised infective pneumonia. Diagnosis can be assisted by bronchoalveolar lavage, bronchial brushings and if necessary, biopsy. Serological tests may also help support the diagnosis. The management of pneumonia in immunocompromised individuals is essentially the same as in the non-immunocompromised, although the range of potential infective agents is greater. Always seek advice on the likely pathogens, appropriate investigations and initial treatment. Common first-line agents are as follows:

Pneumocystis pneumonia. High-dose co-trimoxazole (Septrin) and steroids to reduce the inflammatory response.

Fungal pneumonia. High-dose fluconazole or (liposomal) amphotericin.

Cytomegalovirus (CMV). Ganciclovir. Beware of nephrotoxicity and bone marrow suppression.

Tuberculosis

Most tuberculosis infections are treated with triple or even quadruple therapy. Isoniazid, rifampicin, ethambutal, streptomycin and other agents are frequently used in combination. Many strains of tuberculosis are multi-drug resistant; seek advice from your microbiologist and local infectious diseases consultant.

Patients with impaired conscious level, cough or gag reflexes are at risk of aspiration of gastric contents into the airway. Aspiration may present with acute airway obstruction if the aspirated matter is solid. More commonly it presents as gradual onset of respiratory distress and respiratory failure, either due to bacterial infection of the lungs or due to the inflammatory effects of acid aspiration. Some patients will develop ALI following aspiration (see ALI, p. 154).

If a patient is known to have aspirated gastric contents, e.g. during an anaesthetic, management is as follows:

Suction the trachea to remove debris. If possible suction should be applied before any form of positive pressure ventilation.

Consider bronchoscopy and lavage if available.

Monitor clinical condition and oxygen saturation. Give humidified oxygen as required.

Avoid antibiotics unless there is evidence of infection. If necessary, antibiotic therapy should cover the normal respiratory pathogens plus Gram-negatives and anaerobes. A combination of broad-spectrum cephalosporin and metronidazole is appropriate initially. Further treatment should be guided by the results of microbiological investigation.

There is no role for routine prophylactic steroids.

Treat bronchospasm appropriately. If wheeze persists, consider possible foreign body aspiration and the need for rigid bronchoscopy.

If the patient’s condition deteriorates, ventilatory support may be necessary.

Asthma occurs principally in young people and the incidence of this potentially life-threatening condition is increasing. Asthma involves increased airway reactivity, often triggered by an environmental stimulus, or following infection. An inflammatory process results in narrowing of small airways, mucus plugging, expiratory wheeze and air trapping. Severe asthma is a medical emergency. It may be rapidly progressive and clinical signs may be misleading. The clinical signs of severe asthma are shown in Box 5.4.

Management

Give high flow humidified oxygen and monitor oxygen saturation continually.

Give nebulized β-agonists (salbutamol 2.5–5 mg neb.) and anticholinergics (ipratropium bromide 0.5 mg neb.). Repeat as frequently as required. Ensure nebulizers are given in oxygen not air.

Give i.v. corticosteroids to suppress the inflammatory response. Hydrocortisone 200 mg bolus then 100 mg 6-hourly.

There is no role for antibiotics unless there is clear evidence of a precipitating bacterial infection.

Commence i.v. fluid, to correct dehydration.

If there is no improvement, commence i.v. β-agonist, either salbutamol 4 μg / kg loading dose over 10 min followed by infusion 5 μg / min or aminophylline 5 mg / kg loading dose over 10 min followed by infusion 0.5 mg kg h.

Consider a single bolus dose of magnesium sulphate 1.2–2 g i.v. over 20 min.

If there is no improvement or the patient’s condition is life-threatening, consider need for ventilation. Indications for ventilation are shown in Box 5.5.

Box 5.5 Indications for ventilation in asthma

Exhaustion

PaO₂ < 8 kPa

PaCO₂ > 6.5 kPa

pH < 7.3

Cardio-respiratory arrest

Asthma is unlike other forms of respiratory failure in that the problem is not immediately solved by intubation and ventilation. Airway obstruction may be initially worsened by tracheal intubation and attending staff are faced with a paralysed intubated patient who cannot be ventilated!

