352 CHAPTER 22 Respiratory disorders Atelectasis and pulmonary collapse A collapsed lobe or segment is usually visible on a ches t X-ray. Macroatelectasis is also evident as volume loss. In microatelectasis, the chest X- ray may be normal, but the A \200\223aDO2 will be high. Atelectasis reduces lung compliance and PaO2, and increases work of breathing. This may result in poor gas exchange, increased airway pressures, reduced tidal volume and, if severe, circulatory collapse. Causes \200 Collapsed lobe/segment \200\224bronchial obstruction (e.g. sputum retention, foreign body, blood clot, vomitus, misplaced endotracheal tube). Macroatelectasis \200\224air space compr ession by heavy, oedematous lung tissue, external compression (e.g. pleural effusion, haemo thorax), sputum retention. Microatelectasis \200\224inadequate depth of respiration, nitrog en washout by 100% oxygen with subsequent absorption of oxygen occurring at a rate greater than replenishment. Sputum retention Excess mucus (sputum) normally stimulates coughing. If ciliary clearance i s reduced (e.g. smoking, sedatives) or mucus volume is excessive (e.g. asthma, bronchiectas is, cystic \201 brosis, chronic bronchitis), sputum reten- tion may occur. Sputum retenti on may also be the result of inadequate coughing (e.g. chronic obstructive pulmonary diseas e, pain, neuromus- cular disease) or increased mucus viscosity (e.g. hypovolaemia, inadequa te humidi \201 cation of inspired gas). Preventive measures \200 Sputum hydration \200\224maintenance of systemic hydration and humidi \201 cation of inspi red gasses (e.g. nebulised saline/bronchodilators, heated water bath, heat-moisture exchang ing \201 lter). Cough \200\224requires inspiration to near total lung capacity, glottic c losure, contraction of abdominal muscles, and rapid opening of the glottis. Dynamic compres sion of the airways and high velocity expiration expels secretions. The process is limited if total lung capacity is reduced, abdominal muscles are weak, pain limits contraction, or small airways collapse on expiration. It is usual to \202 ex the abdomen on coughing, and this should be simulated in supine patients by drawing the knees up. This also limits pain in patients with an upper abdominal wound. Physiotherapy \200\224postural drainage, percus sion and vibration, hyperin \202 ation, intermittent positive pressure breathing, incentiv e spirometry, or manual hyperin \202 ation. Maintenance of lung volumes \200\224increased VT, CPAP, PEEP, positioning to reduce compression of lung tissue by oedema. Management Speci \201 c management depends on the cause and should be corrective. All meas ures taken for prevention should continue. If there is lobar or segmental collapse with obs truction of proximal airways, bronchoscopy may be useful to allow directed suction, foreign body removal, and saline instillation. Patients with high FIO2 may deteriorate due to the effects of excessive lavage or suction reducing minute ventilation. ATELECTASIS AND PULMONARY COLLAPSE 353 See also: Fibreoptic bronchoscopy, p88; Chest physiotherapy, p90; Bronchodilators, p254; Ch ronic air \202 ow limitation, p354; Acute weakness, p440; Critical care neuromuscular diso rders, p460; Pain, p618; Post-operative critical care, p620. 354 CHAPTER 22 Respiratory disorders Chronic air \202 ow limitation Many patients requiring ICU admission for community-acquire d pneu- monia have chronic respiratory failure. An acute exacerbation (which may or may not be infection-related) results in decompensation and sympto- matic deterioration. Such infe ctions include viruses, Haemophilus in \202 u- enzae, Klebsiella, and Staphylococcus aureu s, in addition to Streptococcus pneumoniae, and rarely, Mycoplasma pneumoniae and Legionell a pneu- mophila. Otherwise, patients are admitted with coincidental chronic air \202 ow li mitation (CAL) or as a prophylactic measure in view of their limited respiratory function, e.g. for elective post-operative ventilation. Problems in managing CAL patients on the ICU \200 \200 Disability due to chronic ill health. Fatigue, muscle weakness, and decreased physiological reserve leading to earlier need for ventilatory support, increased dif \201 culty in wean ing, and greater physical dependency on support therapies. Psychological dependency on supp ort therapies. More prone to pneumothorax. Usually have greater levels of sputum production . Right ventricular dysfunction (cor pulmonale). \200 \200 \200 Notes \200 Trials of non-invasive ventilatory support 9 respiratory stimulants such as doxepram have s hown considerable success in avoiding intubation and mechanical ventilation. Decisions on w hether or not to intubate should be made in consultation with the patient (if possible), th e family, and a respiratory physician or GP with knowledge of the patient. The patient shou ld be given the bene \201 t of the doubt, and intubated