theoretically cause less ventilator-associated lung injury: large studies are underway to d e \201 ne its role in adult ARDS. Perhaps the ultimate means of resting the injured lung i s to perform Extra Corporeal Oxygenation. This technique requires that the patient \200\231 s blood passes across a membrane to supplement gas exchange. Because of associated com- pli cations, this has traditionally been used as a salvage therapy, which is only of proven ben efit in children. However, newer devices such as the Novalung require a less invasive app roach and less anticoagulation, suggesting that this and similar devices may have an increa sing role in the future. Ventilator-associated lung injury Experiments carried out 30 \200\22340 years ago demonstra ted that high tidal volume and high pressure ventilation caused lung injury in healthy anim als, and that previously damaged lung was particularly susceptible to these effects. Simila r models implicated the effects of overdistension (volutrauma) as opposed to high airway pr essure (baro- trauma). and demonstrated the injurious effects of cyclic expansion and colla pse of lung units de \201 cient in surfactant activity (atelectotrauma). The \200\230biot rauma hypothesis \200\231 addresses the question of how the effect of injurious mechanical ventilation affects mortality, when only a small minority of patients succumb to respirator y failure. The hypothesis is supported by clinical studies demonstrating that injurious, as opposed to protective, mechanical ventilation was associated with the detection of increas ed concentrations of in \202 ammatory mediators in bronchoal- veolar lavage and plasma. Fr om these studies it can be inferred that injurious mechanical ventilation stimulates the pr oduction of in \202 ammatory mediators that overspill from the lung into the systemic circ ulation and contribute to multiple organ failure. Adjuncts to ventilatory support In many cases of ARDS, especially those with an indirect no n-pulmonary cause, there is a predominance of collapse and consolidation in dependent lung regions. Turning patients from supine to prone improves ventilation \200\223 perfusion matc hing and signi \201 cantly affects gas exchange in 2/3 cases of ARDS. Furthermore, the we ight of the mediastinum is removed from the left lower lobe, secre- tion clearance may be e nhanced and ventilator-associated lung injury may be mitigated. Large studies have failed t o demonstrate a bene \201 t in terms of survival or duration of mechanical ventilation wit h prone positioning, whilst the procedure is labor intensive and associated with tube displ acement and a higher incidence of pressure sores. Inhaled vasodilators, nebulized prostacyc lin or Nitric Oxide (NO) also improve oxygenation in 2/3 cases of lung injury, but have re peatedly failed to improve survival in multi-center clinical trials. Recommendations for instituting invasive mechanical ventilation in patients with ARDS It is not possible to describe ideal ventilator parameters for all patients with ARDS; mechanica l ventilation settings need to be individualized and changed with time to suit the patient \200\231s condition. This is best achieved with an empirical approach and patience; however , some guidelines may be applied: \200 Ventilation strategy It is now accepted that mechanical ventilation is inevitably damaging to the injured lung and it is neither necessary nor desirable to strive to achieve normal A BGs in patients with ARDS. The ARMA study demonstrated improved survival by selecting a tid al volume target of 6 as opposed to 12ml/ kg predicted body weight (PBW). However, it is no t known whether 6ml/kg is the optimal tidal volume and there does not appear to be a thresh old, or safe plateau pressure, below which there is no advantage in decreasing tidal volume . PEEP recruits collapsed lung, reduces intrapulmo- nary shunting and improves oxygenation, making it a central part of the mechanical ventilation strategy in ARDS, because large par ts of the lung are collapsed owing to de \201 - cient surfactant activity. PEEP also has d etrimental effects primarily by overdistending compliant alveoli or by decreas- ing venous return, RV function and oxygen delivery. In patients being ventilated with a target tidal v olume of 6ml/kg, there was no bene \201 t in using high (14mm Hg) against low (8mm Hg) PEE P in the ALVEOLI ARDS network study. Similarly, the application of high airway pressure for a limited period (recruitment maneuvers) confers short- term physiological bene \201 t on ly, but may be useful to rescue patients with life-threatening hypoxia. Tidal volume of 6ml/kg predicted body weight (PBW), calculated as follows: for men, PBW = 5 0.0 + 0.91 (height in cm \200\223 152.4); and for women, PBW = 45.5 + 0.91 (height in cm \200\223 152.4). If the plateau pressure is >30cm H2O, try to decrease tidal volume further if gas exchange targets can still be met. This may be unnecessary if there is an extrapulm onary cause of restriction, e.g. abdominal distension. Respiratory rate of 20/min, which wi ll tend to mitigate respiratory acidosis but ensure that expiration is com- pleted before t he subsequent inspiration starts in order to avoid breath stacking. Accept a pH >7.2 and do not worry about hypercapnia unless there is concurrent intracranial hypertension or other contraindications. Respiratory acidosis is generally well tolerated unless the rise in carb on dioxide tension is rapid. Oxygen saturation target of 88 \200\22392% to minimize oxygen toxicity. Set PEEP between 14 and 8mm Hg, start at a high level and decrease, until the com pliance or oxygenation deteriorates. Alternative modes of respiratory support There is very little evidence to favor one ventila tory mode over another in adult patients with ARDS. High frequency ventilation aims to mini mize tidal volume whilst maintaining recruitment through a high mean airway pressure. This mode improves oxygenation and should 261 CHAPTER 17.7 ARDS: ventilatory management Whilst muscle relaxants and full sedation may be required initially, these should be withdr awn or minimized as soon as possible to avoid neuromuscular sequelae. Refractory hypoxaemia may be improved by prone positioning, recruitment maneuvers and the adminis- tration of an inhaled vasodilator such as NO, although none of these interventions can be recommended fo r routine use. Ferguson ND, Villar J, et al. Understanding high-frequency oscillation: lessons from the an imal kingdom. Intensive Care Med 2007; 33: 1316 \200\2238. Gattinoni L, Caironi P, Cressoni M, et al. Lung recruitment in patients with the acute resp iratory distress syndrome. N Engl J Med 2006; 354: 1775 \200\22386. Guerin C, Gaillard S, Lemasson S, et al. 2004. Effects of systematic prone positioning in h ypoxemic acute respiratory failure: a rand- omized controlled trial. JAMA 292: 2379 \200 \22387. Hager DN, Krishnan JA, Hayden DL, et al. Tidal volume reduction in patients with acute lung injury when plateau pressures are not high. Am J Respir Crit Care Med 2005; 172: 1241 \200 \2235. Further reading Acute Respiratory Distress Syndrome Network. Ventilation with lower tidal v olumes as compared with traditional tidal volumes for acute lung injury and the acute respi ratory distress syndrome. N Engl J Med 2000; 342: 1301 \200\2238. Pinhu L, Whitehead T, Evans,T, et al. Ventilator-associated lung injury. Lancet 2003; 361: 332 \200\22340. Ranieri VM, Giunta F, Suter PM, et al. Mechanical ventilation as a mediator of multisystem organ failure in acute respiratory distress syndrome. JAMA 2000; 284: 43 \200\2234. Brower RG, Lanken PN, MacIntyre N, et al. Higher versus lower positive end-expiratory press ures in patients with the acute respiratory distress syndrome. N Engl J Med 2004; 351: 327 \200\22336. 262 S SINGH Asthma A chronic in \202 ammatory disorder of the airways in which many cell types play a role, i n particular mast cells, eosi- nophils and T lymphocytes. In susceptible individuals, this in \202 ammation causes recurrent episodes of wheezing, breath- lessness, chest tightness and cough, particularly at night and/ or in the early morning. These symptoms are usually a ssoci- ated with widespread but variable air \202 ow limitation that is at least partly re versible either spontaneously or with treatment. The inflammation also causes an associated increase in airway responsiveness to a variety of stimuli. The diagnosis is a clinical one and not always simple. There is no con \201 rmatory blood test, radiographic sign or his- topathological feature. The diagnosis can usually be made by a combination of history (par ticularly if typical), pulmonary function testing, spirometry, serial measurements of peak expiratory \202 ow rates (PEFR) or bronchial provocation testing by metha- choline or exe rcise. A therapeutic trial of bronchoodilators often aids diagnosis by the above methods. T he differential diagnosis includes respiratory and non- respiratory conditions that may cau se similar symptoms, co-exist or worsen asthma severity. Allergic rhinitis (in most allergi c asthma and 50% of non-allergic asthma) may present as post-nasal drip syndrome. Gastro-oe sophageal re \202 ux can exacerbate asthma symptoms. Variable air \202 ow obstruction is characteristic of asthma. A non-smoker with cough, shortness of breath and/or wheezing who has expiratory air \202 ow obstruction that reverses to normal with treatment or over time probably has asthma. In contrast, the person with symptoms with consistently normal spirom etry probably does not have asthma, and alternative diagnoses (e.g, recurrent bronchitis) s hould be sought. Examination: key points \200 