vinson - thorax · after vinson's paper the majority of reports in the 1930's were...

Thorax (1949), 4, 44.

THE PULMONARY COMPLICATIONS OF DYSPHAGIA

BY

J. R. BELCHERHospital for Consumption and Diseases of the Chest, London

INTRODUCTIONThis paper is concerned with the pulmonary

-aspiration phenomena associated with mechanicaldysphagia, and the term "dysphagia pneumo-nitis" is used for the syndrome. Lesions due tocentral dysphagia and secondary to broncho-oesophageal fistulae have been excluded. In 1927Vinso"n reported a case of achalasia vhich wascomplicated by a lung abscess, and since then 38others have been described. These, together witha further collection of nine cases hitherto unpub-lished, form the basis of this article.

After Vinson's paper the majority of reports inthe 1930's were published by French otolaryngo-logists as single unusual histories. But from 1938onwards more have appeared in the Americanliterature, some have been described by clinicians,and others by radiologists. Weens (1944) col-lected five and reviewed the literature, Bird-Acosta (1944) described a further three, and Hawesand Soule (1945) two cases. Six have been pub-lished in the British journals by Cummins andWilliams (1933), Schrier (1938), Robson andWilkinson (1946), and Wooler (1948); others havebeen described incidentally in reviews of differentconditions. Jackson and Jackson (1933), in dis-cussing pulmonary symptoms of oesophageal dis-ease, cite three cases, and Keefer (1934) reportedone aspiration lung abscess in a paper describingseventeen examples of oesophageal carcinomaassociated with pulmonary lesions. Harrington(1945) and Lahey (1946), in their large series ofpharyngeal diverticula, each mention four casescomplicated by lung abscesses.The association of dysphagia with the presence

of non-pathogenic acid-fast bacilli in the sputumand with lipoid pneumonia has led to the publica-tion of a further six cases (Rothstein and Pirkle,1946; Baldwin, 1942; Thomas and Jewett, 1936;Warring and Rilance, 1943; Cummins and Wil-liams, 1933 ; Tcherthoff, 1941), and Wooler (1948),in his paper on cardiospasm, refers to threeexamples of " dysphagia pneumonitis."

CASE HISTORIESThe summaries of the nine cases given below

include examples of the main causative factorsand of the commoner resulting pulmonary lesions.

Case 1. Achalasia complicated by collapse.-Awoman aged 65 had thirteen years' history of dys-phagia due to achalasia. She was investigated inNovember, 1947, and a gross mega-oesophagus wasdiscovered (Plate Ia). In January, 1948, she wasadmitted to hospital with three weeks' history of pro-ductive cough, fever, and dyspnoea. A radiograph(Plate Ib) showed a collapsed right lower lobe. Herclinical condition improved and an oesophago-gastrotomy was performed (N. R. Barrett) in March,1948. The operation was complicated by totalatelectasis on the right side. The upper lobe re-expanded after aspiration of food particles througha bronchoscope, but the lower lobe collapse persisted.Case 2. Achalasia complicated by pneumonitis with

acid-fast bacilli in spatum.-A man aged 41, from1940 to 1945 complained of slight dysphagia on hurry-ing food. In 1945 he developed " pneumonia." Acid-fast bacilli were found in the sputum. A radiograph(Plate Ila) showed bilateral mid-zone infiltration witha suggestion of cavitation on the right side. Rapidclinical and radiological improvement ensued until hisradiograph was almost clear six months later. InMarch, 1948, a Heller's operation was performed(N. R. Barrett) for increasing dysphagia. He had nopulmonary symptoms in the interim, the radiographwas then clear (Plate Ilb) and no acid-fast bacilli werefound in his oesophagus or sputum.Case 3. Achalasia associated with " typical"

fibrosis.-A man aged 50, whose abnormality wasdiscovered on mass radiography (Eley, 1948), had hadslight dysphagia for years with recent dyspnoea andrepeated bronchitis. The radiograph (Plate Illa) ischaracteristic of the condition; this and his symptomshave now remained unchanged for a year.Case 4. Carcinoma of lower third of oesophagus

and lung abscess.-A man aged 69 gave a three weeks'history of cough and purulent sputum. A radiographshowed a left dorsal-lobe lung abscess with a fluidlevel. He improved until he was symptom-free onemonth later. The radiograph now showed no cavity,

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but there was residual fibrosis in the fissure area. Twomonths later his dysphagia became overt and a bariumswallow and oesophagoscopy revealed a carcinoma ofthe lower third of the oesophagus. There was noevidence of a fistula.