in an acute situation where a prec ise history and quality of life are not known. Accept lower target levels of PaO2 or SpO2 ( e.g. 88 \200\22392%). Accept higher target levels of PaCO2 if patient is known or suspected to have chronic CO2 retention (e.g. elevated plasma bicarbonate levels on admission to hos pital). \200 Weaning the patient with CAL \200 \200 An early trial of extubation may be worthwhile. Weaning may be a lengthy procedure. Daily t rials of spontaneous breathing may reveal faster-than-anticipated progress. Provide plentif ul encouragement and psychological support. Setting daily targets and early mobilization ma y be advantageous. Do not tire by prolonged spontaneous breathing. Consider gradually incre asing periods of spontaneous breathing interspersed by periods of rest. Ensure a good night \200\231s sleep, ideally by natural means. Use patient appearance and lack of symptoms (e. g. tachypnoea or fatigue) rather than speci \201 c blood gas values to judge duration of s pontaneous breathing. Early tracheostomy may bene \201 t when dif \201 culty in weaning i s expected. The patient may cope better with a tracheostomy mask than CPAP. Extrinsic PEEP or CPAP may prevent early airway closure reducing the work of breathing. However, there is a risk of air trapping. Consider heart failure as a cause of dif \201 culty in weaning. \200 \200 CHRONIC AIRFLOW LIMITATION 355 Key papers Brochard L, Mancebo J, Wysocki M, et al. (1995) Non-invasive ventilation for acu te exacerbations of chronic obstructive pulmonary disease. N Engl J Med 333: 817 \200\22322 . Antonelli M, Conti G, Rocco M, et al. (1998) A comparison of non-invasive positive-pressure ven- tilation and conventional mechanical ventilation in patients with acute respiratory f ailure. N Engl J Med 339: 429 \200\22335. Epstein SK, Ciubotaru RL. (1998) Independent effects of etiology of failure and time to rei ntuba- tion on outcome for patients failing extubation. Am J Respir Crit Care Med 158: 489 \200\22393. See also: Oxygen therapy, p38; Positive end expiratory pressure (1), p66; Continuous positi ve airway pres- sure, p70; Non-invasive respiratory support, p76; Chest physiotherapy, p90; Blood gas analysis, p156; Bronchodilators, p254; Respiratory stimulants, p256; Antimicrobi als, p326; Acute chest infection (1), p356; Pneumothorax, p368. 356 CHAPTER 22 Respiratory disorders Acute chest infection (1) Patients may present with or may develop infection as a complicat ion of critical care management. Typical features include fever, cough, purulent sputum pro - duction, breathlessness, pleuritic pain, and bronchial breathing. Urgent investi- gation includes arterial gasses, chest X-ray, blood count, cultures of blood and sputum. In commun ity-acquired pneumonia, acute phase antibody titres and urinary antigen (e.g. S. pneumoniae , L. pneumophilia) should be measured. If Panton-Valentine Leukocidin (PVL) producing S. au reus is suspected (necro- tising pneumonia, especially in younger patients), perform PCR te sting Diagnosis and initial antimicrobial treatment Basic resuscitation is required if there is c ardiorespiratory compromise. Appropriate treatment of the infection depends on chest X-ray and micro- biology \201 ndings, and although empiric, \200\230best guess \200\231 antibi otic treatment may be started before culture results are available. Treatment includes phys iotherapy and methods to aid sputum clearance. Clear chest X-ray Acute bronchitis is associated with cough, mucoid sputum, and wheeze. In the previously healthy, a viral etiology is most likely, often with an upper respiratory pr odrome. Symptomatic relief is often all that is needed. Likely organisms in acute-on-chroni c bronchitis include S. pneumoniae, H. in \202 uenzae or S. aureus. Use appropriate antibi otics, e.g. cefuroxime or ampicillin 9 \202 ucloxacillin. Bacteria in sputum may confuse viral pneumonia although secondary bacterial infection is common. Consolidation on chest X-ray Recent history is important for deciding the cause of pneumoni a (see \201 gure 22.1): \200 Hospital-acquired pneumonia \200\224enteric (Gram-negative) organisms treated with ceftazid ime and gentamicin, or carbapenems if extended spectrum beta-lactamase (ESBL) producing; S. aureus is treated with \202 ucloxacillin (or teicoplanin/vancomycin/linezolid if resista nt). Recent aspiration \200\224anaerobic or Gram-negative infection treated with clindamyci n or cefuroxime and metronidazole. Community-acquired pneumonia in a previously healthy ind ividual \200\224for S. pneumoniae (often lobar, acute onset) or atypical pneumonia (insidio us onset, known community outbreaks, renal failure, and electrolyte disturbance in Legionna ire \200\231s disease), treat with cefuroxime and clarithromycin. Treat PVL-positive S. aur eus pneumonia with clindamycin and linezolid. Both S. aureus and H. in \202 uenzae are com mon in those