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 Diagnostic pleural sampling: All patients with a pleural effusion in association with sepsi s or a pneumonic illness require pleural \202 uid aspiration. All patients with unexplain ed fever or rising CRP should have aspiration or re-aspiration of a pleural effusion. Faile d aspi- ration is an indication for an ultrasound scan. Normally effusions <1cm on X-ray (o r ultrasound) can be safely observed but require repeated imaging. Aspiration should be per formed with full sterile technique. Fluid should be sent, before antibiotic therapy is com- menced, for the following: \200 \200 Streptococcal (Streptococcus milleri) Staphylococcus aureus Escherichia coli Pseudomonas sp ecies Haemophilus in \202 uenzae Klebsiella spp. More rarely an anerobic or mixed growth can be found Staphylococcus aureus is most commonly found in associa- tion with nosocomial empyemas, post-operative empye- mas and in the immu nocompromised. Microbiology Gram stain and culture, acid- and alcohol-fast bacilli (AAFB) staining and cul ture Protein, glucose, lactate dehydrogenase (LDH) Cytology pH ( \202 uid should be collec ted in a heparinized syringe avoiding the presence of air and measured in a blood gas analy zer) Stages of empyema In 1962, the American Thoracic Society described three stages of empyema, which continue to be applied in the classi \201 cation of the disease): 1 Exudative (acut e) stage: protein-rich pleural \202 uid remains free \202 owing. High neutrophil count, normal glucose and pH levels. This stage lasts for 24 \200\22372h. Drainage of the effusio n and appropriate antimicrobial therapy are normally suf \201 cient for treatment. \200 \200 Frank pus should not be put through a blood gas analyzer as pH yields no additional informa tion (drainage is already indicated) 2 Fibrinolytic (transitional) stage: increasing \202 uid viscosity, activation of coagula tion factors and \201 broblast activity. Glucose and pH levels start to fall. This stage lasts for 7 \200\22310 days. Natural history If left untreated or with inappropriate or delayed treatment, empyema resul ts in signi \201 cant morbidity. The presence of purulent \202 uid and pleural thickenin g results in restriction of movement and expansion of the lung. Atelectasis of the underlyi ng lung results in ventilation \200\223perfusion mismatch. As a result of the above, gas ex change is severely impaired, resulting in hypoxia and hypercapnia. Even with treatment, the 30-day post-operative mortality after video-assisted tho- racoscopy (VATS) debridement and open decortication has been reported to range between 1.3 and 6.6%. 3 Organizing (chronic) stage: loculated pus in the pleural space with adherence to the visc eral and parietal pleura. This may progress with the formation of pleural peels in which th e pleural layers are indistinguishable. Clinical approach History: key points \200 Symptoms are non-speci \201 c and include: chest pain, fever, sweating, shortness of breat h, malaise, loss of appetite, weight loss. Delayed clinical improvement or relapse of pneum onia A recent history of chest drain insertion, pleural aspira- tion, interventional endoso copy, thoracoscopy, cardiac or thoracic surgery Complications of empyema \200 Empyema necessitans: A swelling appears over the chest wall, which has a positive cough imp ulse, in communica- tion with the underlying empyema. Resolves with treat- ment of the unde rlying empyema. \200 269 CHAPTER 17.11 Empyema culture and sensitivity results. Patients with suspected nosocomial infection require broad er spectrum antibiotic cover, including for MRSA. There are no controlled trial data to add ress optimal length of treatment with antibiot- ics; depending on response, most patient ar e treated for at least 21 days Fibrothorax: Adhesion of the two layers of pleura, so that the lung is covered by a thick l ayer of non-expansi- ble \201 brous tissue BPF Management The choice of the appropriate treatment depends on the nature of the underlying disease, stage of the empyema and the patient \200\231s co-morbidity. The aims of treatment are to control infection, clear infection from and prevent recur- rence of infection withi n the pleural space, and to restore normal pulmonary function. In addition, there is good e vidence that optimizing nutrition will improve prognosis. The cornerstones of management ar e: \200 \200 \200 \200 Medical thoracoscopy Can be used as a drainage procedure and can be per- formed early in th