Respiratory emergencies: the acutely breathless patient

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Chapter 8 Respiratory emergencies

the acutely breathless patient

Craig Hore, John Roberts

GENERAL PRINCIPLES

Exclude airway compromise, which may be subtle, as the cause of acute breathlessness. Management of airway problems always comes first. Dyspnoea is a sensation which has multiple aetiologies and can be difficult to assess.

There may be several reasons why the patient with comorbidities experiences dyspnoea. This patient may require comprehensive treatment strategies to optimise their condition and thus relieve their symptoms.

Initial goals in assessment and management are:

1. To identify and treat life-threatening abnormalities of gas exchange, acute onset or deterioration of hypoxia and hypercarbia.

2. To commence non-invasive ventilation in the form of bi-level positive airway pressure (BiPap) or continuous positive airway pressure (CPAP) where indicated.

3. To identify when intubation and ventilation is required and initiate this therapy.

4. To identify and commence specific treatment to relieve respiratory distress based on initial history and examination.

5. To formulate a plan of investigation and management of cases where the exact cause of respiratory distress is unknown or uncertain.

Triage all patients presenting with a respiratory system emergency to a monitored acute bed. Obtain IV access. Arterial blood gases (ABGs), chest X-ray (CXR) and BiPap services should be available.

OXYGEN THERAPY

Delivery of oxygen is one of the most common therapies in the emergency department and an important component of resuscitation. Acute hypoxaemia is immediately life-threatening and the ‘first-line drug’ for hypoxaemia is oxygen! It is a safe drug: the complications of oxygen therapy are concentration- and time-dependent, uncommon and take time to develop. Other aspects of oxygen delivery may also need to be improved in the hypoxaemic patient, especially cardiac output, haemoglobin, tissue perfusion and reducing tissue O₂ requirements.

Table 8.1 The haemoglobin–oxygen (Hb–O₂) dissociation curve

SaO₂ (%)	P_aO₂ (mmHg)	Level
98	100	Arterial blood
90	60
75	40	Venous blood
50	26
∼33	∼20	Tissue

SaO₂, oxygen saturation; P_aO₂, partial pressure of oxygen in arterial or venous blood or tissue

Note: When SaO₂ ≈ 60–90%, there is a linear relationship between SaO₂ and P_aO₂.

Essentially, oxygen should be delivered to all patients who have acute respiratory failure to maintain a partial pressure (P_aO₂) of 60–80 mmHg (or a P_aO₂ > 55 mmHg in chronic respiratory failure). The lowest fraction of inspired oxygen (FiO₂) that provides an acceptable P_aO₂ should be chosen. Choosing the right mode of delivery is also important.

Oxygen delivery systems

Simple delivery systems

These are variable performance systems—the FiO₂ delivered not only depends upon the oxygen flow rate, but also on the rate and depth of respiration. The FiO₂ delivered by various systems can be estimated (Table 8.2).

Table 8.2 Estimation of the fraction of inspired oxygen (FiO₂) achieved by simple delivery systems

Flow rate (L/min)	FiO₂
2 (nasal prongs)	0.25
3 (nasal prongs)	0.28
4 (nasal prongs)	0.30
6	0.40
8	0.45
15	0.65
15 (reservoir mask)^∗	0.70

∗ If a double wall supply is used, a flow rate of 30 L/min and FiO₂ up to 0.90 can be achieved.

Nasal prongs. These are easy to use and usually well tolerated by the patient, allowing them to eat, drink and talk without interrupting oxygen delivery. They are ineffective if the patient has blocked nasal passages or is an obligate mouth breather. Flow rates > 4 L/min can lead to mucosal drying and are less well tolerated.

Hudson mask. A simple and easy way to deliver oxygen but delivery is variable (see above). Flow rates < 4 L/min are not recommended as rebreathing can occur.