Patients with severe life-threatening asthma are often dehydrated and have high levels of endogenous catecholamines. When anaesthesia is induced to facilitate intubation, the cardiovascular depressant effects of the drugs, the reduction in endogenous catecholamines and the effects of dehydration and acidosis can lead to profound cardiovascular collapse.

Following intubation ensure adequate analgesia and sedation. The presence of an endotracheal tube in the larynx of an inadequately sedated asthmatic is a potent source of irritation and continued bronchoconstriction. Standard sedative regimens are generally sufficient. There may be a role for ketamine infusion both as a sedative agent and as a bronchodilator in refractory bronchospasm. Muscle relaxation may be required initially in severe cases. Avoid agents likely to release histamine, such as atracurium or mivacurium. Cisatracurium, vecuronium or pancuronium are less likely to cause direct release histamine.

During ventilation, severe bronchoconstriction may result in air trapping and hyperinflation. This may lead to difficulty in ventilating the patient adequately using conventional ventilator settings. High airway pressure may be required, with the risk of barotrauma and development of a pneumothorax.

To minimize these problems, ventilator settings should be adjusted to allow adequate time for expiration. The optimal combination of ventilation settings in any individual patient is best determined by trial. In general, set a slow rate and prolonged expiratory time (I:E, 1:3–1:4) to allow adequate time for full expiration. The short inspiratory time may result in higher peak airway pressure. This is partly offset by the slower rate. In severe cases it may be necessary to accept a higher PaCO₂ rather than increase inspiratory pressures.

The role of PEEP in asthma is controversial. In theory, adding PEEP increases FRC and may worsen air trapping in patients who are hyperinflated. Judicious levels of PEEP have, however, been used to recruit airways and improve ventilation. In practice, try adding PEEP cautiously and observe the response (see PEEP, p. 126).

If severe hyperinflation becomes a problem it may be necessary to disconnect the patient from the ventilator and manually ventilate with a long expiratory time. Manual compression of the chest wall has been used to expel trapped air and improve respiratory mechanics. Volatile anaesthetic agents may be useful in severe bronchospasm. These can be either given through an anaesthetic machine but the attached ventilators are often incapable of ventilating such patients. There are specialized pumped injector delivery systems for volatile agents into ICU ventilator circuits. Occasional patients can be managed with ECMO or related technology, though this is likely to require transfer to a specialist centre, which may be problematic or impossible in the patient with severe acute bronchospasm. Simple systems for extracorporeal CO₂ removal are available (e.g. Novalung®) that can be used outside specialist centres to reduce a high PaCO₂.

Chronic obstructive pulmonary disease (COPD) is a broad ‘description’ applied to patients with chronic bronchitis and emphysema. These conditions frequently coexist, and in severe cases may result in respiratory failure, which may be precipitated by intercurrent viral or bacterial respiratory infection.

Acute exacerbation

Patients with so-called acute exacerbations of COPD are generally managed in A&E and on medical wards with a combination of antibiotics, bronchodilators, controlled oxygen therapy (usually 24–35% oxygen by a fixed performance, Venturi system) and non-invasive ventilation. Pathophysiologically, there is some overlap between chronic obstructive pulmonary disease and asthma, with features of airway reactivity occurring in both diseases. Some patients may genuinely suffer both conditions. There are increasing numbers of respiratory units that provide high dependency care to this group of patients, who are, therefore, only likely to be admitted to an ICU when these measures have failed and tracheal intubation and full ventilatory support is required. (See Non-invasive ventilation, p. 122.)

Management

Due to the effects of long-term compensatory mechanisms, these patients often tolerate markedly deranged blood gases (hypoxia and hypercapnia) very well. Therefore, it is the clinical condition of the patient rather than blood gases that determines the need for ventilatory support. Assess the patient clinically. If able to talk, and not distressed, the patient is unlikely to need immediate ventilation, regardless of the blood gas picture.