e course of the disease, under sedation, with local anesthesia, is less expensive and avoid s the need for general anesthesia. It is useful in patients at high surgical risk. Surgical intervention Surgery should be considered in all patients with a locu- lated effus ion, those who are not responding to drainage and once the effusion has become organized (s tage III). Primary treatment strategy of VATS is associated with a higher ef \201 cacy, sh orter hospital duration and less cost than a treatment strategy that utilizes catheter-dire cted \201 brino- lytic therapy. VATS debridement is associated with less pain and shorter recovery period than open thoracotomy. The time frame between onset of symptoms and surger y where VATS debridement can be performed with success has been shown to be between 1 and 2 weeks For pleural empyema in an organizing phase, full thoracot- omy with decortication re mains the treatment of choice. Perfusion and spirometry improve signi \201 cantly in patie nts after the decortication, but the function of the affected lung remains impaired. Drainage Antibiotics Early surgical intervention Nutritional supplementation Indications for drainage \200 Pus on aspiration \200 Cloudy or turbid \202 uid \200 Organisms seen on Gram stain/culture \200 Clear \202 uid with pH <7.2 \200 Pleural \202 uid LDH >1000 \200 Positive culture and glucose <2.2mmol/l \200 Poor clinical pro gress during treatment with antibiotics alone Loculated effusion Effusion with pleural thic kening \200 Summary of treatment according to stage: 1 Exudative: treat with antibiotics and thoracocen tesis or Choice and siting of drain Stage I and II effusions may be managed by antibiotics and close d drains. Drains can be inserted under ultrasound or CT guidance to improve position. Small bore 12 \200\22316F Seldinger-type chest drains can be used and are well tolerated, but ma y block and should be \202 ushed regularly. Large bore chest drains block less often but are less well tolerated, Multiple drains may be needed to manage loculated effusions. Pleur al adhesions may form quickly as drainage progresses, leading to the formation of undrained loculations. Frequent cross-sectional imaging is needed to detect such loculae so that add itional drainage catheters may be placed if needed. chest tube drainage. 2 Fibrinolytic: treat with \201 brinolysis via chest tube or tho- racoscopic (VATS) debri dement. VATS is preferred in good-risk patients 3 Organizing: requires formal decortication by thoracot- omy in order to prevent recurrence and restriction. Further reading Davis CW, Gleeson FV, Cavies RJ. BTS guidelines for the manage- ment of pleural infection. Thorax 2003; 58 Suppl 2: ii18 \200\22328. Evans AL, Gleeson FV. Radiology in pleural disease: state of the art. Respirology 2004; 9: 300 \200\22312. Light RW. Parapneumonic effusions and empyema. Proc Am Thorac Intrapleural \201 brinolytics Fibrinolytics may be used in the treatment of pleural infec tion. Intrapleural urokinase or tissue-type plasminogen activator in combination with caref ul image-guided place- ment of chest tubes may be effective However, a double- blind RCT de monstrated that intrapleural administration of streptokinase does not improve mortality, th e rate of surgery or the length of the hospital stay among patients with pleural infection. Soc 2006; 3: 75 \200\22380. Maskell NA, Davies CW, Nunn AJ, et al. U.K. controlled trial of intrapleural streptokinase for pleural infection. N Engl J Med. 2005; 352: 865-74. Rzyman W, Skokowskia J, Romanowicz G, et al. Decortication in chronic pleural empyema \200 \224effect on lung function. Eur J Cardiothorac Surg 2002; 21: 502 \200\2237. Tassi GF, Davies RJO, Noppen M. Advanced techniques in medical thoracoscopy. Eur Respir J 2006; 28: 1051 \200\2239. Wait MA, Sharma S, Hohn J, et al. A randomized trial of empyema Antibiotics All patients should receive antibiotics as soon as pleural infection is identi \201 ed, and this should cover community- acquired bacterial pathogens, including anaerobe s, pending therapy. Chest 1997; 111: 1548 \200\22351. Wurnig PN, Wittmer V, Pridun NS, et al. Video-assisted thoracic surgery for pleural empyema . Ann Thorac Surg 2006; 81: 309 \200\22313. 