debilitated by chronic disease (e.g. alcoholism, diabetes, chronic air \202 o w limitation, or the elderly). S. aureus pneumonia complicates in \202 uenza. Immunosuppre ssed \200\224opportunistic infections (e.g. tuberculosis, Pneumocystis carinii, Herpes viru ses, CMV, or fungi). Pulmonary cavitation on chest X-ray Cavitation should alert to the possibility of anaerobic infection (sputum is often foul-smelling) (see \201 gure 22.2). S. aureus, K. pneumoniae or tuberculosis are also associated with cavitation. Appropriate antibiotics include metro ni- dazole or clindamycin for anaerobic infection, \202 ucloxacillin for S. aureus, and c eftazidime and gentamicin for K. pneumoniae. A foreign body or pulmonary infarct should als o be considered where there is a single abscess. ACUTE CHEST INFECTION (1) 357 Fig 22.1. X-ray showing left (L) basal consolidation (arrow). Fig 22.2. X-ray showing right upper zone cavitation (arrow). See also: Blood gas analysis, p154; Respiratory imaging, p158; Full blood count, p220; Bact eriology, p224; Virology, serology and assays, p226; Antimicrobials, p326; Respiratory fail ure, p350; Chronic air \202 ow limitation, p354; Acute chest infection (2), p358; Infectio n \200\224diagnosis, p552; HIV-related disease, p566; SARS, VHF, and H5N1, p570. 358 CHAPTER 22 Respiratory disorders Acute chest infection (2) Laboratory diagnosis The following samples are required for labor atory diagnosis: \200 Sputum (e.g. cough specimen, endotracheal tube aspirate, protected brush specimen, bronchoa lveolar lavage specimen). \200 Blood cultures. \200 Serology and PCR (in community-acqu ired pneumonia). \200 Urine for antigen (if Legionella, Pneumococcus, or Candida suspecte d). In severe pneumonia, blind antibiotic therapy should not be withheld while awaiting res ults. However, specimens should be taken before starting anti- biotics. Microbiological yield is usually very low, especially if antibiotic therapy has started before sampling. Where cultures are positive, there is often multiple growth. Separating pathogenic organisms from colonizing organisms may be dif \201 cult. In hospital-acquired pneumonia, known nosocomial pathogens are the likely source, e.g. local Gram-negative \202 ora, MRSA. Continuing treatment Antibiotics should be adjusted according to sensitivities once availab le. Failure to respond to treatment in 72h should prompt consideration of infections more c ommon in the immunocompromised. Hospital-acquired pneumonia requires treatment with appropriate anti- biotics for 24h after symptoms subside (usually 3 \200\2235 days). Some Critical Care Units use longer courses, but a multicentre study showed no differ- ence in outcome between 7 and 14 days \200\231 tr eatment. In atypical or pneumococcal pneumonia, 10 \200\22314 days antibiotic treat- ment is usual ( though no evidence base exists to indicate optimal duration of therapy). ACUTE CHEST INFECTION (2) 359 Antimicrobial treatment Drug Dose Organism Aciclovir 10mg/kg 8-hourly IV Herpes viruses Amphotericin B 250mg \200\2231g 6-hourly IV Fungi Ampicillin 500mg \200\2231g 6-hourly IV H. in \202 uenzae Gram-negative spp. Benzylpenicillin 1.2g 2 \200\2236 hourly IV S. pneumoniae Ceftazidime 2g 8-hourly IV K. pneumoniae P. aeruginosa Gram-negative spp. Cefuroxime 750mg \200\2231.5g 8-hourly IV S. pneumoniae H. in \202 uenzae Gram-negative spp. Clarithromycin 500mg 12-hourly IV (250 \200\223500mg 12-hourly PO if less severe) Atypical pneumonia S. pneumoniae Erythromycin 1g 6 \200\22312 hourly (500mg 6- hourly PO if less severe) Atypical pneumonia S. pneumoniae Clindamycin 300 \200\223600mg 6-hourly IV Anaerobes Gram-negative spp. Cotrimoxazole 120mg/kg/d IV Pneumocystis carinii Flucloxacillin 2g 6-hourly IV (500mg \200\2231g 6- hourly PO if less severe) S. aureus Ganciclovir 5mg/kg 12-hourly IV (over 1h) CMV K. pneumoniae, P. aeruginosa Gram-negative spp. Gentamicin 1.5mg/kg stat IV (thereafter by levels, usually 80mg 8-hourly) Anaerobes Metronidazole 500mg 8-hourly IV or 1g 12- hourly PR Teicoplanin 400mg 12-hourly for 3 doses, then 400mg daily Methicillin-resistant S. aureus Vancomycin 500mg 6-hourly (monitor levels) Methicillin-resistant S. aureus Linezolid 600mg 12-hourly IV or PO Methicillin-resistant S. aureus Key papers Iregui M, Ward S, Sherman G, et al. (2002) Clinical importance of delays in the initiation of appro- priate antibiotic treatment for ventilator-associated pneumonia. Chest 122: 262 \200\2238. Chastre J, for the PneumA Trial Group. (2003) Comparison of 8 vs 15 days of antibiotic ther apy for ventilator-associated pneumonia in adults: a randomized trial. JAMA 290: 2588 \200 \22398. See also Bacteriology, p224; Virology, serology and assays, p226; Antimicrobials, p326; Acu te chest infection (1), p356; HIV related disease, p566; SARS, VHF, and H5N1, p570. 