Entrainment systems

Venturi masks. This system uses the Bernoulli effect to entrain a fixed amount of air to mix with oxygen. This is an example of a fixed performance system—the FiO₂ delivered is more independent of patient factors. Nonetheless, it may vary in patients with very high peak inspiratory flow rates. One commonly used system delivers the following options: 24/28/35/40/50/60% oxygen. The lower concentrations are especially useful for patients with chronic obstructive pulmonary disease (COPD) and CO₂ retention.

Partial rebreathing systems

Reservoir masks. These can achieve a higher FiO₂ than simple masks but it is essential to keep the reservoir inflated with O₂. This can require high flow rates. This is a good initial choice for most conscious, unwell, hypoxaemic patients in the emergency department.

Anaesthetic circuits. Mentioned for completeness; rarely used in the emergency department setting.

Non-rebreathing systems

Resuscitation bags (e.g. Laerdal, Baxter). The commonly used bags are self-inflating, and have a series of one-way valves and a reservoir bag. The aim is to keep the reservoir bag at least 75% inflated with O₂. An FiO₂ of close to 100% can be delivered if 15 L/min O₂ is used and the reservoir bag is inflated (50% without a reservoir bag). There is a growing trend to use disposable, single-use bags to help overcome the problem of incorrect assembly and sterilisation. The ability to use a bag–mask system is a vital skill that should be learned and mastered early!

Gas-driven inflating valves (e.g. Oxy-viva).

Others

• Positive pressure ventilators

• Non-invasive positive pressure ventilation (e.g. CPAP, biPAP)

• Hyperbaric oxygen (HBO) therapy

Other delivery systems are dealt with in more detail in other chapters of this text.

INVESTIGATIONS IN RESPIRATORY EMERGENCIES

Arterial blood gases: oxygenation and ventilation

Arterial blood gases (ABGs) reflect oxygenation (P_aO₂), ventilation (P_aCO₂) and acid–base status. The last is dealt with in more detail in Chapter 27, ‘Metabolic disorders’.

Oxygenation

Remember that, even for ‘normal’ lungs, the P_aO₂ varies with the following parameters.

The inspired O₂ concentration (FiO₂). Never take ABGs, or try to interpret ABGs, without noting the FiO₂. If room air, this is 21% (i.e. FiO₂ = 0.21).

Age. P_aO₂ falls with age. As a rough guide to what to expect at a given age, use the following estimation:

Altitude. P_aO₂ falls by ∼ 3 mmHg for each 1000 feet (∼300 m) above sea level. Temperature. For each degree Celsius rise (or fall) in temperature, the P_aO₂ will rise (or fall) by ∼ 5%.

pH. For each 0.1 decrease (or increase) in pH, the P_aO₂ will increase (or decrease) by ∼ 10%.

Do not take oxygen off a hypoxic patient to perform ABGs. Perform the ABGs with the patient on oxygen and note the FiO₂. The A-a gradient (the difference between alveolar and arterial oxygen pressure, P_A-aO₂) is calculated from the alveolar gas equation:

P_AO₂ is the alveolar oxygen tension and R is the respiratory quotient (usually 0.8). The partial pressure of inspired oxygen (PiO₂) is determined by the atmospheric pressure, which varies with altitude. Usually, it is assumed that the patient is breathing at sea level, that atmospheric pressure is 760 mmHg and that the water vapour pressure is 47 mmHg. There is usually a small difference between the P_AO₂ and the P_aO₂—the A-a gradient or P_A-aO₂.

• P_A-aO₂ < 15 mmHg is normal.

• P_A-aO₂ = 20–30 mmHg reflects mild pulmonary dysfunction.

• P_A-aO₂ > 50 mmHg reflects severe pulmonary dysfunction. Note that pulmonary embolism is only one of many causes of an increased P_A-aO₂.

The gradient varies with age: add 3 for each decade over the age of 30 years.

The P_AO₂ can also be quickly estimated using one of the following rules of thumb:

• If breathing room air,

• If breathing supplemental O₂,

The causes of hypoxia

There are four main types of hypoxia:

1. stagnant hypoxia resulting from decreased cardiac output

2. anaemic hypoxia resulting from decreased haemoglobin

3. histotoxic hypoxia resulting from decreased oxygen-binding capacity

4. hypoxaemic hypoxia resulting from decreased O₂ saturation.