270 F CHUA & P SHAH Haemoptysis Selective bronchial angiography, when available, can local- ize the bleeding site relativel y accurately, characterize the nature of the vascular lesion and guide embolotherapy. Haemoptysis, the expectoration of blood from the respira- tory tract, is potentially life-t hreatening. It should be distinguished from haematemesis or bleeding from the nasal \200 \223pharyngeal compartment. Mortality related to acute haemoptysis is in \202 uenced by th e quantity and rate of blood loss Massive haemoptysis is the loss of blood at a rate that p oses an immediate threat to life. Quantitatively, this may equate to the expectoration of a s little as 200 \200\223600ml of blood/24h. This is because the nature of haemoptysis is un predictable and its severity dif \201 cult to ascertain clinically. Sentinel bleeds may be inconspicuous, and the magnitude of bleeding may be underestimated by blood retention with in the lower airways. The bronchial circulation is the most common source of bleeding (90%) , followed by the pulmonary (5%) and non- bronchial systemic (5%) circulation. In many case s the culprit vessels are fragile anastomoses that link the bron- chial and pulmonary circu lation. Pulmonary hemorrhage may be complex if bleeding involves the pleurae. The most comm on causes of haemoptysis in non-Western countries include complications of pulmonary tuberc ulosis (including bronchiectasis and ruptured Rasmussen \200\231s aneu- rysms), lung absces ses and bronchogenic carcinoma. In Western countries, bronchial neoplasms, in \202 ammator y lung disorders (e.g. chronic bronchitis, infections including fungal lung disease, pulmon ary vasculitides, fungal, cystic \201 brosis and non-TB bronchiectasis), thromboembolism, coagulopa- thies as well as iatrogenic causes are encountered. Bleeding pulmonary AV malfo rmations, ruptured aortic aneurysms and unusual disorders (e.g. bronchial Kaposi \200\231s sarcoma) make up the rest. Death due to massive haemoptysis usually results from asphyxiati on (loss of gas exchange surface) rather than exsanguination. Diagnostic evaluation Key poi nts \200 Clinical management Immediate measures Priorities of clinical management are: (1) securing the upper airway, (2) preserving gas exchange and (3) replacing lost circulating volume. Ad minister high- \202 ow oxygen and continuously monitor SpO2, blood pressure and pulse rate . Secure IV access with large-bore peripheral cannulae; don \200\231t waste time attempting central venous cannulation. Infuse colloid or crystalloid \202 uids unless blood, either matched or group O negative, is available. If immediate tracheal intubation is necessary, use an ETT (size 8 \200\22310) large enough to pass a \202 exible \201 breoptic bron- c hoscope. Positioning the patient with the culprit lung dependent is an intuitive (but unpro ven) maneuver. Enlist anesthetic or ICU help immediately. Medical treatment Aggressively identify and treat any coagulopathy. Beware of the patient w ith co-existing liver or renal disease, or those on antithrombotic or antiplatelet agents. The empiric use of tranexamic acid to inhibit \201 brinolysis is popular in minor haemopt ysis but its value remains unproven. The role of antitussive agents in haemoptysis is also controversial; in theory, they may help to decrease cough-related shear forces within the a irways. Use desmopressin and related vasoconstrictors cautiously; their systemic haemodynam ic effects may be unacceptable to individuals with coronary artery disease or hypertension. Antimicrobial agents should be targeted against the likely pathogen, either bacterial or f ungal. The use of conservative measures alone in signi \201 cant haemoptysis is associated with very high mortality. Whilst awaiting bronchoscopic or angiographic intervention, judg e whether early cardiothoracic input is necessary. Rigid vs \202 exible bronchoscopy Early bronchoscopy, compared with a deferred procedure, is more likely to identify the site of bleeding. A rigid bron- choscope has a larger lumin al caliber, providing superior suction, but is more limited in its reach, particularly to t he upper lung lobes and peripheral airways. Rigid bronchos- copy also requires general anes thesia. In contrast, \202 exible bronchoscopy affords greater maneuverability and can be performed on the ward. In cases where iatrogenic haemo- ptysis has arisen due to bronchosco pic lesional biopsies, the instrument must be kept advanced in the airway but a short dista nce away from the site of bleeding so as not to disrupt and clot formation and still facili tate suctioning of the airways. Plain radiography is readily available and may reveal pulmonary masses and cavities. Howeve r, it has a low overall sensitivity in diagnosing haemoptysis or localizing the site of