Anaesth. Intens. Care (1975), 3, 19
UNILATERAL PULMONARY OEDEMA FOLLOWING RE-EXPANSION OF PNEUMOTHORAX M.
X.
SHANAHAN,* IAN MONKt AND
H. ].
RrCHARDst
Departments of Cardiothoracic Surgery, St. Vincent's Hospital and Royal North Shore Hospital, Sydney SUMMARY
Unilateral pulmonary oedema is a rare complication in the routine management of spontaneous pneumothorax. Previous reports have emphasized excessive negative intrapleural pressure, rapid re-expansion of the lung and bronchial obstruction as major factors in the pathogenesis. We have encountered four cases, and at least one of these factors have been absent in each case. Review of the literature, and our own experience suggests that the major factor is chronic and total lung collapse resulting in hypoxia and increased alveolar-capillary membrane permeability. Other factors which may be contributory are discussed. INTRODUCTION
Spontaneous pneumothorax is a benign condition under most circumstances, and the treatment is generally uncomplicated. The objectives of treatment are to promote the early re-expansion of the lung, the sealing of an air leak when this is persistent and the production of a pleurodesis if the pneumothorax has been recurrent. These objectives are generally accomplished by the insertion of an intercostal catheter connected to an underwater seal system, and in most cases, to a controlled suction apparatus to ensure full re-expansion of the lung. In some cases with recurrent pneumothorax or persistent air leak, thoracotomy, surgical control of the air leak and gauze abrasion pleurodesis may be necessary (Clagett 1968). On four occasions, the authors have encountered severe unilateral pulmonary oedema occurring as a complication of such treatment in spontaneous pneumothorax. The circumstances of presentation, the initial management and the
* F.R.A.C.S., F.R.C.S., Honorary Cardiothoracic Surgeon, St. Vincent's Hospital. t M.S., F.RC.S., F.RA.C.S., Honorary Surgeon, Royal North Shore Hospital. :j: F.R.C.S., F.RA.C.S., Honorary Surgeon, Royal North Shore Hospital. Address for reprints: Dr. Mark X. Shanahan, 4th Floor, St. Vincent's Medical Centre, 376 Victoria Street, Darlinghurst, N.S.W., 2010, Australia.
mechanisms of re-expansion differed in each case. In no case was excessive negative intrapleural pressure applied, a circumstance which has been implicated in previously reported cases (Ziskind, Weill and George 1965, Childress, Moy and Mottram 1971, Trapnell and Thurston 1970). Case 1 is reported in detail to highlight the extremely severe degree of systemic shock, which can be associated with this complication. Case 2 is the first report in the literature of unilateral pulmonary oedema as a complication of thoracotomy and pleurodesis. Case 3 was the least severe, and was comparable to previous cases reported in the literature, and is not reported in detail. Case 4, the oldest patient so far reported in the literature, was complicated by the development of bronchopneumonia in spite of intermittent positive pressure ventilation, and died on the fifth day. CASE REPORTS
Case 1 B.D., a 20 year old bank officer presented to the emergency department on 19.1. 71. He had experienced a sudden pain in the right anterior chest five days prior to this, and the pain had persisted. For three days, he had been mildly short of breath on exertion, and this also was progressive. A chest X-ray taken on the 19.1.71 showed a total right pneumothorax (Figure 1). The right lung was opaque and completely collapsed. An air bronchogram of
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the right lung was clearly evident. There was no mediastinal shift and the left lung appeared normal. An intercostal catheter, size 20 French, was inserted in the right second intercostal space anteriorly, and was connected to an underwater seal bottle. There was no air leak, and a repeat chest X-ray showed that the lung was still collapsed. The tube was clamped and the patient transferred to the ward where he arrived
ized cyanosis, but the central venous pressure was not raised. The trachea was markedly deviated to the right. There was reduced air entry over the right chest and coarse crepitations were audible over the right side. The left lung was free of crepitations. Blood gas analysis revealed an arterial P0 2 of 50 mmHg, PC0 2 of 32 mmHg, and the pH was 7 ·29 with a base excess of -10. A further chest X-ray revealed an opaque consolidated right lung, with minimal aeration and mediastinal shift to the right (Figure 2). The left lung was hyperinflated but showed no opacification or consolidation. Suction on the chest tube was reduced and maintained at 10 cm of water. During the next hour, expectoration produced 2,000 ml of pink frothy straw-coloured fluid and 1,500 ml of a similar fluid drained via the intercostal
FIGURE I.-A postero-anterior chest film (I !l.l. 71) shows complete collapse of the right lung clue to spontaneous pncmllothorax. .\11 anterior intercostal catheter has been inserted but no suction applied. There is a well-llmrked air bronchogram of all lobes of the lung, excluding the presence of bronchial obstruction.
in no distress. One hour after insertion, the intercostal catheter was connected to a controlled suction unit, set at a negative pressure of 25 cm of water. On the institution of suction, the tube bubbled briefly and then continued to swing with respiration, without any further air leak. Shortly thereafter the patient became distressed and dyspnoeic. Paroxysmal coughing occurred and was productive of 30 ml of straw-coloured frothy fluid every fl'w minutes. He became progressively cyanosed and shocked with gross dyspnoea. Similar straw-coloured fluid drained from the intercostal catheter. The blood pressure fell to 60 mmHg systo\ic, the pulse rose to 160 beats/min and was weak and thready. He was cold and sweaty with general-
2.--An antero-posterior chest fIlm taken two hours after Figure 1. Suction had been applied and shock became evident. There is gross pulmonary oedema of the right lung, with mediastinal shift to the right side, and marked hn)crinfiation of the left lung. FIGURE
catheter. An emergency tracheostomy was performed, and intermittent positive pressure respiration instituted. An intravenous infusion of 5 per cent dextrose in water and serum albumin was maintained, and intravenous hydrocortisone 1,000 mg was also given. In spite of intense resuscitation measures, deterioration continued for six hours. Hypotension,
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UNILATERAL PULMONARY OEDEMA
cyanosis and peripheral vasoconstriction continued for 12 hours before improvement began. 100 per cent oxygen was necessary to maintain an arterial P0 2 of 100 mmHg. On 20.1.71 repeat chest X-ray showed persistent opacification of the right lung with a small residual pneumothorax in spite of suction. There was a persistent small air leak, but fluid loss at this time had become minimal Improvement continued slowly (Figure 3) and assisted ventilation was discontinued on the 26.1.71. By 27.1.71 his chest X-ray showed full expansion of his right lung with clearance of the oedema, but there remained a persistent air leak from the intercostal catheter until 5.2.71. On 8.2.71 the intercostal catheter was removed. Three hours later, repeat chest X-ray showed complete collapse of the right lung once again. An intercostal catheter was re inserted but no suction was applied. Thoracotomy was performed on 9.2.71. There was a thin-walled cyst measuring 3 cm in diameter at the apex of the right upper lobe. Apart from some pleural thickening at the site of the initial intercostal catheter, the chest appeared otherwise normal.
21
No lung biopsy was taken. A gauze abrasion pleurodesis was performed, and the chest closed with drainage. Convalescence was thereafter uneventful and he was discharged on 20.2.71 and has remained well since. Case 2 P.L. This 18 year old student presented to another hospital on 6.1.73 with left chest pain and dyspnoea of several days duration. A chest X-ray showed a left pneumothorax with 60 per cent collapse of the lung. A size 28 French Malecot catheter was inserted in the second left intercostal space anteriorly and connected to an underwater seal apparatus. No suction was applied. Chest X-rayon 7.1.73 showed some re-expansion of the lung, but subsequent X-rays on the 8.1.73 and 10.1.73 showed complete collapse of the lung. He was transferred to Royal North Shore Hospital on 11.1.73 and without further interference, thoracotomy was carried out early on 12.1.73. Chest X-ray prior to this procedure showed the lung to be still completely collapsed. Through a limited 6th intercostal space incision, a small
(a) (b) 3.-(a). A portable machine chest film (22.1.71) shows diffuse atelectasis of the right lung following temporary interruption, after three days, of positive pressure ventilation via a tracheostomy tube. This occurred in spite of 10 cm of water negative pressure applied to the intercostal catheter. (b) A later chest film .(24.1.71) after I.P.P.V. had resumed still shows diffuse" ground-glass" opacification, unlike the fluffy opaCIficatIOn of pulmonary oedema. This is presumed to be due to widespread microscopic atelectasis. FIGURE
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cyst at the apex of the upper lobe was ligated, and a gauze abrasion pleurodesis was performed. The lung which was still collapsed, was then manually inflated with positive pressure via the endotracheal tube. After closure of the chest, the patient failed to regain consciousness. He was cyanosed after extubation in spite of apparent good respiratory effort and intranasal oxygen. He was reintubated. Copious pulmonary oedema fluid was then aspirated from the endotracheal tube. He was given frusemide 40 mg and dexamethazone 16 mg by intravenous injection. Ventilation was difficult, even with muscle relaxation. The blood pressure was 70/50 mmHg, and the pulse rate was 104/min. Blood gas analysis showed an arterial P0 2 of 48 mmHg and PC0 2 of 29 mmHg with a base excess +8. Chest X-ray showed unilateral pulmonary oedema of the left lung (Figure 4). Apical and basal pleural drains which were connected to an underwater seal apparatus showed no air leak, and normal respiratory oscillation. Ko negative suction had been applied to the tubes. The patient was
conscious but in respiratory distress one hour later. He continued to improve and was extubated 6 hours after the operative procedure. He had a cough with expectoration of small amounts of pink frothy sputum for several hours after extubation. On admission to the Intensive Care Ward one hour after operation, suction of 20 cm of water was applied to the chest tubes without any worsening of his condition. On 13.1.73 he seemed well and was breathing normally, but blood gas analysis 36 hours after the onset of pulmonary oedema, showed an arterial P0 2 of 72 and PC0 2 of 56 in spite of intranasal oxygen (4l/min). On 14.1.73, radiological clearing of pulmonary oedema had occurred, and the patient thereafter had a normal convalescence and remains well.
