re-expansion pulmonary oedema - thorax · re-expansion pulmonary oedema fig. 1. case 1....

Thorax (1975), 30, 54.

Re-expansion pulmonary oedemaM. WAQARUDDIN and A. BERNSTEIN

Department of Thoracic Medicine, Hope and Ladywell Hospitals, Salford M6 8HD

Waqaruddin, M. and Bernstein, A. (1975). Thorax, 30, 54-60. Re-expansionpulmonary oedema. Clinical details are given of two patients who developed ipsilateralpulmonary oedema following re-expansion of their spontaneous pneumothoraces byintercostal drainage of air. The possible mechanisms underlying the oedema are

discussed, and prior literature is analysed. Reference is made particularly to its pre-

dictability and to precautions recommended to minimize the frequency of this potentiallyfatal complication in the management of spontaneous pneumothorax.

CASE REPORTS

CASE 1. A 21-year-old man was admitted toLadywell Hospital on 13 February 1973. Fiveweeks prior to admission he had had an influenza-like illness associated with cough, sputum pro-duction, and dyspnoea. His general conditionimproved after one week, but his dyspnoeapersisted and became gradually worse on exertion.There was no history of chest pain nor any pasthistory of chest disease.On examination he was comfortable at rest.

The heart rate was regular at 80 beats per minute,and blood pressure 130/80 mmHg. The physicalsigns suggested left-sided pneumothorax, and achest radiograph confirmed this, showing com-plete left-sided pulmonary collapse with somemediastinal shift towards the right side (Fig. 1).On the following day an intercostal tube wasinserted in the second left intercostal spaceanteriorly on the left side and a Heimlich valvewas attached to the distal end of the catheter. Animmediate egress of air through the valve wasobserved. Within minutes the patient had a boutof severe coughing productive of small amountsof clear sputum. His cough persisted, and althoughthere was no deterioration in his general con-dition, his sputum showed a pink discolourationwithin ten minutes. Examination at this stagerevealed fine crepitations audible over the leftmiddle and lower chest. An anteroposterior chestradiograph taken one hour after intubationshowed almost complete expansion of the leftlung but with an homogenous infiltration involv-ing the left middle and lower zones (Fig. 2).Within two hours of intubation he appeared paleand anxious with tachypnoea, sweating, and a

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tachycardia of 100 beats per minute. His bloodpressure fell to 90/60 mmHg. A pink serous fluidwas seen to be draining from the intercostal tubeand this was therefore reconnected to an under-water seal system because of the possibility ofblockage of the Heimlich valve cusps. His generalcondition improved spontaneously over the next24 hours, and during this period about one litreof serous fluid drained into the underwater sealbottle. Serial chest radiographs over the follow-ing five days showed clearing of the pulmonaryinfiltration. Within six days his radiograph re-turned to normal (Fig. 3) and the intercostal tubewas removed on the seventh day. Full expansionwas maintained thereafter. He was discharged on2 March 1973 and has subsequently remainedsymptom-free.

CASE 2. A 24-year-old man was admitted toLadywell Hospital on 28 August 1973. Three daysprior to his admission he developed left-sided chestpain of sudden onset accompanied by dyspnoea.There was no previous history of chest disease.On examination he was dyspnoeic at rest. He

had signs suggesting a left-sided pneumothorax,and a chest radiograph confirmed this, showingalmost complete pulmonary collapse with somemediastinal shift towards the right side (Fig. 4).An intercostal tube was inserted in the fifth leftintercostal space in the anterior axillary line, anda Heimlich valve was attached to the distal endof the catheter. An immediate egress of airthrough the valve was observed. The patient'sdyspnoea was considerably relieved, but withinthree hours crepitations were audible over theleft lung posteriorly, and an anteroposterior chest

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Re-expansion pulmonary oedema

FIG. 1. Case 1. Posteroanterior chest radiograph prior tointubation.

radiograph taken at this time showed a fullyexpanded left lung, though with diffuse shadowingthroughout the whole lung field, excluding onlythe apical region (Fig. 5).

Serous fluid was seen draining from the inter-costal tube, and therefore the drainage systemwas changed to an underwater seal system. Thepatient's condition did not deteriorate at anytime, and by the fifth day there was completeradiological clearing of the left lung. Extubationwas performed and the lung remained fullyexpanded (Fig. 6). He was discharged on 4September 1973.He was re-admitted to another hospital on

26 September 1973 with a further complete left-sided pneumothorax. Intercostal drainage tounderwater seal was carried out, and althoughsatisfactory expansion was achieved, initial chest

radiographs showed pulmonary infiltration, whichagain spontaneously resolved.

DISCUSSION

The earliest accounts of pulmonary oedemaoccurring in a re-expanded lung are those ofFoucart in 1875 and Ortner in 1899-both citedby Carlson et al. (1959)-and of Riesman (1902).The oedema followed aspiration of large volumesof pleural fluid. In 1906 Hartley reported 35similar cases all occurring within one hour ofthoracocentesis.

Carlson et al. (1959) first reported this complica-tion following re-expansion of the collapsed lungdue to pneumothorax, and since then 11 furthercases including the present report have beendescribed (see Table).