ble eding. Contrast-enhanced CT may identify tell-tale aetiological signs (tumor, bronchiectasi s, aneurysm) or localize the site of hemorrhage. Even so, it fails to reveal the cause of h aemoptysis in up to 10% of cases. CT angiography using multi-detector row helical CT (MDCT) enhances the identi \201 cation of bleeding arteries over conventional CT. It is believed to achieve comparable sensitivity to conventional angiography for distinguishing bleeding from the bronchial and non-bronchial systems. Laboratory tests. A full hematology pro \201 le, renal and liver biochemistry, in \202 ammatory markers and clotting panel as well as urinanalysis comprise the primary labora- tory work-up of any patient with haemoptysis. Add itional tests may be ordered to narrow speci \201 c diagnoses such as vasculitis, infectio ns or pulmonary \200\223renal syndromes. Bronchoscopy is a widely available and versatile t ool. Although its diagnostic accuracy in localizing bleeding sites is reduced by \200\230n ormal \200\231 chest imaging, it enables a range of endobronchial therapies to be administe red. Therapeutic intervention via \202 exible bronchoscopy The initial bronchoscopic goal in m anaging haemoptysis is identi \201 cation of the bleeding lung segment so that the tip of the bronchoscope can be wedged within it. However, massive haemoptysis often obscures endos copic visualiza- tion of the \201 eld. Maintain high- \202 ow suction to remove blood an d instill ice-cold saline and epinephrine (1:100 000 dilution) to promote vasoconstriction. Endobronchial application of tranexamic acid and \201 brin \200\223thrombin agents has n ot produced consistent results. 271 CHAPTER 17.12 Haemoptysis The most established maneuver to occlude a bleeding pulmonary segment is to produce tampona de using a Fogarty balloon-tip catheter. A small catheter (size 4 \200\2237F) may be passed through the inner channel of the broncho- scope for this purpose. A larger catheter will n eed to be advanced in parallel to the bronchoscope via an in situ ETT. This method frees th e endoscopic channel for suctioning and drug instillation. However, catheter-induced bronch ial blockade provides only temporary reprieve and carries recognized ischaemic airway compl ications. We advise occlusion of the segmental or lobar bronchus for 2 \200\2234min at a t ime. The balloon should be gradually de \202 ated to check if fresh bleeding has ceased, a nd re-in \202 ated if bleeding persists, and further checks made at 5min intervals. If a b alloon catheter has already been advanced into the airways prior to placement of an ETT, th e bronchoscope will have to be removed before the ETT can be placed. Both single-lumen and double-lumen tubes have been used to protect the bronchial tree in life-threatening haemopt ysis. The former isolates the contralateral bron- chus by shielding access to the bleeding side. With the lat- ter, the higher (tracheal) cuff acts as a proximal blocker while the lo nger endobronchial arm is positioned \200\230cuffed \200\231 within the contralateral bron chus to ventilate the non- bleeding lung. Secure placement of a double-lumen ETT requires c onsiderable skill. and AV shunting. Dye extravasation is an unusual \201 nding. A variety of embolization ma terials are used, including polyvinyl alcohol foam, absorbable gelatin particles and stainl ess steel platinum coils. BAE is not without risk; recognized complications range from tran sient visceral ischaemia (e.g. chest pain or dys- phagia) to catastrophic spinal infarction . Surgical management of haemoptysis Emergency surgery for acute massive haemoptysis carries a signi \201 cant risk of death. Indications for emergency thora- cotomy have decreased wi th advances in bronchoscopic and radiological intervention. However, surgery remains the ma nagement of choice for haemoptysis resulting from leaking aortic anerysms, traumatic chest injuries, pulmonary vessel hemorrhage and bleeding from a mycetoma unsuc- cessfully control led by other means. Further reading Dweik RA, Stoller JK. Role of bronchoscopy in massive hemoptysis. Clin Chest Med 1999; 20: 89 \200\223105. Gottlieb LS, Hillberg R. Endobronchial tamponade therapy for intractable hemoptysis. Chest 1975; 67: 482 \200\2233. Hirshberg B, Biran I, Glazer M, et al. Hemoptysis: etiology, evalua- tion and outcome in a tertiary referral hospital. Chest 1997; 112: 440 \200\2234. Mal H, Rullon I, Mellot F, et al. Immediate and long-term results of bronchial artery embol ization for