Colloids Human albumin Human albumin solution is available as 5 or 20%, the former being us ed for hypovolaemia, the latter for the treatment of hypoalbuminaemia in the presence of sa lt and water overload. In the UK, human albumin is expensive and there are concerns over th e risk of transmission of infections, as with any blood product. A Cochrane systematic revi ew showed no bene \201 t in terms of mortality when albumin was used for resuscitation. Th is review was mainly made up of patients from the SAFE trial, which showed no difference in outcome between normal saline and human albumin when given as a bolus in 7500 patients. Performing a \202 uid challenge To test this mechanism requires a variable amount of \202 uid. Filling pressures represent the net effect of preload, ven- tricular compliance a nd afterload. The initial \202 uid challenge technique proposed by Weil and Henning in 19 79 meas- ured CVP at 10min intervals after 100 \200\223200ml of \202 uid. If the change i n CVP was <2mm Hg, the \202 uid was continued. If it Gelatins Gelatins are produced by the hydrolysis of bovine collagen and then cross-linked w ith urea to produce Haemaccel or 245 CHAPTER 16.3 Fluid challenge succinylated to produce Gelofusine. They remain in the circulation for 2h, with renal excr etion occurring within 48h. They are isotonic and the amount of chloride is lower than norm al saline (145). Haemaccel has a significant amount of calcium (Ca 6.25) and so should not be infused through the same giving set as citrated blood. Gelatins also have the potential to cause allergic reactions. Hypertonic saline Hypertonic solutions are considered to expand intravascu- lar volume by c ausing an osmotic shift of \202 uid from the extracellular and interstitial compartments to the intravas- cular space, thereby increasing blood pressure. The per- ceived advantage is that a small amount can be given over a short period with less risk of interstitial oede ma. In par- ticular it may be the \202 uid of choice in head injuries where the patient i s hypovolaemic, as an increased MAP is required to maintain CPP, but not at the expense of a large \202 uid load that may result in interstitial oedema and brain swelling. The osmo tic gradient may even draw water out of the brain tissue, thereby reducing ICP. However, if the blood \200\223brain barrier is interrupted, the hypertonic saline may in fact pass acr oss, drawing excessive amounts of water with it and thereby increasing intracranial pressur e. Hypertonic solutions may also prevent interstitial oedema whenever there is acute lung i njury such as after trauma or surgery. There are data in animals and humans to suggest that hypertonic saline has a favorable effect on haemaody- namic variables, ICP, and gut and re spiratory function. However, there are no conclusive RCTs in humans at present. Dextrans Dextrans are polysaccharides derived from fermentation of sucrose which is then hy drolysed and fractionated into different molecular weights. Dextran 40 has a molecular weig ht of 40 000Da. It is hyper- tonic and is not used for the treatment of hypovolaemia. It ca n cause renal tubular obstruction and renal failure. Dextran 70 is produced as a 6% solutio n in normal saline or 5% dextrose. Its average molecular weight is 70 000Da. Osmolality is 335mosm/kg and is therefore mildly hyper- tonic. Plasma half-life is 6h. It can precipitate anaphylactic reactions and interfere with haemostasis. Hyroxyethyl starches Hydroxyethyl starches are prepared by hydroxyethyl sub- stitution of a mylopectin, a glucose polymer. They are gen- erally presented in solution in normal saline and so may cause a hyperchloraemic acidosis. They vary in molecular weight but remain in th e intravascular space for at least 6h. Hydroxyethyl starches may have adverse effects on co agu- lation and may also cause intractable itching if large vol- umes are used. Further reading Bunn F, Alderson P, Hawkins V. Colloid solutions for \202 uid resuscita- tion. Cochrane Database Syst Rev 2003; (1): CD001319. Bunn F, Roberts I, Tasker R, et al Hypertonic versus near isotonic crystalloid for \202 uid resuscitation in critically ill patients. Cochrane Database Syst Rev 2004; (3): CD0020 45. Crystalloids Normal saline Normal saline has long been used for resuscitation. However, the high chloride present will result in a hyper- chloraemic acidosis when given in large volu mes. The hyperchloraemic acidosis is caused by the high chloride content of normal saline ( 154mmol). This excess of nega- tive chloride ions lead to a decrease in the strong ion dif- ference, which causes a normal anion gap anion gap metabolic acidosis. Finfer S, Bellomo R, Boyce N, et al. A comparison of albumin and saline for \202 uid resu scitation in the intensive care unit. N Engl J Med 2004; 350: 2247 \200\22356. Roberts I, Alderson P, Bunn F, et