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Review Articles Pulmonary Oedema Associated with Airway Obstruction

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Review Articles Pulmonary Oedema Associated with Airway Obstruction 210 Review Articles Pulmonary oedema associated with airway Scott A. Lang MD, Peter G. Duncan Mo FRcPc, David A.E. Shephard MB FRCPC, obstruction Hung C. Ha MO ~CPC The purpose of this review is to describe the pathogenesis of analysons rimportance sur l'attitude d prendre devant une pulmonary oedema associated with upper airway obstruction, obstruction des voies adriennes. Les mdcanismes sous-jacentes summarize what is known of its clinical presentation, and reflect d, ce type d'oeddme pulmonaire sont multiples, le principal upon its implications for the clinical management of airway demeurant toutefois la presence de pressions intrapleurales obstruction. The pathogenesis of pulmonary oedema associated ~ tr~s ~, n~gatives. L' incidence du phdnom~ne demeure difficile d with upper airway obstruction is multifactorial. However, as the ~valuer mais il semble bien que chez les enfants, prds de 50 pour phrase "negative pressure pulmonary oedema" suggests, mark- cent des ~pisodes se produisent dans des cas de laryngite ou edly negative intrapleural pressure is the dominant pathophysi- d'~piglottite ndcessitant une intubation tandis que chez les ological mechanism involved in the genesis of pulmonary adultes, on en retrouve une proportion semblable associ~e aux oedema associated with upper airway obstruction. The frequen- laryngo~pasmes survenant d l'dmergence de l'anesth~sie ou cy of the event is impossible to ascertain from the literature but dans les cas de tumeurs situdes haut clans les voies a~riennes. paediatric cases requiring airway intervention for croup or Une fois identifi~es, les victimes potentielles devraient dtre epiglottitis and adults requiring airway intervention for emer- observdes de pros tant que le risque persiste m~me sice sont les gence laryngospasm or upper airway tumours account for over premieres minutes qui suivent le d~veloppement ou la rdsolution 50 per cent of the documented cases in each age group, d'une obstruction aigu~ qui sont les plus critiques. Ce type respectively. Individuals at risk should be observed closely d'ced~me pulmonaire est transitoire, s'estompant en quelques while they remain at risk. The majority of cases present within heures. S'il survient, on doit s'assurer de la permdabilitd des minutes either of the development of acute severe upper airway voies a~riennes et faire respirer de l'oxygdne quoique dans pr~s obstruction or of relief of the obstruction. Resolution is typically de la moiti~ des cas, la ventilation mdcanique avec pression rapid, over a period of a few hours. Rarely is anything more positive en fin d'expiration s'avdrera ndcessaire. required for management than the maintenance of a patent airway, supplemental oxygen, and, in approximately 50per cent of cases, mechanical ventilation and positive end-expiratory Fatalities from upper airway obstruction are usually due to pressure. asphyxia from markedly diminished or absent airflow. However, rapid re-establishment of the airway does not Dans cet article, nous d~crivons la pathogdndse de l'oed~me guarantee improvement in gas exchange. It has recently pulmonuire associ~ d l'obstruction de la partie sup~rieure des been recognized that morbidity may result from the voies respiratoires. Nous en revoyons les aspects cliniques et, en delayed effects of the obstruction. As early as 1927 an association between upper airway Key words obstruction and the development of pulmonary oedema AIRWAY: obstruction; was suggested in spontaneously breathing dogs exposed COMPLICATIONS: oedema, pulmonary; to inspiratory resistive loads, t These dogs' lungs were LARYNX: spasm; found at autopsy to be "boggy." However, the pathophys- LUNG: oedema. iological correlation between these events was not recog- nized until 1942, 2 and the first description of pulmonary From the Department of Anaesthesia, University of Saskatche- oedema associated with upper airway obstruction did not wan, University Hospital, Saskatoon, Saskatchewan, appear until 1973. 3 The first report of the clinical Canada. significance of this phenomenon was published in 1977. 