The take-home message from this list is that the patient can be ‘hypoxic’ with a normal O₂ saturation. Perhaps the most obvious example is histotoxic hypoxia resulting from CO poisoning.

Acute respiratory failure is generally associated with hypoxaemic hypoxia. The problem is getting the oxygen from the lungs into the capillaries. Ventilation/perfusion (V/Q) mismatch is the commonest cause. At one extreme of V/Q mismatching, there is normal ventilation, but abnormal perfusion (dead space ventilation). This mismatching affects the exchange of O₂, resulting in hypoxaemia. Hypercarbia occurs to a lesser extent as CO₂ diffuses more easily than O₂. The classic example is pulmonary embolism. At the other extreme, there is normal blood flow but abnormal ventilation (shunt). This is most commonly a result of venous admixture where capillary blood and alveolar gas do not equilibrate, such as when blood is flowing through a consolidated lung. The larger the shunt, the less responsive it is to supplemental O₂.

Ventilation

Hypercarbia (↑P_aCO₂)

The commonest cause of hypercarbia is alveolar hypoventilation. This can be due to a variety of problems, e.g. airway obstruction, narcotics, CNS disorders, PNS disorders, chest wall disorders. Remember there are other uncommon causes of hypercarbia including: V/Q inequality (e.g. COPD, emphysema); increased CO₂ production (e.g. hyperpyrexia, hypercatabolism, thyrotoxicosis, inappropriate carbohydrate load); and increased dead space (e.g. physiological—V/Q mismatch or ‘dead space ventilation’, equipment—long ventilator tubing and circuitry).

The clinical effects of hypercarbia

Respiratory drive will typically be increased, unless it is suppressed due to the underlying cause of the hypercarbia (e.g. CNS disorders, narcotics). There is a rise in endogenous catecholamines leading to tachycardia, hypertension, increased CO, increased cerebral blood flow and raised intracranial pressure (ICP). Peripheral vasodilatation typically occurs. The patient initially becomes anxious and restless, followed by a decreased level of consciousness and eventually coma if it remains uncorrected.

The ‘chronic CO₂ retainer’

Some patients with chronic respiratory disorders (e.g. COPD) have a chronically elevated P_aCO₂. The chemoreceptors adjust to this elevated level and essentially become less ‘sensitive’ to fluctuations in P_aCO₂, relying more on changes in P_aO₂—the so-called ‘hypoxic drive’. A high FiO₂ could depress ventilation by decreasing this hypoxic stimulus. This is the theory, but clinically it actually rarely occurs in patients with acute respiratory failure. Hypoxia can kill quickly, so give oxygen to the hypoxaemic patient. If the patient may have chronic CO₂ retention, still give oxygen, accepting a P_aO₂ of 50–60 mmHg or even less.

Other investigations in respiratory emergencies

The chest X-ray

The chest X-ray (CXR) is one of the most useful investigations in the patient with respiratory failure. In order to interpret the film correctly, and to avoid missing important findings, a good routine for assessing the CXR is a must. The principles of chest radiography, and other chest imaging modalities, are dealt with in more detail in Chapter 4, ‘Diagnostic imaging in emergency patients’.

The lung can react in a similar fashion to a variety of insults. Therefore, there are no absolute rules in terms of radiological patterns that allow us to distinguish between these insults with 100% accuracy. It is important to always interpret the chest X-ray in the light of your clinical history and examination findings! There will be times when an acutely short of breath patient presents to the emergency department and is found to be hypoxaemic without any significant changes seen on chest X-ray. The differential here includes pulmonary vascular disease (e.g. emboli), respiratory problems (e.g. asthma, early COPD, early chronic lung disease, early pneumonia) and non-respiratory problems (e.g. compromised airway, high oxygen consumption, hyperthermia, intracardiac shunt).

