Postoperative pulmonary atelectasis

POSTOPERATIVE PULMONARY ATELECTASIS W. Associate

E.

ADAMS, M.D.

Professor of Surgery, CHICAGO,

A

LTHOUGH a century has passed since its first recognition and experimentaI production, puImonary ateIectasis stiI1 constitutes the most common puImonary complication foIIowing intraabdomina1 operations. RinkG1 (1938) recentIy stated that from a series of reported cases, puImonary compIications occurred in 14 per cent of the abdomina1 operations and in onIy about I per cent of nonabdomina1 operations, and that the Iatter as a ruIe were other than puImonary atejectasis. These statistics are in accord with those of King38 (1933) who reported an incidence of 14.3 per cent for the abdomina1 group and 1.2 per cent for a11 others. The importance of ateIectasis is more appreciated when its reIationship to postoperative pneumonia is considered. It is now an estabIished fact, based on experimenta and cIinica1 evidence, that unIess effective earIy treatment is instituted postoperative ateIectasis is IikeIy to deveIop into pneumonia. The proof of this statement wiI1 be presented Iater in the discussion deaIing with pathoIogic physioIogy. The term, ateIectasis, is derived from two Greek words, “ateIes,” meaning imperfect, and “ ektasis,” meaning expansion. It was first applied by Jorg3j*16 in 1832, on ideas gained from his father, to a condition of the Iungs observed in newborn infants after death. It was not recognized as a (puImonary) compIication foIIowing abdomina1 operations unti1 aImost seventy-five years Iater when Pasteur5’s5* (Igo8 to IgI I) pubIished a series of articIes on the subject. The term, “massive coIIapse of the Iung,” was originated by Pasteur to designate a type * From the Department

University

of Chicago

ILLINOIS

of atejectasis which invoIved an entire Iung Iobe as compared to patchy ateIectasis. This differentiation unfortunateIy was on an etioIogica1 basis and subsequentIy Ied to considerabIe confusion when attempts were made to reproduce the condition in experimenta1 animaIs. To Sir James Barr5 (1907) goes the credit of diagnosing the condition as a postoperative compIication. After ruIing out pIeurisy with effusion by attempted thoracentesis, a diagnosis of ateIectasis was made and the patient “under a course of respiratory recovered gymnastics.” ETIOLOGY

It is not the purpose of this paper to go into great detai1 concerning the historica background of the theories pertaining to the etioIogy of postoperative puImonary ateIectasis. These theories have been thoroughIy reviewed by severa authors incIudothers, ChurchiII14 ( 1g25), ing, among Brunn and BriII1o~ll (Ig3o), more recently by Moore52 (1939) and will onIy be mentioned here in connection with various etioIogica1 factors as they are now recognized. AIthough the etioIogy of ateIectasis has been debated for almost a century, a universa1 agreement was not forthcoming unti1 within the past two decades. Much of the argument has been as to what factors are most important and which are secondary. The schooIs of thought have been divided into three groups and wiI1 be discussed as such. I. Bronchial Obstruction. As earIy as 1853, Gairdne? was aware of the frequency of “coIIapse of the Iung” and recog-

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nized both the “diffused and Iobular” types. He beheved that bronchia obstruction which was dependent on a number of secondary factors (i.e., mucus in the bronchi, weakness or ineffrciency of the inspiratory power and inability to cough and expectorate) was the essentia1 etioIogical factor in the production of ateIectasis. He thought that the obstruction was of a ball-vaIve type and that the air was removed by way of the air passages. BarteIQ ( I86 Ij also favored bronchial obstruction as the primary etiologica1 factor but agreed with Fucks25 ( I 849) who was the first to point out that the entrapped air was probably absorbed by the blood. It remained for Lichtheim?” (I 878)) through ingenious and painstaking experiments, to prove that the entrapped air following bronchial obstruction was absorbed by the bIood. He demonstrated that when the blood vessels were tied no atelectasis occurred. In addition he determined the rate of coIIapse, and found that complete absorption of pure oxygen occurred from the lungs within forty-five minutes while nitrogen required at least twenty-four hours. As pointed out by SewalY (192 I), these experiments did not disprove the possibility of the air being removed from the lung by the ball-vaIve action of the bronchia pIug. Elliott and Dingleyzl (1914) in a review of eleven patients were among the first to recognize ateIectasis as an important postoperative complication. A viscid mucopurulent secretion was found in all instances and bronchial obstruction was thought to be essential for the production of ateIectasis, ahhough immobility of the diaphragm was considered as a secondary factor. More recently an abundance of both clinical and experimental evidence (Jackson and Lee33 (1925), Andrus3 (1925), Hearn and CIerf30 (1927), Lee et a1.40,41v42(1928), CorylloslX ( 1930)) Adams and Livingstone’ (1931), Karol”’ (1931)) has left no doubt that bronchial obstruction is the one primary factor essential for the production of pulmonary atelectasis.