al. Colloids versus crystalloids for \202 uid resuscita tion in critically ill patients. Cochrane Database Syst Rev 2004; (4): CD000567. Vincent JL, Weil MH. Fluid challenge revisited. Crit Care Med 2006; 34: 1333 \200\2237. Weil MH, Henning RJ. New concepts in the diagnosis and \202 uid treatment of circulatory shock. Thirteenth annual Becton, Dickinson and Company Oscar Schwidetsky Memorial Lecture. Anesth Analg 1979; 58: 124 \200\22332. Hartmann \200\231s solution. Hartmann \200\231s solution has a lower chloride concentration than normal saline but is mildly hypotonic, so may exacer- bate cerebral oedema in those w ith brain injury. However, its main bene \201 t is that its use is not associated with a n or- mal anion gap acidosis. This page intentionally left blank 247 Chapter 17 Respiratory disorders Chapter contents Upper airway obstruction 248 Respiratory failure 250 Pulmonary collapse and atelectasis 252 Chronic obstructive pulmonary disease (COPD) 254 ARDS: diagnosis 256 ARDS: general managem ent 258 ARDS: ventilatory management 260 Asthma 262 Asthma: ventilatory management 264 Pneu mothorax 266 Empyema 268 Haemoptysis 270 Inhalation injury 272 Pulmonary embolism 274 Commu nity-acquired pneumonia 276 Hospital-acquired pneumonia 278 Pulmonary hypertension 280 248 A KAPILA Upper airway obstruction There are few medical conditions that are as rapidly and predictably lethal as the loss of upper airway patency. Because of the relative infrequency with which upper airway obstructi on (UAO) is encountered by most physicians, opportunities to acquire signi \201 cant clini cal experience are limited. This, combined with the frequently subtle presenta- tion of UAO and the clinician \200\231s inability to visualize the upper airway in its entire extent t hrough routine physical examina- tion, may hamper diagnosis of this condition until a crisi s results. Trauma Burns Neoplasm \200 \200 Pharyngeal, laryngeal and tracheobronchial carcinoma Vocal cord polyposis Congenital \200 \200 Vascular rings Laryngeal webs, laryngocoele Miscellaneous \200 \200 \200 \200 Pathophysiology The sites of UAO may be within the airway lumen, in the walls or extrinsic to the airway. Further, sites of UAO maybe can be divided into supraglottic, glottic and in fraglottic above the carina. Finally, UAO will behave differently during inspiration and ex piration if intrathoracic or extrathoracic. The intrathoracic airway dilates during inspira tion as it is exposed to outward force of negative intrapleural pressure. Positive intraple ural pressure during expiration causes compression and narrowing. The compliant extrathorac ic airway, not exposed to intrapleural pressure, collapses dur- ing inspiration and increas es in diameter during expiration. UAO is likely to occur at sites of anatomic narrowing suc h as the hypopharynx at the base of the tongue, and the false and true vocal cords at the l aryngeal opening. Cricoarytenoid arthritis Achalasia of the esophagus Hysterical stridor Myxoedema Clinical presentation and initial evaluation May be complete or partial. Complete UAO \200 Rapidly progressing series of events. Patient is unable to breathe, speak or cough, and may hold the throat between the thumb and index \201 nger (the universal chok- ing sign). An xious and agitated. Vigorous attempts at respiration with intercostal and supraclavicular r etrac- tion. Heart rate and blood pressure raised. Patient becomes rapidly cyanosed, Respir atory efforts diminish, loss of consciousness, bradycardia and hypotension. Cardiac arrest. Death is inevitable if the obstruction is not relieved within 2 \200\2235min of the onset, Causes Functional causes \200 \200 CNS depression Peripheral nervous system and neuromuscular abnor- malities Recurrent laryng eal nerve interruption (post-operative, in \202 ammatory, tumor in \201 ltration) Obstruc tive sleep apnoea Laryngospasm Myasthenia gravis Guillain \200\223Barre polyneuritis Hypoca lcaemia (causing vocal cord spasm) Tetanus Partial UAO \200 \200 Stable, or progressive deterioration, Signs and symptoms may be mild but as they worsen the y include coughing, inspiratory stridor, crowing or noisy respiration, dysphonia, aphonia, choking, drooling and gagging. Dyspnoea, feeble cough, respiratory distress and signs of hy poxaemia and hypercarbia such as anxiety, confusion, lethargy and cyanosis may be present a s the obstruction worsens. Powerful inspiratory efforts against an obstruction may produce dermal petechiae and subcutaneous emphysema. Partial airway obstruction that is worsening s hould be aggressively managed and, if rapidly progressing, immediate preparation for treatm ent as complete obstruction should be made. In stable, non-progressing cases of partial obs truction, speci \201 c diagnostic evaluation may be undertaken provided the patient is str ictly observed for any signs of