life-threatening hemoptysis. Chest 1999; 115: 996 \200\2231001. Additional measures Successful use of recombinant factor VIIa to promote haemostasis has be en described in case reports of patients with signi \201 cant haemoptysis. However, its ef \201 cacy has yet to be con \201 rmed in a controlled trial. Laser photocoagula- tion an d radiotherapy have no role in the emergency treatment of haemoptysis. Meijer K, de Graaff WE, Daenen SM, et al. Successful treatment of massive hemoptysis in acu te leukemia with recombinant factor VIIa. Arch Intern Med 2000; 160: 2216 \200\2237. Naidich DP, Funt S, Etenger NA, et al. Hemoptysis: CT \200\223broncho- scopic correlations in 58 cases. Radiology 1990; 177: 357 \200\22362. Remy-Jardin M, Bouaziz N, Dumont P, et al. Bronchial and non- bronchial systemic arteries a t multi-detector row CT angiogra- phy: comparison with conventional angiography. Radiology 2004; 233: 741 \200\2239. Percutaneous angiography and bronchial artery embolization (BAE) Selective bronchial angiog raphy may provide vital diagnostic information in the pre-operative setting or immediately prior to therapeutic embolotherapy. In skilled hands, BAE is highly successful in controlli ng life-threatening haemopt- ysis in patients unsuitable for surgery. Typical angiographic \201 ndings in large-volume haemoptysis include vessel tortu- osity, hypertrophy, hyperva scularity, aneurysmal dilatation Yoon YC, Lee KS, Jeong YJ, et al. Haemoptysis: bronchial and non-bronchial systemic arterie s at 16-detector row CT (MDCT). Radiology 2005; 234: 292 \200\2238. Yoon W, Kim JK, Kim YH, et al. Bronchial and nonbronchial systemic artery embolization for life-threatening hemoptysis: a compre- hensive review. Radiographics 2002; 22: 1395 \200 \223409. 272 J HANDY Inhalation injury Presentation Presentation will vary according to the severity and type of injury and presen ce or absence of cutaneous burn. History (e.g. \201 re in enclosed space) is essential in identifying the risks of carbon monoxide and cyanide poisoning, signi \201 cant inhalatio n injury and airway compromise. Signs and symp- toms can develop up to 36h after inhalation injury. Smoke inhalation injury occurs in about one-third of patients with major burns, and contrib utes signi \201 cantly to their mortality. It is the most frequent cause of death at the s cene of a \201 re. Injury to the airway and tracheobronchial tree may also result from in halation of chemicals (such as chlorine gas), drugs and biological weapons. Systemic distur bances are common, but depend on the nature and toxicity of the inhaled substance. Assessment Initial assessment should take the form of the trauma primary survey. The presen ce or absence of cutaneous burns does not predict the potential for airway or respira- tory compromise. The speci \201 c causes of hypoxia should be sought and treated. Pathophysiology Discreet pathophysiological phases of lung injury may be seen. An exudative phase is characterized by neutrophil in \202 ux, formation of oxygen free radicals, macro phage acti- vation and production of in \202 ammatory mediators with an increase in pulmon ary capillary permeability. Injury to type II pneumocytes results in decreased surfactant p roduction. Hyaline membranes may form on the denuded alveolar basement membranes. Transpulm onary \202 uid \202 ux increases, with an increase in EVLW and increased pulmonary shun t fraction. Upregulation of NO has been implicated in the pathogenesis of associated lung i njury. In some patients the exudative phase may be followed by uncomplicated repair and res olution; however, others may develop a \201 brotic phase. During this \201 brosing alve olitis, neoangiogenesis and increased collagen deposition is seen. Overall, injury results from damage due to heat, hypoxia and toxins (local and systemic): Airway Obstruction or risk of obstruction must always be consid- ered early while administe ring high flow humidified oxygen. It is a clinical diagnosis; blood gas analysis and oximet ry should not be relied upon. Decreased oxygen saturation is a late and pre-terminal sign o f airway and breathing compromise. Hoarse voice, carbonaceous sputum on deep cough, singed facial and nasal hair, and erythema and oedema of the mucosa in the mouth should raise susp icions of potential airway compromise. Swelling may not reach its maximum until 24h after i njury, and may occur rapidly during \202 uid resuscitation. Paradoxical (abdominal) breat hing pattern, tracheal tug and intercostal