Correct hypoxia by incremental increase in FiO₂. Aim to achieve PaO₂ 7–8 kPa, SaO₂ ≥ 90% or that which is normal for the patient.

In some patients with COPD and type 2 respiratory failure, chronic hypercapnia results in loss of the normal ventilatory responsiveness to CO₂. In these patients hypoxia is the main stimulus to respiration. High concentrations of inspired oxygen can result in the loss of the stimulus to respiration and precipitate respiratory arrest. Look at the bicarbonate concentration on the blood gas. If this is normal, or only slightly raised (<30 mmol / L), chronic CO₂ retention is unlikely to exist and the patient should not be dependent on hypoxic drive. Increase the inspired oxygen concentration as necessary and repeat the blood gases after 30 min.In cases where the patient is dependent on hypoxic drive, the PaCO₂ may rise and the need for assisted ventilation may be precipitated earlier.

Avoid respiratory stimulants such as doxapram. These generally do not help and can result in patients becoming exhausted and requiring ventilation. Consider use of CPAP or non-invasive ventilation.

Give nebulized β-agonists (salbutamol 2.5–5 mg neb.) and anticholinergics (ipratropium bromide 0.5 mg neb.). Repeat as frequently as required. Ensure nebulizers are given in oxygen not air.

Give i.v. corticosteroids (hydrocortisone 200 mg bolus then 100 mg 6-hourly) to suppress the inflammatory response.

There is no role for antibiotics unless there is clear evidence of a precipitating infection.

Commence i.v. fluid, to correct dehydration.

If there is no improvement, commence i.v. β-agonist, either salbutamol 4 μg/kg loading dose over 10 min followed by infusion 5 μg/min or aminophylline 5 mg/kg loading dose over 10 min followed by infusion 0.5 mg/ kg/ h.

If the patient remains severely hypoxic, becomes increasingly hypercapnic, acidotic or clinically exhausted, urgent ventilation is likely to be necessary.

Most patients with acute exacerbations of COPD who require a short period of ventilation do well and leave hospital. Patients in end-stage respiratory failure, however, particularly those that have been ventilated before and who have been difficult to wean from ventilators, may not be suitable for further admission to intensive care. This decision should be taken by a senior doctor in consultation, where possible, with the patient and / or the next of kin. Seek senior advice.

Intensive care management

These patients are typically very distressed and have a high level of sympathetic catecholamine activity. Anaesthetic drugs used to intubate may abolish this and unmask relative hypovolaemia, with subsequent cardiovascular collapse. In addition, there are frequently coexisting medical problems such as ischaemic heart disease. Therefore:

Where possible transfer the patient directly to the ICU for intubation and ventilation rather than attempting this on the ward.

If the patient’s condition allows, site an arterial line and institute arterial pressure monitoring before induction.

Consider giving a fluid bolus (e.g. 500 mL of colloid) prior to induction. Have adrenaline (epinephrine) available for resuscitation.

After securing the airway, institute IPPV. SIMV mode is usually adequate. Avoid hyperventilation. Rapid lowering of the PaCO₂ may further reduce sympathetic drive and lower the blood pressure.

Continue antibiotic therapy according to local protocol. (See Pneumonia, p. 141, and Empirical antibiotic therapy, p. 336.)

Give nebulized bronchodilators. Salbutamol 2.5 mg and ipratropium bromide 0.5 mg.

Consider intravenous bronchodilator therapy. Aminophylline 5 mg / kg loading dose (if not on long-term theophylline and not already loaded) followed by infusion aminophylline 0.5 mg / kg / h. Check levels.

Corticosteroids. Hydrocortisone 200 mg initially then 100 mg 6-hourly.

Many of these patients require a relatively short period of ventilation and wean easily from the ventilator. Weaning can often be facilitated by the use of non-invasive ventilation techniques such as BIPAP. Some patients, however, particularly those with type 2 respiratory failure, may be more difficult to wean and early tracheostomy may be considered to facilitate tracheal toilet and improve patient comfort while allowing a reduction in sedative drugs. Once stable, patients on BIPAP via mask or tracheostomy may be transferred to medical wards or weaning units for further weaning (see Weaning from artificial ventilation p. 135).