Tests of forced expiration

These tests are effort- and technique-dependent and may not be able to be properly performed when the patient is acutely breathless.

Peak expiratory flow rate (PEFR) is measurable using a simple, portable flow meter. It is reproducible by most patients after several practice efforts. PEFR may be reduced in COPD, asthma and respiratory muscle weakness. PEFR may be normal or increased in restrictive lung diseases such as fibrosis. It is perhaps most useful as a monitor for asthmatic patients in the outpatient/home setting. It may also be helpful in the emergency department as one of the means to assess discharge suitability of asthmatic patients (e.g. PEFR should be at least 75% of predicted or best).

Forced vital capacity (FVC) is the volume of air that can be exhaled with maximum force following a full inspiration. It varies with age, sex, height and general physique.

Forced expiratory volume in 1 second (FEV₁) is the maximum amount of air that can be forcibly exhaled in 1 second following a full inspiration. FEV₁ is reduced in disease that affects airflow, lung elasticity and/or the state of the chest wall, including respiratory musculature. If FEV₁ improves by > 15–20% following bronchodilator therapy, there is said to be reversible airway obstruction. FEV₁ normally accounts for > 75% of the FVC. In obstructive airway disease, FEV₁/FVC is classically < 70%. In restrictive lung disease, FEV₁/FVC is classically normal or increased.

Microbiological methods

Treatment of suspected severe respiratory infections should not be delayed while awaiting the results of laboratory tests. A causal pathogen is found in less than 50% of cases of community-acquired pneumonia. This percentage decreases even further if the cultures are taken after antimicrobials have been given.

Blood cultures can often be collected in the emergency department before antimicrobial therapy is commenced. Ideally, two sets should be taken at least 1 hour apart. The second set may not be possible when rapid empirical therapy is indicated.

The value of sputum culture is limited but may be improved if the sputum is purulent, properly collected—not contaminated by the upper respiratory tract (e.g. saliva, epithelial cells) and, where possible, taken before antibiotics are given—and transported to the lab within 2 hours of collection. Where bacterial infection is not likely (e.g. many upper respiratory tract infections), cultures are usually not indicated. Respiratory syncytial virus (RSV) immunofluorescent-labelled antibody examination of exfoliated cells in nasopharyngeal secretions may be undertaken in paediatric acute bronchiolitis.

The nature of the sputum may be helpful: copious, pink frothy sputum is characteristic of acute left ventricular failure; copious, purulent, pungent sputum of lung abscess; clear, watery sputum of alveolar cell carcinoma; and rusty, mucoid sputum of pneumococcal pneumonia.

Invasive respiratory investigations

Invasive techniques such as percutaneous needle biopsy, diagnostic bronchoscopy, transbronchial biopsy and bronchoalveolar lavage are rarely undertaken in Australasian emergency departments. An exception is diagnostic and/or therapeutic thoracentesis. Pleural fluid is normally a pale yellow colour. It is turbid in the setting of empyema or parapneumonic effusion. Blood in pleural fluid may be due to trauma, malignancy or pulmonary infarction. Other common analyses of pleural fluid include: protein (pleural fluid protein < 30 g/L represents a transudate; > 30 g/L represents an exudate); lactate dehydrogenase (LDH) (pleural fluid:serum LDH ratio < 0.6 represents a transudate; > 0.6 represents an exudate); white cell count (leukocytes may be due to a parapneumonic effusion, pulmonary embolus or empyema; lymphocytes may be due to tuberculosis, malignancy or a vasculitis); glucose (pleural fluid glucose may be < 50% serum glucose levels in bacterial infections, malignancy, rheumatoid arthritis and systemic lupus erythematosus (SLE)); cytology (malignant cells, mesothelial cells); and culture.

LIFE-THREATENING CONDITIONS PRESENTING WITH BREATHLESSNESS

Acute asthma

Initial management

1. Give oxygen and salbutamol or other short-acting beta-2 agonist immediately, if not already commenced, after taking a brief history and physical examination.