Case 5. Pharyngeal diverticulum with patchypneumonitis.-A man aged 65 who had had bron-chitis for years developed "pneumonia" eight yearsago and had had repeated attacks since then. He alsonoticed dysphagia for six to eight years, which wasgetting gradually worse. In August, 1947, he devel-oped a patch of infiltration at the apex of his rightlung, and acid-fast bacilli were found in the sputumon one occasion. The symptoms cleared rapidly, butthe pneumonia recurred in December, 1947; he hasremained sputum-negative since then. His diverticu-lum was excised in June, 1948 (C. Price Thomas).His bronchitis persists, but there are no othersymptoms, and the infiltration in the radiograph isnow clearing.

Case 6. Pharyngeal diverticulum with lung abscess.-A man aged 46 complained of one year's history ofdysphagia. In September, 1947, he developed pneu-monia, and two months later during a second attackhe was diagnosed as having a lung abscess. He wasadmitted to hospital in January, 1948, and was shownto have a pharyngeal diverticulum associated with aleft upper-lobe lung abscess and collapse of the leftlower lobe. One month later he developed a patchof "pneumonitis " in the right lower lobe whichcleared with chemotherapy. His general conditionimproved, and the radiograph cleared, but the leftlower lobe collapse persisted. In February, 1948,the pouch was excised and he was discharged muchimproved one month later. At that time the collapseand abscess had cleared, leaving areas of pulmonaryfibrosis.Case 7. "Short" oesophagus associated with

bilateral bronchiectasis.-A child aged 6 gave a historyof frequent coughs, colds, and pain in chest since theage of 1 year. She had "pneumonia" when aged2 years and 3 years, and thereafter continuous non-foetid sputum. She was investigated in 1945 andfound to have almost total bronchiectasis on the rightside. She- was seen again six months later when shehad started "vomiting" white phlegm and was notgaining weight. Another bronchogram at this timeshowed lingular bronchiectasis. One year later thevomiting was much worse and a barium swallowshowed dilated " short " oesophagus, probablysecondary to peptic ulceration.Case 8. Achalasia in association with pulmonary

fibrosis.-A man aged 35 who had had an empyemadrained in 1930 developed " influenza " in November,1940. He was investigated in 1941 and found to havemega-oesophagus secondary to achalasia and bilateralmid-zone infiltration of the lungs. During the nexttwo years the infiltration waxed and waned on alter-nate sides due to recurrent attacks of " pneumonitis."In January, 1943, he was admitted to hospital with a

history of occasional haemoptyses, minimal cough,and regurgitation. Clubbing was present. The radio-graph (Plate IIIb) shows mid-zone shadows and amega-oesophagus. The achalasia was treated bydilatation of the cardia with a hydrostatic bag. Thelung fields remained unchanged on radiography, butthe oesophageal dilatation was improved.

Case 9. Achalasia associated with lipoid pneu-inonia.-A woman aged 19 complained of threeyears' history of sickness after meals. Bougies werepassed at intervals with partial improvement for oneyear. She then developed rheumatism in the hands,and radiograph of the chest showed "abnormalitysecondary to dysphagia." Two years later radiographyshowed lipoid pneumonia (Plate IVa), and bouginagewas continued. One year later, in 1945, a Heller'soperation was performed. The diagnosis of lipoidpneumonia was made from the radiographs and froma history of inhalation .of liquid paraffin.

DIscussIoNINCIDENCE.-The frequency with which patho-

logical conditions of the oesophagus are associ-ated with abnormalities of the lungs is difficult toassess; there is little doubt that it is considerablygreater tthan the number of cases recorded in theliterature suggest. Weens (1944) found that inhis series of fifteen cases of achalasia of the cardia,five developed pulmonary lesions, but-Eley (1948)only found one example in 60,000 mass radio-graphs. The eight patients described by Harring-ton (1945) and Lahey (1946) give an accurate ideaof the incidence in their series of 349 pharyngealdiverticula.