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2. Decreased Inspiratory Force. Pasteur ~~~~~~~~~~~ (1890 to 19 14) who was the first strong supporter of this theory, was much influenced by observing pulmonary atelectasis in a number of patients with postdiphtheritic paralysis of the diaphragm. He also believed that paralysis of the bronchia muscles might in some way aid in the production of ateIectasis and was among the first to recognize its importance as a postoperative complication. Briscoe” also beIieved that quiet breathing in the supine position in patients who did not fix their chest with the abdominal muscles, wouId normahy lead to ateIectasis. Likewise Bradford8 (1917 to 19 19) after observing a number of patients with atelectasis foIlowing and on the opposite side to trivia1 war wounds of the chest wall, was inclined to believe that reflex immobility and retraction of the chest wall were the primary etiologic factors. The fact that ateIectasis is bv far the most frequent pulmonary complication of abdominal operations (Mastics et al.ln (i927), Scott”” (1927)) is supportive evidence for this theory since it has been repeatedly demonstrated (Churchill and McNeil’” (r927j, Muller et al.“’ (1929), Carlson (1932)) that Operations, especially in the upper abdomen, reduce both vital capacity (as much as 50 to 60 per cent) and inspiratory effort to a considerable degree. However, the fact that diminished inspiratory force due to paralysis of the diaphragm or immobilization of the chest wall is insuffrcient in itself to produce ateIectasis is being demonstrated continua1I-y in the surgical treatment of pulmonary tuberculosis. Thus it must be regarded as contributory in nature. 3. Nervous ReJlex Contraction of the Lung. In 1903, Dixon and BrodielY produced ateIectasis experimentally by the direct action of drugs, and by reflex vagal stimujation causing bronchoconstriction. In order to obtain these results, artificia1 respiration with IittIe force and with the expiratory phase prolonged was required. If the reverse were tried (i.e., much force

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and a Iong inspiratory phase), distention of the lung resuIted. Scrimger6g (192 I) and ScotV5 (1923) also beheved that nervous reflex production of contraction of the bronchial muscles, such as that demonstrated by Carlson and Luckhardt12 (1920) was the major etiologica1 factor in the evoJution of ateIectasis. Support for this theory is found in the report by Bergamini and Shepard’ of two fatal cases of bilateral total ateIectasis which occurred during surgery and in whom no bronchia obstruction or secretions were demonstrable at necropsy. More recently Thomas’O (1938) has reported the experience of Mr. J. E. H. Roberts, who observed the sudden development of ateIectasis through an open thorax when intratracheal aspiration was started. It was pointed out by Thomas that cases of atelectasis produced by this reflex mechanism represent a smaI1 minority, probably Iess than IO per cent, the vast majority resulting from bronchia obstruction by retained secretions. AIthough, as stated by CoryIlos,“j no one has given “an exact and precise description of the reflex invoIved or of the nature of the stimuJus itseIf,” it is yet to be proved that a smaI1 minority of cases are not the resuIt of this mechanism. PATHOLOGIC

HISTOLOGY

AND

PHYSIOLOGY

Distribution. Postoperative ateIectasis may vary markedly in amount and distribution. The Iower Iobes are more commonIy invoIved and may present onIy smaI1 patches of airless parenchyma or the entire lobe may be flabby and contain no air. The process may involve a11 of both Iower Iobes as reported by Ball4 (1928), or as is not infrequentIy seen may incIude an entire Iung. The amount and distribution of invoIvement may vary from hour to hour (Hearn and CIerf) either increasing or decreasing, and may shift from one side to the other by “interna drainage” (FauIkner,24 1932). DoubtIessIy many cases with the patchy variety of atelectasis clear spontaneousIy

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by the routine changing of the patient’s position in bed, with IittIe evidence of its manifested. When pathogenic presence organisms are dammed back by the obstruction, symptoms soon appear. In 1918, WhippIe found that a pneumococcus of the type IV group couId be cuItured from most patients having this compIication. Whether these are secondary invaders from the nasopharyngeal flora is not definiteIy known. However, most avaiIabIe information indicates that they are primary in nature as a result of interference with drainage of the Iung. Since the prognosis of postPathology. operative ateIectasis is usuaIIy good, IittIe necropsy materia1 has been available for study. If ateIectasis of a Iobe is complete, the lung Iobe wiI1 be markedIy shrunken, flabby as a piece of muscle, of a dark reddish-purple coIor and will sink when pIaced in water. Microscopic sections revea1 approximation of aIveoIar waIIs with some mucus in the bronchioIes. If micro-organisms are trapped by the obstruction, Ieukocytes and Iymphocytes may be seen in the air passages and alveoli. Later stages may show edema of the parenchyma, but it is questionable whether this does not represent the deveIopment of pneumonia. Coryllos” (rgq) believed that not only was there a cIose reIationship between postoperative bronchitis, ateIectasis and pneumonia, but that the three conditions represented three stages of a single process. He demonstrated experimentaIIy the simiIaritv of the microscopic appearance and the disturbed circulation observed in atelectasis and pneumonia. CIinicaI experience has reveaIed the co-existence of the two conditions. Furthermore, differentiation between the two by means of symptoms, physica and x-ray signs is not infrequently very difficult especiaIIy when dealing with the patchy type of ateIectasis. Thus it is obvious that when these facts are considered, postoperative ateIectasis assumes a much more important r8le. Physiologic Considerations. In the presence of patchy ateIectasis without wide