2. Focus on delivering oxygen, reversing the bronchospasm and relieving symptoms as soon as possible in a high acuity, well supervised, monitored area with IV access.

Assess severity

Assess severity as mild, moderate or severe and life-threatening using signs of physical exhaustion, cyanosis, speech, PEFR, spirometry (the most accurate test, but may not be possible initially), oxygen saturation, heart rate, respiratory rate and pulsus paradoxus (abnormal decrease in blood pressure on inspiration). Refer to Table 8.3.

Table 8.3 Initial assessment of acute asthma in adults

Features of severe and life-threatening asthma include: paradoxical chest wall movement, exhaustion, sweating, vomiting, panic, speaking in short phases or words only, pulse rate > 120/min, pulsus paradoxus >12 mmHg, central cyanosis, quiet, NOT wheezy chest, PEFR < 50% predicted or < 100 L/min, FEV₁ < 50% predicted or < 1 L, pulse oximetry < 90%.

Difficult to treat patients are usually those who have delayed presentation and/or deteriorated despite outpatient steroid treatment.

Also observe carefully the patient who has childhood onset of asthma, is steroid dependent, has previously been intubated or has a history of severe episodes, especially requiring ICU admission, as they are at increased risk.

Further treatment

1. Hydrocortisone 250 mg IV or equivalent (maximum adult dose) in severe and life–threatening cases; repeat 6-hourly and review at 24 hours.

2. Oral steroids for moderate severity, e.g. prednisolone at 0.5–1.0 mg/kg daily.

3. Salbutamol nebulised, 1 mL of 5 mg/mL solution + 3 mL saline every 15–30 minutes.

4. If not responding, give salbutamol 250 μg (0.5 mL of 500 μg/mL solution) IV bolus over 1 minute, then IV infusion at 5–10 μg/kg/hour.

5. Ipratropium bromide 2 mL 0.05% (500 μg) with salbutamol 2-hourly (optional in moderate severity, not required in mild cases).

6. Adrenaline 0.5 mg IM or slowly IV in severe, prearrest cases or where anaphylaxis may be present. In these circumstances, adrenaline is best administered in 0.1 mg boluses (1 mL of 1:10,000 solution) or 1 mg in 100 mL burette titrated slowly. Subsequent adrenaline infusions should be prepared and titrated based on local hospital protocols.

Intubation and ventilation, while often seen as a last resort, are required for respiratory arrest or exhaustion leading to an immediate prearrest state. Asthmatic patients who are intubated are at risk of barotrauma and are ventilated using permissive hypercapnoea.

Assess response to therapy

• Use the same criteria used to assess severity.

• Severe and life-threatening cases require ABGs, CXR and electrolytes.

• Observed deteriorations in oxygen saturation monitoring require prompt treatment.

• Continuous metered-dose inhaler (MDI) or nebulised salbutamol can result in blood levels equivalent to therapeutic salbutamol infusions. Patients who are hypoventilating, have mucus obstructed airways or are not responding to nebulised salbutamol may require parenteral therapy.

• Patients with COPD may begin to deteriorate due to hypercarbia associated with high oxygen flow and reduced hypoxic drive, signalling the need for reduced FiO₂ and/or BiPap support.

Admission, discharge, follow-up

Observe until the patient is clearly fit for discharge. Longer periods of observation may be required if the patient presents at night or if review, follow-up and compliance with therapy may be compromised.

Every patient discharged following an acute asthma episode should have a clear follow-up plan, including a review of medications, precipitating factors and need for an asthma action plan.

Acute exacerbation of COPD

Patients with COPD, because of their marginal lung function at diagnosis, are prone to significant symptoms with minor precipitants. The precipitant may include acute infection (most commonly), small pneumothoraces, deteriorations in cardiac performance and arrhythmias and may be complicated by acute anxiety and increasing O₂ consumption.

Smoking is the commonest cause of COPD and acute interventional counselling is as effective as any other measure in reducing smoking in all emergency department patients.