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M. Waqaruddin and A. Bernstein

FIG. 2. Case 1. A nteroposterior chest radiograph one hour afterintubation.

Early evidence of pulmonary oedema may bethe occurrence of cough and chest tightness dur-ing or immediately after aspiration of air(Trapnell and Thurston, 1970), as happened incase 2, and in cases described by Childress, Moy,and Mottram (1971), Ratcliff et al. (1973), andSaini (1974). It is generally agreed that oedemais more likely to occur as a complication of largepneumothoraces and where collapse has beenprolonged for a period of at least three days(Trapnell and Thurston, 1970; Sautter et al.,1971). In the 12 cases recorded, the duration ofpneumothorax (from onset of dyspnoea) averaged18 days with a minimum of three days, apartfrom one patient (Humphreys and Berne, 1970)with metastatic carcinoma in whom the pneumo-thorax apparently complicated an attempt to placea central venous pressure catheter percutaneously,and which was re-expanded within one hour ofthis accident.The fact that negative pressure was applied to

the pleural cavity in no less than five of the 12cases reported suggests that the rapidity withwhich air is removed from the pleural cavity is asecond predetermining factor.

Miller et al. (1973) emphasize both these pointsin their experiments on Rhesus monkeys. Theyfound ipsilateral pulmonary oedema within twohours in all monkeys with induced 80 to 100%pneumothoraces where the pneumothorax hadbeen maintained for three days and where rapidre-expansion was obtained by applying suction of-10 cmHg. In contrast to these, pulmonaryoedema did not develop in two other groups ofmonkeys:

(a) where underwater drainage alone was ap-plied after three days' collapse, and

(b) when the lung was re-expanded after onehour with the application of negative pressure tothe intrapleural cavity.There have been several theories as to the

pathogenesis of the oedema; all are conjectural,

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FIG. 3. Case 1. Posteroanterior chest radiograph. Post-extubationfilm.

and it is probable that all are, to some extent,involved. It is possible, as suggested by Carlsonet al. (1959) and Humphreys and Berne (1970),that anoxic damage to the pulmonary capillaryendothelial cells during collapse is followed byincreased permeability of these capillaries to fluidafter expansion of the lung and restoration of thepulmonary circulation. There is certainly evidencethat capillaries deprived of oxygen for threeminutes show an increased permeability to protein(Barach, Martin, and Eckman, 1938).A second explanation, possibly acting in con-

cert with anoxic capillary damage, is the effect onthese capillaries of a sudden and large increase innegative intrapleural pressure which occurs withrapid pulmonary expansion, especially with theaid of suction applied to the pleural cavity.Warren, Peterson, and Drinker (1942) demon-strated in dogs that a large increase in negativeintrathoracic pressure drew fluid from pulmonary

capillaries into parenchyma, and, under excessiveconditions, not only plasma but red cells left thecapillaries. Robin, Cross, and Zelis (1973), intheir comprehensive review of pulmonary oedema,also drew attention to this factor.

Finally there is the inevitable consideration ofthe effect of alteration of surface tension. Severalauthors (Trapnell and Thurston, 1970; Sautteret al., 1971) suggest that decrease of surfactantin the chronically collapsed lung, with a conse-quent rise in alveolar surface tension, may be acontributory factor. However, it has been shownthat pulmonary oedema is not usually associatedwith abnormally high alveolar surface tensionforces, and that oedema can develop in a degassedlobe without an air-liquid interface (Robin et al.,1973).With respect to technique, we originally were

concerned that the use of the Heimlich valve(Bernstein, Waqaruddin, and Shah, 1973) may

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FIG. 4. Case 2. Anteroposterior chest radiograph prior to intubation.

have been a causative factor in the production ofoedema because of the rate of egress of air usingthis method. This fear appears to be obviated bythe recurrence of ipsilateral oedema in case 2during his second admission when the pneumo-thorax was drained to an underwater seal. Thereis the possibility that, for some reason, this patientmay have been prone to develop pulmonaryoedema. The other lung, however, showed noradiological abnormality; plasma proteins werenormal, and examination of the heart and electro-cardiogram were also normal. Further lungfunction tests were not performed.Whatever the mechanisms involved, it seems

that the development of pulmonary oedema is arelatively benign complication, although twofatalities and one near fatality have been re-corded. The case of Trapnell and Thurston (1970)was an 18-year-old boy with impaired intelligencewho exhibited a number of congenital abnor-malities, including webbing of the toes and pigeonchest. Following a three-day history of chest painand dyspnoea he was found to have a left-sidedpneumothorax with complete collapse of the

lung. Underwater drainage failed to produceexpansion, and suction was applied with a Robertspump. Severe pulmonary oedema developed inthe left lung within four hours. In spite of in-tensive therapy he died about seven hours afterthoracocentesis.