360 CHAPTER 22 Respiratory disorders Acute respiratory distress syndrome (1) Acute respiratory distress syndrome (ARDS) is the r espiratory compo- nent of multiple organ dysfunction. It may predominate the clinical pictu re or be of lesser importance in relation to dysfunction of other organ systems. Etiology As part of the exaggerated in \202 ammatory response following a major exogenous insult which may be either direct (e.g. chest trauma, inhalation injury) or distant (e.g. p eritonitis, major hemorrhage, burns). Histology reveals aggregation and activation of neutr ophils and platelets, patchy endothelial and alveolar disruption, interstitial oedema, and \201 brosis. Classically, the acute phase is characterized by increased capillary perme- ability and the \201 broproliferative phase (after seven days) by a predominant \201 br otic reaction. However, recent data suggest such distinctions are not so clear-cut; evidenc e of markers of \201 brosis is present as early as day 1. De \201 nitions Acute lung injury (ALI): \200 \200 \200 \200 PaO2/FIO2 \211 300mmHg (40kPa). RegardLess of level of PEEP. With bilateral in \201 ltrat es on chest X-ray. With pulmonary artery wedge pressure <18mmHg. Acute respiratory distress syndrome (ARDS): \200 As above but PaO2/FIO2 \211 200 mmHg (26.7kPa). Prognosis Prognosis depends in part on the underlying insult, the presence of other organ d ysfunctions, and the age and chronic health of the patient. Predominant single-organ ARDS c arries a mortality of 30 \200\22350%; there has been outcome improvement over the last deca de. Some deterioration on lung function testing is usually detectable in sur- vivors of ARDS, e ven in those who are relatively asymptomatic. Recent studies indicate that a signi \201 ca nt proportion of survivors of ARDS have physical and/or psychological sequelae at one year. ACUTE RESPIRATORY DISTRESS SYNDROME (1) 361 Key papers Bernard GR for the American-European Consensus Conference on ARDS. (1994) De \201 nitions, mechanisms, relevant outcomes, and clinical trial coordination. Am J Respir C rit Care Med 149: 818 \200\22324. Marshall RP, Bellingan G, Webb S, et al. (2000) Fibroproliferation occurs early in the acut e respira- tory distress syndrome and impacts on outcome. Am J Respir Crit Care Med 162: 17 83 \200\2238. Herridge MS, Cheung AM for the Canadian Critical Care Trials Group. (2003) One-year outcome s in survivors of the acute respiratory distress syndrome. N Engl J Med 348: 683 \200\22393 . Cheung AM, Tansey CM, Tomlinson G, et al. (2006) Two-year outcomes, health care use, and co sts of survivors of acute respiratory distress syndrome. Am J Respir Crit Care Med 174: 538 \200\22344. See also: Acute respiratory distress syndrome (2), p362; Inhalation injury, p374; Systemic in \202 ammation/ multi-organ failure \200\224causes, p556; Multiple trauma (1), p582; Mul tiple trauma (2), p584; Burns \200\224 \202 uid management, p592; Burns \200\224general m anagement, p594; Blast injury, p596. 362 CHAPTER 22 Respiratory disorders Acute respiratory distress syndrome (2) General management 1. Remove the cause whenever pos sible, e.g. drain pus, antibiotics, \201 x long bone fracture. 2. Sedate with an opiate-benzodiazepine combination as mechanical ven- tilation is likely t o be prolonged. Doses should be kept to the lowest possible but consistent with adequate se dation. 3. Muscle relaxation can be used in severe ARDS to improve chest wall compliance and gas exchange. 4. Haemodynamic manipulation with either \202 uid, dilators, pressors, diu- retics and/or inotropes may improve oxygenation. This may be achieved by either increasing cardiac outpu t and thus mixed venous saturation in low output states, or by decreasing cardiac output th ereby lengthening pulmonary transit times in high output states. Care should be taken not t o compromise the circulation. Respiratory management 1. Maintain adequate gas exchange with increased FIO2, and depending on severity, either non-invasive respiratory support (e.g. CPAP, BiPAP) or positive pressu re ventilation. Speci \201 c modes may be utilized such as pressure-controlled ventilation . VT should be targeted at 6 \200\2237mL/kg and plateau inspiratory pressures \211 30cmH2O , if possible. However, there is no consensus regarding the upper desired levels of FIO2 an d PEEP. Greater emphasis is currently placed on higher levels of PEEP (up to 20cmH2O). Whil e the European view generally favors use of high FIO2 (up to 1.0), a common US approach is to keep FIO2 \211 0.60, yet maintain- ing SaO2 with high PEEP. Recent studies assessing hi gh and low levels of PEEP found no mortality bene \201 t. 2. Non-ventilatory respiratory support techniques such as ECCO2R can be used in severe ARDS , but have yet to show convincing bene \201 t over conventional ventilatory techniques. 