AETIoLoGY.-The pulmonary changes associ-ated with dysphagia are due to aspiration ofoesophageal contents into the bronchial tree. Themechanism of aspiration varies with differentoesophageal lesions. During normal deglutitionthe arrival of a bolus of food in the pharynx setsup a reflex mechanism, part of which is concernedwith the onwards transmission of the food, andpart of which prevents its ingress through theglottis. A lesion which interferes with this pro-tective reflex makes aspiration almost inevitable.When deglutiticn is not taking place the coughreflex protects the bronchial tree from contami-nation by liquid in the pharynx or oesophagus.Any lesion which may cause, the retention ofliquid in this area, in the presence of factorswhich tend to dull the cough reflex, renders thepatient liable to " dysphagia pneumonitis."Carcinomata of the upper third of the oeso-

phagus are particularly prone to produce aspira-tion, as they are usually of the stenotic typecausing early dysphagia, and are often compli-

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cated by recurrent nerve palsies. This combina-tion provides the factors of retention of liquid inthe pharynx plus interference with the mechanismnormally responsible for closure of the glottisduring deglutition. Camiel and Lo-we (1941)divided their cases of carcinoma of the oeso-phagus into upper-third and lower two-thirdsgroups, for the purpose of discussion of pul-monary complications. They demonstrated thatcases in the upper third almost invariably died ofaspiration pneumonia (eleven cases out ofthirteen) secondary to vocal-cord paralysis. Theydemonstrated the " spill" in progress during abarium swallow, and considered that it would bepossible to do this in all cases of upper-thirdcarcinoma with vocal-cord paralysis. The remain-ing seventeen cases in their series were in thelower two-thirds of the oesophagus, and of theseonly two gave rise to " dysphagia pneumonitis."The two-conditons most frequently responsible

for the presence of retained liquid in the pharynxare achalasia of the cardia and pharyngeal diverti-culum. Even in advanced cases of mega-oesophagus secondary to achalasia the columnof fluid seldom reaches the glottis when thepatient is in the upright position, and thus it isonly liable to be aspirated in recumbency. Thereare cases on record of patients who had to sleepin- the upright position to prevent the chokingcaused by recumbency (Grey Turner, 1946). Thefact that regurgitation occurs under these condi-tions may be due, as has been suggested by Negus(1942), to incompetence of the cricopharyngealsphincter.The method by which the contents of the

pharyngeal pouches get into the danger area isprobably different. Alteration in position of thehead from side to side may squeeze the retainedcontents of the pouch into the pharynx; duringthe daytime gravity carries the material away fromthe glottis, but during sleep it flows upwards.

Sergent and others (1934) produced an hypo-thesis to account for loss of the normal protectivereflex of the glottis. They described a patientwho was found to have barium in his right lowerlobe after a barium swallow. The patient hadbeen unaware of the passage of liquid into hisbronchial tree. These authors suggested thatrepeated small "insults" dulled the normal reflexand gave rise to aspiration during deglutition.

Brock (1946) explains the predilection of lungabscess for the upper lobes by stating thatbronchial embolism occurs when the coughreflex is diminished during sleep, recumbencyand gravity being responsible for the position of

the abscesses. A large proportion of the cases inhis series had upper-lobe disease.

Anaesthesia also causes abolition of the coughreflex. Post-operative bronchial embolism maybe due to material aspirated from the oesophagusas well as from the much more common sitesabove the glottis. This occurred in Case 1, inwhich the right upper-lobe collapse was due toaspiration of oesophageal contents either duringor soon after operation.

Price Thomas (1948) suggests that in order todiminish the risk of aspiration in- the pre-operative period the pouch or oesophagus shouldbe cleansed with sodium bicarbonate and thenemptied by the patient tipping head downwardsjust before retiring. Emptying the "sump"immediately pre-operatively, either by this methodor by oesophagoscopy as practised by Allison,seems a wise precaution.