Indigenous Australians continue to lose significantly more quality life years because of smoking and COPD.

Initial stabilisation

1. Give oxygen initially, titrated to O₂ saturation > 90%. Monitor carefully for hypercarbia and intervene before significant decrease in LOC or loss of hypoxic drive.

2. Commence nebulised bronchodilator therapy with salbutamol and ipratropium bromide.

3. Give IV hydrocortisone 200 mg.

4. Monitor respiratory rate, ECG, pulse oximetry.

5. Obtain IV access.

6. Assess sputum volume, colour, ABGs, spirometry and CXR.

7. If febrile or appear septic, sputum and blood cultures.

Further treatment

1. Regular nebulised salbutamol 5 mg q4h and ipratropium bromide 500 μg q6h.

2. Antibiotics per Therapeutic Guidelines if evidence of infection. If IV antibiotics are required due to severity, inability to safely swallow, use guidelines for community-acquired pneumonia, usually Class III or IV.

3. Hydrocortisone IV maximum 400 mg/day. Long-term steroid therapy is only indicated where reversible bronchospasm has been identified.

4. Consider additional treatment with nitrates and diuretics if pulmonary oedema is also a factor. Crackles on auscultation may be preexisting due to pulmonary fibrosis rather than pulmonary oedema; check old records.

5. BiPAP is highly effective in acute symptom relief, treatment of hypercarbia and exhaustion. Many intubations have been prevented by early institution of BiPAP.

BiPAP should be initialised with care and consideration of the fact that many of these patients become acutely claustrophobic and take time to adjust to their face being covered and the sensation of the pressure changes.

Patients who have reported good quality of life despite home O₂ therapy may request intubation in the event of respiratory arrest or BiPAP failure, if there is a reversible precipitating factor.

Advanced directives should be checked and respected.

Admission, discharge, follow-up

All but the most minor exacerbations presenting to hospital will require admission.

GP liaison, multidisciplinary community care, pulmonary rehabilitation programs, influenza vaccination and establishment of advanced directives continue to improve patient outcomes and reduce length of stay and readmission rates.

Acute pulmonary oedema

This topic is covered in Chapter 9, ‘Acute pulmonary oedema’.

Pneumonia

• Initially, presentation may be subtle, with fever and malaise.

• Pleuritic chest pain, sputum and dyspnoea may not occur until more advanced, unless there is a significant preexisting respiratory comorbidity.

• Pneumonia presenting with respiratory distress generally represents a severe case likely to require ICU monitoring and management.

• CXR may not be helpful until later in the course of the illness and after rehydration.

• The immediate threats to life are hypoxaemia and systemic sepsis.

Management

1. Initiate high flow oxygen.

2. Obtain IV access.

3. Initiate goal-directed sepsis management if examination reveals signs of severe sepsis.

4. Blood culture from a minimum of two sites and sputum culture are helpful to potentially rationalise and target antibiotic therapy.

5. Commence antibiotic therapy as soon as cultures taken in high parenteral doses using antibiotic guidelines and Pneumonia Severity Index Score (Figure 8.1).

Figure 8.1 The Pneumonia Severity Index

The Pneumonia Severity Index is used to determine a patient’s risk of death. The total score is obtained by adding to the patient’s age (in years for men or in years – 10 for women) the points assigned for each additional applicable characteristic.

Based on Fine MJ, Auble TE, Yealy DM et al. A prediction rule to identify low-risk patients with community-acquired pneumonia. N Engl J Med 1997; 336:243-250, as presented in Halm EA, Teirstein AS. Management of communityacquired pneumonia. N Engl J Med. 2002; 347(25):2039-2044

Consider that respiratory symptoms may be secondary to severe sepsis from another source.

Be aware of the aggressive therapy required for the immunosuppressed patient or hospital-acquired pneumonia.

Consider severe acute respiratory syndrome (SARS) and Legionella as potential causes, particularly in rapidly deteriorating cases associated with respiratory failure.