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distribution, little alteration of cardiorespiratory function may be effected. However, when an entire lung or only one lobe becomes entirely atelectatic, marked changes may be manifested and may vary directly with the rate of lung collapse. Reduction in respiratory function which is already encumbered by a Iowered vital capacity, is apt to produce dyspnea and hyperpnea. This is al1 the more likely because of the associated lowering of blood oxygen saturation. Andrus,3 in 1925, found that thirty minutes following occlusion of the bronchus of an entire lung, the volume flow of blood through that lung was reduced to 3 I .o per cent of the total cardiac output, the latter having been increased 14.0 per cent over the preobstruction 1eveI. Twentyfour hours later this was decreased to 28.0 per cent, and at the end of one month to 8.0 per cent of the preobstruction level. These results have been substantiated more recently by Moores3 (193 I) and also in our laboratory (,Adams et al.,2 Phillips et al.60 (1940). Another striking physiologic alteration produced by atelectasis of an entire lobe or lung, takes place in the pleural cavity. The normal intrapleural negative pressure varies in different locations of the pleural space and with the respiratory cycle. Whereas the average normal is about -6.0 mm. of mercury on expiration and -8.0 mm. of mercury on inspiration, El kin”” from measurements made in three clinical patients reported intrapleural pressures as high as - 12.0 mm. of mercury in expiration and - 15. 0 mm. of mercury on inspiration on the efFected side with pressures on the opposite side remaining approximately normal. This is similar to the measurements recorded in our laboratory (Escudero and Adam?“) on dogs with unilateral collapse of an entire lung. Here the intrapleural pressures were altered from a normal of - 6.0 and -8.0 cm. of water to - 14.0 and - 18.0 cm. water on the effected side with aIso a decrease in pressure on the opposite side to -8.0 and - 10.0 cm. water correspondingly on expira-

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tion and inspiration. This discrepancy in pressure changes on the side opposite to that of the collapse occurring in dogs as compared to man is explained likely due to the more mobile mediastinum in the former, thus causing a greater shift of mediastinal structures toward the side of ateIectasis, a finding also present to a lesser degree in children. The rate of production of atelectasis of an entire lobe or lung has been much debated. From experimental studies as well as clinical observations it has been found to \Farq considerably according to the etiological factors, i.e., the type and effectiveness of bronchial obstruction and the character of the respiratory movements which are present in individual cases. Lee and his coworkers3’ (1928) produced atelectasis of an entire lung in dogs within from thirty minutes to three hours by obstructing the bronchus with either IOO per cent acacia or with bronchial secretions removed bronchoscopicallv from a patient having massive atelectasis of the entire left lung. The dogs were under deep narcosis but the respiratory movements became exaggerated on the side of the chest opposite to the side of collapse. Experiments performed on dogs in our laboratory” (19;o) demonstrated conclusively that a straining or grunting type of respiration with a checkvalve type of obstruction markedly shortened the time necessary for the production of atelectasis of an entire lobe or lung. Serial x-rays revealed marked changes present within a two-minute period. This increased rate of production seems logical since the air in the lung has two avenues of escape, i.e., through the bronchus and also by way of the blood stream. Further, in total obstruction with grunting or straining respiration, absorption of the entrapped air by the blood stream is likely to be more rapid than with quiet respiration since gas absorption varies directly with its partial In experiments performed at a pressure. later datez2 (1933) complete bronchial obstruction in the presence of a normal type of respiration without sedation or

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narcosis produced tota ateIectasis of an entire Iung Iobe within a three-hour period. CLINICAL

PICTURE

AND

DIAGNOSIS

Postoperative ateIectasis characteristicaIIy makes its appearance twenty-four to seventy-two hours after surgery but may deveIop as Iate as seven to ten days postoperativeIy. It may be sudden or insidious in onset and varies from miId to severe in its course. There is usuaIIy a sharp rise in temperature, puIse and respiratory rate accompanied by various degrees of dyspnea. A cough is usuaIIy present and may or may not be productive of sputum. OccasionaIIy, a chiI1 wiI1 accompany the rise in temperature, and in severe cases cyanosis may be present. Pain is a variabIe compIaint and whether this represents a combination of ateIectasis and pneumonia with pIeurisy is not known. As a ruIe a11 of these symptoms are not present in each individua1 case, however, eIevation of temperature, puIse and respiration are usuaIIy present. As stated by Brunn and BriII’O (Ig3o), “the chief characteristic of the physica findings is their VariabiIity.” They may vary from hour to hour according to the amount of invoIvement and the type of or absence of bronchia obstruction. It is generaIIy agreed that the most important finding on physica examination for making the diagnosis of ateIectasis is dispIacement of the heart and mediastinum toward the side of invoIvement. Unfortunately, this is not aIways easy to determine in postoperative patients by physica examination and therefore portabIe x-rays are indicated when the condition is suspected. The above findings are usuaIIy accompanied by eIevation of the diaphragm on the invoIved side with Iimitation of motion of the chest waI1 and narrowing of the interspaces, the degree of which wiI1 be somewhat determined by the amount of Iung tissue invoIved. If the Iesion is biIatera1, or of the patchy variety, the above findings may be Iess striking or minima1 in degree. In the case of patchy