deteriora- tion and facilities for skilled airway managemen t are immediately available. \200 \200 \200 \200 \200 Mechanical causes \200 Foreign body aspiration Infections \200 \200 \200 \200 \200 \200 \200 \200 Epiglottitis Supraglottitis Retropharyngeal cellulitis or abscess Parapharyngeal abscess Lu dwig \200\231s angina Diphtheria Bacterial tracheitis Laryngotracheobronchitis Special investigations Laryngoscopy and bronchoscopy Laryngoscopy using \202 exible naso- endoscopy in a stable, cooperative patient is useful in diagnosing foreign bodies, retropha ryngeal or laryngeal masses and other glottic pathology. In skilled hands it is quick, simp le and atraumatic. If laryngoscopy is conducted using a \202 exible intubating laryngosco pe or bronchoscope, de \201 nitive airway control can be achieved at conclusion of examina tion by railroading Laryngeal oedema \200 \200 Allergic Hereditary angioedema Hemorrhage and haematoma \200 \200 \200 Post-operative Anticoagulation therapy Coagulopathy 249 CHAPTER 17.1 Upper airway obstruction and Rightward Pressure) may improve laryngeal visualiza- tion. Pre-loading the ETT onto a b ougie will minimize apnoeic time. Use of a CO2 detector (capnography or single use device) will ensure correct placement of the ETT in the trachea. If appropriate skills are availabl e then \202 exible endoscopic techniques (FOI) may be considered. This can be achieved th rough an LMA, for example, or under local anesthesia if time permits. Siting of a cricothyr oid cannula beforehand can provide oxygenation using transtracheal jet ventilation during t he intubation attempt and can remove the sense of extreme urgency from the situation. Care with allowing time for exhalation and not overin \202 ating the lungs will avoid barotraum a, especially in the presence of severe UAO. In the presence of blood and excessive secreti ons, FOI may be impossible. Retrograde tracheal intubation over a J-tip guide wire passed c ranially via the cricothyroid membrane can be useful in this scenario. an ETT into the trachea. Disadvantages are need for a skilled operator, time to achieve loc al anesthetic topicali- zation of the airway and a cooperative patient. It can be very dif \201 cult in the presence of blood and secretions. It is a traumatic procedure and may lea d to worsened swelling, bleeding and oedema, and catastrophic loss of the airway. Radiographic imaging AP and lateral plain neck radiographs can be useful in detecting radio paque foreign bodies, retropharyngeal masses and epiglottitis. A lateral view should be obt ained during inspiration with the neck fully extended. CT scanning in stable patients enabl es assessment of the integrity of the thyroid, cricoid and arytenoid cartilages, as well as the status of the airway lumen. Management A myriad of techniques using a huge variety of equipment have been described for management of UAO. The key principles are to have agreed a set number of techniques and to provide training and equipment for these for each institution. Surgical airway Indicated when earlier airway plans have failed or at the outset if endotra cheal intubation is not possible (e.g. bleed- ing into an oral surgery microvascular \202 ap with severe UAO) or if an unstable cervical spine is threatened by avail- able airway t echniques. The key principle here is to recog- nize the need for a surgical airway early an d not wait till the patient is already severely hypoxic. Percutaneous transtracheal jet ven tilation using one of the proprietary needle cannula/catheters/jet ventilation systems (e.g . VBM Manujet \204 ) inserted through the crico- thyroid membrane can be achieved relativel y quickly. Cricothyrotomy with a wide bore cannula or even an ETT with a minimum internal d iameter of 5mm will allow ade- quate gas exchange through a normal breathing circuit. The c ricothyroid space is 9mm by 30mm in an adult; therefore, up to a size 8.5mm outer diameter tube should avoid com- plications such as laryngeal fracture and vocal cord damage. Complic ations such as subglottic stenosis, thyroid fracture, hemorrhage and pneumothorax are uncom mon. Emergency tracheostomy is rarely required. Formal surgical tracheostomy under local an esthesia may be a prudent approach under some controlled conditions General measures Reverse hypoxia with 100% oxygen. Gain IV access as soon as practicable. C ontinuous monitoring and observation with the most skilled personnel available. Assess the airway carefully to delineate where and what type of UAO is present. Plan the approach to a irway management with Plan A and subsequent back-up plans in the event of failure. Airway e quipment should be readily available, ideally in a movable trolley with an agreed contents list that is maintained regularly. Such a list would include a choice of laryngoscopes, bla des and ETTs, \201 breoptic bronchoscope