Widespread, high-pitched, polyphonic wheezes. More commonly in expiration. These are distin guishable from monophonic wheezes of \201 xed airway narrowing or upper airway sounds hea rd over the neck. Nasal polyps, which appear as glistening, gray, mucoid masses within the nasal cavities, should prompt ques- tioning about concomitant aspirin sensitivity and chron ic sinusitis. Inhaler technique, as part of full assessment. Classi \201 cation \200 \200 Acute asthma, status asthmaticus Chronic asthma; mild, mild intermittent, mild persistent, moderate persistent, severe Allergic ( \200\230extrinsic \200\231) or non-allergic ( \200 \230intrinsic \200\231) \200\230Brittle asthma \200\231 Corticosteroid-resistant asthma Oc cupational asthma Cough variant asthma Factitious asthma (paradoxical vocal cord motion) \200 \200 \200 \200 \200 Investigations \200 Pulmonary function testing \200\224FEV1/FVC <0.7; PEFR reduction with bronchodilator revers ibility (>15%) Total serum IgE and peripheral blood eosinophilia Allergy sensitivity testin g \200\224to common inhaled allergens by skin testing or speci \201 c IgE (RAST). Methacho line testing (PC20 = concentration causing a 20% fall in FEV1) Chest radiograph \200\223 e xclude other diagnoses Exhaled NO \200\224marker of airway in \202 ammation under evaluati on \200 \200 Clinical approach History: key points \200 \200 Management Chronic asthma Goals of treatment are freedom from symptoms of asthma, minimizin g exacerbations, eliminating impairment of daily activities, reducing pharmacological side effects, optimizing lung function (FEV1 and/or PEFR >80% predicted or best) and patient/car er education about asthma, its prevention and early treatment. These are achievable through : \200 \200 \200 \200 Cough, wheeze, breathlessness (classic triad), Chest tightness, chronic cough, recurrent \200\230infections \200\231 (often a misdiagnosis leading to a new diagnosis of asthma), Ep isodic symptoms; time course hours \200\223days, particulary nocturnal symptoms (or early m orning wakening). Triggers; exercise, cold air, allergen exposure (e.g. animal hairs, house dust mite, molds, pollens, cockroaches) and non-speci \201 c irritants (e.g. cigarette smo ke or fumes), Atopy; personal or family history, in association with symptoms, favors a dia gnosis of asthma, Childhood symptoms of asthma, \200\230wheeziness \200\231, recurrent \200\230bronchitis \200\231 or eczema favor diagnosis of asthma, Occupational history, Drug history; aspirin/NSAIDs/ -adrenergic antagonists may exacerbate asthma. Regular monitoring of symptoms/lung function (PEFR) Avoiding and controlling asthma trigger factors Appropriate pharmacological therapy Patient education (including asthma management plans) Pharmacological treatments A stepwise approach aims to abolish symptoms and optimize lung f unction by initiating treatment at the level/dosing most appropriate to achieve this. As sy mptoms emerge, early con- trol and maintaining it by stepping up treatment as necessary and stepping down when good control established. \200\231Relievers \200\231: short-acting agonists (SABAs) for short-lived relief in all with symptomatic asthma. Anticholinergics ca n be added in acute excerbations. \200\230Preventers \200\231: inhaled corticosteroids (IC S) should be used regularly. Sodium cromoglycate works in some patients. Theophylline or le ukotriene receptor antagonists can be used as \200\230add-on \200\231 treatments at \211 step 3 (see below). \200 Features that suggest an alternative diagnosis to asthma include: \200 \200 Lack of response to bronchodilators or corticosteroids, Onset after 50 years \200\224althou gh late-onset asthma is well recognized, Greater than 20 pack year smoking history suggests increasing likelihood of COPD. 263 CHAPTER 17.8 Asthma Speci \201 c therapies: sublingual immunotherapy, monoclonal anti-IgE (e.g, omalizumab); s eek specialist advice. Clinical features Management Immediate treatment: O2 (high \202 ow), nebulized bron- chodilator (salbutamol 5mg ipratropium bromide 500mcg (O2 driven), Hydrocortisone IV 100mg bd \200\223qds (pre dnisolone 30 \200\22340mg PO). Review: monitor PEFR, O2 sats, repeat ABG if no improve- men t, check serum K+. If no response, further back-to-back nebulized bronchodilators (or every 15min). Life-threatening: IV magnesium Mg2+ (20ml 10% MgSO4) over 20min and/or SC terbutal ine (5mg in 10ml normal saline) over 24h or IV salbutamol (250mcg slow bolus) and/or IV ami nophylline 500 \200\223750mg in normal saline over 24h (monitor levels). Good \202 uid re suscitation. Discuss with ICU; need for intubation and mechanical ventilation. Only conside r NIV in an ICU setting with senior experts and only if no indication for immediate intubat ion. Stepwise approach Step 1: mild intermittent asthma; SABA as required. Step 2: regular preve nter therapy; ICS 