Case 3 P.B. This 23 year old long distance runner experienced sudden right-sided chest pain associated with dyspnoea three weeks prior to his admission to St. Vincent's Hospital in 1962. He presented because of increasing disability,
(a) (b) 4.-(a) An antero-postcrior chest film (11.1.73) shows complete collap,e of the left lung. (b) After left thoracotomy a chest film, which has been reversed, shows diffuse oedema of the left lnng. The right lung is hyperinflatcd with mediastinal shift to the left. Positive pressure ventilation via an endotracheal tube was llsed to inflate the collapsed left lung . FIGURE
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UNILATERAL PULMONARY OEDEMA
and his chest X-rayon admission showed complete collapse of the right lung (Figure 5). A readily visible air bronchogram was present, and the patient had no cough or sputum. An intercostal catheter was inserted and connected to an underwater seal system, with 20 cm of water suction. He complained of pain in the chest and developed respiratory distress, which persisted in spite of reduction in the suction to 10 cm of water. Amber coloured fluid drained
23
powder was carried out on the sixth day following his admission. His progress thereafter was satisfactory and he remains well to this time. Case 4 This 84 year old male presented on 26.3.74. He had a two-week history of dyspnoea, cough and purulent sputum. His initial signs were those of pneumonia and responded to parenteral penicillin. Ten days prior to admission he had become more acutely dyspnoeic and breath sounds were noted to be absent over the right chest. No X-ray was taken at that time but on admission it revealed a total right pneumothorax (Figure 7a). An intercostal catheter was inserted and the lung gradually expanded. No suction was applied to the underwater seal apparatus. One hour later the X-ray showed partial opacification of the expanded lung and
FIGURE 5.-A postero-anterior chest film (1962) shows complete collapse of the right lung following a spontaneous pneumothorax.
from the chest tube and he began to expectorate copious white frothy sputum. A further chest X-ray showed extensive unilateral pulmonary oedema on the right side (Figure 6). He was pale and sweaty and the blood pressure fell to 90 mmHg systolic. Suction was discontinued and he was given intravenous Aminophylline and intranasal oxygen with some improvement. He continued to have an air leak from the intercostal catheter and a further chest X-ray showed partial collapse of the consolidated right lung. Suction was therefore recommenced without producing further distress and his condition had returned to normal within 24 hours of the onset of the oedema. Radiological clearing of the oedema was present in four days. Because of a persistent air leak, thoracoscopy and pleurodesis by the instillation of iodised talcum
FIGURE 6.-An antero-posterior chest film. three hours after suction had been applied to an intercostal catheter, shows diffuse patchy oedema of the right lung. The left lung appears normal.
was thought to represent acute pneumonia. Two hours later he had deteriorated further. There was cyanosis, tachycardia, widespread crepitant rales, and a blood pressure of 60 mmHg systolic. X-ray opacification was more widespread (Figure 7b). He was then seen by members of the Thoracic Unit and a diagnosis of unilateral pulmonary oedema was made. The patient was breathing 28 per cent oxygen via a face mask, and blood
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(a) (b) 7.-(a) A portable chest film (26.3.74) shows collapse of most of the right lung due to a pneumothorax. A bullous cyst of the upper lobe is faintly vi-;ib1e. (b) Two hours later an intercostal catheter has been inserted and rc-expansion of the right lung has taken place, without the use of any negative intrapleural pressure. There is some patchy opacification of the right lower lobe. The left lung is relatively normal for this age group.
FIGURE
gas analysis revealed an arterial P0 2 of 50 mmHg and PC0 2 of 31 mmHg. Oxygen concentration was increased but deterioration continued and Pa0 2 fell to 41 mmHg. Digitalis and diuretics were given. An oral endotracheal tube was inserted and intermittent posltl\'e pressure ventilation with 100 per cent oxygen in:;tituted. Twelve hours after the onset cardiac arrest occurred, at which time the arterial P0 2 was 30 mmHg and pH 7 ·on. Resuscitation was achieved and tracheostomy was performed. Secretions which were frothy became thick and purulent. There was some improvement thereafter but in spite of intensive therapy, deterioration and death occurred on the fifth day. Autopsy showed extensive atelectasis of both lungs (Figure 8), and widespread bronchopneumonia. At no time was suction applied to the intercostal catheter during management. DISCUSSION
Unilateral pulmonary oedema is a rare but serious complication following the treatment of spontaneous pneumothorax. \Ye haye been able to find only fiye preyious reports of this complication. The first of these was Carlson, Classen and Gollan (1959) followed by Ziskind
et al. (19n5), Humphreys and Berne (1970), Trapnell and Thurston (1970) and Childress et al. (1971). The cases reported by these authors are summarized in Table 1. A similar complication was not uncommon early this century when the Potain apparatus, which applied high negative pressure to a needle, was commonly used for the aspiration of pleural fluid (Reisman 190~). In many of these cases the pulmonary oedema was associated with " massiye albuminous expectoration" as occurred in onc of our cases (Case 1). Hartley (190.'1) reported 35 such cases and in 29 of these the onset occurred immediatelv after or within onc hour of the thoracentesis. ;\Iore recent reports were by Cameron (1948) and Luisada and Cardi (1956). The literature on pulmonary oedema and its mechanisms of development, is voluminous and at times controversial and contradictory. Pulmonary oedema is seldom caused by any one single factor, but rather is due to a combination of several factors Adriani ct al. (1967); Yisscher, Hadd and Stephens (1956) and Luisada and Cardi (1956). A single factor may appear to be the underlying cause, but usually it is only the precipitating factor out of several
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(a) (b) 8.-(a) A chest film, after the onset of more acute respiratory distress, shows widespread oedema of the right lung. Changes in the left lung are still minimal. (b) Four days later, in spite of continued intermittent positive pressure ventilation with oxygen, the chest film (30.3.74) shows widespread opacification of both lungs. Histology showed widespread patchy atelectasis of the right lung and bronchopneumonia of both lungs. FIGURE
additional co-existing factors (Drinker 1954). A particular set of circumstances may precipitate pulmonary oedema on one occasion, but not on another, under seemingly similar circumstances. This generalization is equally applicable to unilateral pulmonary oedema following the treatment of a pneumothorax, as innumerable patients have had re-expansion of a collapsed lung without developing pulmonary oedema. In trying to determine the aetiology of this condition therefore, one must look for a number of factors, not all of which may be present in anyone particular case. Six of the reported cases were young, healthy individuals under 25 years of age, with no evidence of co-existent disease or abnormality. One must therefore assume that the factors producing unilateral pulmonary oedema are related solely to the involved lung, the extent and duration of collapse, and the method of re-expansion. In most of the cases reported in the literature, the lung was completely collapsed on presentation, or became so, before re-expansion was actively produced. In all but one case the collapse had been present for at least three days. In the one exception (Humphreys and Berne 1970) the patient was ill and cachectic, opacifica-
tion of the lung was present on the side of the iatrogenic pneumothorax before re-expansion and the appearances were consistent with pneumonitis which then responded to antibiotic treatment. The first pre-requisite therefore is presumed to be chronic collapse of the lung. This point was stressed by Trapnell and Thurston (1970) who suggested that" if the lung or part of it was compressed and airless for a longer period (1-3 days) and if aspiration of large quantities of air or fluid is then undertaken, oedema will develop ". The development of acute unilateral pulmonary oedema after re-expansion of an induced pneumothorax was studied by Miller et al. (1973) in Rhesus monkeys. When the induced complete pneumothorax was maintained for three days re-expansion by applying suction produced marked acute pulmonary oedema within two hours in all animals. Re-expansion by underwater seal alone in six other animals did not result in pulmonary oedema. When the pneumothorax was maintained for only one hour re-expansion using suction, even at a pressure of -10 cm mercury, did not result in any oedema.
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TABLE 1
A Summary of relevant Clinical Details of Cases of Cuilateral Pulmonary Oedema Following He-Expansion of Pneumothorax, Previously Described in the l_itcratuyc, Together with Corresponding j)ctails of Cascs Prescnted ill this R~poyt (Shanalian 1974) Author and Year Carlson 1!l59* .. Ziskind 1!l65 Humphrcys 1970 ~
I Age
I
I
;j
=~_. .)
I
!
I!l
1_ COllll:letc
67
I
ti3
1
:'lcthod of Ee- Expansion
Duration of Lung Collapse
Lung Collapse
-1--1--31 Complete
---- ---- I
;:;
'"~
:-;umber of Cases
I
,j
weeks
J
.'i
days
Complete Partial
:? weeks :? hours
I
Degree of Pulmonary Oedema-
Additional Comments
Pump suction
Severe
Consolidation lasted 8 days persistent pneumothorax
with
High negative suction
:\Ioderate dyspnoea
Clearance 111 6 hours. expectoration
Low suction Needle aspiration
Severe with shock X-I{ay evidence only
Clearance in 3 days Patient cachectic. Other factors involved
Pink frothy
,.....
-~---.-----
3-4 :'Ionths
55
S days
No suction
:\fodcrate dyspnoea
18
Complete
± days
High negative suction
Gross with shock
U
Complete
6 days
High negative suction
Severe with shock
X-Ray clearance in 6 days. frothy expectoration
20
comPlcte---1
,j
days
25 cm water suction
Gross with shock
~
18
Complete
4 days
...... ...... .......
:23
Complete
3 weeks
Positi ve pressnre Gcneral anaesthesia 1 Open thoracotom~ ' 20 Cln water suction
Tracheostomy. IPPR. Consolidation lasted 8 days. Massive albnminons expectoration Clearance in :? days
84
Complete
4
56 58
;:,
"......
;::.
1:l days
~.
'"Cl
."'=
Childress I !l71 .. Shanahan 1974 ..