or laryngoscope, bougies, a choice of supraglott ic airway devices such as LMA \204 and intubating laryngeal mask airway (ILMA \204 ) and e quipment necessary for a surgical airway (cricothyroidotomy set, tracheostomy tray and equi pment for trans tracheal jet ventilation), emergency drugs and good suction, Principles of airway management techniques Airway maneuvers Try simple maneuvers to open ai rway, jaw thrust, inser- tion of an oropharyngeal or nasopharyngeal airway may be effective in the unconscious or obtunded patient. Consider the coma position to maintain the airway if the cervical spine is clear. Further reading American Society of Anesthesiologists Task Force on Management of the Dif \201 cult Airway. Practice Guidelines for Management of the Dif \201 cult Airway: An Updat ed Report by the American Society of Anesthesiologists Task Force on Management of the Dif \201 cult Airway. Anesthesiology 2003; 98: 1269 \200\22377. Endotracheal intubation If UAO persists, the key principle in gaining formal airway control is not to lose oxygenation during the intubation attempts. Supraglottic airway devices suc h as the LMA and ILMA can provide a means of oxygenation and a conduit for endotracheal int ubation. If a full stomach is likely and a rapid sequence intubation indicated, then carefu l head and neck positioning and cricoid pressure with the BURP maneuver (Backward, Upward Dif \201 cult Airway Society, http://www.das.uk.com/ Henderson JJ, Popat MT, Latto IP, et al (2004). Dif \201 cult Airway Society guidelines for management of the unanticipated dif \201 cult intubation. Anesthesia 59: 675 \200\22394. Langeron O. Trauma airway management. Curr Opin Crit Care 2000; 6: 383 \200\2239. 250 L CAMPORATA & A JONES Respiratory failure De \201 nition Respiratory failure is a condition in which the respiratory system is unabl e to maintain adequate gas exchange to satisfy metabolic demands, i.e. oxygenation of and/o r elimi- nation of carbon dioxide from mixed venous blood. The respiratory system consists of a gas-exchanging organ (the lungs) and a ventilatory pump (respiratory muscles/ thorax) either or both of which can fail and precipitate respiratory failure. Qs/Qt= (CcO2 \200\223CaO2)/(CcO2 \200\223 CvO2) or more simply as; Qs/Qt= (1 \200\223 SaO2)/(1 \200\223 SvO2) Where CcO2 = capillary oxygen content; CaO2 = arterial oxygen content; CvO2 = venous oxygen content CcO2 = capillary oxygen content; SaO2 = arterial oxygen saturation; SvO2 = mixed v enous oxygen saturation. In practice, it is dif \201 cult to distinguish between true shun t and V/Q mismatch, and they often occur simultaneously. V/Q mismatch results in hypoxaemia because the distribu- tion of alveolar oxygen tension is uneven. However, when breathing F iO2 1.0, the alveolar oxygen tension becomes uniform with V/Q mismatch, whereas there is no effect in true shunt, and, therefore, it may be possible to distinguish the two processes. Diffusion impairment occurs when the movement of oxygen from the alveolus to the pulmonary capillary is impaired and there is insuf \201 cient time for oxygenation to occur. This i s invariably related to extensive and/or destructive lung disease where V/Q mismatch is als o a signi \201 cant factor, and in its pure form occurs rarely in clinical practice. Reduc ed inspired oxygen concentration is not a problem in conventional practice (outside of extr eme environ- ments), and is easily overcome by increasing the FiO2. Initially, the hypoxaem ia present in type I respiratory failure is frequently associated with an increase in the v en- tilation, and therefore decreased PaCO2. However, as the condition persists or progress es, fatigue of the respiratory muscles or CNS impairment can lead an increase in PaCO2. Ano ther factor that may contribute to hypoxaemia is low mixed venous oxygen saturation (SvO2). Normally, only 20 \200\22330% of the delivered oxygen is extracted by the tissues, and the resulting venous oxygen levels can be measured using a central venous catheter (central ve nous oxygen saturation, ScvO2) or in the pulmonary artery using a pul- monary artery cathet er (mixed venous oxygen saturation, SvO2). SvO2 values of 65 \200\22375% represent an opti mal bal- ance between global oxygen supply and demand. It is clear that the lower the SvO2 the greater will be the effect of shunt or low Va/Q ratio on PaO2. Increasing SvO2 with ear ly use \202 uids, blood transfusion and inotropic support to optimize cardiac output, can have a favorable effect on arterial oxygenation and also survival. Classi \201 cation Respiratory failure is generally classi \201 ed into: \200 Hypoxaemic (type I). This is the most common form of respiratory failure and is invariably associated with parenchymal lung diseases (Table 17.2.1). It is character- ized by a PaO2 < 8.0kPa (60mm Hg) with a normal or low pCO2. Ventilatory (type II). This is secondary to fai lure of the ventilatory pump, and characterized by hypoventilation with hypercapnia (PaCO2 >6.0kPa (45mm Hg)), which in the absence of supplemental oxygen is invariably associ- ated with hypoxaemia (Table 17.2.1). Table 17.2.1 Common causes of respiratory failure Type I: hypoxaemic Type II: hypercapnic Pneumonia ARDS/ALI Pulmonary \201 brosis Pulmonary oedema Asthma COPD Pneumothorax Pulmon ary embolus Obesity COPD Severe asthma Drug overdose (opiates) CNS insult (trauma, CVA) Primary muscle disorder s Myasthenia gravis Poliomyelitis Kyphoscoliosis Polyneuropathies Pulmonary hypertension Obesity hypoventilation syndrome Pathophysiology Hypoxaemic \200\224type I Type I respiratory failure derives from the effec ts of one or more of the following four pathophysiological mechanisms: ventilation/perfusio n mismatch, true shunt, diffusion impair- ment or reduced inspired oxygen concentration. Ve ntilation/perfusion (V/Q) mismatching occurs when alveolar units are poorly ventilated in r elation to their perfusion (low V/Q units). As the degree of V/Q maldistri- bution increase s, hypoxaemia worsens because a greater proportion of the cardiac output will be poorly oxy genated. This effect is ampli \201 ed because the sigmoid shape of the hemoglobin dissocia tion curve means that high or normal V/Q alveolar units cannot compensate for the units at low V/Q ratio. True shunt occurs when deoxygenated mixed venous blood bypasses ventilated a lveoli, resulting in \200\230venous admixture \200\231. The quantity of blood which would be required to reduce the saturation of the pulmonary end-capillary blood to the observed v alue of PaO2 is called the shunt fraction (Qs/Qt) and can be calculated as; Hypercapnic \200\224type II In normal conditions PaCO2 is maintained within strict limits ( 4.8 \200\2235.9kPa (36 \200\22344 mmHg)). Hypercapnic respira- tory failure may occur eithe r acutely, insidiously or acutely upon chronic CO2 retention. The common denominator in typ e II respiratory failure is reduced effective alveolar ventilation (VA) for a given CO2 pro duction (VCO2). The relationship between end-tidal CO2 and VCO2 is: [end-tidal CO2] = VCO2/VA; [end tidal CO2] = VCO2/(VE(1 \200\223 VD/VT) end-tidal concentration in % approximates to end-tidal value in kPa. Partial pressure can b e substituted and there 251 CHAPTER 17.2 Respiratory failure \200 FBC Septic screen (sputum, blood culture) is a close but unpredictable relationship between PaCO2 and end-tidal CO2, so the equation can be rewritten Several indices are used in clinical practice to assess and monitor gas exchange in ventila ted and non-ventilated patients. P(A \200\223a)O2 gradient: the alveolar to arterial (A \200\223a) oxygen gradient is calculated by subtracting the PaO2 from the alveolar PAO2, ca lculated using the alveolar gas equation: PaCO2 = VCO2/(VE(1 \200\223 VD/VT) \227f) Where VE is minute ventilation and VD is dead sp ace ventilation, VT is tidal volume and f is respiratory frequency. Under conditions where VCO2 remains unchanged, the resulting pCO2 will depend on the interaction between respirato ry rate, tidal volume and the degree of dead space ventilation. Although the latter is ofte n assumed to be \201 xed, in reality the physiological dead space may vary within a given patient and depends on the interaction between alveolar and pulmonary vascular pressures. This can be particularly important in critically ill patients where the precarious cardiova scular status interacts with the need for positive pressure ventilation. VCO2 is rarely the limiting factor in normal lungs (see below), but even normal (carbohydrate-based feeds) or slightly increased (increased work of breathing) VCO2 may be a problem with extensive lung disease. Clinically, type II (hypercapnic) respiratory failure occurs under four circumsta nces. \200 PAO2 = PIO2 \200\223 (PaCO2/R) The normal A \200\223a gradient varies with age and FiO2. Hypoventilation can be differenti ated from other causes of hypoxaemia by the presence of a normal A \200\223a gradient. P(a/ A)O2 ratio or respiratory index: this is calculated by dividing the P(A \200\223a)O2 gradie nt by PaO2. Unlike the P(A \200\223 a)O2 gradient it is relatively unaffected by the FiO2. The normal P(a/A)O2 ratio varies from 0.74 \200\2230.77 when FiO2 is 0.21, to 0.80 \200\223 .82 when FiO2 is 1. PaO2/FiO2 ratio: this is probably the most widely used index, being eas y to calculate and a good estimate of shunt fraction. A PaO2/FiO2 ratio of <200mm Hg (26.6k Pa) indi- cates ARDS and relates to a shunt fraction of >20%, and <300mm Hg (40kPa) de \201 nes ALI. Oxygenation index (OI): this index takes into account the mean airway pressur e and is calculated as: Central CNS depression with reduction of the respira- tory drive (e.g. drugs, CNS diseases) Impaired respiratory muscle