PATHOLOGYGeneral.-Certain aspects of the pathology of

the pulmonary lesions secondary to the aspirationof oesophageal contents differ from those secon-dary to aspiration from the upper respiratorytract and mouth. There are two reasons for this:the aspirations of oesophageal contents frequentlytake the form of repeated small insults to thebronchial tree, rather than of large " spills" ; andsecondly the material aspirated is less liable tocontain pathogenic organisms. Where there isulceration of the oesophageal lesions, as in thecase of carcinomata, pulmonary complicationsoccur earlier than in achalasia where ulcerationis a late and inconstant feature.The pulmonary lesions with which the patients

have presented in this series have been as follows:Lung abscess .. .. 18BronchiectasisFibrosis" Lipoid pneumonia" . ." Pneumonitis "

Collapse

6.. 10

48

..2

Total .. 48

As the aetiology of these lesions is fundament-ally the same, no hard-and-fast line should bedrawn between them; each is a manifestation ofan incident in the course of the disease. As pul-monary abscess formation is the most seriouscomplication, the largest number of cases werediscovered at this stage. At least five of theseabscesses gave rise to residual fibrosis, and twopatients who were discovered at the stage of

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TABLE ISUMMARY OF HISTORIES OF PATIENTS WITH PNEUMONMTlS

CourseAuthor Age Sex Cause Effect Site and Presentation

comments

Cummins and 30 F Achalasia Pneumonitis Right Acid-fast bac- DysphagiaWilliams illi, clubbing

Bird-Acosta.. 58 M Achalasia Pneumonitis 2nd and 5th Cleared com- Recurrentright inter- pletely pneumoniaspace

Weens .. 18 F Achalasia Pneumonitis Both tases Cleared 1 year Dysphagia 2 yearsJackson 42 M Achalasia Pneumonitis Right lower Cleared Dysphagia, regurgi-

lobe tation, cough, andsputum 8 years

Jackson . 1 F Stricture Pneumonitis Diffuse Cleared com- Regurgitation andpletely cough since birth

Tucker .. 13 M Achalasia Pneumonitis R ight upper Cleared com- Chronic coughlobe . - pletely

Wooler .. 16 F Achalasia Collapse with Right mid-zone Minimal dys- Cough haem o-pneumonitis and right phagia ptysis

lower lobeCase 2 .. 41 M Achalasia Pneumonitis Mid-zones max- Acid-fast bac- Pneumonia

imal on right illi, clearedCase5 .. 65 M Diverticulum JPneumonitis Right second Acid-fast bac- Dysphagia and re-

inter-space illi, cleared current pneumonia8 years

fibrosis gave histories suggestive of abscessformation.

Tracheo-bronchitis.-This lesion can cause recurrent.cough long before the development of frank pul-monary lesions, and a low-grade tracheo-bronchitisis inevitable whenever irritating material is repeatedlyaspirated in small quantities. This is responsible forthe long-standing cough often associated with dys-phagia. It has been mrentioned specifically by Jacksonand Jackson (1933) and by Tucker (1933); the formerauthors proved the presence of tracheo-bronchitis onbronchoscopy.

"Pneumonitis."-The term " dysphagia pneumo-nitis" is used in the broad sense to cover all pul-monary lesions associated with dysphagia. In thissection "pneumonitis " is taken to mean non-specificinflammation of the interstitial tissue of the lung; ithas occurred as a separate entity and also in associa-tion with fibrosis (Case 8) and with lung abscesses(Case 6). In nine cases (three of which were associ-ated with acid-fast bacilli in the sputum) it has pre-sented as a separate entity, and the impression givenby the histories is that the aspirations responsiblewere minimal, sporadic, and of short duration (as inCase 2).

" Pneumonitis " has been mentioned as occurringin association with fibrosis on five occasions. Itcleared subsequently and must have been due to anexacerbation of the process causing the fibrosis. Thefeatures common to these patients were. that they allcleared up completely, some after treatment of their

dysphagia, and all had had single or recurrent attacksof " pneumonia "' with fever, cough, sputum, and painin the chest. The distribution of the lesions waspredominantly right-sided and in the mid-zones. Theoriginal radiograph of Case 2 is similar to those pub-lished by Warring and Rilance, both of whose patientswent on to fibrosis. In Case 2 complete clearingtook place, and the relative shortness of history andpaucity of symptoms accounts for this difference,although it is possible that in all cases of " pneu-monitis" some degree of fibrosis takes place, butthat only in old-standing ones is it sufficiently denseto be radio-opaque.