The clinical signs of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are those of increasing respiratory distress, with associated tachycardia, tachypnoea and onset of cyanosis. Blood gases indicate severe hypoxaemia. The CXR shows acute bilateral interstitial and alveolar shadowing. The non-cardiogenic nature of the alveolar oedema can be confirmed by pulmonary artery catheterization (PAOP < 18 mmHg, CI > 2 L / min / m3) or echocardiography and infective processes excluded by BAL.

The principal diagnostic criterion used to distinguish ALI and ARDS is the degree of hypoxaemia, as shown in Table 5.15.

Pathophysiology

A large number of conditions have been associated with the onset of ALI / ARDS, as indicated in Box 5.6.

Box 5.6 Common conditions associated with ALI/ARDS

Physical	Infective	Inflammatory/immune
Trauma	Pneumonia	Blood transfusion
Acid aspiration	Septicaemia	Cardiopulmonary bypass
Fat embolism	Pancreatitis	Anaphylaxis
Smoke inhalation

It is clear that an ALI can develop in response to a wide range of insults. The exact processes by which this occurs are not fully understood. It is characterized by proliferation of inflammatory cells, increased permeability of the alveolar capillaries and leak of proteinaceous fluid into the alveoli (so-called ‘non-cardiogenic pulmonary oedema’). This protein-rich material precipitates, forming hyaline membranes. In survivors, the acute inflammatory process gradually subsides and healing occurs. This may result in widespread interstitial lung fibrosis. Not all patients who have ALI go on to develop severe ARDS. There is a spectrum of disease ranging from mild to severe.

Although used primarily as a research tool, a scoring system for grading the severity of ALI / ARDS has been devised. This is shown in Table 5.16.

TABLE 5.16 Scoring system for acute lung injury

Component	Assign value
Chest X-ray appearance
No alveolar consolidation Alveolar consolidation in 1 quadrant Alveolar consolidation in 2 quadrants Alveolar consolidation in 3 quadrants Alveolar consolidation all 4 quadrants	0 1 2 3 4
Hypoxaemia score (PaO2/FiO2 mmHg)*
>300 225–299 175–224 100–174 <100	0 1 2 3 4
Compliance (mL/ cmH2O)
>80 >60 >40 >20 <20	0 1 2 3 4
PEEP (cm H2O)
<5 6–8 9–11 12–14 >15	0 1 2 3 4
Score generated by dividing sum of component values by number of components used
Score = 0 Score < 2.5 Score > 2.5	No lung injury Mild to moderate lung injury Severe lung injury (ARDS)

* for kPa divide by 7.5

Source: Murray JF, Matthay MA, Luce JM, Flick MR 1989 American Review of Respiratory Disease139: 1065.

Management

Severe ARDS is associated with a high mortality ranging from approximately 25 to 80% in different series. The best outcomes have been reported from centres using strict protocols for management. In general:

Treat the underlying cause, as appropriate.

Institute invasive cardiovascular monitoring (arterial line, CVP, pulmonary artery catheter or equivalent) and use inotropes / vasopressors as appropriate to optimize CO, perfusion pressure and oxygen delivery.

Artificial ventilation is usually necessary. Reduced pulmonary compliance results in high inflation pressures, which are associated with increased risks of barotrauma. Current ventilatory strategies are intended to limit ventilator-associated lung damage while providing for alveolar recruitment. Pressure control ventilation, with longer inspiratory times (reversed I:E ratio) may be used to limit peak airway pressure. Tidal volumes should not exceed 6 mL / kg. Increased levels of PEEP are used to promote alveolar recruitment and improve oxygenation (see Ventilation strategy, p. 127).

The FiO₂ should be kept to the minimum necessary to maintain acceptable oxygenation (PaO₂ 7–8 kPa, SaO₂ ≥ 90%) in order to reduce lung damage associated with oxygen toxicity. Moderate levels of hypercapnia may be tolerated (permissive hypercapnia) if excessive ventilatory pressures would otherwise be required.