~
a
4
10 days
...... '11
...~
~
S1 ..... -
r
UNILATERAL PULMONARY OEDEMA
27
the application of high negative intrapleural suction, and stated that both these factors appeared to be necessary for the production of the pulmonary oedema. Blockage of the major bronchi by preventing the inflow of air into the alveoli, allows the negative pressure to persist in the alveolar sacs. This increases the gradient between the capillaries and the alveolar sacs and favours the transudation of fluid. Neff (1972) emphasized the importance of an air bronchogram in the collapsed lung, stating that it should be present and that" its absence (1) Negative intrapleural pressure is highly suggestive of an occlusive bronchial It is only in recent years that negative intra- lesion". If "its absence" is the case, he pleural pressure has again come into vogue for recommended that bronchoscopy should be the treatment of spontaneous pneumothorax, performed before significant suction is applied resulting in rapid re-expansion of collapsed lung to the pleural space. Felson (1960) stated that tissue even at relatively low levels of negative " the absence of an air bronchogram is of little suction. However, the occurrence of unilateral significance, since it indicates either that the pulmonary oedema in cases in whom no suction lesion is extrapulmonary, or that it is intrawas applied (Cases 2 and 4) or in whom only low pulmonary but that the bronchi are no longer levels of suction were used to achieve air filled". re-expansion, indicates that it is not so much In two of our cases, excellent air bronchograms the level of negative pressure (Ziskind et al. were present in the collapsed lung excluding 1965, Fenn 1951) but the rate of re-expansion significant bronchial obstruction. In the third which is critical (Humphreys and Berne 1970). case, tenacious sputum was first aspirated Ziskind et al. (1965) pointed out that if high before pink frothy fluid was obtained. This negative pressure is applied to the great veins patient had clinical evidence of respiratory tract and pulmonary vascular bed, the pulmonary infection and a productive cough prior to arterial inflow is greatly increased and over- thoracotomy. However, his lung was expanded filling of arteries and capillaries occurs. by positive endobronchial pressure during anaesHumphreys and Berne (1970) quoted experi- thesia and oedema occurred before any negative mental work of Barach, Martin and Eckman pressure was applied to the pleural cavity. In (1938) which demonstrated that expansion of a four of the cases which have been reported the lung in a negative pressure chamber results in free expectoration of large amounts of oedema rapid increase in pulmonary capillary pressure fluid would appear to exclude significant and flow. This rapid return of pulmonary obstruction of the bronchi to the affected lung blood flow at a high pressure may result in fluid tissue. transudation across the capillary and alveolar In experimental studies in which the clinical membranes, as well as the accummulation of phenomenon of unilateral pulmonary oedema interstitial oedema fluid. This oedema can be was reproduced, Carlson et al. (1959) and Miller reduced by the use of positive pressure ventila- et al. (1973) were unable to demonstrate any bronchial obstruction, either grossly or on tion. histological examination. Re-collapse of the (2) Airway obstruction lung which did occur in some animals was An open bronchial system in the presence of related to intra-alveolar blockage producing negative pressure should not under normal diffuse microscopic atelectasis and was a self circumstances allow an abnormal pressure limiting phenomenon which resolved in five to gradient to develop between the pulmonary seven days, and for which bronchoscopy was not capillaries and the alveolar space, as the rapid indicated. This is discussed later in relation to influx of air into the alveoli causes instant re- changes in alveolar surfactant. expansion of the lung and consequent obliteration of the pleural space. This is what (3) Increased alveolar-capillary membrane permeprobably occurs in the majority of cases where ability no pulmonary oedema occurs. In a general discussion of factors which may Childress et al. (1971) stressed the significance contribute to the development of pulmonary of blockage of the bronchus, in combination with oedema, Luisada and Cardi (1956) stressed the
Other factors which existed in these cases and which may have been contributory are listed and discussed below: (1) Negative intrapleural pressure. (2) Airway obstruction. (3) Increased alveolar-capillary membrane permeability. (4) Loss of tissue surfactant. (5) Fluid shift from periphery to pulmonary vascular bed due to peripheral vasoconstriction, or increased venous return.
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importance of increased permeability of the pulmonary capillaries. Among the many factors which may favour this, they mentioned tissue hypoxia. Drinker (1954) strongly emphasized the importance of " anoxia" as a contributing factor in the formation and persistence of pulmonary oedema. In the earliest known reports of unilateral pulmonary oedema Foucart (1875) and Ortner (1899) postulated that the mechanism was the presence of chronic " anoxia" of the endothelial cells of the pulmonary capillaries secondary to compression collapse of the lung by pleural fluid. Reisman (1902), Cameron (1948) and Humphreys and Berne (1\)70) referred to this mechanism in explaining the development of unilateral oedema. That hypoxic damage to alveolar capillaries does occur in association with chronic atelectasis was demonstrated by Coryllos and Birnbaum (1929). They studied the short-term effect of ligation of the bronchus in the dog, and concluded that the blood flow into the lung was reduced in proportion to the degree of lung collapse. They stated that the obstruction to blood liO\y took place at the capillary level, and they demonstrated disintegration of the capillarie,; after several days, followed by the formation of hyaline membranes within the alveoli after some weeks. Tooley (19(;3) also measured Jlulmonary blood flow following bronchus ligation and found that the flow fell essentially to zero in 12 to 24 hours following the bronchus ligation. It may be concluded that collapse of the lung, of Illore than one day duration, produces a direct hypoxic effect on the pulmonary capillary membrane, increasing capillary permeability and hence contributing to the leakage of oedema fluid when re-expansion occurs. The se\'erity of the oedema is related to the degree of hypoxic damage as well as to other factors already discussed, particularly negative intrapleural pressure. (4) Loss of tisslle surfactant Studies on pulmonary surface tension in experimental atelectasis have been reported by Avery and Chernick (1963) and Finley et al. (19G4). The concept that the alveoli are lined and stabilized by a substance, the surface tension of which ~·aries as the alveolar volume and surface area, was first proposed by Clements, Brown and Jolmson (UJ58). This substance, now clearly defined, is called surfactant. Avery reported (hat an increase in surface tension of lung extracts occurred in the collapsed lung
only after more than 24 hours of induced pneumothorax. Studies in Vil'O showed that rapid expansion resulted firstly in oedema and then further atelectasis, with recovery taking place, as early as two hours in some, and much longer in others. On the other hand, control lungs kept airless under refrigeration for up to one week, had normal surface tension characteristics. These and other studies in both rabbits and mice suggest that airlessness per se is not the cause of the alterations in surface tension in collapsed lungs, but that it is the associated ischaemia which mediates the change. Finley et al. (1964) studied the effects of pulmonary artery occlusion and showed an earlier increase in the surface tension of the lung followed by atelectasis after an interval of 24 hours. Clearly the rise in surface tension, or the loss of surfactant, is due to a reduction in pulmonary blood flow which was shown by Tooley (l!Hi3) to be a sequel to atelectasis. Loss of tissue surfactant has also been shown to occur as a result of pulmonary oedema (Said et al. 1967). It is therefore unlikely that loss of surfactant is related to the deVelopment of the unilateral oedema after re-expansion of pneumothorax, but it is likely to be responsible for the phenomenon of recollapse of the lung, due to diffuse microscopic atelectasis, which was stressed by Carlson (1 H5B) and which was such an outstanding feature of our Cases 1 and 4 (Figures ;{ and R). (5)
Fluid shift from periphery to plllmonary 7'asclllar bed due to peripheral vasoconstriction or increased venous return. An increased venous return and pulmonary arterial inflow certainly occurs in those cases in whom a sudden negative pressure is applied to the pleural cavity (Ziskind et al. 19(i5, Barach et al. 1938) and this would contribute to the severity of the pulmonary oedema when other factors were co-existent to initiate its development. However, there seems little likelihood that an increased pulmonary inflow alone could initiate oedema. Peripheral vasoconstriction has not been noted prior to the onset of the oedema in any reported cases. However, in severe cases the oedema mav be associated with a fall in blood pressure and shock and peripheral vasoconstriction can then become marked. It is likely that such a state of shock perpetuates the oedema in the affected lung by virtue of resultant fluid shift and generalized hypoxia (Gould 1955). If fluid shift were a major primary factor however, one would expect both lungs to be involved, even if not equally.