function (e.g. neuromus- cular diseases, malnutrition, drugs, skeletal deformities, respiratory muscle dysfunction or fatigue from excessive mechanical l oad) V/Q mismatch (high V/Q, with increase in dead space ventilation) Increased CO2 product ion in extreme cases (malignant hyperthermia) can be the sole cause OI = (FiO2 \227 Paw \227 100/PaO2) Principles of treatment Respiratory failure is managed by a combination of speci \201 c an d supportive measures. General principles are the fol- lowing. \200 \200 \200 \200 Acute vs chronic respiratory failure Acute type II respiratory failure develops over minute s to hours and is invariably associated with an acidosis (pH <7.35). In chronic type II res piratory failure, hypercapnia develops over a much longer period, allowing time for renal c ompensation with an increase in bicarbonate con- centration and minimal change in pH. The d istinction between acute and chronic hypoxaemic (type I) respira- tory failure cannot easil y be made on the basis of arterial blood gasses, but clinical markers of chronic hypoxaemia , such as polycythaemia or cor pulmonale, suggest a long- standing disorder. Ensure airway patency Administer oxygen to maintain SaO2 >90% Correct hypoperfusion and ane mia Correct reversible causes (e.g. drain pleural effusion or pneumothorax) Pharmacological management to treat infection, bron- choconstriction Physiotheraphy to mobilize secretions Consider non-invasive ventilatory support (CPAP/ bilevel) to improve oxygenation, reduce w ork of breath- ing and reduce hypercapnia Early assessment for mechanical ventilation if no n-inva- sive respiratory support contraindicated or failed. \200 Clinical assessment The assessment of a patient with suspected respiratory failure requires a thorough clinical history and examination in conjunction with speci \201 c investigatio ns, with individual \201 ndings dependent on the precipitating cause. The degree to which this is feasible may depend on the severity and rapidity with which the patient is deterio rating, and it is not uncommon for some of this process to occur following the instigation of empirical therapy and sometimes ventilatory support. None the less, this process should be completed as soon as is practicable. Repeated clinical observation, including pulse oxim etry monitoring may be necessary. Further reading Hess DR, Kacmarek RM. Indices of oxygenation and ventilation. In: Hess DR, Kacmarek RM, eds. Essentials of mechanical ventilation. New York: McGraw-Hill, 2002: 240 \200\2235. Lumb AB. Nunn \200\231s applied respiratory physiology, Elsevier, 2005. Mellemgaard K. The alveolar-arterial oxygen difference: its size and components in normal man. Acta Physiol Sc and 1966; 67: 10 \200\22320. Rivers E, Nguyen B, Havstad S, et al. Early goal-directed ther apy in the treatment of severe sepsis and septic shock. N Engl J Med 2001; 345: 1368 \200 \22377. West JB Respiratory physiology \200\224the essentials, 7th edn. Baltimore: Essential investigations \200 \200 \200 Williams and Wilkins, 2004. Wood LD. The pathophysiology and differential diagnosis of acute respiratory failure. In: H all JB, Schmidt GA, Wood LD, eds. Principles of critical care. New York: McGraw-Hill, 2005: 417 \200\22326. Arterial blood gas analysis ECG CXR 252 K BRIGNALL & A JONES Pulmonary collapse and atelectasis Clinical features Presenting features will depend on speed of onset, cause and severity of the atelectasis. Many patients may be asymptomatic, but common symptoms include breath- les sness, cough and chest pain, and some may report systemic features. A full medical history may help identify the etiology. The terms atelectasis and collapse are often used inter- changeably. Pulmonary collapse can affect any anatomical division of the lung, i.e. the whole lung, a single lobe or segments or subsegments of a lobe. It occurs due to a reduction or complete cessation of ventilatio n. Causes Obstructuve (resorptive) atelectasis. Intrinisic obstruction of the airway with dist al resorption of air obstruction: inhaled foreign body, aspiration, neoplasms, mucus plugs (asthma, bronchiectasis, allergic bronchopul- monary aspergillosis (ABPA), secretions (pneu monia), endobronchial intubation. Examination \201 ndings \200 \200 \200 \200 \200 \200 \200 \200 Fever, tachycardia Tachypnoea Low SaO2 Reduced expansion on the affected side Trachea devia ted towards the side of the collapse \210\227 Dull percussion note over affected area \210 \227 Reduced breath sounds over affected area \210\227 Other signs that the patient is at r isk of collapse, i.e. chest and abdominal wounds, abdominal distension, neuromus- cular abn ormalities. Relaxative (passive) atelectasis Interruption of the negative pressure holding visceral and parietal pleura in close contact causes the lung to retract: pneumothorax, pleural effusio ns. Compressive