muscle recession with inability to speak are sig ns of imminent airway obstruction. Heat Exposure to the mucous lining of the airway and tracheo- bronchial tree results in imm ediate erythema, oedema and ulceration. Airway compromise due to oedema is a signi \201 - cant risk. Thermal damage is usually limited to the supra- glottic region due to the heat e xchanging capacity of the upper airway. Dry gasses have a lower speci \201 c heat capacity than saturated gasses with less potential to cause injury. Distal thermal damage is rare, but can result from inhala- tion of superheated particles or saturated gasses. Breathing Respiratory distress due to inhalation injury usually takes several hours to deve lop. If evident on presentation, airway compromise must be excluded. Clinical signs include tach- ypnoea, intercostal recession, accessory muscle use, wheeze and bronchorrhoea. Soot or burn discoloration and the potential presence of carboxyhaemoglobin render cyanosis an u nreliable sign. Circulation/disability/exposure Cardiovascular, neurological and external signs will vary a ccording to the extent and type of other injuries. Reduced conscious level in the absence o f head injury and following resuscitation should prompt investigation for systemic toxins. Oxygen Environmental hypoxia occurs due to the consumption of oxygen during combustion. Toxins Toxins causing direct damage to the epithelium of the airways include sulfur dioxide , nitrogen dioxide, chlorine and ammonia. Their effects result from pH or free radical dama ge. Distal carriage can occur in the presence of carbon particles. Increased alveolar capil lary permeability and lung water contribute to decreased lung compliance. Epithelial cast f ormation and sloughing, mucociliary dysfunction and oedema result in increased airway resis tance, airway obstruction, atelectasis and predisposition to bacterial overgrowth and the d evelopment of pneumonia. Ventilation \200\223 perfusion mismatch with increased pulmonary s hunt results. Systemic toxins include the asphyxiants carbon monoxide, hydrogen cyanide and hydrogen sul \201 de. These bind to mitochondrial cytochromes causing disruption of the e lec- tron transportation chain. Carbon monoxide has a higher af \201 nity for hemoglobin t han oxygen, preventing binding of the lat- ter and impairing oxygen carriage. Other systemi c toxins include hydrocarbons, organophosphates and metal fumes. Monitoring Vital signs should be monitored continuously during the assessment and initial m anagement phase. Pulse oximetry can give erroneously high readings in the presence of signi \201 cant carboxyhaemoglobin. Speci \201 c investigations Arterial blood gas analysis wi th co-oximetry is essential to assess carboxyhaemoglobin levels. Blood should be drawn for cyanide levels; however, the results may take several days to be ascertained. Cyanide toxic ity should be suspected and treated in patients with persistent high blood lactate levels, acidaemia, high mixed venous oxygen saturation, low oxygen extraction ratio and deteriorati ng neurological and cardiac function despite appropriate resuscitation. Corrected anion gap and osmolar gap should be calculated if acidaemia persists. Toxicology screen should be co nsidered, 273 CHAPTER 17.13 Inhalation injury Cardiovascular support primarily involves \202 uid resuscita- tion. This can be extremely dif \201 cult to assess, particularly if large burns co-exist. Widespread increases in ca pillary permeability result in \202 uid redistribution into the intersti- tium, including that of the lung and airway. Patients with major burns and inhalation injury require far g reater \202 uid resuscitation than those with either injury alone. Limitation of \202 u id resuscitation in victims of smoke inhalation has not been supported in clinical trials. Crystalloid resuscitation for the \201 rst 24h is based on historic evidence, but its use in preference to colloids and blood should be balanced against other injuries. New colloid s are available and in development which may alter the recommended \202 uid resuscitation regimes. Lung injury is a trigger of SIRS and multiple organ dysfunction. Inotrope and vas opressor therapy may be required. Adrenal insuf \201 ciency should be considered in patien ts refractory to vasopressor therapy, and replacement therapy commenced if appropriate. Imp rovement in cardiac output and blood pressure may enhance oxygenation through improved lung perfusion and reduced intrapulmonary shunt. Hypoxic pulmonary