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UNILATERAL PULMONARY OEDEMA COMMENT
The radiological demonstration of an airless and collapsed lung does not constitute an emergency situation unless there is associated evidence of tension or bleeding within the pleural cavity. Therefore re-expansion of the lung can be allowed to occur gradually after the introduction into the pleural cavity of an intercostal catheter connected to a valve or an underwater seal apparatus (Trapnell and Thurston 1970). There is no indication, other than that of expediency, to apply negative suction to the pleural cavity unless a persistent air leak prevents full re-expansion of the lung. If full re-expansion does not occur in the absence of a persistent air leak, then bronchoscopy and aspiration of secretions may be necessary to exclude or treat retained or tenacious sputum. If chronic collapse of the lung is suspected then the application of negative intrapleural pressure to the intercostal catheter should be deferred for several hours and reexpansion encouraged by coughing and physiotherapy. In some cases of prolonged collapse, such as Case 4 in whom oedema developed without any suction, gradual staged reexpansion, allowing a small amount of pleural air to be expressed at half-hourly intervals, may be advisable. Successful intercostal catheter suction depends upon the volume of air beinG withdrawn from the pleural space exceeding the volume being drawn through the pulmonary defect. As long as this relationship is maintained the lung should re-expand and fill the pleural space. This need not occur rapidly but if an air leak is present some suction is essential. If the air leak is such that re-expansion will not occur with a negative pleural pressure of 25 cm water, then surgical closure of the pulmonary defect is indicated. CONCLUSION
Unilateral pulmonary oedema after reexpansion of a chronic complete pneumothorax is now a well documented clinical entity. Persistence of complete collapse of some lung tissue for several days is an essential pre-requisite for its development. Two deaths, one in a previously healthy young male, and several instances of severe systemic shock have occurred in association with this complication. It is therefore essential that the factors be recognized and the development of unilateral pulmonary oedema prevented. Large amounts of air should never be rapidly removed, and negative
pressure should be avoided during re-expansion whenever possible. If unilateral pulmonary oedema does occur most cases will respond to the usual treatment for pulmonary oedema, but severe cases may require intubation and intermittent positive pressure ventilation with high concentrations of oxygen, to overcome systemic hypoxaemia. REFERENCES
Adriani, J., Zepernick, R, Harwon, W., and Hiern, B. (1967): "Iatrogenic Pulmonary Oedema in Surgical Patients ", Surgery, 61, 183. Avery, M. E., and Chernick, V. (1963): "Alterations of the Alveolar Lining Layer in Rabbits ", J. Pediat., 63, 762. Barach, A. L., Martin, J., and Eckman, M. (1938): " Positive Pressure Respiration and its Application to the Treatment of Acute Pulmonary Oedema", Ann. Intern. Med., 12, 754. Cameron, G. R (1948): "Pulmonary Oedema (Sydney Ringer Memorial Lecture) ", Brit. Med. J., I, 965. Carlson, H.. 1., Classen, K. L., Gollan, F. (1959): "Pulmonary Oedema Following the Rapid ReExpansion of a Totally Collapsed Lung Due to a Pneumothorax; A Clinical and Experimental Study", Surg. Forum, 9, 367. Childress, M. E., Moy, G., and Mottram, M. (1971) : "Unilateral Pulmonary Oedema Resulting from Treatment of Spontaneous Pneumothorax", A mer. Rev. Resp. Dis., 104, 119. Clagett, O. (1968): "The Management of Spontaneous Pneumothorax ", Editorial. J. Thorac. and Cardiovas. Surg., 55, 76l. Clements, J. A., Brown, E. S., and Johnson, R. P. (1958): "Pulmonary Surface Tension and the Mucus Lining of the Lungs-Some Theoretical Considerations ", J. Appl. Physiol., 12, 262. Coryllos, P. M., and Birnbaum, G. L. (1929): "Circulation in Compressed Atelectatic Pneumonic Lung .. (Pneumothorax - Apneumatosis - Pneumonia), A~ch. Surg., 19, 134. Drinker, C. K. (1954): The Clinical Physiology of the Lungs, C. C. Thomas, Springfield, Illinois, pp. 21-37. Felson, B. (1960): Fundamentals of Chest Roentgenology, W. B. Saunders Co., Philadelphia, p. 52. Fenn, VV. D. (1951): "Mechanics of Respiration' Amer. J. 1vled., 10, 77. Finley, J. N., Hill, T. R, and Bonica, J. J. (1963) : "Effect of Intrapleural Pressure on Pulmonary Shunt Through Atelectatic Dog Lung ", Amer. J. Physiol., 205, 1187. Finley, T. N., Tooley, W. H., Swenson, E. W., Gardner, R E., and Clements, J. A. (1964): "Pulmonary Surface Tension in Experimental Atelectasis ", Amer. Rev. Resp. Dis., 89, 372. Foucat, A. (1875): De la Morte Subite ou Rapide Apres la Thoracocentise, Paris. Gould, D. M., and Torrance, D. J. (1955): "Pulmonary Oedema ", Amer. J. Roentgen, 73, 366. Hartley, P. H-S. (1905): "Albuminous Expectoration Following Paracentesis of the Chest", St. Bartholomew's Hospital Reports, 41, 77. Humphreys, R L., and Berne, A. S. (1970): "Rapid Re-Expansion of Pneumothorax. A Cause of Unilateral Pulmonary Oedema ", Radiology, 96, 509.
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Luisada, A. A., and Cardi, L. (1956): "Acute Pulmonary Oedema; Pathology, Physiology and Clinical :.\Ianagement ", Circulation, 13, 113. Miller, 'vV. C., Toon, R., Palat, H., and Lacroix, J. (1973) : "Experimental Pulmonary Oedema Following Re-Expansion of Pneumothorax", A mer. Rev. Resp. Dis., 108, 664. Neff, T. A. (1\J72): "Unilateral Pulmonary Oedema Resulting from Treatment of Spontaneous Pneumothorax. Correspondence ", Amer. Rev. Resp. Dis., 105, 318. Ortner, N. (18!)!)) : "\Viner Kleinische \Vochenschrift ", 44, 10UO. Reisman, D. (190J): "Albuminous Expectoration Following Thoracentesis ", Amer. f. j[ed. Sci., 123, 620.
Said, S. J., Banerjee, C. M. Harlan, W. K, and Avery, ;\1. E. (lU67): "Pulmonary Oedema as a Cause of Surfactant Deficiency", fap. Heart. j., 8, 742. Tooley, 'vV. H., Discussion of Avery, M. E., and Chernick, V. (IU63): j. Pediat., 63, 763. Trapnell, D. H., and Thurston, J. G. (1970): "Unilateral Pulmonary Oedema After Pleural Aspiration ", Lancet, 1, 1367. \,isscher, :'11. 13., Hadd, F. J., and Stephcns, G. (1056) : "The Physiology and Pharmacology of Lung Oedema ", Pharmacal. Rev., 8, 389. Ziskind, :'11. :'11., WeiIJ, H., and George, K A. (1U65) : " Acute Pulmonary Oedema Following the Treatment of Spontaneous Pneumothorax with Excessi\"(, Negati\'e Intrapleural Pressure ", A Iller. Rev. Resp. Dis., 92, 63J.
Future Meetings 1975 February 14-18, Park City, Utah, u.s.,\: 20th .\nnual .\nesthcsiology· Course. Information: Dept. of Anesthesiology, Uniy. of Utah ;\Iedical Centcr, 50 :\'th :'IIedical Drive, Salt Lake City, Utall, 84[32, U.s..\. March :ll, Crewe, Cheshire, U.K.: Spring ~Ieeting Oustctric .\nacsthetists ,\ssocn. of C.l\:. Information: Dr. 1. :\Iullock, Leighton Hospital, Crewe, Cheshire, U.K. June S l:!, Florence, Italy: Sixth International Cungress of :\'cpllrology. Information: Scient. PH).". Committee-Nephrology llialysis Dept., S. Ursola university Hosp., \'ia Cllassarenti 9, 401:IS Dologna, Italy. Social Prog. CommittceIn'ititute of urology, Univ. of Florence, Viale Peiraccini 18, 50139 Fircnze, Hall'. June, b,t w"ck, Salamanca: V. Spanish Portuguese Congress of .\naesthesiology. For information: Proi'. Dr. :\1. A. Nalda F., Uni\'ersicJ"d de Salamanca, Facultaci de :'IIedicina. Salamanca, Spain. July 7-1~, Qulu: l:!th :\Iceting of the Scandinavian Anaesthesia Society. For information: Dept. of .~naesthesiology, Univ. of Oulu, P.O. Box 240, 90101 Oulu 10, Finland. July 14-18, Johannesburg: South African Congress of ,\nacsthesiology. For information: Dr. J. A. Gcrber, P. O. Box 23660, Johannesburg, South .~frica.
July 20--25, Helsinki, Finland: 6th International Congress of Pharmacology. Information: Secretariat, 6th fnt'l Congress of Pharmacology, Siltavourenpenger 10, SF-00270 Helsinki 17, Finland. August, Copenhagen: 13th Congress of the International Society of Orthopaedic Surgery and Tranmatology. Information: S.I.C.O.T., 43 rue des Champs Elysees, 1050, Bruxelles, Belgique. August 25-29, Quito: XIII. Latinamerican and I. Ecuadorian Congress of Anaesthesiology. Information: Dr. Vigilio Paez, Casilla 237 A, Quito, Ecuador, Latinamerica. September 2-4, Balatonfured, Hungary: 1st Int!. Congress of Anaesthesiology and Reanimation. Information: Office for Conference Organization
of i'-cderation of Hungarian .\ledical Societies (:\lotcsz), 1-[ 1361, l3udapest, 1'013:12, Hungary. Septemuer 10-13, Bremen: 14tll :\Iel'ting of the Austrian, (~ennan and Swiss Societies of Anaesthesiologists. Information: Dr. \V. F. Henschcl, Zentralkrankenhaus St. J iirgen, Stalic, 13remen (FRG). September 1:l, 13radford, Yorks, U.l';:.: Autumn ;\Ieeting Oustetric Anaesthetists Assocn. of C.l\:. information: Dr. J. D. Holdsworth, Dewsbury Postgraduate Medical Centre, General Hospital, DcwslJUry, \V. Yorks, \YFI:l :!LE, G.1\:. Papers by 1st July. September 18-19, Cardiff: .\nnual Scientific Meeting of the .~ssociation of .~nacsthetists of (;reat Britain and ireland. Information: Eoom 475, Tadstock Honse South, Tavistock Square, London WC1H 9HH., England. October 11-15, Chicago: ,\nnual Cllecting of the American Society of Anacsthesiologists. Information: A.S.A.-Headquarters, 5\;3 Busse Highway, Park Ridge, lllinois 60068, U.s.A. October 25-30, Melbourne, Australia: 34th Annual Gencral Meeting of the Australian Society of Anaesthetists. Information: Hon. Fed.· Secretary, A.S.A., P.O. Box 5:l5, Potts Point, N.S.W., 2011, Australia.
1976 April 25 to Cllay 1, :\lcxico: Sixth World Congrcss of Anaesthesiologists. Information: DL G. Vasconcelos, Amsterdam Xo. 14-303, Mexico 11, D. F. :'I16xico. October 9-13, San Francisco: Annual ;\lceting of the American Society of Anaesthesiologists. Information: A.S.A.-Headquarters, 51;, Busse Highway, Park Ridge, Illinois 60068, 1;.S.A.
1977 May, last week, l3ratislava: VIII. International Congress of Anaesthesiology. October liJ-19, New Orleans: Annual ;\Ieeting of the American Society of Anaesthesiologists. Information: A.S.A.-Hcadquartcrs, 515 Busse Highway, Park Ridge, Illinois 60068, C.S.A.
Anaesthesia and Intensive Care, Vol. Ill, No. 1, February, 1975
UNILATERAL PULMONARY OEDEMA FOLLOWING RE-EXPANSION OF PNEUMOTHORAX M.
X.