BAL should be performed to identify infection, and, if appropriate, antibiotics started.

Although in ARDS pulmonary oedema is classically thought of as non-cardiogenic, these patients often have multiple organ failure. It is estimated that 25% may develop myocardial failure, and fluid overload is common. Diuretics may be given to ‘dry’ the patient and may help to reduce the extent of pulmonary oedema.

Nitric oxide

Nitric oxide is a naturally occurring vasodilator produced by the endothelium of blood vessels. If added to the inspiratory gases in concentrations of 5–20 v.p.m., it results in pulmonary vasodilatation in those areas of the lung that are well ventilated. Blood is diverted away from poorly ventilated areas. Ventilation–perfusion mismatch is reduced and there is an improvement in oxygenation. At the same time pulmonary hypertension and the risk of right heart failure is reduced. Nitric oxide has a short half-life when inhaled and is generally safe for the patient. It is, however, a toxic gas, and should only be used according to the protocols established in your unit. Although nitric oxide may produce an improvement in oxygenation and therefore allow reduced FiO₂ and airway pressures, there is little evidence that it improves outcome.

Prone positioning

Turning the patient prone may improve V / Q mismatch and blood gases. The response in individual patients is unpredictable. The benefit tends to be temporary (24–48 h) and patients may need to be turned alternately prone and supine. The risks of turning large patients include injury to staff and the patient, accidental tracheal extubation, and loss of venous access, chest drains, etc. There is little evidence to show improved outcome. (See Practical procedures, p. 425.)

ECMO

Extracorporeal membrane oxygenation is a technique that allows oxygenation to be maintained while the lungs recover. The benefits are well recognized in neonatal and paediatric practice, but are less well established in adult practice, although a recent study in adults has reported favourable results [Conventional ventilation or ECMO for Severe Adult Respiratory Failure (CESAR) Trial. www.cesar-trial.org]. In the UK, ECMO is only provided in a limited number of centres and the transfer of patients with severe hypoxaemia is hazardous. Evidence suggests that to be of benefit it should be started within 5–7 days of artificial ventilation being commenced.

Steroids in ARDS

The traditional view was that therapeutic doses of steroids were of no benefit in ARDS. Despite a resurgence of interest in the use of steroids in ARDS, there is currently little evidence for any outcome advantage from therapeutic (high) dose steroids either in the acute or convalescent phase of illness.

Outcome from ALI / ARDS

Mortality in patients with ARDS is high; however, many of these patients die from the effects of multiple organ failure rather than directly from hypoxaemia. Lung function in survivors of ALI / ARDS often slowly improves over weeks or months but in severe cases lasting lung damage may persist.

The combination of tracheal intubation or tracheostomy and IPPV makes interpretation of classic respiratory signs in the noisy environment of the ICU very difficult. The CXR therefore assumes additional importance when evaluating the patient’s condition.

You must be able to recognize the typical abnormal appearances seen in intensive care, particularly those that relate to complications of procedures. It is best, therefore, to have a standard system for evaluating the chest X-ray:

Check name, date and orientation of film. The normal CXR orientation is posteroanterior (PA). That is, the X-rays are passed through the patient from behind towards the film, which is in front. Films taken in intensive care are generally anteroposterior (AP). This alters the magnification of structures.

Check penetration and rotation of film.

Check mediastinal structures, including cardiac shadow, lung hilum and pulmonary vessels.

Check lung fields. Note position of diaphragms.

Check bones and soft tissues.

All tracheal tubes, central venous and pulmonary artery catheters, nasogastric tubes and any drains visible by CXR should be checked for both correct placement and evidence of complications. In particular, note the following:

Endotracheal tube, correct position above the carina, not endobronchial.

Central venous catheters. Check intrathoracic placement with the tip positioned in a site consistent with the superior vena cava, above the pericardial reflection (see p. 376).

Pulmonary artery catheter. Check tip lying in the pulmonary artery, preferably on the right side and not too distal (within 2 cm of edge of the spinal column).

Nasogastric tube in the stomach.

A number of CXR patterns are common in intensive care.