200 \200\223800mcg/day beclomethasone dipropionate equivalent. Step 3: ad d-on therapy; Add long-acting agonists (LABAs) or combination ICS \200\223LABA. Increase the ICS dose if required. Consider sequential add-on therapies. Step 4: persistent poor co ntrol; increase ICS up to 2000mcg/day and/or add-on therapies. Stop ineffective add-on ther apies. Consider review asthma, and specialist referral. Step 5: frequent or continuous oral corticosteroids. Consider trials of steroid-sparing agents if long-term oral corticosteroi ds likely. Specialist monitoring. Acute severe asthma Acute severe asthma and status asthmaticus or near-fatal asthma remain important causes of preventable mortality. The predictors of morbidity include underpercept ion of severity, poor asthma management and previous ICU admission. International guideline s for management are published. Follow-up Transfer of care from ICU through to the respiratory ward, and asthma clinic foll ow-up, with close monitoring, discharge planning and management planning. Further reading British Thoracic Society/Scottish Intercollegiate Network. British guidelin e on the management of Asthma. Thorax 2003; 58 Suppl: 1 \200\22394. Moderate exacerbation Acute severe Life threatening Global Initiative for Asthma Management and Prevention. NHLBI/ WHO Workshop Report, US Depa rtment of Health and Human Services. National Institutes of Health, Bethesda, 1995; Pub #95 -3659. PEFR Respiratory effort/rate (RR) 50 \200\22375% 33 \200\22350% RR >25/min <33% RR >25/min http://www.ginasthma.com;www.thoraxjnl.com Feeble effort/silent chest Cannot complete sentence in a breath HR \211 110/min Heart rate (HR) HR \211 110/min; arrythmias, bradycardia, hypotension SpO2 <92% SpO2 >92% Arterial blood gas (ABG) PaO2 >8kPa PaCO2 4.6 \200\2236.0kPa normal PaO2 <8kPa PaCO2 4.6 \200\2236.0kPa normal >6.0kPa Other features exhaustion, confusion, coma 264 S SINGH Asthma: ventilatory management Some patients with severe acute asthma/status asthmaticus develop respiratory failure and r equire supportive care with mechanical ventilation. Approximately 4% of all patients hospit alized for acute asthma require mechanical ventila- tion. Although life-saving, mechanical ventilation and its associated interventions (e.g, sedatives, paralytics) can also cause mo rbidity and mortality. The median duration of mechanical ventilation is 3 days. The indica tions for intubation and mechanical ventilation are clinically rather than guideline determ ined. Thus, a reduced level of consciousness, impending respira- tory failure and cardiores piratory arrest are undisputed indications. Where possible, intubation should be performed semi-electively, by someone with experience in airway management, and preferably with a lar ge bore ETT (e.g. size 8mm). Manipulation of the airway can cause increased air \202 ow ob struction due to exaggerated bronchial respon- siveness. Hence, adequate venous access, non -invasive monitoring, and sedation should be optimized prior to intubation. Table 17.9.1 Typical ventilator setting for severe asthma Respiratory rate Tidal volume 10 \200\22314 breaths/min \211 8ml/kg 80 \200\223100l/min \211 80% of the intrinsic PEEP Inspiratory \202 ow Extrinsic positive end- expiratory pressure (extrinsic PEEP) Minute v entilation \211 115ml/kg <30cm H2O Inspiratory Pplat PEEP can be detrimental and should be generally avoided in ventilated and paralyzed patient s. Intrinsic PEEP increases the magnitude of the drop in airway pressure that the patient m ust generate to trigger a breath, thereby increas- ing the patient \200\231s workload. Care ful application of extrinsic PEEP at levels less than the intrinsic PEEP will reduce this g radient and the work of breathing. Thus, ventilator-set PEEP levels up to 80% of intrinsic PEEP are often helpful in spontaneously breathing pa tients if set, monitored and adjusted at the bedside. Note that measurements of intrin- sic PEEP may be underestimated in severe widespread airway closure, due to impedance of end-expiratory alveolar pressures. In view o f the potential for further dynamic hyperin \202 ation, which may go unrecognized, one sho uld be prepared to decompress manually if necessary (by disconnecting from the ventilator t ubing momentarily). 