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ateIectasis physica examination may be practicaIIy norma or consist 0nIy of some diminution in breath sounds with or without the presence of rbIes. However, in the Iobar type or when an entire Iung is invoIved, the percussion note wiI1 be duI1 or ffat and breath sounds wiI1 be aItered. If the bronchi are compIeteIy occIuded, no breath sounds or rhIes are demonstrabIe and tactiIe fremitus is diminished or absent. When the bronchia obstruction is reIeased, Ioud moist rbIes and bronchia breathing are present and tactiIe fremitus wiI1 be restored. Many of these findings are simiIar to those of e?rIy pneumonia especiaIIy of the bronchia type and for this reason the Iesion has undoubtedIy been diagnosed as pneumonia when IittIe shift of the heart was noticeabIe. From experimenta work on dogs, CoryIIos and Birnbaum” (1929) concIuded that ateIectasis represented a stage in the deveIopment of pneumonitis. At the present time it is generaIIy beIieved from cIinica1 observations that more serious compIications such as Iung abscess and pneumonia deveIop from ateIectasis if the Iatter is not promptIy diagnosed and properIy treated. For this reason, as mentioned above, x-rays of the chest are frequentIy indispensabIe. Here also the evidence is not aIways concIusive, for patchy ateIectasis has in the past been frequentIy diagnosed as bronchopneumonia. Other Iaboratory tests may be of IittIe heIp in differentiation between the two conditions since the white bIood ceIIs in Iobar ateIectasis are usuaIIy increased to 15,000 or 20,000; and aIthough the sputum is often, tenacious in character, it may be quite thin, scanty or abundant and usuaIIy contains a pneumococcus of (one of) the type IV group. Factors which aid most in diagnosis are: (I) awareness of incidence after abdomina1 operations; (2) time of onset-twenty-four to forty-eight hours after operation; (3) sudden rate of deveIopment and severity of symptoms; (4) shift of heart and mediastinum on physica and x-ray examination, and (5) bronchoscopic fInding of bronchia obstruction.

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TREATMENT

The treatment of postoperative puImonary atelectasis may be divided into prophylactic and active. Since the incidence of ateIectasis foIlowing operations can be materially reduced by attention being given to etioIogicaI factors, the importance of prophylaxis is at once apparent. Proph~rlaxis. As mentioned above the primary etiologica1 factor in most cases of atelectasis is bronchial obstruction usuahy produced by retained secretions. AI1 other factors are secondary but nevertheless may be of just as much importance, and not infrequently two or more factors may be complimentary in the production of the complication. 1. Infection. Since this is an important factor in most pulmonary complications, adequate attention should be given to careful oral hygiene. Furthermore, all major operations of eIection shouId be delayed for some time (severa weeks) when there is a suspicion of an upper respiratory infection. Placing patients in the Trendelenburg position (about IO to 15 degrees) until consciousness returns or even as a routine in major abdominal operations wiI1 aid in the elimination of secretions from the tracheobronchial tree by gravity. The same principle holds in the frequent change of position in bed (at Ieast every four hours) during the first four or five days following operation. 2. Drugs. Since some drugs such as atropine and hyoscine tend to dry secretions, making them more tenacious and dithcult to eliminate, they had best be eliminated even when excessive secretions are present (Mathes and HoIman”g’jo (1929, 1930) and Thomas”’ (1938)). In our experience this has definitely reduced the incidence of postoperative atelectasis. 3. Anesthesia. Since the incidence of this lesion is practicahy the same foIlowing the use of various anesthetic agents, the attention of the anesthetist should be directed toward maintainance of the cough reflex when possibIe and to the early return

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of consciousness folIowing operation. Careful elimination of secretions both during and following operation by gravity drainage or by aspiration through a catheter or a bronchoscope is of paramount importance (Eversole (1940), MouseI”’ (1940)). 4. Operation. It is common knowledge that this complication usually follows abdominal and peIvic operations. Thus greater care shouId be given to this group of patients both in the way of prophylactic treatment as we11 as watching for its early manifestations folIowing operation. 5. Excessive Secretions. In patients with a chronic productive cough due to chronic bronchitis or bronchiectasis particular attention should be given to the elimination of the exudate (secretions) before, during and foIlowing operation. This may be accomplished by postural drainage, encouraging the patient to expectorate or by bronchoscopic aspiration prior to operation. To aid elimination by gravity during operation, the patient IS placed in a TrendeIenburg position by lowering the head end of the operating table to a I o to I 5 degree angle. Aspiration by catheter may be advisabIe during operation in some cases in which the secretions are profuse. FolIowing operation catheter or bronchoscopic aspiration of secretions from the tracheobronchial tree should be as thorough as possible. On return to the pavilion or room repeated catheter aspirations as described by Haight2g (1938) wil1 do much to prevent atelectasis and pneumonia. An indication for aspiration is the presence of loud rhles and ronchi produced by mucus and pus which the patient is unable to expectorate. If this can not be removed by aspiration with a catheter, a bronchoscope should be inserted and the aspiration carried out under direct vision. 6. Diminished Respiratory Force. Since it has been definitery proved that in abdominal operations the respiratory force and vital capacity are markedly reduced, a11 attempts should be made to prevent further reduction of function by abdominal binders and deep sedation. Henderson’~‘*Rz*3D