3. Blood gas values should be aimed at maintaining survival without striving to necessarily achieve normality. Permissive hypercapnia, where PaCO2 values are allowed to rise, sometim es >10kPa, has been associated with outcome bene \201 t. Acceptable levels of SaO2 are con troversial; in general, values 93 \200\22398% are targeted, but in severe ARDS, this may be progressively relaxed to 80 \200\22385% or even lower, provided organ function remains ade quate. 4. Patient positioning may improve gas exchange. This includes kinetic therapy using special rotational beds, and prone positioning with the patient turned frequently through 180*. Care must be taken during turning to prevent tube displacement and shoulder injuries. 5. Inhaled nitric oxide or epoprostenol improves gas exchange in some 50% of patients though no outcome bene \201 t has been shown. 6. High-dose corticosteroids are bene \201 cial in 50 \200\22360% of patients, at least in terms of improving gas exchange. 7. Surfactant therapy is currently not indicated for ARDS. 8. Neutral \202 uid balance (a fter initial resuscitation) improves outcomes. 9. Ventilator trauma is ubiquitous. Multiple pneumothoraces may occur and may require multiple chest drains. They may be dif \201 cult to diagnose by X-ray and, despite the attendant risks, CT scanning may reveal undi- agnose d pneumothoraces and aid drain placement. ACUTE RESPIRATORY DISTRESS SYNDROME (2) 363 Key papers Hickling KG, Walsh J, Henderson S, et al. (1994) Low mortality rate in adult res piratory distress syndrome using low-volume, pressure-limited ventilation with permissive h ypercapnia: a prospec- tive study. Crit Care Med 22: 1568 \200\22378. Meduri GU, HeadLey AS, Golden E, et al. (1998) Effect of prolonged methylprednisolone thera py in unresolving acute respiratory distress syndrome: a randomized controlled trial. JAMA 280: 159 \200\22365. Acute Respiratory Distress Syndrome Network. (2000) Ventilation with lower tidal volumes co mpared with traditional tidal volumes for acute lung injury and the acute respiratory distr ess syndrome. N Engl J Med 342: 1301 \200\2238. Gattinoni L, for the Prone-Supine Study Group. (2001) Effect of prone positioning on the su rvival of patients with acute respiratory failure. N Engl J Med 345: 568 \200\22373. NHLBI Acute Respiratory Distress Syndrome (ARDS) Clinical Trials Network. (2006) Comparison of two \202 uid-management strategies in acute lung injury. N Engl J Med 354: 2564 \200 \22375. Meade MO, for the Lung Open Ventilation Study Investigators. (2008) Ventilation strategy us ing low tidal volumes, recruitment maneuvers, and high positive end-expiratory pressure for acute lung injury and acute respiratory distress syndrome: a randomized controlled trial. JAMA 299: 637 \200\22345. Mercat A, Richard J-C, Vielle B, et al. (2008) Positive end-expiratory pressure setting in adults with acute lung injury and adult respiratory distress syndrome. JAMA 299: 646 \200 \22355. See also: Oxygen therapy, p38; Ventilatory support \200\224indications, p44; IPPV \200\224a djusting the ventilator, p50; IPPV \200\224complications of ventilation, p56; High frequenc y oscillatory ventilation, p64; Positive end expiratory pressure (1), p66; Positive end exp iratory pressure (2), p68; Lung recruitment, p72; Prone positioning, p74; Extracorporeal re spiratory support, p78; Blood gas analysis, p154; Extravascular lung water measurement, p15 6; Nitric oxide, p258; Surfactant, p260; Corticosteroids, p328; Acute respiratory distress syndrome (1), p360; Pneumothorax, p368. 364 CHAPTER 22 Respiratory disorders Asthma \200\224general management Pathophysiology Acute bronchospasm and mucus plugging are often secondary to an insult such as infection. The patient may progress to fatigue, respi ratory failure, and collapse. The onset may develop slowly over days or occur rapidly withi n minutes to hours. Clinical features \200 Dyspnoea, wheeze (expiratory 9 inspiratory), dif \201 culty in talking, use of accessory r espiratory muscles, fatigue, agitation, cyanosis, coma, collapse. Pulsus paradoxus is a poo r indication of severity; a fatiguing patient cannot generate signi \201 cant respiratory swings in intrathoracic pressure. A \200\230silent \200\231 chest is also a late sign sugg esting severely limited air \202 ow. Pneumothorax and lung/lobar collapse. \200 Management of asthma Asthmatics must be managed in a well-monitored area. If clinical fea- tures are severe, they should be admitted to an intensive care unit where rapid institution of mechanical ventilation is available. Monitoring should comprise, as a minimum, pulse ox imetry, continuous ECG, regular blood pressure measurement, and blood gas analysis. If seve re, an intra-arterial cannula 9 central venous access should be inserted. 1. FIO2 to mainta in SpO2 92 \200\22398%. 2. Nebulised B2-agonist (e.g. salbutamol) \200\224may be repeated e very 2 \200\2234h or, in severe attacks, administered continuously. 3. IV corticosteroids for 24h, then oral prednisolone. Nebulised ipratro- pium bromide rare ly gives additional bene \201 t and may thicken sputum. 