2-adrenoceptor agonists are usually delivered to venti- lated patient s by in-line nebulizer. The amount of drug reaching the airways depends on the nebulizer de sign, driving gas \202 ow, characteristics of the ventilator tubing and the size of the e ndotracheal tube. Sedation and Anesthesia Personal experience and local practice account fo r the variation in agents used. Propofol, with its rapid onset and offset is a good agent f or intubation and short-term seda- tion, although additional \202 uid resuscitation is ne cessary to counter its vasodilatory properties. Etomidate is also used, in view of a low ri sk of cardiovascular side effects. Ketamine, with its bronchodilator and sympathomimetic pr operties, is useful for induction and sometimes after intubation in persisting severe bronc hospasm, as an infusion. Caution is warranted in patients with ischaemic heart disease, hyp er- tension, intracranial pathologies and pre-eclampsia, and the associated dysphoria is of ten distressing. Thiopentone is generally avoided due to vasodilation and hista mine releas e. Opiates may be used as co-induction agents, although boluses can cause histamine re leas e and worsen- ing bronchoconstriction. Fentanyl, which causes less hista- mine release than morphine, is more appropriate in the acute setting. Ventilatory strategy The ventilatory strategy for an asthmatic patient is governed by the n eed to prevent dynamic hyperinflation and its consequences. Hypo tension is a common conseq uence of pre-existing hypovolaemia, when positive pressure ventila- tion is applied, in con junction with the use of ana esthetic agents and sedatives. Bronchospasm, airway in \202 a mmation, airway oedema and mucus plugging increase airflow obstruction, decrease expiratory \202 ow and prolong the required complete expiratory time. Dynamic hyperin \202 ation o ccurs when increased airway resistance prolongs expiratory flow, so that the next breath in terrupts exhalation of the tidal volume, leading to air trapping or \200\230breath stackin g \200\231. The consequences of pro- gressive increases in intra-thoracic pressure, due to intrinsic PEEP and elevated inspiratory plateau pressure (Pplat) are cardiovascular collaps e and barotrauma. Hence, ventilation strategies include: low tidal volumes, slow respirator y rate with prolongation of expiratory time, and pressure limitation. This should minimize dynamic hyperin \202 ation, and consequent hypotension and baro- trauma (pneumomediastinum and pneumothorax). The low minute ventilation may lead to relative hypoventilation and res ultant hypercapnia (i.e. permissive hypercapnia). Permissive hypercapnia is generally well tolerated so long as adequate oxygenation is achieved and in the absence of contraindi cati ons, particularly intracranial pathology, or myocardial ischaemia. Other potential complica tions include pneumothorax, often the result of excessive \200\230hand- bagging \200\231, and cardiac dysrrythmias. Ventilatory settings In general, controlled modes of ventilation are pre ferred in the imme diate post-intubation period, in view of the fre- quently difficult airway hyper-reactivity , tendency to dynamic hyperin \202 ation and a desire to rest the fatigued respiratory mus cles. An example of typical ventilator set- tings in a pressure-limited mode of ventilation are shown in Table 17.9.1. Neuromuscular blocking agents Suxamethonium may be used in rapid sequence induction. The us e of neuromuscular agents is sometimes necessary to achieve control of ventilation, and red uce dynamic hyperin \202 ation. Potential additional bene \201 ts include reduc- tion in oxygen consumption, and reduc tion in carbon dioxide 265 CHAPTER 17.9 Asthma: ventilatory management and lactic acid production. The preferred agents are vecuro- nium and pancuronium. Although all these agents may cause histamine release in large boluses, potentially wor sening bron choconstriction, long-term muscle relaxa tion with vecuronium is associated with low levels of histamine release as compared with atracurium. The risk of myositis and myopathy, assoc iated with a rise in creatinine kinase (CK), is greater with the concomitant use of cortico ster- oids than without neuromuscular blockers. Therefore, minimizing the duration of use w ith monitoring is necessary. However, it is not superior to \200\230pure \200\231 2-adrenoceptor agonists and is not recommended for routine use in the treatment of asthma. It may bene \201 t non-responding patients and can be given either nebulized, SC or IV. Heliox There have been few studies of its use in acute severe asthma. Heliox, a blend of he lium and oxygen with a lower density than nitrogen \200\223oxygen mixtures (helium \200\223 oxygen mixture in ratios 80:20 or 70:30), although not recom- mended for routine use, has b een shown to improve airway pressures and gas ex change in intubated patients with asthma. However, it can also cause ventilator malfunc- tion, including inaccurate measurement of ti dal volume and oxygen concentration. Weaning Weaning from ventilation is usually commenced following signs of stabilization of v entilation, and reductions in dynamic hyperin \202 ation. There often appears to be a well de \201 ned time, speci \201 c to patients, at which this occurs, albeit dif \201 cult to predict. Sometimes it is heralded by a lack of need for frequent changes in ventilatory parameters, and the production of