SHANAHAN,* IAN MONKt AND
H. ].
RrCHARDst
Departments of Cardiothoracic Surgery, St. Vincent's Hospital and Royal North Shore Hospital, Sydney SUMMARY
Unilateral pulmonary oedema is a rare complication in the routine management of spontaneous pneumothorax. Previous reports have emphasized excessive negative intrapleural pressure, rapid re-expansion of the lung and bronchial obstruction as major factors in the pathogenesis. We have encountered four cases, and at least one of these factors have been absent in each case. Review of the literature, and our own experience suggests that the major factor is chronic and total lung collapse resulting in hypoxia and increased alveolar-capillary membrane permeability. Other factors which may be contributory are discussed. INTRODUCTION
Spontaneous pneumothorax is a benign condition under most circumstances, and the treatment is generally uncomplicated. The objectives of treatment are to promote the early re-expansion of the lung, the sealing of an air leak when this is persistent and the production of a pleurodesis if the pneumothorax has been recurrent. These objectives are generally accomplished by the insertion of an intercostal catheter connected to an underwater seal system, and in most cases, to a controlled suction apparatus to ensure full re-expansion of the lung. In some cases with recurrent pneumothorax or persistent air leak, thoracotomy, surgical control of the air leak and gauze abrasion pleurodesis may be necessary (Clagett 1968). On four occasions, the authors have encountered severe unilateral pulmonary oedema occurring as a complication of such treatment in spontaneous pneumothorax. The circumstances of presentation, the initial management and the
* F.R.A.C.S., F.R.C.S., Honorary Cardiothoracic Surgeon, St. Vincent's Hospital. t M.S., F.RC.S., F.RA.C.S., Honorary Surgeon, Royal North Shore Hospital. :j: F.R.C.S., F.RA.C.S., Honorary Surgeon, Royal North Shore Hospital. Address for reprints: Dr. Mark X. Shanahan, 4th Floor, St. Vincent's Medical Centre, 376 Victoria Street, Darlinghurst, N.S.W., 2010, Australia.
mechanisms of re-expansion differed in each case. In no case was excessive negative intrapleural pressure applied, a circumstance which has been implicated in previously reported cases (Ziskind, Weill and George 1965, Childress, Moy and Mottram 1971, Trapnell and Thurston 1970). Case 1 is reported in detail to highlight the extremely severe degree of systemic shock, which can be associated with this complication. Case 2 is the first report in the literature of unilateral pulmonary oedema as a complication of thoracotomy and pleurodesis. Case 3 was the least severe, and was comparable to previous cases reported in the literature, and is not reported in detail. Case 4, the oldest patient so far reported in the literature, was complicated by the development of bronchopneumonia in spite of intermittent positive pressure ventilation, and died on the fifth day. CASE REPORTS
Case 1 B.D., a 20 year old bank officer presented to the emergency department on 19.1. 71. He had experienced a sudden pain in the right anterior chest five days prior to this, and the pain had persisted. For three days, he had been mildly short of breath on exertion, and this also was progressive. A chest X-ray taken on the 19.1.71 showed a total right pneumothorax (Figure 1). The right lung was opaque and completely collapsed. An air bronchogram of
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the right lung was clearly evident. There was no mediastinal shift and the left lung appeared normal. An intercostal catheter, size 20 French, was inserted in the right second intercostal space anteriorly, and was connected to an underwater seal bottle. There was no air leak, and a repeat chest X-ray showed that the lung was still collapsed. The tube was clamped and the patient transferred to the ward where he arrived
ized cyanosis, but the central venous pressure was not raised. The trachea was markedly deviated to the right. There was reduced air entry over the right chest and coarse crepitations were audible over the right side. The left lung was free of crepitations. Blood gas analysis revealed an arterial P0 2 of 50 mmHg, PC0 2 of 32 mmHg, and the pH was 7 ·29 with a base excess of -10. A further chest X-ray revealed an opaque consolidated right lung, with minimal aeration and mediastinal shift to the right (Figure 2). The left lung was hyperinflated but showed no opacification or consolidation. Suction on the chest tube was reduced and maintained at 10 cm of water. During the next hour, expectoration produced 2,000 ml of pink frothy straw-coloured fluid and 1,500 ml of a similar fluid drained via the intercostal
FIGURE I.-A postero-anterior chest film (I !l.l. 71) shows complete collapse of the right lung clue to spontaneous pncmllothorax. .\11 anterior intercostal catheter has been inserted but no suction applied. There is a well-llmrked air bronchogram of all lobes of the lung, excluding the presence of bronchial obstruction.
in no distress. One hour after insertion, the intercostal catheter was connected to a controlled suction unit, set at a negative pressure of 25 cm of water. On the institution of suction, the tube bubbled briefly and then continued to swing with respiration, without any further air leak. Shortly thereafter the patient became distressed and dyspnoeic. Paroxysmal coughing occurred and was productive of 30 ml of straw-coloured frothy fluid every fl'w minutes. He became progressively cyanosed and shocked with gross dyspnoea. Similar straw-coloured fluid drained from the intercostal catheter. The blood pressure fell to 60 mmHg systo\ic, the pulse rose to 160 beats/min and was weak and thready. He was cold and sweaty with general-
2.--An antero-posterior chest fIlm taken two hours after Figure 1. Suction had been applied and shock became evident. There is gross pulmonary oedema of the right lung, with mediastinal shift to the right side, and marked hn)crinfiation of the left lung. FIGURE
catheter. An emergency tracheostomy was performed, and intermittent positive pressure respiration instituted. An intravenous infusion of 5 per cent dextrose in water and serum albumin was maintained, and intravenous hydrocortisone 1,000 mg was also given. In spite of intense resuscitation measures, deterioration continued for six hours. Hypotension,
A naesthesia and IlltCl1sivc Care,
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UNILATERAL PULMONARY OEDEMA
cyanosis and peripheral vasoconstriction continued for 12 hours before improvement began. 100 per cent oxygen was necessary to maintain an arterial P0 2 of 100 mmHg. On 20.1.71 repeat chest X-ray showed persistent opacification of the right lung with a small residual pneumothorax in spite of suction. There was a persistent small air leak, but fluid loss at this time had become minimal Improvement continued slowly (Figure 3) and assisted ventilation was discontinued on the 26.1.71. By 27.1.71 his chest X-ray showed full expansion of his right lung with clearance of the oedema, but there remained a persistent air leak from the intercostal catheter until 5.2.71. On 8.2.71 the intercostal catheter was removed. Three hours later, repeat chest X-ray showed complete collapse of the right lung once again. An intercostal catheter was re inserted but no suction was applied. Thoracotomy was performed on 9.2.71. There was a thin-walled cyst measuring 3 cm in diameter at the apex of the right upper lobe. Apart from some pleural thickening at the site of the initial intercostal catheter, the chest appeared otherwise normal.
21
No lung biopsy was taken. A gauze abrasion pleurodesis was performed, and the chest closed with drainage. Convalescence was thereafter uneventful and he was discharged on 20.2.71 and has remained well since. Case 2 P.L. This 18 year old student presented to another hospital on 6.1.73 with left chest pain and dyspnoea of several days duration. A chest X-ray showed a left pneumothorax with 60 per cent collapse of the lung. A size 28 French Malecot catheter was inserted in the second left intercostal space anteriorly and connected to an underwater seal apparatus. No suction was applied. Chest X-rayon 7.1.73 showed some re-expansion of the lung, but subsequent X-rays on the 8.1.73 and 10.1.73 showed complete collapse of the lung. He was transferred to Royal North Shore Hospital on 11.1.73 and without further interference, thoracotomy was carried out early on 12.1.73. Chest X-ray prior to this procedure showed the lung to be still completely collapsed. Through a limited 6th intercostal space incision, a small
(a) (b) 3.-(a). A portable machine chest film (22.1.71) shows diffuse atelectasis of the right lung following temporary interruption, after three days, of positive pressure ventilation via a tracheostomy tube. This occurred in spite of 10 cm of water negative pressure applied to the intercostal catheter. (b) A later chest film .(24.1.71) after I.P.P.V. had resumed still shows diffuse" ground-glass" opacification, unlike the fluffy opaCIficatIOn of pulmonary oedema. This is presumed to be due to widespread microscopic atelectasis. FIGURE
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cyst at the apex of the upper lobe was ligated, and a gauze abrasion pleurodesis was performed. The lung which was still collapsed, was then manually inflated with positive pressure via the endotracheal tube. After closure of the chest, the patient failed to regain consciousness. He was cyanosed after extubation in spite of apparent good respiratory effort and intranasal oxygen. He was reintubated. Copious pulmonary oedema fluid was then aspirated from the endotracheal tube. He was given frusemide 40 mg and dexamethazone 16 mg by intravenous injection. Ventilation was difficult, even with muscle relaxation. The blood pressure was 70/50 mmHg, and the pulse rate was 104/min. Blood gas analysis showed an arterial P0 2 of 48 mmHg and PC0 2 of 29 mmHg with a base excess +8. Chest X-ray showed unilateral pulmonary oedema of the left lung (Figure 4). Apical and basal pleural drains which were connected to an underwater seal apparatus showed no air leak, and normal respiratory oscillation. Ko negative suction had been applied to the tubes. The patient was
conscious but in respiratory distress one hour later. He continued to improve and was extubated 6 hours after the operative procedure. He had a cough with expectoration of small amounts of pink frothy sputum for several hours after extubation. On admission to the Intensive Care Ward one hour after operation, suction of 20 cm of water was applied to the chest tubes without any worsening of his condition. On 13.1.73 he seemed well and was breathing normally, but blood gas analysis 36 hours after the onset of pulmonary oedema, showed an arterial P0 2 of 72 and PC0 2 of 56 in spite of intranasal oxygen (4l/min). On 14.1.73, radiological clearing of pulmonary oedema had occurred, and the patient thereafter had a normal convalescence and remains well.