atelectasis External compression of the lung by chest wall, pleural or mediasti nal structures. Can be localized or regional in nature: neoplasms (primary or secondary), l ymphadenopa- thy (e.g. sarcoid, TB, lymphoma), cardiomegaly (especially affecting left and middle lobe bronchus), loculated pleural collections, abdominal distension (ascites, ileus, abdominal compartment syndrome), obesity, neuromuscular weakness, chest pain (e.g. post-su rgical, trauma). ( \210\227only if signi \201 cant volume of the lung affected) Differential diagnosis It is often dif \201 cult clinically to differentiate collapse from consolidation or pleural \202 uid, and frequently these entities will co-exist (Table 17 .3.1). Investigations \200 \200 Adhesive atelectasis Increased surface tension within the alveoli due to decreased producti on or inactivation of surfactant: ARDS, infant respiratory distress syndrome (IRDS), pulmon ary oedema, near drowning. CXR: ideally a PA \201 lm, but a lateral may be useful. Markers of infection and inflamma tion (FBC, CRP, sputum and blood cultures) as indicated Arterial blood gasses (ABGs) to ass ess the degree of respiratory compromise CT may demonstrate the anatomy and may define caus es, e.g. endobronchial lesion, lymphadenopathy Chest ultrasound may differentiate collapsed lung from a pleural effusion Bronchoscopy: both diagnostic (large airway obstruc- tion, e. g. foreign body, sputum plug, tumor) and thera- peutic Cicratrization atelectasis Loss of lung volume due to parechymal scarring: granulo- matous disease, radiation, necrotizing pneumonia. Rounded atelectasis (folded, trapped lung) A distinct condition associated with in \202 am matory pleural disease, usually asbestosis, with minimal volume loss. Consequences \200 Hypoxaemia \200 \200 Increased work of breathing \200 \200 V/Q mismatching Reduced FRC Table 17.3.1 Radiographic differences between collapse, consolidation and pleural \202 ui d Surfactant dysfunction in collapsed region Decreased thoracoabdominal compliance (passive a nd compressive atelectasis) Increased risk of infection Increased bacterial growth in colla psed region Development of respiratory failure Collapse Consolidation Effusion Marked Marked Minimal Absent Variable Absent Volume loss Compensatory hyperin \202 ation Tracheal shift \200 \200 Towards lesion Absent Away from lesion Away from lesion Not elevated The severity of the changes seen depends on the degree and rapidity of the developing colla pse. Towards lesion Absent Mediastinal shift Diaphragm position Unilateral elevation Not elevated Incidence Pulmonary collapse is not uncommon, the exact frequency depending on the cause. I n patients who have undergone open abdominal surgery the incidence of significant subsegmen tal collapse approaches 20 \200\22325%. Absent Present Absent Air bronchogram 253 CHAPTER 17.3 Pulmonary collapse and atelectasis Radiology Radiographic signs of collapse may be direct or indirect Direct \200 \200 \200 Speci \201 c management options Physiotherapy There is little evidence for the prophylacti c use of physio- therapy for the prevention of atelectasis. However, there is evidence for its ef \201 cacy in treatment. Including manual treatments (percussion, vibration and posi tive pressure assist devices) in conjunction with patient positioning. Displacement of intralobular \201 ssures Loss of aeration Vascular and bronchial crowding Indirect \200 \200 \200 \200 \200 Fibreoptic bronchoscopy Aside from its diagnostic use, bronchoscopy can be used for therape utic intervention, e.g. to remove a foreign body, or, more commonly, remove retained secret ions. It is commonly applied in the ICU, achieving similar results to physiotherapy. Case s eries demonstrate an improvement in PaO2, lung compliance and CXR \201 ndings. It can be con- sidered in lobar and segmental rather than subsegmental collapse, but may be less effe ctive in patients who demon- strate air bronchograms on the preceding chest \201 lm. Elevation of hemidiaphragm Mediastinal displacement Hilar displacement Compensatory hyperin \202 ation of remaining lung Crowding of ribs Lobar collapse is associated with well de \201 ned patterns on the chest radiograph. Howev er, CXR signs can be subtle and easily overlooked by the unwary clinician. Total lung colla pse results in complete opaci \201 cation of the effected hemithorax, with indicators of m arked volume loss on that side, mediastinal shift and hyperin \202 ation of the contralat- eral lung. Subsegmental (plate, discoid) atelectasis may appear as peripheral band-like de nsities perpendicular to the pleural surface. Mucolytics (N-acetylcysteine, DNase) Such therapies aim to reduce the viscosity of secretio ns, making them easier to clear and reducing mucus plugging. Although DNase has been shown to be effective in cystic \201 brosis, de \201 nitive evidence