copious secretions, thought to be related to the loosenin g of trapped sputum plugs as bron- chiolar bronchoconstriction and inflammation settle. Pre paration for extubation comes with recognition of a possible sympathetic response-induced b ronchoconstric- tion. Bronchodilators and inhalational anesthetic agents are often useful i n this situation. Extracorporeal life support The removal of carbon dioxide and maintenance of oxy- genation through an arti \201 cial membrane can be used for patients with severe refractory asthma complicated by refractory respiratory acidosis. However, clinical outcome studies are absen t. Follow-up Patients with status asthmaticus who require mechanical ventilation have increase d in-hospital mortality compared with patients who do not require mechanical ventilation (7 vs 0.2%). Patients who survive to hospital discharge remain at high risk of death Transfer of care from ICU through to the respiratory ward, and asthma clinic follow-up, with close monitoring, discharge planning and management planning are thus vital. Other techniques in severe asthma with mechanical ventilation Despite use of the treatments mentioned above, some patients continue to demonstrate refractory bronchocon- striction, e xtreme overinflation and mucus plugging. Various additional methods have been used to allev iate these factors. The routine use of these adjunctive therapies cannot be recommended on the basis of existing clinical studies. Further reading Abroug F, Nouira S, Bchir A, et al. A controlled trial of nebulized salbuta mol and adrenaline in acute severe asthma. Intensive Care Med 1995; 21: 18 \200\22323. Afessa B. Morales I, Cury JD. Clinical course and outcome of patients admitted to an ICU fo r status asthmaticus. Chest 2001; 120: 1616 \200\22321. General anesthesia Inhalational anesthetic agents such as isoflurane and sevo \202 ur ane are potent bronchodilators and are effective for mask induction in severe asthma. They have been used for mainte nance of anesthesia in refractory cases, although this is limited by the few ICU ventilators which can deliver inhalational anesthetics, and anesthetic ventilat ors, which may not have the capabilities for ventilating patients with very severe airway r esistance. Anzueto A, Frutos-Vivar F, Esteban A, et al. Incidence, risk factors and outcome of barotra uma in mechanically ventilated patients. Intensive Care Med 2004; 30: 612. Krishnan V, Diette GB, Rand CS, et al. Mortality in patients hospital- ized for asthma exac erbations in the United States. Am J Respir Crit Care Med 2006; 174: 633. Mutlu GM. Factor P, Schwarn DE, et al. Severe status asthmaticus: management with permissiv e hypercapnia and inhalation anesthesia. Crit Care Med 2002; 30: 477 \200\22380. Manual decompression During expiration, manual compression may reduce hyper- in \202 ation . However, it has not been fully evaluated in studies. The use of mucolytics, expectorants or chest physiother apy has not been shown to provide any direct bene \201 t. Scoggin CH, Sahn SA, Petty TL. Status asthmaticus: a nine-year experience. JAMA 1977; 238: 1158. Tassaux D, Jolliet P, Thouret JM, et al. Calibration of seven ICU ventilators for mechanica l ventilation with helium \200\223oxygen mixtures. Am J Respir Crit Care Med 1999; 160: 22. Adrenaline Adrenaline has both a bronchodilator effect from its 2- adrenoceptor agonist a ction, and an agonist vasoconstric- tor ef fect, thus possibly reducing mucosal oedema f ormation. 266 A BRAME & A JONES Pneumothorax \200 \200 \200 \200 \200 De \201 nition A pneumothorax is de \201 ned as the presence of air in the pleural cavity , and can be classi \201 ed as either primary or secondary. Subcutaneous emphysema Tachycardia Hypoxia Hypercapnia* Hypotension* Pulsus paradoxus* Primary pneumothorax \200 Patients without clinically apparent lung disease. More common in tall thin males (M:F 5:1) with a peak inci- dence between10 and 30yrs. Most have unrecognized underlying lung diseas e, with subpleural bullae found in almost all patients who undergo thoracotomy. Cigarette s moking increases the risk by 100 times. (*tension pneumothorax/secondary pneumothrax with severe underlying lung disease) Additiona l \201 ndings in ventilated patients \200 \200 Increased peak airway pressures (volume control) Decreased tidal and minute volumes (pressu re- \200\230control- led \200\231 modes) Secondary pneumothorax \200 Spontaneous \200\224underlying lung disease (COPD, asthma, cystic \201 brosis, interstiti al lung disease, TB, lung abscess, PCP). Traumatic \200\224penetrating and non-penetrating thoracic and upper abdominal trauma. Iatrogenic \200\224pleural biopsy or aspiration, centr al venous access, mechanical ventilation, percutaneous tracheos- tomy. Investigations Chest X-ray In the absence of life-threatening cardiovascular compro- mise, it