4. IV bronchodilators, e.g. salbutamol, magnesium sulfate. 5. Exclude pneumothorax and lung /lobar collapse. 6. Ensure adequate hydration and \202 uid replacement. 7. Commence antib iotics (e.g. cefuroxime 9 clarithromycin) if strong evi- dence of bacterial chest infection . Green sputum does not necessarily indicate a bacterial infection. 8. If no response to above measures or in extremis, consider: \200 \200 \200 \200 IV salbutamol infusion. Epinephrine SC or by nebuliser. Mechanical ventilation. Anecdotal s uccess has been reported with sub-anesthetic doses of a volatile anesthetic agent such as i so \202 urane or sevo \202 urane which both calm/sedate and bronchodilate. Indications for mechanical ventilation \200 \200 \200 Increasing fatigue. Respiratory failure \200\224rising PaCO2, falling PaO2. Cardiovascular collapse. Facilitating endotracheal intubation Summon senior assistance. Pre-oxygenate with 100% O2. Perform rapid sequence induction. \200\230Breathing down \200\231 with an inhalational ane sthetic (e.g. iso \202 urane) pre-intubation should only be attempted by an experienced cl inician. To minimize barotrauma, care should be taken to avoid excess air trapping, high ai rway pressures, and high tidal volumes. ASTHMA \200\224GENERAL MANAGEMENT 365 Drug dosages Epinephrine 0.5mL 1:1000 solution SC or 2mL 1:10000 solution by nebuliser Hydrocortisone 100 \200\223200mg qds Ipratropium bromide 250 \200\223500mcg qds by nebuliser Prednisolone 40 \200\22360mg od initially Salbutamol 2.5 \200\2235mg by nebuliser 5 \200\22320mcg/min by IV infusion Magnesium sulfate 1.2 \200\2232.0g IV over 20min Key paper British Thoracic Society Scottish Intercollegiate Guidelines Network. (2008) Brit ish Guideline on the Management of Asthma. Thorax 63 (Suppl 4): 1 \200\223121. See also: Oxygen therapy, p38; Endotracheal intubation, p42; Ventilatory support \200\224in dications, p44; Pulmonary function tests, p148; Blood gas analysis, p154; Bronchodilators, p254; Antimicrobials, p326; Corticosteroids, p328; Asthma \200\224ventilatory management, p 366; Pneumothorax, p368. 366 CHAPTER 22 Respiratory disorders Asthma \200\224ventilatory management 1. Initially give low VT (5mL/kg) breaths at low rate (5 \200\22310/min) to as- sess degree of bronchospasm and air trapping. Slowly increase VT (to 6 \200\2237mL/kg) 9 increase rate, taking care to avoid signi \201 cant air trapping and high inspiratory pressures. Low rates with prolonged I:E ratio (e.g. 1:1) may be advant ageous. Avoid very short expiratory times. Do not strive to achieve normocapnia. 2. Administer muscle relaxants for a minimum 2 \200\2234h until severe bron- chospasm has a bated and gas exchange improved. Although atracurium may cause histamine release, it does n ot appear clinically to worsen bronchospasm. 3. Sedate with either standard medication or with agents such as keta- mine or iso \202 ur ane that have bronchodilating properties. Ketamine given alone may cause hallucinations whi le iso \202 urane carries a theoretical risk of \202 uoride toxicity and can excessively vasodilate. 4. If signi \201 cant air trapping remains, consider ventilator disconnection and forced manual chest compressions every 10 \200\22315min. 5. If severe bronchospasm persists, consider injecting 1 \200\2232mL of 1:10000 epinephrine down ET tube. Repeat at 5min intervals as necessary. Maintenance 1. Ensure adequate rehydration. 2. Generous humidi \201 cation should be given to loosen mucus plugs. Use a heat-moisture exchanger plus either hourly 0.9% saline nebuli sers or instillation of 5mL 0.9% saline down the endotracheal tube or a hot water bath humi di \201 er. 3. Physiotherapy assists mobilization of secretions and removal of mucus plugs. Hyperventilation should be avoided. 4. With improvement, gradually normalize ventilator settings (VT, rate, I: E ratio) to achi eve normocapnia before allowing patient to waken and breathe spontaneously. 5. If acute deterioration, consider pneumothorax or lung/lobar collapse. 6. If mucus pluggi ng constitutes a major problem, instillation of a mu- colytic (N-acetylcysteine) may be con sidered though this may induce further bronchospasm. Bronchoscopic removal of plugs should only be performed by an experienced operator. Assessment of air trapping (intrinsic PEEP, PEEPi) \200 \200 \200 \200 Measure PEEPi by pressing end-expiratory hold button of ventilator. No pause between expira tory and inspiratory sounds. Disconnection of ventilator and timing of audible expiratory w heeze. An increasing PaCO2 may respond to reductions in minute volume which will lower the level of intrinsic PEEP. Weaning \200 Bronchospasm may increase on lightening sedation due to awareness of ET tube and increased coughing. May need trial of extubation while still on high FIO2. Consider extubation under inhalational or short-acting IV sedation. Space out intervals between B2-agonist nebulisers . Convert other anti- asthmatic drugs to oral medication. Theophylline dose (if used) shoul d be adjusted to ensure therapeutic levels. \200 \200 ASTHMA \200\224VENTILATORY MANAGEMENT 367 See also: Ventilatory support \200\224indications, p44; IPPV \200\224modes of ventilation, p48; IPPV \200\224adjusting the venti- lator, p50; IPPV \200\224failure to deliver ventilat ion, p54; IPPV \200\224complications of ventilation, p56; IPPV \200\224 weaning techniques, p58; Positive end expiratory pressure (1), p66; Positive end expiratory pressure (2), p68; Chest physiotherapy, p90; Sedatives and tranquilisers, p308; Muscle relaxants, p310. 