in other conditions is sc arce. Mechanical ventilation The following maneuvers can be considered in isolation or in concert to re-expand collapsed regions/prevent regional (dependent) lung collapse; \200 \200 Generic management Stabilize the patient \200 \200 \200 Oxygen, \200\230ABC \200\231 Assess the need for ventilatory support (invasive or non-inva sive i.e. respiratory rate, ABGs) Higher levels of PEEP/CPAP Recruitment maneuvers: transient application ofhigh levels of PE EP (30 \200\22340cm H2O) Positioning the patient with collapsed segments in non- (less) dep endent position, Identify causes and treat It is important to identify the likely causes of collapse as some are amenable to speci \201 c therapeutic interventions: Further reading Ashizawa K, Hayashi K, Aso N, et al. Lobar atelectasis: diagnostic Intrinsic airway obstruction: \200 \200 pitfalls on chest radiography. Br Radiol J 2001; 74: 89 \200\22397. bronchoscopy to remove the source of obstruction endobronchial stenting for a neoplastic le sion Hansell DM, Armstrong P, Lynch D, et al. Basic patterns of lung disease. In: Imaging of dis eases of the chest. Phillidelphia: Elsevier Mosby, 2005: 69 \200\223141. Removing external sources of compression: \200 \200 \200 Kreider M, Lipson D. Bronchoscopy for atelectasis in the ICU: a case report and review of t he literature, Chest 2003; 124: 344 \200\22350. Schindler MB. Treatment of atelectasis: whe re is the evidence? Drain pleural effusion Treat pneumothorax Drain large ascites Crit Care 2005; 9: 341 \200\2232. Re-expansion of collapsed lung: \200 \200 Stiller K. Physiotherapy in intensive care: towards an evidence- based practice. Chest 2000; 118; 1801 \200\22313. CPAP Mechanical ventilation with PEEP 254 A ZUREK Chronic obstructive pulmonary disease (COPD) De \201 nition COPD is characterized by slowly progressive airflow obstruction that is not fully reversible with treatment. Air \202 ow obstruction is de \201 ned as an FEV1 (forc ed expiratory volume in 1s) of <80% predicted and an FEV1/FVC (forced vital capacity) ratio of <0.7. Smoking is by far the most important cause of COPD. Others include air pollution, occupational dust (e.g. coal) and chemical (e.g. cadmium) exposure, and genetic causes ( 1-antitrypsin de \201 ciency). Severity de \201 ned on the basis of FEV1: Mild: Moderate: Severe: Lung transplantation: single or double lung if FEV1 is <25% predicted and/or cor pulmonale are present plus severe symptoms despite maximal medical therapy. Recipients must be non-sm okers, <65 years old. Lung volume reduction surgery: consider in patients with upper lobe-p redominant emphysema where symp- toms persist despite maximal medical therapy. Lung functio n parameters should be at least 20% predicted and PaCO2 <7.3kPa. Bullectomy for patients wi th signi \201 cant dyspnoea or complications due to a single large bulla. Acute exacerbations of COPD (AECOPD) A major cause of morbidity and mortality accounting fo r 1 in 8 of acute medical admissions. Typically patients present with increased dyspnoea, c ough or wheeze, chest tightness, sputum volume and/or purulence. FEV1 50 \200\22380% predicted FEV1 30 \200\22349% predicted FEV1 <30% predicted Differential diagnosis Asthma, bronchiectasis, cardiac failure, lung cancer, bron- chioliti s. These conditions may also co-exist with COPD. Investigations include CXR, pulse oximetry and measure- ment of acute bronchodilator reversibility plus (where indi- cated) full lung function testing, peak \202 ow diary, FBC, ABGs, ECG, echocardiogram, sputum culture, 1-antitrypsin level and thoracic CT scan. Causes Commonly infective (viral and bacterial), but others include air pollution (nitrogen and sulfur dioxide, ozone and particulates) and temperature changes. In some cases the cau se is unidenti \201 able. The most common bacterial patho- gens are Haemophilus in \202 u enzae, Streptococcus pneumoniae and Moraxella catarrhalis. Viral causes include rhinovirus, in \202 uenza, coronavirus and adenovirus. Management of stable COPD Most treatments for stable COPD aim at controlling symp- toms, pr eventing exacerbations and maintaining or improving exercise capacity and quality of life. Only long-term oxygen therapy (LTOT) in hypoxaemic patients has been shown to reduce mortal ity. Smoking cessation reduces the rate of decline of lung function while lung transplantat ion and lung volume reduction surgery can result in improved lung function. However, surger y is only appropriate and available for a small minority of COPD patients. Current manageme nt of stable COPD includes: \200 Differential diagnosis Pneumonia, pulmonary oedema, PE, pneumothorax, pleu- ral effusion, l ung cancer, UAO, recurrent aspiration. Investigations CXE, ECG, ABGs, FBC, U&Es, CRP plus blood cultures if pyrexial, and theophyl line level if the patient is on oral theophylline therapy.