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( 1920 to I 929) recommended the inhaJation of carbon dioxide-oxygen at intervals following operations in order to re-expand hypoventiJated Jung tissue. This prophyJactic measure has been given an extensive tria1 with reports of its vaJue being variabJe, Scott and CuJter67 (1928), Scott”* (I pg), Brunn’O (1930). H owever, where hypoventiJation is extreme as is the case foJJowing some upper abdomina1 operations, there is JittJe doubt that occasiona hyperventiJation is beneficia1. 7. Cough. Since coughing is probabJy the best natura1 defence against stagnation of secretions in the bronchia tree, every effort shouJd be made to keep it effective. Due to the production of pain on straining the abdomina1 waJ1, the patient is reJuctant to cough and expectorate retained intrabronchial secretions. This can be partiaJJy overcome by spJinting the wound with a binder which does not restrict respiratory movements and aJso by the patient using his hands to support the abdomen during the act of coughing (Sommer64 ( I 94 I )). The use of drugs for the reJief of pain is important but respiratory depressants should be limited. Active Treatment. When once the diagnosis of postoperative ateJectasis is estabJished, active therapeutic measures should be immediateJy instituted in order to obviate more serious compJications. Since bronchia obstruction due to the stagnation of secretions is present in the majority of cases, cJearing of the air passages and re-expansion of the ateJectatic Jung is the first consideration. The amount of Jung tissue invoJved and the severity of the symptoms wiI1 determine to some extent the therapeutic measures indicated and the urgency of their appJication. Since marked hypoventiJation and an ineffective cough are usuaJJy manifested, correction of these factors shouJd be given first attention. Coughing wiJ1 be more effective in a conscious patient with the head rest somewhat eJevated. By supporting the wound with a binder which does not restrict respiratory activity and by

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splinting the abdomen with the hands, the patient may be abJe to raise the obstructing secretions (Saute62 (1927)). Persistent encouragement in this regard is worth whiJe and in the end is often rewarded. Sedation for the contro1 of pain is heJpfu1 in producing an effective cough but respiratory depressants should be used sparingJy. RecentJy, Guisz7T2*(1940) has made use of a paravertebra1 procaine block of the tenth, eJeventh and tweJfth dorsa1 and the first and second Jumbar nerves for the reJief of pain that interferes with cough, and for improving ventiJation of the Jung and increasing vital capacity folIowing upper abdominal operations. Overbreathing or hyperventiJation may also be obtained by the use of a 95 per cent oxygen and 5 per cent carbon dioxide mixture and shouJd be administered for five minutes severa times a day according to the needs of individual patients. This wiJJ not onJy reinflate the hypoventiJated Jower portion of the Jungs but wiJ1 increase the force and effectiveness of the cough and tend to Joosen obstructing secretions. Drainage of the bronchial tree through gravity by pIacing the patient in the TrendeJenburg position and by change of position in bed from side to side and on the abdomen is of great value in the reinflation of an ateJectatic Jung. This is more effective when the secretions are thinned by the use of steam inhaJations or expectorants. If the retained secretions are profuse or very tenaceous and the above measures are insuffrcient to cJear the bronchia tree, aspiration by means of a catheter (No. 16 French urethraI) inserted through the nose and directed into the air passages shouJd be carried out without deJay. The catheter may be introduced more easiJy with the patient in a semisitting position and passed into the trachea as the patient takes a deep breath, as described by Haight and Ransom31a (1941). The patient is then placed in a horizonta1 or sJight TrendeJenburg position for aspiration. By having the patient cough and repeating the suction intermittentJy on severa occasions, effective

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removal of the secretions is IikeIy. The procedure may have to be repeated several times. If this procedure appears to be

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Sedation

postoperativeIy consisted of n1.S. and 0.015 during the first clay and a similar amount the second day.

Gm. 0.010

R

FIG. I. Case 1. A, x-ray of chest before operation. B, s-ray of chest twenty-four hours foIlowing operation.

inefFective, or the severity of the symptoms seem to warrant it, bronchoscopic aspiration should be promptIy carried out iHaight and Ransom31a LeopoId43). This can be accomplished in the patient’s room and may be a life saving measure. Bronchoscopic aspiration has the advantage over catheter aspiration in that the air passages may be more compIeteIy cleared of secretions under direct vision. More recentIy the use of chemotherapy has been found of value in the management of pulmonary ateIectasis. Since bronchopneumonia may readily foIIow the development of ateIectasis, the use of sulfapyradine or sulfathiazoIe during the reinflation of the collapsed Iung is of real importance. The dosage used for this purpose is similar to that employed in the treatment of pneumonia. The following cases illustrate various clinical features and therapeutic measures employed in the management of pulmonary ateIectasis compIicating operations: CASE

REPORTS

CASE I. A white maIe of fifty-six in fair general condition was admitted for treatment of carcinoma of the stomach. On August 13, I 94.1. a partial gastrectomy was made under ethyleneoxygen anesthesia, following M.S. Gm. 0.010 and calcium nembutal Gm. 0.27premeditation.

On August 14 the temperature suddenly became elevated to 104.3'~.(rectal) and the patient feIt chilly; the pulse was 125, respiration thirt,v per minute. A cough with grayishyeIlow sputum was noted. On physical examination the patient appeared somewhat cyanotic. Over the lower right chest posteriorly there was dullness with diminished breath sounds and some coarse &es. The heart was deviated markedIy to the right. Atelectasis or pneumonia was suspected. The sputum contained many organisms including pneumococci. The kvhite bIood count was I 3,800 (preoperative nhite blood count, 6,850). An x-ray revealed the heart and mediastinum markedly deviated to the right and a triangular shadow representing an atelectatic right lower Iobe. The right intercostal spaces were narrowed and the right diaphragm was elevated. (Fig. IB.) Diagnosis: Massive atelectasis of the right lower lobe and patchy atelectasis of the right upper lobe. Coughing was made more effective l>y elevation of the head rest. Hyperventilation was carriedlO out every thirty minutes by rebreathing in a paper bag. Steam inhalations were begun and the patient’s position was changed frequently. Sodium SuIfathiazole Gm. 3.0 were given intravenously and the same dose repeated three hours later. On August 15 the patient was much impro\red. The highest rectal temperature was I02’F. Sulfathiazole (Gm. 3.0) was given intravenously and other therapeutic measures \vere continued.