is advisable to con \201 rm a suspected pneumtothorax with a CXR prior to instigating t reatment. Classically a pneumothorax appears as a sharp white apicolateral line, beyond whi ch there are no lung markings. In the intensive care patient, however, diagnosis may be mor e dif \201 cult, with anteromedial (38%) or subpulmonic (26%) pneumothora- ces being commo n. In addition, pleural adhesions may result in loculated or encysted pneumothoraces which may be indistinguishable from bullae. Radiological \201 ndings associated with pneumothor aces in this population include: \200 \200 \200 \200 \200 \200 \200 Incidence Both primary and secondary pneumothoraces are rela- tively common reasons for med ical consultation and hospital admission. In the critical care population overall, the inci dence of pneumothorax is 3%, although in venti- lated patients the incidence can be much h igher, and predominantly related to ventilator-induced barotrauma, or invasive procedures ( Table 7.10.1). In general, morbidity and mortality are determined by the underlying conditi on. However, in the critically ill, pneumthoraces are associated with increased morbidity a nd mortality. Increased lucency over diaphragm/upper abdomen Deep sulcus sign Visualization of the inferi or surface of the lung Ovoid hypodense regions Fluid level Temporal changes in line and dra in positions Mediastinal air and surgical emphysema Table 17.10.1 Risk factors for pneumothorax in critically ill High plateau pressures Central venous acess ARDS/ALI Asthma/COPD Interstitial lung disease HIV disease (PCP) Low body weight In patients with signi \201 cant surgical emphysema, bullous lung disease or complex chest pathology, CT scanning may be required both for diagnosis and to guide further management. Radiologocal signs of tension pneumothorax \200 \200 Shift of mediastinum to contralateral side Flattening or inversion of ipsilateral diaphragm Clinical features Symptoms and signs Patients commonly present with ipsilateral pleuritic c hest pain and dyspnoea. The severity of the symptoms relates to the size of the pneumothora x (small pneumothoraces may be asymptomatic). Patients with secondary pneumot- horaces or a ny tension pneumothorax may have more dramatic presentations with severe dyspnoea, hypoxia, hypercapnia and cardiovascular instability. This particularly applies to ventilated patien ts with their underlying lung pathology and increased risk of tensioning. Physical examinat ion may reveal; \200 \200 Conditions mimicking a pneumothorax on CXR \200 \200 \200 Bullae Visceral gas within the chest Skin folds Arterial blood gas analysis \200 \200 Hypoxaemia and mild respiratory alkalosis common Hypercapnia and acidosis dictate emergent management Management (Table 17.10.2) Primary spontaneous pneumothoraces: usually well tolerated and, if small (<2 \200\2233cm) and asymptomatic, can be observed and discharged if there is no d eterioration after a period of hours. With larger, symptomatic pneumothora- ces, aspiration should be attempted, and can be repeated if not fully effective initially. If aspiration f ails, intercostal drain insertion with underwater seal is then recommended. Tachypnoea (may be missing in ventilated patients) Asymmetrical chest wall movement (decrea sed expan- sion on affected side) Hyper-resonance on percussion Tracheal deviation \200\224 towards affected side in simple pneumothorax; away from affected side in tension pneumothor ax. \200 267 CHAPTER 17.10 Pneumothorax Secondary pneumothorax: intercostal drainage is agreed \201 rst-line management in most s ymptomatic patients. Iatrogenic pneumothoraces, in the absence of signi \201 cant underlyi ng lung disease, may be treated with simple aspira- tion. Otherwise an intercostal drain sh ould be considered. Table 17.10.3 Indications for surgical referral Air leak after 2 \200\2234 days in secondary and 3 \200\2235 days in primary pneumothoraces Second ipsilateral pneumothorax \200 Contralateral pneumothorax \200 Bilateral pneumoth oraces \200 Spontaneous haemothorax \200 High risk activities, e.g. diving, \202 ying Table 17.10.2 Acute management of symptomatic pneumothorax High \202 ow oxygen \200 If life-threatening cardiovascular compromise consider needle decompression, 2nd intercostals space, mid-clavicular line on the affected side. Leave in s itu until intercostal drain in place Prevention In the critically ill, pneumothoraces are associated with increased morbidity an d mortality. The following strategies to reduce risks should be considered. \200 \200 Drainage Aspiration primary pneumothorax >2 \200\2233 cm Intercostal drain primary pneumothorax not responding to aspiration secondary pneumothoraces mechanically ven tilated patients Adherence to lung protective ventilation strategies Ultrasound-guided insertion of CVCs Post-drainage CXR Special