Spontaneous pneumothorax

Traumatic pneumothoraces are treated more aggressively and are covered in Chapter 3, ‘Resuscitation and emergency procedures’.

The classic presentation is that of the thin, tall young man with pleuritic chest pain and dyspnoea. Spontaneous pneumothoraces occur in families and can be recurrent.

Illness such as COPD and asthma may be associated with spontaneous pneumothorax, especially in association with acute exacerbations where the pneumothorax may have precipitated the presentation.

Initial stabilisation

The immediate threat to life is the tension pneumothorax which, if untreated, will lead to circulatory collapse. Circulatory collapse is preceded by extreme and rapidly deteriorating respiratory distress.

Tension pneumothorax leading to significant compromise will be obvious clinically.

The presence of tension is independent of the size of the pneumothorax, although it will progressively enlarge unless there is marked gas trapping in the affected lung. The patient may be agitated and confused and appear restless with dyspnoea, tachypnoea and cyanosis. The affected hemithorax will appear hyperinflated, neck veins distended.

The patient will be tachycardic and hypotensive. Tracheal shift, if palpable, will be away from the side of the pneumothorax. Auscultation reveals reduced or absent breath sounds on the affected side. The affected hemithorax is hyperresonant to percussion. Subcutaneous emphysema, if present, may become suddenly worse.

• Identify the affected hemithorax and place a 12-gauge IV cannula in the 2nd intercostal space, midclavicular line. Attach it to a flutter valve or leave it open to air.

• Needle thoracostomies with IV cannulae are prone to block or kink and may be too short to drain reliably unless a longer than standard cannula is used.

• Placement of the cannula commits to a formal tube thoracostomy.

• Experienced practitioners adept at rapid insertion of tube thoracostomy will be less likely to need needle thoracostomy. Nonetheless, the patient must not be allowed to deteriorate or remain untreated if a slow process of tube thoracostomy is anticipated.

• Initiate high flow oxygen.

• Obtain IV access for sedation and analgesia in the case of tube thoracostomy.

Specific treatment

Treatment options are available, depending on the patient’s underlying condition and the response of the pneumothorax.

1. Conservative management as an outpatient

Suitable for patients with a small pneumothorax, no preexisting lung disease, mild symptoms and no hypoxia. The pneumothorax is treated with high flow oxygen while being assessed, but is not drained. The patient is discharged after remaining stable for 4–6 hours of observation.

The patient is advised to seek follow up X-rays (12–48 hours, shorter if a repeat X-ray is not taken prior to discharge) and full resolution and clearance is required before flying or diving. Discharge is not advised if any doubts exist as to the patient’s ability to return promptly to hospital.

2. Aspiration of pneumothorax

Suitable for patients with moderate symptoms and a 20–40% pneumothorax with no underlying lung disease (secondary spontaneous pneumothorax).

An IV cannula and three-way tap or other catheters designed for the purpose may be used.

A pigtail catheter inserted using Seldinger technique may be safer and also effective if continuous drainage is required.

The pneumothorax is aspirated using a three-way tap and then X-rays are repeated.

If the pnuemothorax has recurred on repeat CXR, a formal tube thoracostomy should be performed or, if a suitable catheter was used initially, it may be connected to an underwater drain and low suction.

3. Tube thoracostomy

The best choice for those with a large pneumothorax or significant underlying lung disease.

Place the tube in the 4th–5th intercostal space and directed superiorly.

Avoid placing the tube where lung adhesions may be present as seen on CXR. Use the 2nd intercostal space midcostal line if necessary. Connect to low suction.

Large pneumothoraces are regarded as > 2–3 cm of collapse; however, treatment decisions regarding ‘smaller’ pneumothoraces should be based on the patient’s stability, as determinations of pneumothorax size from CXR are notoriously inaccurate.

Male smokers have a 20-fold increased risk of primary spontaneous pneumothorax.

COPD and cystic fibrosis patients have increased risk and associated mortality.

Recurrent spontaneous pneumothoraces (i.e. same hemithorax) should be referred to a thoracic surgeon for possible thorascopic treatment.