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On August 16 he continued to improve, rectal temperature was IOO’F. Physical and Auoroscopic examination revealed the right

On the foIlowing day the temperature was lower and the sputum was raised more easily. On January 3 the white blood count was

Iung to be cIear. There was an uneventfu1 convaIescence thereafter and the patient was discharged thirteen days postoperativeIy. CASE II. A white maIe of seventy-nine entered the hospital complaining of jaundice of two weeks’ duration. Three months before admission he had a severe coId which persisted for a month. His genera1 condition was onIy fair, having Iost twenty pounds in weight during the preceding three months. On physical examination his chest was found normaI. (Fig. 2~.) On December 27, 1939, a choIecystgastrostomy for a carcinoma of the head of the pancreas was made under ethyIene-oxygen anesthesia foIIowing M.S. Gm. 0.010 premedication. Postoperative sedation consisted of M.S. Gm. 0.020 during the first day and a similar amount on the second day. On December 29 the patient was coughing and had a recta1 temperature of 103’~. PhysicaI examination reveaIed dullness, decreased breath sounds and coarse’rbles over the midportion of the right lung posteriorIy. The heart was shifted to the right. The white bIood count was 13,200. The sputum contained a type XX pneumococcus. CIinicaI diagnosis: PartiaI ateIectasis of the right lung. HyperventiIation with 90 per cent of oxygen and IO per cent of carbon dioxide was carried out and the patient’s position in bed was changed frequently. K.I. IO ggts was administered t.i.d. to make coughing more effective.

10,900. The patient continued to improve but an x-ray of the chest reveaIed a persistence of the atelectasis of the right Iung with deviation of heart and mediastinum to the right. (Fig. 2~~) Sulfapyradine Gm. 1.0 was given every four hours. On January 7 the white bIood count was 9,440. An x-ray of the chest was normaI on January 14. (Fig. 2c.) The patient had an uneventfu1 course thereafter and was discharged on January 21. CASE III. A white male of sixteen was admitted for a plastic operation on the right mandible. He was in good genera1 condition and on physica examination the Iungs were entireIy normaI. On February 22, 1941, a bone graft from the right ninth and tenth ribs to the right mandible was made under avertin and ether anesthesia, the Iatter being administered by intranasal catheter folIowing induction by the drop method. No premeditation was given. Postoperative sedation consisted of M.S. Gm. 0.010 on the first day, M.S. Cm. 0.010 and nembuta1 Gm. 0.09 the second day and M.S. Gm. 0.020, nembuta1 Gm. 0.09 and codeine Gm. 0.12 on the third day. On February 24 the rectal temperature became eIevated rapidIy to IOS’F. He became dyspneic and cyanotic; p&e was rgo, respirations 35 per minute. PhysicaI examination reveaIed duIIness to Aatness over the Ieft chest with breath sounds aImost absent and a few &es present at the apex. The heart was shifted over to the Ieft axiIIa. The sputum contained

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staphylococci, streptococci and pneumococci. The white bIood count was 19,200. An x-ray of the chest reveaIed marked shifting of the heart and mediastinum to the Ieft with diuseff spotty graying of the lower three-fourths of the left lung field. (Fig. 3.) Diagnosis: Massive coIIapse of the Ieft Iower lobe with patchy atelectasis of the left upper lobe. Oxygen was given by nasa1 catheter. Hyperventilation with oxygen and carbon dioxide was begun and the patient’s position changed frequently to aid aeration of the Iung by gravity drainage. Sulfathiazole Gm. 2.0 were given intravenously and followed by Gm. 1.0 ever? four hours. There was definite improvement on February 25. The rectal temperature was down to 103’~. and the white blood count was 15,600. The following day the temperature was normal. Physical examination reveaIed a normal chest and the white bloocl count was 9,750. An x-rayrevealed only patchy areas of nonaerated lung with no deviation of mediastinal structures. The course was uneventfu1 thereafter and the patient was discharged on March 5. A white female of twenty-six in ChSE IV. good general condition was admitted for a

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expectoration of cIear mucus (no other complaints) ; temperature 102.2’~., pulse I 30, respiration, 38 per minute. Physical examina-

FIG. 3. Case I,,. X-ray of chest made with patient on a pneumonia bed t\vo days following operation.

tion revealed a few &es and an inspirator) stridor over the right chest anteriorIv. The white blood count was 15,800 and pneumonia was suspected. The sputum containecl a type 19 pneumococcus. An .x-ray of the chest revealed

R

FIG. 4. Case IV. A, x-ray of chest twenty-four hours following operation. R, s-rag of chest made thirteen cla\s following operation.

pelvic operation. There was a history of an occasional pain in the chest with chronic wheezing. Ori September 6, 1939, an incompIete hysterectomy and bilateral saIpingo-o8phorectomy was made under ethylene-oxygen-ether anesthesia after M.S. Gm. 0.020 and hyoscine Gm. 0.00075 premeditation given in two doses. M.S. Cm. 0.010 was given foIlowing operation to control pain. On September 7 there was some cough with

an opaque shadow at the right apex, being concave inferiorly. The right diaphragm was elevated. Diagnosis: Postoperative massive atelectasis of the right upper lobe. (Fig. 4~.) Cough was made more effective by the use of steam inhalations and K.I. IO ggts t.i.d. HyperventiIation of the lungs was instituted and the patient’s position in bed was changed frequently. Sulfapyradine Gm. 4.0 were given and folIowed by Cm. 1.0 every four hours.