circumstances Air transportation/ \202 ying \200 A patient with an untreated, closed pneumothorax should not \202 y due to the risk of gas expansion and wors- ening clinical condition. If air transportation is essential, a functi oning intercostal drain is essential. Current guidelines recommend a period of 6 weeks foll owing either a de \201 nitive surgical procedure or a CXR showing complete resolution befo re \202 ying. In patients with underlying lung disease, without de \201 ni- tive surgery , recurrence risk remains signi \201 cant up to a year later, and alternative transportati on measures may need to be considered. Chest drain management \200 In simple pneumtohoraces there is no evidence that large tubes (20 \200\22324F) are better than smaller tubes (10 \200\22314F). Large bore drains are reserved for those with complex pneumothraces (hydro/haemothoraces), large air leaks, e.g. bullous lung disease, mechanical ventilation. For larger bore drains, the use of a trocar is not recom- mended, and the dra in should be placed using blunt dissection. Intercostal drains should not be removed unless the air leak has resolved (no bubbling) and there is radiographic resolution. There is no place for the routine clamping of chest drains. Complications of drain insertion include pe netration of major organs or vessels and ultrasound guidance, failure of resolution, pleura l infection and surgical emphysema. If there is signi \201 cant surgical emphysema, consid er a mal- positioned, kinked or blocked tube, or an air leak too large for the capacity of the drain. The British Thoracic Society recommends specialist refer- ral for anyone with a pneumothora x who takes part in high risk activities such as diving or frequent \202 ying (pilots, \202 ight crew). Further reading Baumann MH, Strange C, Heffner JE, et al. Management of sponta- neous pneum othorax, An American College of Chest Physicians Delphi Consensus Statement. Chest 2001; 11 9 55590 \200\223602 In patients with an ongoing air leak despite a larger sized drain, high volume, low pressur e ( \200\22310 to \200\22320cm H2O) suction can be considered in the appropriate setting. In the non- mechanically ventilated patient, a persisting air leak beyond 2 \200\2235 days should prompt a chest physician/thoracic surgical involvement (Table 17.10.3). Surgical ple urodhesis (pleurectomy, abrasive) is the most effective approach to resolve persistent leak s and for preventing recurrence. Chemical pleurodhesis with talc slurry is less effective, but may be preferred in those too frail for surgery. British Thoracic Society guidelines for the management of spon- tanoues pneumothorax. Thora x 2003; 58 Suppl 2: 39ii \200\22358ii. (www. brit-thoracic.org.uk/guidelines_since_1997. ht ml) British Thoracic Society guidelines for the insertion of a chest drain. Thorax 2003; 58: 53 \200\22359. (www.brit-thoracic.org.uk/ guidelines_since_1997.html) de Lassence A, Timsit JF, Taf \202 et M, et al. Pneumothorax in the inten- sive care unit: incidence, risk factors and outcome. Anesthesiology 2006; 104: 5 \200\22313. Rankine JJ, Thomas AN, Fluetcher D, et al. Pneumothorax in critically ill adults. Postgrad Med J 2000; 76: 399 \200\223404. 268 C RAYNER Empyema Empyema is a condition in which purulent \202 uid accumu- lates in a body cavity. The nam e comes from the Greek word empyein meaning pus-producing. Empyema in the pleural cavity is sometimes called empyema thoracis, or empyema of the chest, to distinguish it from empyema elsewhere in the body. An empyema develops when the \202 uid in the pleural space is inf ected and progresses from free- \202 owing \202 uid to a complex in \202 ammatory colle ction. Examination: key points \200 \200 \200 Tachycardia Percussion note dull Absent breath sounds Special investigations Imaging of the pleural space is a key element in assessment and mana gement \200 \200 CXR to detect effusion Ultrasound may detect small effusions not clearly seen on CXR and ma y also demonstrate the presence or absence of septae within the pleural \202 uid collecti on Contrast-enhanced CT of the chest provides the most information, and will demonstrate \202 uid, loculation and thickening of the pleural membranes CT and ultrasonography can be used in the placement of drainage catheters MRI is rarely used in the imaging of pleural ef fusion and empyema Empyemas may develop in association with the following: \200 \200 \200 \200 \200 \200 \200 \200 \200 Infection of parapneumonic effusion Rupture of lung abscess Thoracic trauma Complicating th oracic surgery Complication of chest drains Complication of diagnostic pleural \202 uid a spiration Oesophageal rupture Spread of infection from mediastinum Bronchopleural \201 st ulae (BPFs) The following aerobic Gram-positive and Gram-negative organisms can cause infection \200 \200 \200 \200 \200 \200 