Pulmonary embolism

This topic is covered in Chapter 10, ‘Pulmonary emboli and venous thromboses’.

Acute lung injury (noncardiogenic pulmonary oedema)

This represents a range of conditions characterised by inflammation or injury causing increased permeability of lung tissue and exudation of fluid into the alveoli.

Wet, stiff lungs make gas exchange and ventilation difficult.

The condition may not become apparent until the patient starts to decompensate and tire, hours after the initial insult. Further decompensation is likely and should be anticipated.

Respiratory dysfunction may become apparent as late as 48 hours or longer after the initial insult and may take weeks or months to resolve.

Causes include pulmonary contusion, aspiration, chemical pneumonitis, narcotic overdose, near drowning, transfusion of blood products, SARS, avian influenza and severe sepsis.

When invasive ventilation is required, care should be taken to avoid further ventilator-associated lung injury, as these patients are particularly at risk, especially from barotrauma.

Anaphylaxis with bronchospasm

(See also Chapter 40, ‘Dermatological presentations to emergency’.)

• Anaphylaxis may present with respiratory distress with or without shock as a result of the type 1 hypersensitivity reaction.

• Initial management is as for acute severe asthma; however, these patients require adrenaline, at least subcutaneous 0.3 mg for mild cases and IM 0.5 mg and/or titrated IV adrenaline for more severe cases.

• They can be identified by known history of allergy and precipitants, airway involvement with signs of oedema and voice changes, urticaria and pruritis. Suspect also when ‘asthma’ is of sudden onset without obvious precipitant.

• Following this initial therapy the patient should also receive IV hydrocortisone 200 mg and antihistamine therapy.

• Observe the patient for up to 12 hours because of the risk of late relapse.

Hyperventilation

• Organic causes of hyperpnoea and hypocapnea must be considered and excluded initially.

• A chest X-ray will be normal and ABGs will show respiratory alkalosis.

• Patients may present with non-exertional chest pain, blurred vision, palpitations, paraesthesiae, carpopedal spasm, fear, panic and hysteria.

• Treatment is with patient education and relaxation techniques, the goal being to achieve self control.

• A short course of benzodiazepines may be useful.

• Antidepressants possibly have a role in recurrent cases but should not be initiated in the emergency department.

• Mitral valve prolapse may present with atypical chest pain, palpitations, dyspnoea, anxiety and panic attacks so, if a typical click is heard, associated ECG changes seen, an outpatient echocardiogram should be arranged.

• ‘Paper bag breathing’ is not recommended.

EDITOR’S COMMENTS

• ABC—beware of breathing, deterioration can be subtle—look for trends in observations and tests.

• Respiratory rates are very good measures of the degree of respiratory compromise.

• Pulse oximetry—respond if low or drops.

RECOMMENDED READING

Blackwell N., Foot C., Thomas C. Examination intensive care and anaesthesia. Elsevier Australia; 2007.

Hillman K., Bishop G., editors. Clinical intensive care and acute medicine, 2nd edn., Cambridge: Cambridge University Press, 2004.

McKenzie DK, Abramson M, Crockett IJ et al. The COPD-X Plan: Australian and New Zealand guidelines for the management of chronic obstructive pulmonary disease 2007. Online. Available: http://www.copdx.org.au/search.asp?zoom_query=management; December 2008.

National Asthma Council of Australia. Asthma management handbook 2006. Online. Available: http://www.nationalasthma.org.au/cms/index.php; December 2008.

Sigillito R.J., DeBlieux P.M. Evaluation and initial management of the patient in respiratory distress. Emerg Med Clin N Am. 2003;21:239-258.

Warrell D.A., Cox T.M., Firth J.D., editors. Oxford textbook of medicine, 4th edn., Oxford: Oxford University Press, 2003.

Webb A.J., Shapiro M.J.. Singer M., et al, editors. Oxford textbook of critical care. Oxford: Oxford University Press, 1999.

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