Pulmonary abscess.-A major spiHl of materialfrom the oesophagus, in some cases containing viru-lent organisms, is the probable cause of developmentof pulnonary abscesses. Of the eighteen casescollected in this series three have been multiple andten have been described as foetid. The localizationof the lung abscesses has been as follows:

Right upper lobe ... ... ... 11Right middle lobe ... ... 0Right lower lobe ... ... ... 5Left upper lobe ... ... 1Left lower lobe ... ... 3

Of those occurring in the lower lobes four have beenin the apical segments; that is, of the total twentyabscesses in eighteen cases, sixteen have occurred inthe sites most liable to bronchial embolus duringrecumbency.The positions in which a group of patients slept

were recorded twice a night in order to see whether

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TABLE IISUMMARY OF HISTORIES OF PATIENTS W1TH PULMONARY ABSCESS

CourseAuthor Age Sex Cause Effect Site and Presentation1~-.. ]comments

Putrid abscess

Putrid abscess

Abscess

Abscess

Abscess

Foetid abscess

Foetid abscess

Non-foetid ab-scess

Foetid abscess

Foetid abscess

Foetid abscess

Foetid abscess

Chronic abscess

Foetid abscess

Foetid abscess

Foetid abscess

Abscess collapseAbscess

Right upperlobeRight upperlobeRight upperlobe; left lowerlobeRight upperlobe

Right upperlobeRight upperlobe

Right dorsallobeRight upperlobeRight upperlobeRight upperlobeRight lowerlobeRight upperlobeLeft dorsallobeRight lowerlobeRight upperlobe, rightdorsalRight lowerlobe

Left upper lobeLeft dorsal lobe

Fibrosis

Asymptomatic;lung stone

Acid-fast bac-illi, fibrosis

No full des-cription

Acid-fast bac-illi, fibrosis10 years mini-mal dyspha-gia

Fibrosis"Silent" dys-phagia

10 years' dysphagiaand regurgitationLung abscess

10 years' dysphagiaand regurgitation

Dysphagia

Dysphagia and re-gurgitationLung abscess

10 years' dysphagia

Lung abscess

20 years bron- Dysphagia 9 yearschitis, clearedNo fistula Dysphagia; short

history15 years' cough Dysphagia 15 years

and regurgitationCleared com- Lung abscesspletely

Recurrent pro- Dysphagia 16 yearsductive cough

Cleared up Lung abscess

£Cleared up Dysphagia and re-gurgitation

Cleared up Broncho-pneumonia

Fibrosis Dysphagia I yearCleared- fib- Lung abscessrosis-"sil-ent" dys-phagia

the predominance of right-sided lesions could beaccounted for by gravity. The results were asfollows:

Right side ... ... ... 579Left side 429

Back . ... ... ... 302The straightness of the right main bronchus tends tomake aspirated material go to the right side when thepatient lies on his back, and thus lesions on the rightside should be twice as common as those on the left.In fact the proportion is higher.

In this series not one of the pulmonary abscesseshad to be drained; of those in which details weregiven, three died, five led to fibrosis with disappear-ance of the cavity (Case 4), two led to chronic

abscesses (one with a "lung stone" but no symp-toms), and five cleared up completely. The clinicalcourse is different from the other types of aspirationabscess-in which chronicity is so much more common.

Abscess formation is an incident in the course ofthe disease. Where there has been a very long historythe likely end result will be fibrosis; where the historyhas been short complete clearing appears to be morelikely.

Pulmonary fibrosis.-A prolonged series of aspira-tions extending over many years gives rise to pul-monary fibrosis, and it-is the most frequent end resultof dysphagia pneumonitis. Ten cases were first diag-nosed- at this stage, and five of the pulmonary abscesses

Vinson

Sampson

Rothstein arPirkle

Keefer

Baldwin

Weens

Bird-Acosta . .