Consolidation and collapse

These terms are often used incorrectly and even interchangeably. The X-ray appearances of consolidation and collapse are, however, quite distinct (Fig. 5.4).

Fig. 5.4 Chest X-ray features of collapse and consolidation.

Typical features of consolidation are:

opacification of a lobe or segment (may be patchy)

no loss of lung volume

mediastinal and diaphragmatic borders partially preserved

air bronchograms may be present.

Typical features of collapse include:

loss of volume on side of collapse

compensatory hyperinflation of remaining lobes

shift of mediastinal structures towards side of collapse

cardiac and diaphragmatic boarders obscured.

Collapse of a lung

An extreme example of collapse is collapse of an entire lung. In intubated and ventilated patients this may occur as a result of obstruction of the bronchus (e.g. by mucus plugging) or following endobronchial intubation. The anatomy of the bronchial tree is such that endotracheal tubes are more likely to pass down the right main bronchus than the left. This commonly leads to collapse of the left lung, the typical appearances of which are shown in Fig. 5.5.

Fig. 5.5 Collapse of left lung.

Pleural effusion / haemothorax

The classic feature of a pleural effusion in an upright patient is that of uniform opacification in the pleural space, typically obscuring the costodiaphragmatic recess, with an obvious meniscus or fluid level. In critically ill patients, CXRs are generally taken with the patient supine, often in the presence of positive pressure ventilation or CPAP. Therefore the classic appearance of pleural effusion may be missed. The only evidence of a small or moderate pleural effusion may be a general white haze to the whole lung field (imagine the fluid lying posteriorly in the pleural space). Larger effusions may have classic features or may present with a ‘white-out’ of that side, with shift of mediastinal structures towards the other side (Fig. 5.6).

Fig. 5.6 Chest X-ray appearances of pleural effusion.

Pneumothorax

Pneumothorax should be suspected in any patient who deteriorates while on a ventilator, particularly if there is associated trauma or recent insertion of a tracheostomy, central line or other practical procedure in the chest or neck. The typical appearances are that of a visible lung edge and translucent free air in the pleural space, as shown in Fig. 5.7.

Fig. 5.7 Chest X-ray showing bilateral pneumothorax with lung edge. Right lung has not expanded despite chest drain. Check drain not blocked or kinked (presence of respiratory swing). Consider low suction. Similar changes on left but less marked.

The appearance may not, however, always be so obvious. In the critically ill supine patient with a small pneumothorax, free air may lie anteriorly over the lung and there may be no visible lung edge on CXR. (This is analogous to small pleural effusions lying posteriorly.) The only evidence may be that of an increased translucency (blackness) anteriorly, as shown in Fig. 5.8. If in doubt a lateral CXR or CT scan may help.

Fig. 5.8 Chest X-ray appearance of anterior pneumothorax.

Surgical emphysema and mediastinal air

Air may leak outside the pleural cavity, presenting as surgical emphysema and / or as mediastinal air on CXR. Surgical emphysema typically develops in the face, neck, mediastinum, pericardium, abdomen and scrotum and has a ‘tissue paper’ feel on palpation. It is visible on X-ray as black air shadows in the soft tissues of the upper body and chest wall, often outlining the pectoral muscles. Mediastinal air is visible on CXR as black translucent areas usually outlining the mediastinal shadows.

Pulmonary oedema

Pulmonary oedema is common on the intensive care unit and may indicate heart failure, fluid overload or evidence of acute lung injury. There is a spectrum from mild interstitial oedema to gross alveolar shadowing. Features include:

interstitial shadowing (Kerley B lines)

perihilar shadowing

alveolar shadowing

fluid in fissures (particularly horizontal fissure)

Pleural effusions.

ALI / ARDS

The CXR appearances of ALI and ARDS are not specific. The common response to lung injury is leaking of capillaries, accumulation of alveolar fluid and subsequent development of areas of collapse and consolidation. The features are therefore a combination of those described above. A typical example is shown in Fig. 5.9.

Fig. 5.9 Chest X-ray showing typical features of severe ARDS.