Case 3 P.B. This 23 year old long distance runner experienced sudden right-sided chest pain associated with dyspnoea three weeks prior to his admission to St. Vincent's Hospital in 1962. He presented because of increasing disability,
(a) (b) 4.-(a) An antero-postcrior chest film (11.1.73) shows complete collap,e of the left lung. (b) After left thoracotomy a chest film, which has been reversed, shows diffuse oedema of the left lnng. The right lung is hyperinflatcd with mediastinal shift to the left. Positive pressure ventilation via an endotracheal tube was llsed to inflate the collapsed left lung . FIGURE
.. Inaesthesia and Intensive Care, 1',,1. 111, No. /, February, 197.5
UNILATERAL PULMONARY OEDEMA
and his chest X-rayon admission showed complete collapse of the right lung (Figure 5). A readily visible air bronchogram was present, and the patient had no cough or sputum. An intercostal catheter was inserted and connected to an underwater seal system, with 20 cm of water suction. He complained of pain in the chest and developed respiratory distress, which persisted in spite of reduction in the suction to 10 cm of water. Amber coloured fluid drained
23
powder was carried out on the sixth day following his admission. His progress thereafter was satisfactory and he remains well to this time. Case 4 This 84 year old male presented on 26.3.74. He had a two-week history of dyspnoea, cough and purulent sputum. His initial signs were those of pneumonia and responded to parenteral penicillin. Ten days prior to admission he had become more acutely dyspnoeic and breath sounds were noted to be absent over the right chest. No X-ray was taken at that time but on admission it revealed a total right pneumothorax (Figure 7a). An intercostal catheter was inserted and the lung gradually expanded. No suction was applied to the underwater seal apparatus. One hour later the X-ray showed partial opacification of the expanded lung and
FIGURE 5.-A postero-anterior chest film (1962) shows complete collapse of the right lung following a spontaneous pneumothorax.
from the chest tube and he began to expectorate copious white frothy sputum. A further chest X-ray showed extensive unilateral pulmonary oedema on the right side (Figure 6). He was pale and sweaty and the blood pressure fell to 90 mmHg systolic. Suction was discontinued and he was given intravenous Aminophylline and intranasal oxygen with some improvement. He continued to have an air leak from the intercostal catheter and a further chest X-ray showed partial collapse of the consolidated right lung. Suction was therefore recommenced without producing further distress and his condition had returned to normal within 24 hours of the onset of the oedema. Radiological clearing of the oedema was present in four days. Because of a persistent air leak, thoracoscopy and pleurodesis by the instillation of iodised talcum
FIGURE 6.-An antero-posterior chest film. three hours after suction had been applied to an intercostal catheter, shows diffuse patchy oedema of the right lung. The left lung appears normal.
was thought to represent acute pneumonia. Two hours later he had deteriorated further. There was cyanosis, tachycardia, widespread crepitant rales, and a blood pressure of 60 mmHg systolic. X-ray opacification was more widespread (Figure 7b). He was then seen by members of the Thoracic Unit and a diagnosis of unilateral pulmonary oedema was made. The patient was breathing 28 per cent oxygen via a face mask, and blood
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SHANAHAN ET AL.
(a) (b) 7.-(a) A portable chest film (26.3.74) shows collapse of most of the right lung due to a pneumothorax. A bullous cyst of the upper lobe is faintly vi-;ib1e. (b) Two hours later an intercostal catheter has been inserted and rc-expansion of the right lung has taken place, without the use of any negative intrapleural pressure. There is some patchy opacification of the right lower lobe. The left lung is relatively normal for this age group.
FIGURE
gas analysis revealed an arterial P0 2 of 50 mmHg and PC0 2 of 31 mmHg. Oxygen concentration was increased but deterioration continued and Pa0 2 fell to 41 mmHg. Digitalis and diuretics were given. An oral endotracheal tube was inserted and intermittent posltl\'e pressure ventilation with 100 per cent oxygen in:;tituted. Twelve hours after the onset cardiac arrest occurred, at which time the arterial P0 2 was 30 mmHg and pH 7 ·on. Resuscitation was achieved and tracheostomy was performed. Secretions which were frothy became thick and purulent. There was some improvement thereafter but in spite of intensive therapy, deterioration and death occurred on the fifth day. Autopsy showed extensive atelectasis of both lungs (Figure 8), and widespread bronchopneumonia. At no time was suction applied to the intercostal catheter during management. DISCUSSION
Unilateral pulmonary oedema is a rare but serious complication following the treatment of spontaneous pneumothorax. \Ye haye been able to find only fiye preyious reports of this complication. The first of these was Carlson, Classen and Gollan (1959) followed by Ziskind
et al. (19n5), Humphreys and Berne (1970), Trapnell and Thurston (1970) and Childress et al. (1971). The cases reported by these authors are summarized in Table 1. A similar complication was not uncommon early this century when the Potain apparatus, which applied high negative pressure to a needle, was commonly used for the aspiration of pleural fluid (Reisman 190~). In many of these cases the pulmonary oedema was associated with " massiye albuminous expectoration" as occurred in onc of our cases (Case 1). Hartley (190.'1) reported 35 such cases and in 29 of these the onset occurred immediatelv after or within onc hour of the thoracentesis. ;\Iore recent reports were by Cameron (1948) and Luisada and Cardi (1956). The literature on pulmonary oedema and its mechanisms of development, is voluminous and at times controversial and contradictory. Pulmonary oedema is seldom caused by any one single factor, but rather is due to a combination of several factors Adriani ct al. (1967); Yisscher, Hadd and Stephens (1956) and Luisada and Cardi (1956). A single factor may appear to be the underlying cause, but usually it is only the precipitating factor out of several
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UNILATERAL PULMONARY OEDEMA
25
(a) (b) 8.-(a) A chest film, after the onset of more acute respiratory distress, shows widespread oedema of the right lung. Changes in the left lung are still minimal. (b) Four days later, in spite of continued intermittent positive pressure ventilation with oxygen, the chest film (30.3.74) shows widespread opacification of both lungs. Histology showed widespread patchy atelectasis of the right lung and bronchopneumonia of both lungs. FIGURE
additional co-existing factors (Drinker 1954). A particular set of circumstances may precipitate pulmonary oedema on one occasion, but not on another, under seemingly similar circumstances. This generalization is equally applicable to unilateral pulmonary oedema following the treatment of a pneumothorax, as innumerable patients have had re-expansion of a collapsed lung without developing pulmonary oedema. In trying to determine the aetiology of this condition therefore, one must look for a number of factors, not all of which may be present in anyone particular case. Six of the reported cases were young, healthy individuals under 25 years of age, with no evidence of co-existent disease or abnormality. One must therefore assume that the factors producing unilateral pulmonary oedema are related solely to the involved lung, the extent and duration of collapse, and the method of re-expansion. In most of the cases reported in the literature, the lung was completely collapsed on presentation, or became so, before re-expansion was actively produced. In all but one case the collapse had been present for at least three days. In the one exception (Humphreys and Berne 1970) the patient was ill and cachectic, opacifica-
tion of the lung was present on the side of the iatrogenic pneumothorax before re-expansion and the appearances were consistent with pneumonitis which then responded to antibiotic treatment. The first pre-requisite therefore is presumed to be chronic collapse of the lung. This point was stressed by Trapnell and Thurston (1970) who suggested that" if the lung or part of it was compressed and airless for a longer period (1-3 days) and if aspiration of large quantities of air or fluid is then undertaken, oedema will develop ". The development of acute unilateral pulmonary oedema after re-expansion of an induced pneumothorax was studied by Miller et al. (1973) in Rhesus monkeys. When the induced complete pneumothorax was maintained for three days re-expansion by applying suction produced marked acute pulmonary oedema within two hours in all animals. Re-expansion by underwater seal alone in six other animals did not result in pulmonary oedema. When the pneumothorax was maintained for only one hour re-expansion using suction, even at a pressure of -10 cm mercury, did not result in any oedema.
Anaesthesia and Intensive Care, Vol. 111, No. 1, February, 1975
~ ~
TABLE 1
A Summary of relevant Clinical Details of Cases of Cuilateral Pulmonary Oedema Following He-Expansion of Pneumothorax, Previously Described in the l_itcratuyc, Together with Corresponding j)ctails of Cascs Prescnted ill this R~poyt (Shanalian 1974) Author and Year Carlson 1!l59* .. Ziskind 1!l65 Humphrcys 1970 ~
I Age
I
I
;j
=~_. .)
I
!
I!l
1_ COllll:letc
67
I
ti3
1
:'lcthod of Ee- Expansion
Duration of Lung Collapse
Lung Collapse
-1--1--31 Complete
---- ---- I
;:;
'"~
:-;umber of Cases
I
,j
weeks
J
.'i
days
Complete Partial
:? weeks :? hours
I
Degree of Pulmonary Oedema-
Additional Comments
Pump suction
Severe
Consolidation lasted 8 days persistent pneumothorax
with
High negative suction
:\Ioderate dyspnoea
Clearance 111 6 hours. expectoration
Low suction Needle aspiration
Severe with shock X-I{ay evidence only
Clearance in 3 days Patient cachectic. Other factors involved
Pink frothy
,.....
-~---.-----
3-4 :'Ionths
55
S days
No suction
:\fodcrate dyspnoea
18
Complete
± days
High negative suction
Gross with shock
U
Complete
6 days
High negative suction
Severe with shock
X-Ray clearance in 6 days. frothy expectoration
20
comPlcte---1
,j
days
25 cm water suction
Gross with shock
~
18
Complete
4 days
...... ...... .......
:23
Complete
3 weeks
Positi ve pressnre Gcneral anaesthesia 1 Open thoracotom~ ' 20 Cln water suction
Tracheostomy. IPPR. Consolidation lasted 8 days. Massive albnminons expectoration Clearance in :? days
84
Complete
4
56 58
;:,
"......
;::.
1:l days
~.
'"Cl
."'=
Childress I !l71 .. Shanahan 1974 ..