Lallemant andOrdioni

Sergent

Sergent

Mallory

Pruvost andLeblancChabrol andCachin

Sergent

Walle

Jackson

Case 6Case 4

42

40

41

63

24

29

53

38

64

45

64

48

7

44

4669

M

M

F

M

F

M

F

F

M

M

M

M

9

F

M

M

MM

Achalasia

Achalasia

Achalasia

Carcinom aupper onethird

Achalasia

Achalasia.

Achalasia

Achalasia

Stricture

Carcinomaupper third

Achalasiaandcarcinoma

Diverticulum

Achalasia

Diverticulum

Stricture

Stricture

DiverticulumCarcinomalower third

48

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TABLE IIISUMMARY OF HISTORIES OF PATIENTS WITH PULMONARY FIBROSIS AND LIPOID PNEUMONIA


comments

Hawes and 57 M Achalasia Fibrosis Mid-zone max- One haemo- Dysphagia and re-Soule illary right ptysis gurgitationHawes and 31 M Achalasia Fibrosis Mid-zone No pulmon- Dysphagia and re-Soule ary symptoms gurgitationWeens .. 37 F Achalasia Fibrosis Maxillary right No dysphagia Productive coughWeens 26 F Achalasia Fibrosis Right maxil- Clubbing Dysphagia and re-

lary zone both gurgitationlower

Bird-Acosta.. 39 M Achalasia Fibrosis Mid-zone Aspirated via Productive cough 2bronchoscope years

Warring and 65 F Achalasia Fibrosis Maxillary right Acid-fast bac- Dysphagia and re-Rilance illi gurgitation 19 yrs.Robson and 13 F Achalasia Fibrosis All zones max- Post-mortem Dysphagia and re-Wilkinson illary right confirmation gurgitation 6 yearsHeaton 51 F Achalasia Fibrosis Mid-zones max- Previous his- Dysphagia and re-

illary right tory of ab- gurgitation 30 yrs.scess

Case 3 .. 50 M Achalasia Fibrosis Mid-zones max- Recent bron- Dysphagia and re-illary right chitis gurgitation 20 yrs.

Case 8 .. 35 M Achalasia Fibrosis Mid-zones max- Mega-oeso- Cough and dys-illary right phagus and pnoea

regurgitationCase 9 .. 19 F Achalasia Lipoid pneu- Mid-zones History of Dysphagia 3 years

monia use of liquidparaffin

Thomas .. 32 M Achalasia Lipoid Right mid-zones Recurrent Dysphagia 4 yearspneumonia left base pneumonia

Wooler .. 31 F Achalasia Lipoid Left lower lobe Due to liquid Dysphagia and re-pneumonia paraffin gurgitation

Tcherthoff .. 77 M Diverticulum Lipoid Left lower lobe Improved, due "Bronchial carci-pneumonia to excess milk noma"

led to residual fibrosis. Heaton's (1948) case had anold history of lung abscess, and several others eithershowed areas on their radiographs suggestive of cavityformation or had histories of febrile attacks associ-ated with cough, sputum, and haemoptyses. Thediagnosis has been radiological, the presence offibrosis alone often giving rise to no symptoms orto a non-productive cough, febrile incidents beingassociated with superadded " pneumonitis" or abscessformation.The characteristic radiological picture is one of

bilateral mid-zone infiltration greater on the rightthan on the left, and often sharply demarcated belowby the fissures (for example, Plates Illa and IVa) andmaxinial at the hilum.The patient described by Robson and Wilkinson

(1946) died after the performance of a Heller's opera-tion; at necropsy the lungs showed widespread nodu-lar fibrosis of all zones, reaching a maximum in theright upper lobe; this suggests that fibrosis may bemore diffuse than is apparent radiologically. Fibrosisalone in this series had not given rise to much dis-ability; dyspnoea and clubbing are recorded, but nocases have developed right heart failure.