4 Address correspondence to: Dr. S. Lang, Department of Since then there have been 77 case reports of pulmonary Anaesthesia, University Hospital, Saskatoon, Saskatchewan oedema associated with upper airway obstruction (Tables S7N 0X0. I and II). CAN J ANAESTH 1990/ 37:2/pp210-8 Lang etal.: AIRWAY OBSTRUCTION AND PULMONARY OEDEMA 211 TABLE 1 Adult cases (n = 32) Time to onset of pulmonary oedema following airway Resolution of Common obstruction (rains) pulmonary oedema PEEP or Mechanical Age (yr) M : F obstructive events n = 25* (hrs) n = 26 Intubation CPAP ventilation Mean 37.6 --- SD 16.6 1.2: I Laryngeal spasm Mean 25.6 • SD 38.8 Mean 29.7 • SD 19. I 27/32 .I 2/32 19/32 18/32 Range 12-79 Aiway tumour Range 3-150 Range 6-72 7/32 Mode 5 Mode 24 *Time to recognized resolution. Excludes cases complicated by pneumothorax, pneumonia, aspiration or heart failure. SD = standard deviation. PEEP = positive end-expiratory pressure. CPAP = continuous positive airway pressure. n = 32 unless otherwise stated. References: 4, 6, 10, I I, 42, 43, 45-47, 50, 52, 64-78. TABLE II Paediatric cases (-< 10 yr) (n = 45) Time to onset of pulmonary oedema following airway Resolution of M : F Common obstruction (mins) pubnonary oedema PEEP or Mechanical Age (yr) n = 30 obstructive events n = 30 (hrs) n = 30* Intubation CPAP ventilation Mean 3.0.4- SD 2.4 2.4: I Epiglottitis 15/45 Mean 33.3 - SD66. I Mean 42.4 -.+ SD 30.8 41/45 16/30 14/30 Range 1/12-10 Group 18/45 Range 5-240 Range 2-96 Foreign body 4/45 Mode 5 Mode 12 *Time to recognized resolution. Excludes cases complicated by pneumothorax, pneumonia, aspiration or heart failure. SD = standard deviation. PEEP = positive end-expiratory pressure. CPAP = continuous positive airway pressure. n = 45 unless otherwise stated. (Galvis 61 does not give full information on 15 patients.) References: 3, 5, 44, 49, 54-63. The true incidence of pulmonary oedema associated influence the movement of fluid across the pulmonary with airway obstruction is not known. However, the capillaries. 7-9 The major factors favouring formation of incidence of pulmonary oedema associated with airway pulmonary oedema fluid are: obstruction has been estimated at 12 and I 1 per cent in 1 The hydrostatic pressure in the pulmonary microvascu- paediatric and adult populations requiring active airway lature (Pc). intervention (intubation or tracheostomy) for acute upper 2 The negative hydrostatic pressure in the pulmonary airway obstruction of varying aetiology. 5'6 Therefore, interstitium (Pi). considering the relative infrequency with which it has 3 The colloid osmotic pressure of the pulmonary interstit- been reported, in contrast to the frequency of presentation ium (~i). of perianaesthetic airway obstruction, pulmonary oedema The major factors retarding the formation of pulmonary associated with upper airway obstruction may go unrec- oedema fluid are pulmonary capillary colloid osmotic ognized. The purpose of this review is to describe the pressure (~c) and pulmonary capillary integrity. When pathogenesis of the syndrome, summarize what is known capillary integrity is impaired fluid movement into the of its clinical presentation, and reflect upon its implica- interstitium is favoured. Capillary endothelial permeabili- tions for the clinical management of airway obstruction. ty is represented by the hydraulic conductance K (the flow rate of fluid per unit pressure gradient across the endothe- Pathogenesis lium), and the reflection coefficient (r (a measure of the Figure 1 is a brief review of the Starling forces that ability of the endothelial membrane to prevent the 212 CANADIAN JOURNAL OF ANAESTHESIA movement of solute, principally albumin, across the membrane). A value of unity for the reflection coefficient Starling Forces in the Lung * indicates total reflection of solute and corresponds to zero Alveolus / colloid osmotic pressure in the pulmonary interstitium. A P, : 0 value of zero for the reflection coefficient indicates free Inlerstltlum premeability of the capillary membrane to proteins and P,:-4 m:9 therefore excludes colloid osmotic pressure from having Arterial Cspill,ly Venous any influence on the movement of water in the lungs. End Pc * IT rrc TM 24 Pc = 12 End The pathogenesis of pulmonary oedema associated KA[(Pc - Pi ) - O (rrc -rn)] with upper airway obstruction is multifactorial, z~ = the rate ot IIuid Iransfer to the interstitium K = hydraulic conductance (ie.the rain ol Ilow per unit Recent advances in methodology have facilitated our pressure gradlenl across Ihe endothellum) understanding of the pathogenesis of this seemingly Pc = hydrostatic pressure In the pulmonary infrequent event. ~2-~6 The principal factors in the patho- microvasculalure Pl = hydroslanc pressure In Interstitium genesis of pulmonary oedema associated with upper = rellncllon coefficient for albumin airway obstruction are shown in Table Ill. ~c = osmotic pressure within pulmonary mlcrovasculature = osmotic pressure within InterstlUum A = capillary surface area Haemodynamic changes secondary to negative PA = alveolar pressure intrathoracic pressure * All pressures expressed In mmHg Pulmonary oedema associated with airway obstruction has been called negative pressure pulmonary oedema HGURE I (NPPE) because most of the proposed pathogenetic mechanisms relate directly to the development of marked- pressure can cause pulmonary oedema associated with ly negative intrapleural pressure (i.e., sustained peak upper airway obstruction.
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