~
a
4
10 days
...... '11
...~
~
S1 ..... -
r
UNILATERAL PULMONARY OEDEMA
27
the application of high negative intrapleural suction, and stated that both these factors appeared to be necessary for the production of the pulmonary oedema. Blockage of the major bronchi by preventing the inflow of air into the alveoli, allows the negative pressure to persist in the alveolar sacs. This increases the gradient between the capillaries and the alveolar sacs and favours the transudation of fluid. Neff (1972) emphasized the importance of an air bronchogram in the collapsed lung, stating that it should be present and that" its absence (1) Negative intrapleural pressure is highly suggestive of an occlusive bronchial It is only in recent years that negative intra- lesion". If "its absence" is the case, he pleural pressure has again come into vogue for recommended that bronchoscopy should be the treatment of spontaneous pneumothorax, performed before significant suction is applied resulting in rapid re-expansion of collapsed lung to the pleural space. Felson (1960) stated that tissue even at relatively low levels of negative " the absence of an air bronchogram is of little suction. However, the occurrence of unilateral significance, since it indicates either that the pulmonary oedema in cases in whom no suction lesion is extrapulmonary, or that it is intrawas applied (Cases 2 and 4) or in whom only low pulmonary but that the bronchi are no longer levels of suction were used to achieve air filled". re-expansion, indicates that it is not so much In two of our cases, excellent air bronchograms the level of negative pressure (Ziskind et al. were present in the collapsed lung excluding 1965, Fenn 1951) but the rate of re-expansion significant bronchial obstruction. In the third which is critical (Humphreys and Berne 1970). case, tenacious sputum was first aspirated Ziskind et al. (1965) pointed out that if high before pink frothy fluid was obtained. This negative pressure is applied to the great veins patient had clinical evidence of respiratory tract and pulmonary vascular bed, the pulmonary infection and a productive cough prior to arterial inflow is greatly increased and over- thoracotomy. However, his lung was expanded filling of arteries and capillaries occurs. by positive endobronchial pressure during anaesHumphreys and Berne (1970) quoted experi- thesia and oedema occurred before any negative mental work of Barach, Martin and Eckman pressure was applied to the pleural cavity. In (1938) which demonstrated that expansion of a four of the cases which have been reported the lung in a negative pressure chamber results in free expectoration of large amounts of oedema rapid increase in pulmonary capillary pressure fluid would appear to exclude significant and flow. This rapid return of pulmonary obstruction of the bronchi to the affected lung blood flow at a high pressure may result in fluid tissue. transudation across the capillary and alveolar In experimental studies in which the clinical membranes, as well as the accummulation of phenomenon of unilateral pulmonary oedema interstitial oedema fluid. This oedema can be was reproduced, Carlson et al. (1959) and Miller reduced by the use of positive pressure ventila- et al. (1973) were unable to demonstrate any bronchial obstruction, either grossly or on tion. histological examination. Re-collapse of the (2) Airway obstruction lung which did occur in some animals was An open bronchial system in the presence of related to intra-alveolar blockage producing negative pressure should not under normal diffuse microscopic atelectasis and was a self circumstances allow an abnormal pressure limiting phenomenon which resolved in five to gradient to develop between the pulmonary seven days, and for which bronchoscopy was not capillaries and the alveolar space, as the rapid indicated. This is discussed later in relation to influx of air into the alveoli causes instant re- changes in alveolar surfactant. expansion of the lung and consequent obliteration of the pleural space. This is what (3) Increased alveolar-capillary membrane permeprobably occurs in the majority of cases where ability no pulmonary oedema occurs. In a general discussion of factors which may Childress et al. (1971) stressed the significance contribute to the development of pulmonary of blockage of the bronchus, in combination with oedema, Luisada and Cardi (1956) stressed the
Other factors which existed in these cases and which may have been contributory are listed and discussed below: (1) Negative intrapleural pressure. (2) Airway obstruction. (3) Increased alveolar-capillary membrane permeability. (4) Loss of tissue surfactant. (5) Fluid shift from periphery to pulmonary vascular bed due to peripheral vasoconstriction, or increased venous return.
Anaesthesia and Intensive Care, Vol. 111, No. 1, February, 1975
28
M. X.
SHANAHAN ET AL.
importance of increased permeability of the pulmonary capillaries. Among the many factors which may favour this, they mentioned tissue hypoxia. Drinker (1954) strongly emphasized the importance of " anoxia" as a contributing factor in the formation and persistence of pulmonary oedema. In the earliest known reports of unilateral pulmonary oedema Foucart (1875) and Ortner (1899) postulated that the mechanism was the presence of chronic " anoxia" of the endothelial cells of the pulmonary capillaries secondary to compression collapse of the lung by pleural fluid. Reisman (1902), Cameron (1948) and Humphreys and Berne (1\)70) referred to this mechanism in explaining the development of unilateral oedema. That hypoxic damage to alveolar capillaries does occur in association with chronic atelectasis was demonstrated by Coryllos and Birnbaum (1929). They studied the short-term effect of ligation of the bronchus in the dog, and concluded that the blood flow into the lung was reduced in proportion to the degree of lung collapse. They stated that the obstruction to blood liO\y took place at the capillary level, and they demonstrated disintegration of the capillarie,; after several days, followed by the formation of hyaline membranes within the alveoli after some weeks. Tooley (19(;3) also measured Jlulmonary blood flow following bronchus ligation and found that the flow fell essentially to zero in 12 to 24 hours following the bronchus ligation. It may be concluded that collapse of the lung, of Illore than one day duration, produces a direct hypoxic effect on the pulmonary capillary membrane, increasing capillary permeability and hence contributing to the leakage of oedema fluid when re-expansion occurs. The se\'erity of the oedema is related to the degree of hypoxic damage as well as to other factors already discussed, particularly negative intrapleural pressure. (4) Loss of tisslle surfactant Studies on pulmonary surface tension in experimental atelectasis have been reported by Avery and Chernick (1963) and Finley et al. (19G4). The concept that the alveoli are lined and stabilized by a substance, the surface tension of which ~·aries as the alveolar volume and surface area, was first proposed by Clements, Brown and Jolmson (UJ58). This substance, now clearly defined, is called surfactant. Avery reported (hat an increase in surface tension of lung extracts occurred in the collapsed lung
only after more than 24 hours of induced pneumothorax. Studies in Vil'O showed that rapid expansion resulted firstly in oedema and then further atelectasis, with recovery taking place, as early as two hours in some, and much longer in others. On the other hand, control lungs kept airless under refrigeration for up to one week, had normal surface tension characteristics. These and other studies in both rabbits and mice suggest that airlessness per se is not the cause of the alterations in surface tension in collapsed lungs, but that it is the associated ischaemia which mediates the change. Finley et al. (1964) studied the effects of pulmonary artery occlusion and showed an earlier increase in the surface tension of the lung followed by atelectasis after an interval of 24 hours. Clearly the rise in surface tension, or the loss of surfactant, is due to a reduction in pulmonary blood flow which was shown by Tooley (l!Hi3) to be a sequel to atelectasis. Loss of tissue surfactant has also been shown to occur as a result of pulmonary oedema (Said et al. 1967). It is therefore unlikely that loss of surfactant is related to the deVelopment of the unilateral oedema after re-expansion of pneumothorax, but it is likely to be responsible for the phenomenon of recollapse of the lung, due to diffuse microscopic atelectasis, which was stressed by Carlson (1 H5B) and which was such an outstanding feature of our Cases 1 and 4 (Figures ;{ and R). (5)
Fluid shift from periphery to plllmonary 7'asclllar bed due to peripheral vasoconstriction or increased venous return. An increased venous return and pulmonary arterial inflow certainly occurs in those cases in whom a sudden negative pressure is applied to the pleural cavity (Ziskind et al. 19(i5, Barach et al. 1938) and this would contribute to the severity of the pulmonary oedema when other factors were co-existent to initiate its development. However, there seems little likelihood that an increased pulmonary inflow alone could initiate oedema. Peripheral vasoconstriction has not been noted prior to the onset of the oedema in any reported cases. However, in severe cases the oedema mav be associated with a fall in blood pressure and shock and peripheral vasoconstriction can then become marked. It is likely that such a state of shock perpetuates the oedema in the affected lung by virtue of resultant fluid shift and generalized hypoxia (Gould 1955). If fluid shift were a major primary factor however, one would expect both lungs to be involved, even if not equally.