368 CHAPTER 22 Respiratory disorders Pneumothorax Signi \201 cant collection of air in the pleural space that may occur spontan e- ously or following trauma (including iatrogenic), asthma, and chronic lung disease. It i s a common result of ventilator trauma. Clinical features \200 \200 \200 May be asymptomatic. Dyspnoea, pain. Decreased breath sounds, hyper-resonant, asymmetric ch est expansion \200\224may be dif \201 cult to assess in a ventilated patient. Respiratory failure and deterioration in gas exchange. Increasing airway pressures and dif \201 culty to ventilate. Cardiovascular deterioration with mediastinal shift (tension). \200 \200 Diagnosis Chest X-ray \200\224most easily seen on erect views where absent lung mark- ings are seen lateral to a well-de \201 ned lung border. Tension pneumo- thorax results in mark ed mediastinal shift away from the affected side. Pneumothorax must be distinguished from b ullae, especially with long- standing emphysema; inadvertent drainage of a bulla may cause a bron- chopleural \201 stula. Advice should be sought from a radiologist. Since ventilated patients are often imaged in a supine position, pneu- mothorax may be miss ed as it may be anterior to normal lung, giving lung markings on the radiograph. A lateral chest X-ray may help. Supine pneu- mothorax should be considered if the following are seen (see \201 gure 22.3): \200 \200 \200 \200 Ultrasound \200\224may be helpful but i s operator-dependent. CT scan \200\224very sensitive and may be useful in dif \201 cult si tuations, e.g. ARDS, and to direct drainage of a localized pneumothorax. Management 1. Incr ease FIO2 if hypoxaemic. 2. If life-threatening with circulatory collapse, aspirate air on affected side Hyperlucent lung \201 eld compared to the contralateral side. Loss of clarity of the diap hragm outline. \200\230Deep sulcus \200\231 sign, giving the appearance of an inverted dia phragm. A particularly clear part of the cardiac contour. with a needle, followed by formal chest drain insertion. 3. Repeated needle aspiration may be suf \201 cient in spontaneously breath- ing patients without respiratory failure. 4. Chest drain insertion. This may need to be done under ultrasound or CT guidance if localized due to surrounding lung \201 brosis. A small pneumothorax (<10% hemithorax) may be left undrained, but prompt action should be i nstituted if cardiorespiratory deterioration occurs. Patients should not be transferred bet ween hospitals, particularly by airplane, with an undrained pneumothorax. Drains may be rem oved if not swinging/bubbling for several days. Bronchopleural \201 stula Denoted by cont inual drainage of air. Usually responds to conservative treatment with continual applicatio n of 5kPa negative pressure; this may take weeks to resolve. For severe leak and/or comprom ised ventilation, high frequency jet ventilation and/or a double-lumen endobronchial tube m ay be considered. Surgical intervention is rarely necessary. PNEUMOTHORAX 369 Lung rim Clear cardiac contour Deep sulcus Fig 22.3. Chest X-ray appearance. See also: Chest drain insertion, p84; Respiratory imaging, p158; Dyspnoea, p346; Respirator y failure, p350. 370 CHAPTER 22 Respiratory disorders Haemothorax Usually secondary to chest trauma or following a procedure, e.g. cardiac surger y, chest drain insertion, central venous catheter insertion. Spontaneous haemothorax is rar e, even in patients with clotting disorders. Clinical features \200 Stony dullness. \200 Decreased breath sounds. \200 Hypovolaemi a and deterioration in gas exchange (if large). Diagnosis \200 Erect chest X-ray \200\224blunting of hemidiaphragm and progressive loss of basal lung \201 eld. Supine chest X-ray \200\224increased opacity of affected hemithorax plus decrease d clarity of cardiac contour on that side. Large-bore needle aspiration to con \201 rm pre sence of blood. A small- bore needle may be unable to aspirate a haemothorax if it has clot ted. Management 1. If small, observe with serial X-rays and monitor for signs of cardiores- piratory deterioration. 2. Ensure any coagulopathy is corrected by administration of fresh frozen plasma and/or platelets or other blood products as indicated. 