Sautter et al. (1971) gave details of a 69-year-old man with a large right-sided pneumothoraxof 21 days' duration. He had a past history ofhypertension and aortic incompetence with manyepisodes of left ventricular failure. The lung ex-panded satisfactorily following drainage, butwithin one hour he was found to be severely dis-tressed and cyanosed. Unilateral pulmonaryoedema was demonstrated radiologically, anddeath occurred 24 hours later despite intensiveresuscitative measures.The patient described by Ratcliff et al. (1973)

survived only with the help of intensive therapy,including mechanical ventilation with positiveend-expired pressure.Pulmonary oedema occurs more commonly

than the dearth of reports would appear to indi-cate. The three episodes described occurred over

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FIG. 5. Case 2. A nteroposterior chestradiograph three hours afterintubation.

FIG. 6. Case 2. A nteroposterior chestradiograph. Post-extubation film.

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TABLE

Author/Year No. of Patients Duration' Suction Outcome

Carlson et al. 1 2 5 weeks + Recovered(1959)

Ziskind et al. 1 3 days + Recovered(1965)ReordHumphreys and Berne 2 2 weeks Recovered(1970) 1 hour Recovered

Trapnell and Thurston 2 8 days Recovered(1970) 3 days ± Died

Childress et al. 1 6 days + Recovered(1971)

DeSautter et al. 1 81 days Died(1971)

Ratcliff et al. 1 3 days + Recovered(1973)

Saini (1974) 1 7 days _ RecoveredWaqaruddin and Bernstein 2 5 weeks Recovered

(present report) 3 days _ Recovered

'Duration of symptoms prior to intubation.'Five cases mentioned, only one described in detail.

a period extending from April 1971 to May 1974,during which time we have actively treated atotal of 34 pneumothoraces, using a Heimlichvalve in 25 of these. It would, therefore, seemlogical to suggest frequent and careful clinicalobservation for at least the first four hours afterintubation in those patients with large pneumo-thoraces present for more than three days. Apost-intubation radiograph taken within two tofour hours is recommended, especially if theapplication of suction is considered necessary.

It may well be worth while controlling theremoval of air by means of a gate clamp appliedproximally to the underwater bottle or, if aHeimlich valve is used, attached to a tubeconnected to the distal end of the valve.

REFERENCES

Barach, A. L., Martin, J., and Eckman, H. (1938).Positive pressure respiration and its applicationto the treatment of acute pulmonary edema.Annals of Internal Medicine, 12, 754.

Bernstein, A., Waqaruddin, M., and Shah, M. (1973).Management of spontaneous penumothorax usinga Heimlich flutter valve. Thorax, 28, 386.

Carlson, R. I., Klassen, K. L., Gollan, F., Gobbel,W. G. Jr., Sherman, D. E., and Christensen,R. 0. (1959). Pulmonary oedema following therapid re-expansion of a totally collapsed lung dueto a pneumothorax: a clinical and experimentalstudy. Surgical Forum, 9, 367.

Childress, M. E., Moy, G., and Mottram, M. (1971).Unilateral pulmonary edema resulting from treat-ment of spontaneous pneumothorax. AmericanReview of Respiratory Disease, 104, 119.

Hartley, P. H-S. (1906). Albuminous expectorationfollowing paracentesis of the chest. St.Bartholomew's Hospital Reports, 41, 77.

Humphreys, R. L. and Berne, A. S. (1970). Rapid

re-expansion of pneumothorax. Radiology, 96,509.

Miller, W. C., Toon, R., Palat, H., and Lacroix, J.(1973). Experimental pulmonary edema followingre-expansion of pneumothorax. American Reviewof Respiratory Disease, 108, 654.

Ratcliff, J. L., Chavez, C. M., Jamchuk, A., Forestner,J. E., and Conn, J. H. (1973). Re-expansionpulmonary edema. Chest, 64, 654.

Riesman, D. (1902). Albuminous expectoration follow-ing thoracentesis. A merican Journal of MedicalScience, 123, 620.

Robin, E. D., Cross, C. E., and Zelis, R. (1973).Pulmonary edema. The New England Journalof Medicine, 288, 239 and 292.

Saini, G. S. (1974). Unilateral pulmonary oedemaafter drainage of spontaneous pneumothorax.British Medical Journal, 1, 615.

Sautter, R. D., Dreher, W. H., MacIndoe, J. H.,Myers, W. O., and Magnin, G. E. (1971). Fatalpulmonary edema and pneumonitis after re-expansion of chronic pneumothorax. Chest, 60,399.

Trapnell, D. H. and Thurston, J. G. B. (1970).Unilateral pulmonary oedema after pleuralaspiration. Lancet, 1, 1367.

Warren, M. F., Peterson, D. K., and Drinker, C. K.(1942). The effects of heightened negativepressure in the chest, together with further ex-periments upon anoxia in increasing the flow oflung lymph. American Journal of Physiology,137, 641.

Ziskind, M. M., Weill, H., and George, R. A. (1965).Acute pulmonary edema following the treatmentof spontaneous pneumothorax with excessivenegative intrapleural pressure. American Reviewof Respiratory Diseases, 92, 632.

Requests for reprints to: Dr. A. Bernstein, Depart-ment of Thoracic Medicine, Hope and LadywellHospitals, Salford M6 8HD.

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