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On September 8 the temperature was onIy and the cough was much more productive. On the foIIowing day there was marked clinicaI improvement; the temperature was IOO’F., white bIood count, I 1,500. On September IO, symptoms and signs of ateIectasis had disappeared, white bIood count was 7,250 and suIfapyradine was discontinued. The patient’s course was uneventfu1 thereafter and she was discharged on September I 8. An x-ray made on September IgreveaIeda norma chest. (Fig. 4~.) 100.4’F.

REFERENCES I. ADAMS, W. E. and LIVINGSTONE, H. M. Obstructive puhnonary ateIectasis. Arch. Surg., 23: 500, 193’. 2. ADAMS, W. E., HRDINA, L. S. and DOSTAL, L. E. Vascular changes in experimental atelectasis. J. Tboracic Surg., 4: 377, 1935. 3. ANDRUS, W. DEW. Observations on the cardiorespiratory physioIogy folIowing the coIIapse of one Iung by bronchia Iigation. Arch. Surg., IO: 506522, 1925. 4. BALL, R. P. Bilateral Iobar atelectasis. Arch. Surg., 17: 82-90, 1928. 5. BARR, J. The pleurae: pleural effusion and its treatment. &it. M. J., 2: 1289, 1907. 6. BARTELS. Bemerkungen iiher eine im Frtihjahre 1860 in der PoIikIinik in KieI beobachtete Masernepidemie, mit besonderer Berticksichtigung der dabei vorgekommenen Lungenaffectionen. Vircbow’s Arch. f. path. Anat., 21: 129-156, 1861. 7. BERGAMINI, H. and SHEPARD, L. A. Bilateral ateIectasis (massive coIIapse) of the Iung. Ann. surg., 86: 35-40, 1927. 8. BRADFORD, JOHN ROSE. Massive cohapse of the lung as a result of gunshot wounds, with especia1 reference to wounds of the chest. Quart. J. Med., 12: 127-150, IgIg. g. BRISCOE, J. C. The mechanism of postoperative massive cdlapse of the Iungs. Quart. J. Med., 13: 293-336, rgrg-20. IO. BRUNN, HAROLD and BRILL, SELLING. Observations on postoperative puImonary atelectasis. Ann. Surg., 92: 801-837, 1930. II. BRUNN, HAROLD and BRILL, SELLING. AteIectasis. A review of its history, significance and treatment. West. J. Surg., 38: 647, 1930. 12. CARLSON, A. J. and LUCKHARDT,A. B. Studies on the visceral sensory nervous system. III. Lung automatism and Iung reflexes in reptilia. Am. J. Pbysiol., 54: 261-306, 1920. 13. CARLSON, H. A. Inhibition of respiration as a factor in the pathogenesis of postoperative puImonary complications. J. Tboracic Surg., 2: 196, 1932. 14. CHURCHILL, E. D. PuImonary ateIectasis, with especia1 reference to massive collapse of the lung. Arch. Surg., I I : 489-3 18, 1925. 15. CHURCHILL, E. D. and MCNEIL, D. The reduction of vita1 capacity following operation. Surg., Gynec. Ed Oh., 44: 483. 1927.