vasoconstriction combined wi th increased thromboxane release following smoke inhalation may result in pulmonary hyperte nsion and RV dysfunction. particularly in patients with reduced or inconsistent neuro- logical levels. Bronchoscopic examination is useful in assessing the tra- cheobronchial tree of patients who are stable a nd have undergone endotracheal intubation. It can be combined with therapeutic lavage CXR s igns may lag behind the clinical course of the patient. A normal chest radiograph does not exclude signi \201 cant, early inhalation injury. Management Initial management Attention to airway, breathing and circulatory abnormali- tie s forms the central tenet of initial management. Airway swelling and obstruction is progres sive, and may be exacerbated during \202 uid resuscitation, emphasizing the need for cons tant reassessment. High \202 ow humidi \201 ed oxygen should be administered to all pati ents in the \201 rst instance. If airway compromise is anticipated, expert endotracheal i ntubation should be performed with prior preparation for dif \201 cult or failed intubatio n. Respiratory management should focus on oxygen delivery. Inhalation injury commonly trigg ers ALI and ARDS; however, this may develop insidiously over a period of hours or days. If mechanical ventilation is required, standard recruitment and lung protection measures shoul d be employed. High frequency oscillatory ventilation has been associated with improved out come and reduced incidence of pneumonia. Early bronchoscopy is recommended to record level and degree of injury. Lavage should be per- formed if pulmonary contamination is present; h owever, consideration should be given to the fact that excessive saline lavage may induce l ung injury. Regular administration of aerosolized bronchodilators should be considered. Neb ulized heparin and NAC have been used to reduce cast formation, distal airway obstruc- tion and atelectasis. Antibiotic and steroid therapies have no proven prophylac- tic role but m ay be required in speci \201 c situations. Pneumonia is the most common cause of death in hospitalized patients suffering from inhalation injury. Carboxy-Hb levels >10% should be tr eated with 100% inspired oxygen therapy. The half-life of carboxy-Hb is reduced from 240min at an inspired oxygen concentration (FiO2) of 21% to 80min at an FiO2 of 100%. Hyperbaric therapy should be considered in patients with carboxy-Hb >40%, or 20% if pregnant and in p atients who have had lowered conscious level from no other cause. Suspicion of cyanide pois oning (see above) should prompt empiric treatment. Sodium thiosulfate acts slowly by cata- lysing the metabolism of cyanide. Sodium nitrite reduces cyanide binding by oxidation of he moglobin to methaemo- globin. Methaemoglobin levels of 40% should be targeted. Cyanide-bin ding agents such as dicobalt edetate or hydrox- ycobalamin may be used, though the former m ay induce cardiac arrhythmias and instability if used in the absence of cyanide poisoning. Longer term management considerations Chest physiotherapy remains widely accepted manage- m ent despite a lack of evidence to support it. Tracheostomy should be considered in patients requiring long-term mechanical ventilation or pulmonary toilet. ALI and ARDS from any caus e is associated with increased resting energy expenditure; dramatically so if burns are als o present. Careful attention to nutritional management should be considered at an early sta ge and reviewed continuously. Therapies employed in the management of long-term critically ill and mechanically ventilated patients should be considered. Examples include the use of prophylaxis against venous thromboembolism and GI stress ulceration. Further reading Enkhbaatar P, Traber DL. Pathophysiology of acute lung injury in combined b urn and smoke inhalation injury. Clin Sci 2004; 107: 137 \200\22343. Freitag L, Long WM, Kim CS, et al. Removal of excessive bronchial secretions by asymmetric high-frequency oscillations. J Appl Physiol 1989; 67: 614 \200\2239. Heimbach DM, Waeckerle JF. Inhalation injuries. Ann Emerg Med 1988; 17: 1316. Herndon DN, Barrow RE, Traber DL, et al. Extravascular lung water changes following smoke i nhalation and massive burn injury. Surgery 1987; 102: 341 \200\2239. Herndon DN, Tranber DL, Traber LD. The effect of resuscitation on inhalation injury. Surgery 1986; 100: 248 \200\22351. Orzel RA. Toxicological aspects of \201 resmoke: polymer pyrolysis and combustion. Occup Med 1993; 8: 414 \200\22329.