3. Ensure crossmatched blood is available for urgent transfusion if necessary. 4. If signi \201 cant in size or patient becomes symptomatic, insert large-bore chest drai n, e.g. size 28Fr. The drain should be directed postero-inferi- orly toward the dependent a rea of lung and placed on 5kPa suction. 5. If drainage exceeds 1000mL or >200mL/h for 3 \200\2234h despite correcting any coagulopathy, contact a thoracic surgeon. 6. Factor VIIa may be considered for intractable bleeding though only an- ecdotal reports of bene \201 t exist. 7. Drains inserted for a haemothorax may be removed after 1 \200\2232 days if no further bleeding occurs. Perforation of an intercostal vessel during chest drain insertion may cause considerable bl eeding into the pleura. If deep tension sutures around the chest drain fail to stem blood l oss, remove the chest drain and insert a Foley urethral catheter through the hole. In \202 ate the balloon and apply traction on the catheter to tamponade the bleeding vessel. If th ese meas- ures fail, contact a thoracic surgeon. HAEMOTHORAX 371 See also: Chest drain insertion, p84; Coagulants and anti \201 brinolytics, p322; Bleeding disorders, p468; Multiple trauma (1), p582; Multiple trauma (2), p584. 372 CHAPTER 22 Respiratory disorders Haemoptysis \200 May range from a few specks of blood in expectorated sputum to massive pulmonary hemorrhage . Likely to disrupt gas exchange before hypovolaemia is life-threatening. May be a presenti ng feature of a patient admitted to intensive care or may result from critical illness and its treatment. \200 Causes Massive haemoptysis \200 Disruption of a bronchial artery by acute in \202 ammation or invasion (e.g. pulmonary neo plasm, trauma, cavitating TB, bronchiectasis, lung abscess, and aspergilloma). Rupture of a rterio-venous malformations and bronchovascular \201 stulae. Pulmonary infarction seconda ry to prolonged pulmonary artery catheter wedging or pulmonary artery rupture. \200 Minor haemoptysis \200 \200 Intrapulmonary in \202 ammation or infarction (e.g. pulmonary embolus). Endotracheal tube trauma (e.g. mucosal erosion, balloon necrosis, trauma from the tube tip, trauma to a trach eostomy stoma, trauma from suction catheters). Tissue breakdown in critically ill patients (e.g. tissue hypoperfusion, coagulopathy, poor nutritional state, sepsis, and hypoxaemia). Investigation and assessment Assess cardiorespiratory function and monitor closely. Massive haemopt- ysis may require resuscitation and urgent intubation. The diagnosis may be sugges ted by the history and a chest X-ray may identify a cavitating lesion. Lower lobe shadowing on a chest X-ray may be the result of overspill of blood from elsewhere in the bronchial t ree. Early surgical intervention should be prompted by a changing air- \202 uid level, per sistent opaci \201 cation of a previous cavity, or a mobile mass. Early bronchoscopy may i dentify the source of haemoptysis although only while bleeding is active. Blood in multiple bronchial ori \201 ces may be confusing but saline lavage may leave the source visible. R igid bronchoscopy is useful in massive haemoptysis allowing oxygenation and wide bore sucti on. Management \200 Basic resuscitation (high FIO2, endotracheal intubation, and blood transfusion) is needed f or cardiorespiratory compromise. Correction of coagulopathy is a priority. Bronchoscopy all ows direct instillation of 1 in 200,000 epinephrine if the source of hemorrhage can be foun d or, alternatively, endobronchial tamponade with a balloon catheter. In cases of severe he morrhage from one lung, a double-lumen endotracheal tube may prevent some overspill to the other lung while de \201 nitive treatment is organized. De \201 nitive treatment may incl ude radiological bronchial artery embolisation or surgical resection. Induced hypotension m ay be useful in bronchial artery hemorrhage. In cases of pulmonary artery hemorrhage, PEEP may be used with mechanical ventilation to reduce pulmonary bleeding. \200 \200 HAEMOPTYSIS 373 See also: Positive end expiratory pressure (1), p66; Positive end expiratory pressure (2), p68; Continuous positive airway pressure, p70; Fibreoptic bronchoscopy, p88; Coagulation mo nitoring, p222. 374 CHAPTER 22 Respiratory disorders Inhalation injury Causes include smoke, steam, noxious gasses, and aspiration of gastric co n- tents. Clinical features \200 \200 \200 \200 \200 \200 \200 \200 Dyspnoea, coughing. Stridor (if upper airway obstruction). Bronchospasm. Signs of lung/loba r collapse (especially with aspiration). Signs of respiratory failure. Cherry-red skin colo r (carbon monoxide). Agitation, coma. ARDS (late). General principles of management 1. High \202 ow, high concentration O2 targeting an SaO2 of 92 \200\22398%. 2. Early intubation if upper airway is compromised or threatened. 3. Ea rly bronchoscopy if inhalation of soot, debris, vomit suspected. Speci \201 c conditions Smoke inhalation \200 