AteIectasis 16. CORYLLOS, P. N. and BIRNBAUM,G. L. Obstructive massive ateIectasis of the Iung. Arch. Surg., 16: sol-559, 1928. its reIation to 17. Idem. BronchiaI obstruction: atelectasis, bronchopneumonia and Iobar pneumonia. Am. J. Roentgenol., 22: 401-430, 1929. 18. CORYLLOS, P. N. Postoperative puImonary comphcations and bronchial obstruction. Surg., Gynec. Ed Obst., 50: 795, 1930. 19. DIXON, W. E. and BRODIE, T. G. Contributions to the physioIogy of the Iung. Part I. The bronchia muscIes, their innervation and the action of the drugs upon them. J. Pbysiol., 29: 97-173, 1903. 20. ELKIN, D. C. Intra-pIeural pressure in postoperative atelectasis. Ann. Surg., 86: 885-889, 1927. 21. ELLIOTT, T. R. and DINGLEY, L. A. Massive colIapse of the Iung folIowing abdominal operations. Lance& I : 1305-1309, 1914. 22. ESCUDERO, L. and ADAMS, W. E. Spontaneous pneumothorax associated with massive collapse. Arch. Int. Med., 63: 29, 1939. 23. EVERSOLE,U. H. and LAHEY, F. H. Aspiration of respiratory passages as aid in prevention and treatment of postoperative complications. Labey Clin. Bull., 2: 26, 1940. 24. FAULKNER, WILLIAM B. and FAULKNER, EDWARD C. Internal drainage. Causative factor in production of postoperative massive coIIapse of Iung (pulmonary atelectasis). Suggestions as to prevention and treatment. Acta cbir. Scandinac., 69: 105, 1932. 25. FUCHS, C. F. Die Bronchitis der Kinder. Leipzig, 1849. 0. Wigand. 26. GAIRDNER, W. T. On the pathological anatomy of bronchitis, and the diseases of the Iung connected with bronchia obstruction. &it. ti For. h4. Rev., I I: 355-375, 1853. 27. Gurs, J. A. Postoperative ateIectasis and reIated pulmonary complications. Internat. Abstr. Surg., 71: 65, 1940. 28. Gurs, J. A. Paravertebral procaine bIock in treatment of postoperative atelectasis. Surgery, 8: 832, 1940. 29. HAIGHT, C. Intratracheal suction in the management of postoperative puImonary complications. Ann. Surg., 107: 218, 1938. 30. HEARN, W. P. and CLERF, L. H. Postoperative massive coIlapse of the Iung: report of bronchoscopic observations. Ann. Surg., 85: 54-60, 1927. 31. HENDERSON, Y., HAGGARD, H. W. and COBURN, R. C. The therapeutic use of carbon dioxide after anaesthesia and operation. J. A. hf. A., 74: 783-786, 1920. 31~. HAIGHT, C. and RANSOM, H. K. Observations on the prevention and treatment of postoperative ateIectasis and bronchopneumonia. Ann. Surg., 114: 243, 1941. 32. HENDERSON, Y. The physioIogy of ateIectasis. J. A. M. A., 93: g&98, 1929. 33. Idem. HyperventiIation of the Iungs as a prophyIactic measure for pneumonia. J. A. M. A., 92: 434-436. 1929. 34. JACKSON, C. and LEE, W. E. Acute massive colIapse of the lungs. Tr. Am. Surg. Ass., 43: 723-766, 1925.

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35. J~~Rc, E. De Pulmonum Vitio organico. Quoted by Lord. Lipsiae, 1832. 36. ldem. Quoted by Willshire, W. H. Brif. C+For. M. Rec., 12: 402-403, r853. 37. Ko~or, EPHKAIM. The aetioIogy and mechanics of massive atelrctasis. Am. Rev. Tuberc., 24: 276, ‘931. 38. KIM;, D. S. Postoperative puImonary complications. I. A statistical study based on two years’ personal observation. Surg., Gynec. e* Obsr., 56: 39. to.

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55. PASTEL R, W. Respiratory paralysis after diphtheria as a cause of pulmonary complications, with suggestions as to treatment. Am. J. M. SC., 100: 242-257 /I ,890. 56. Idem. Cases iIIustrating the association of respiratory paralysis with cardiopulmonary symptoms in diphtheritic multipIe paralysis. Chin. Sot. Tr., 28: 11I-Ip, London, 1895. 57. Idcm. Massive collapse of the lung. I.ancer, 2: ‘351-1355, 1908. 58. Idem. Active Iobar collapse of the lung afterabdominal operations. Lancer, 2: I&-1083, ,910. 59. Idcm. Massive coIlapsc of the lung. (Syn. active labor collapscj. &it. J. Surg., I : 587-601, 1913-1914. 60. PHILLIPS, F. J., ADAMS, \I;. E. and HRDINA, L. S. Physiologic adjustment in sublethal reduction of lung capacity in dogs. Surgery, 9: 25-39, 1941 . 61. TIIOMAS, C. P., MAXWELL, J. and RINK, E. II. Discussion on massive coIlapse of the lung as a complicatron of surgrcn1 operatmns. I’roc. Rqr-. Sot. Med., 3 I : I 247, 1938. 62. SAUTE. 1.. R. hlassive (atelectatic) collapse of the reference to t rc:itmcnt. lung, with especial J. A. i&f. A., 88: 1539-1542, 192”. 63. SEWAIL, II. Pulmonary atclectasis as a source 01 confusion in physical examination of’ chest. Am. Rec. Tubers., 4: 81 I, 1921. 64. SOMMI~.R,G. N. J., JR. Prevention and treatment of postoperative complications. J. .2f. Snc. Neal Jersey, 38: 67, 1941. 65. SCOTT, W. .J. Al. Postoperative massive collapse of the lung. Arch. Surg., IO: 73-1 16, 1925. 66. Scorr, W’. .J. \I. and JOEI_SO&, J. J. Postoperative massive atclectasis: the inffuencc of post urc. Arch. Surg., 15: 8555870, 1927. 67. SCOTT, \V. J. nl. and CUTLER, E. C. Postoperative massive atelectasis: effect of hypcrvcntilation with carbon dioxide. J. A. M. #4., 90: 175c)-1763, I 928. 68. Scorn, W. J. M. Rlassive atelectasis and postoperative pneumonia: prophylaxis and treat mcnt. J. A. M. A., 93: 101-103, 1929. 69. SCRIMGER, F. A. C. Postoperative massive collapse of t hc lung. Surg., Gynec. 0’ Ohsf., 32: 480, ,921. 70. THOM is, C. P., ~IAXWELL, J. and RIZK, 11. I I. Discussion on massive collapse of the lung as :L compIicatmn of surgical operations. I’roc. Z