Anaesthesia and Intensive Care, Vol. Ill, No. 1. February, 1975
29
UNILATERAL PULMONARY OEDEMA COMMENT
The radiological demonstration of an airless and collapsed lung does not constitute an emergency situation unless there is associated evidence of tension or bleeding within the pleural cavity. Therefore re-expansion of the lung can be allowed to occur gradually after the introduction into the pleural cavity of an intercostal catheter connected to a valve or an underwater seal apparatus (Trapnell and Thurston 1970). There is no indication, other than that of expediency, to apply negative suction to the pleural cavity unless a persistent air leak prevents full re-expansion of the lung. If full re-expansion does not occur in the absence of a persistent air leak, then bronchoscopy and aspiration of secretions may be necessary to exclude or treat retained or tenacious sputum. If chronic collapse of the lung is suspected then the application of negative intrapleural pressure to the intercostal catheter should be deferred for several hours and reexpansion encouraged by coughing and physiotherapy. In some cases of prolonged collapse, such as Case 4 in whom oedema developed without any suction, gradual staged reexpansion, allowing a small amount of pleural air to be expressed at half-hourly intervals, may be advisable. Successful intercostal catheter suction depends upon the volume of air beinG withdrawn from the pleural space exceeding the volume being drawn through the pulmonary defect. As long as this relationship is maintained the lung should re-expand and fill the pleural space. This need not occur rapidly but if an air leak is present some suction is essential. If the air leak is such that re-expansion will not occur with a negative pleural pressure of 25 cm water, then surgical closure of the pulmonary defect is indicated. CONCLUSION
Unilateral pulmonary oedema after reexpansion of a chronic complete pneumothorax is now a well documented clinical entity. Persistence of complete collapse of some lung tissue for several days is an essential pre-requisite for its development. Two deaths, one in a previously healthy young male, and several instances of severe systemic shock have occurred in association with this complication. It is therefore essential that the factors be recognized and the development of unilateral pulmonary oedema prevented. Large amounts of air should never be rapidly removed, and negative
pressure should be avoided during re-expansion whenever possible. If unilateral pulmonary oedema does occur most cases will respond to the usual treatment for pulmonary oedema, but severe cases may require intubation and intermittent positive pressure ventilation with high concentrations of oxygen, to overcome systemic hypoxaemia. REFERENCES
Adriani, J., Zepernick, R, Harwon, W., and Hiern, B. (1967): "Iatrogenic Pulmonary Oedema in Surgical Patients ", Surgery, 61, 183. Avery, M. E., and Chernick, V. (1963): "Alterations of the Alveolar Lining Layer in Rabbits ", J. Pediat., 63, 762. Barach, A. L., Martin, J., and Eckman, M. (1938): " Positive Pressure Respiration and its Application to the Treatment of Acute Pulmonary Oedema", Ann. Intern. Med., 12, 754. Cameron, G. R (1948): "Pulmonary Oedema (Sydney Ringer Memorial Lecture) ", Brit. Med. J., I, 965. Carlson, H.. 1., Classen, K. L., Gollan, F. (1959): "Pulmonary Oedema Following the Rapid ReExpansion of a Totally Collapsed Lung Due to a Pneumothorax; A Clinical and Experimental Study", Surg. Forum, 9, 367. Childress, M. E., Moy, G., and Mottram, M. (1971) : "Unilateral Pulmonary Oedema Resulting from Treatment of Spontaneous Pneumothorax", A mer. Rev. Resp. Dis., 104, 119. Clagett, O. (1968): "The Management of Spontaneous Pneumothorax ", Editorial. J. Thorac. and Cardiovas. Surg., 55, 76l. Clements, J. A., Brown, E. S., and Johnson, R. P. (1958): "Pulmonary Surface Tension and the Mucus Lining of the Lungs-Some Theoretical Considerations ", J. Appl. Physiol., 12, 262. Coryllos, P. M., and Birnbaum, G. L. (1929): "Circulation in Compressed Atelectatic Pneumonic Lung .. (Pneumothorax - Apneumatosis - Pneumonia), A~ch. Surg., 19, 134. Drinker, C. K. (1954): The Clinical Physiology of the Lungs, C. C. Thomas, Springfield, Illinois, pp. 21-37. Felson, B. (1960): Fundamentals of Chest Roentgenology, W. B. Saunders Co., Philadelphia, p. 52. Fenn, VV. D. (1951): "Mechanics of Respiration' Amer. J. 1vled., 10, 77. Finley, J. N., Hill, T. R, and Bonica, J. J. (1963) : "Effect of Intrapleural Pressure on Pulmonary Shunt Through Atelectatic Dog Lung ", Amer. J. Physiol., 205, 1187. Finley, T. N., Tooley, W. H., Swenson, E. W., Gardner, R E., and Clements, J. A. (1964): "Pulmonary Surface Tension in Experimental Atelectasis ", Amer. Rev. Resp. Dis., 89, 372. Foucat, A. (1875): De la Morte Subite ou Rapide Apres la Thoracocentise, Paris. Gould, D. M., and Torrance, D. J. (1955): "Pulmonary Oedema ", Amer. J. Roentgen, 73, 366. Hartley, P. H-S. (1905): "Albuminous Expectoration Following Paracentesis of the Chest", St. Bartholomew's Hospital Reports, 41, 77. Humphreys, R L., and Berne, A. S. (1970): "Rapid Re-Expansion of Pneumothorax. A Cause of Unilateral Pulmonary Oedema ", Radiology, 96, 509.
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M. X.
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Luisada, A. A., and Cardi, L. (1956): "Acute Pulmonary Oedema; Pathology, Physiology and Clinical :.\Ianagement ", Circulation, 13, 113. Miller, 'vV. C., Toon, R., Palat, H., and Lacroix, J. (1973) : "Experimental Pulmonary Oedema Following Re-Expansion of Pneumothorax", A mer. Rev. Resp. Dis., 108, 664. Neff, T. A. (1\J72): "Unilateral Pulmonary Oedema Resulting from Treatment of Spontaneous Pneumothorax. Correspondence ", Amer. Rev. Resp. Dis., 105, 318. Ortner, N. (18!)!)) : "\Viner Kleinische \Vochenschrift ", 44, 10UO. Reisman, D. (190J): "Albuminous Expectoration Following Thoracentesis ", Amer. f. j[ed. Sci., 123, 620.
Said, S. J., Banerjee, C. M. Harlan, W. K, and Avery, ;\1. E. (lU67): "Pulmonary Oedema as a Cause of Surfactant Deficiency", fap. Heart. j., 8, 742. Tooley, 'vV. H., Discussion of Avery, M. E., and Chernick, V. (IU63): j. Pediat., 63, 763. Trapnell, D. H., and Thurston, J. G. (1970): "Unilateral Pulmonary Oedema After Pleural Aspiration ", Lancet, 1, 1367. \,isscher, :'11. 13., Hadd, F. J., and Stephcns, G. (1056) : "The Physiology and Pharmacology of Lung Oedema ", Pharmacal. Rev., 8, 389. Ziskind, :'11. :'11., WeiIJ, H., and George, K A. (1U65) : " Acute Pulmonary Oedema Following the Treatment of Spontaneous Pneumothorax with Excessi\"(, Negati\'e Intrapleural Pressure ", A Iller. Rev. Resp. Dis., 92, 63J.
Future Meetings 1975 February 14-18, Park City, Utah, u.s.,\: 20th .\nnual .\nesthcsiology· Course. Information: Dept. of Anesthesiology, Uniy. of Utah ;\Iedical Centcr, 50 :\'th :'IIedical Drive, Salt Lake City, Utall, 84[32, U.s..\. March :ll, Crewe, Cheshire, U.K.: Spring ~Ieeting Oustctric .\nacsthetists ,\ssocn. of C.l\:. Information: Dr. 1. :\Iullock, Leighton Hospital, Crewe, Cheshire, U.K. June S l:!, Florence, Italy: Sixth International Cungress of :\'cpllrology. Information: Scient. PH).". Committee-Nephrology llialysis Dept., S. Ursola university Hosp., \'ia Cllassarenti 9, 401:IS Dologna, Italy. Social Prog. CommittceIn'ititute of urology, Univ. of Florence, Viale Peiraccini 18, 50139 Fircnze, Hall'. June, b,t w"ck, Salamanca: V. Spanish Portuguese Congress of .\naesthesiology. For information: Proi'. Dr. :\1. A. Nalda F., Uni\'ersicJ"d de Salamanca, Facultaci de :'IIedicina. Salamanca, Spain. July 7-1~, Qulu: l:!th :\Iceting of the Scandinavian Anaesthesia Society. For information: Dept. of .~naesthesiology, Univ. of Oulu, P.O. Box 240, 90101 Oulu 10, Finland. July 14-18, Johannesburg: South African Congress of ,\nacsthesiology. For information: Dr. J. A. Gcrber, P. O. Box 23660, Johannesburg, South .~frica.
July 20--25, Helsinki, Finland: 6th International Congress of Pharmacology. Information: Secretariat, 6th fnt'l Congress of Pharmacology, Siltavourenpenger 10, SF-00270 Helsinki 17, Finland. August, Copenhagen: 13th Congress of the International Society of Orthopaedic Surgery and Tranmatology. Information: S.I.C.O.T., 43 rue des Champs Elysees, 1050, Bruxelles, Belgique. August 25-29, Quito: XIII. Latinamerican and I. Ecuadorian Congress of Anaesthesiology. Information: Dr. Vigilio Paez, Casilla 237 A, Quito, Ecuador, Latinamerica. September 2-4, Balatonfured, Hungary: 1st Int!. Congress of Anaesthesiology and Reanimation. Information: Office for Conference Organization
of i'-cderation of Hungarian .\ledical Societies (:\lotcsz), 1-[ 1361, l3udapest, 1'013:12, Hungary. Septemuer 10-13, Bremen: 14tll :\Iel'ting of the Austrian, (~ennan and Swiss Societies of Anaesthesiologists. Information: Dr. \V. F. Henschcl, Zentralkrankenhaus St. J iirgen, Stalic, 13remen (FRG). September 1:l, 13radford, Yorks, U.l';:.: Autumn ;\Ieeting Oustetric Anaesthetists Assocn. of C.l\:. information: Dr. J. D. Holdsworth, Dewsbury Postgraduate Medical Centre, General Hospital, DcwslJUry, \V. Yorks, \YFI:l :!LE, G.1\:. Papers by 1st July. September 18-19, Cardiff: .\nnual Scientific Meeting of the .~ssociation of .~nacsthetists of (;reat Britain and ireland. Information: Eoom 475, Tadstock Honse South, Tavistock Square, London WC1H 9HH., England. October 11-15, Chicago: ,\nnual Cllecting of the American Society of Anacsthesiologists. Information: A.S.A.-Headquarters, 5\;3 Busse Highway, Park Ridge, lllinois 60068, U.s.A. October 25-30, Melbourne, Australia: 34th Annual Gencral Meeting of the Australian Society of Anaesthetists. Information: Hon. Fed.· Secretary, A.S.A., P.O. Box 5:l5, Potts Point, N.S.W., 2011, Australia.
1976 April 25 to Cllay 1, :\lcxico: Sixth World Congrcss of Anaesthesiologists. Information: DL G. Vasconcelos, Amsterdam Xo. 14-303, Mexico 11, D. F. :'I16xico. October 9-13, San Francisco: Annual ;\lceting of the American Society of Anaesthesiologists. Information: A.S.A.-Headquarters, 51;, Busse Highway, Park Ridge, Illinois 60068, 1;.S.A.
1977 May, last week, l3ratislava: VIII. International Congress of Anaesthesiology. October liJ-19, New Orleans: Annual ;\Ieeting of the American Society of Anaesthesiologists. Information: A.S.A.-Hcadquartcrs, 515 Busse Highway, Park Ridge, Illinois 60068, C.S.A.
Anaesthesia and Intensive Care, Vol. Ill, No. 1, February, 1975