D*

Lipoid pneumonia.-Tcherthoff (1941) reviewed the140 published cases of this disease; he stated that allwere secondary to some form of defective swallowingand gave a long history of injections of some oilysubstance; mineral oils in particular were responsible.In the final stages mid-zone fibrosis with an excess ofoil in the lungs develops. He described one case inwhich the disease followed excessive ingestion of milkin a man of 77 suffering from a pharyngeal diverticu-lum. Two others have been described in associationwith achalasia; Case 9 in this series makes the totalup to four. The radiological opacities which are inthe mid-zones (Plate IVa) are mainly due to fibrosisand the oily deposits are coincidental. These casesare examples of pulmonary fibrosis secondary to dys-phagia with the added factor of a high fat content inthe material retained in the oesophagus; sooner orlater aspiration of this fatty material leads to thedevelopment of lipoid pneumonia.

Collapse.-There are two possible causes ofcollapse; a large- "bolus" may be aspirated caus-ing flooding of a bronchus; this was responsible forthe upper-lobe and lower-lobe collapse in Case 1. Thealternative is that a bronchus becomes occluded by

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the dilated oesophagus pressing upon it from behind.Plummer and Vinson (1921) record cases with post-prandial dyspnoea which in their opinion were due todilatation of the oesophagus, and Bird-Acosta recordsan enormous mega-oesophagus causing a bulge in theposterior wall of the trachea which was observed atbronchoscopy. Wooler is of the opinion that thelatter mechanism is responsible for the collapse, asre-expansion took place after dilatation of the cardiacsphincter in his case.

CLINICAL FEATURES

Grey Turner (1946) has stated that achalasiaof the cardia may present as a chronic cough.Examples have occurred in this series which pre-sented as pulmonary disease with completely" silent " dysphagia, and there were others inwhich the pulmonary lesions were revealed onlyon routine radiography during investigation ofdysphagia. Many intermediate examples havebeen reported. The patients in this series havebeen divided into three clinical groups: those whopresented with major pulmonary and minor dys-phagic symptoms; those who presented as dys-phagia with subsequent development of pulmonarylesions; and a few cases in which these symptomsappeared almost simultaneously.The patients with " silent dysphagia " constitute

an important group. They may be defined asthose who have a definite obstruction to normaldeglutition but who have had no subjective diffi-culty in swallowing. There have been eightdescribed, and unless it is recognized thatmechanical obstruction of the oesophagus suffici-ent to lead to aspiration with consequent pul-monary lesions can exist without symptoms ofwhich the patient is conscious, the real aetiologyof the pulmonary lesion may be overlooked.Cases 4 and 7 are examples of " silent dysphagia,"but in those described by Pruvost and Leblanc(1935) and Lallemant and Ordioni (1945) the oeso-phageal lesions were discovered fortuitously whentransnasal bronchography was performed. Ineach, some of the iodized oil went past the glottis;in the first a hitherto unsuspected pharyngealdiverticulum, in the second an achalasia of thecardia which had been symptomless, becameapparent. Both these patients had presented withright upper-lobe lung abscesses.Asymptomatic pulmonary lesions are of less

importance, but the presence- of radiologcalchanges in the lung fields in association with dys-phagia makes active treatment of the latter morenecessary in order that serious pulmonary lesionsmay be avoided. The presence of bilateral mid-

zone fibrosis in association with achalasia wasrecognized in a case described by Hawes andSoule (1945), and it was not until two years laterthat an haemoptysis with purulent foetid sputumdeveloped.

Eighteen patients presented with predominantlypulmonary symptoms. The eight "silent dys-phagias" are included in this number, and theremaining ten had varying degrees of dysphagia,but often they had become accustomed todysphagia and only admitted its presence onquestioning.A long-standing cough in association with the

dysphagia has been a frequent feature, and it inaybe the only clinical indication of a pulmonarylesion. Jackson and Jackson (1933) are of theopinion that there is a "tussive centre" at thelower end of the oesophagus, and that any lesionor pressure from a column of liquid on this areamay be responsible for a reflex cough. It is alsoprobable that even in the early stages of achalasiasmall aspirations take place which cause tracheo-bronchitis and an irritating cough. In the fourcases in which the onset of pulmonary anddysphagic symptoms has been simultaneous, thismechanism may have been responsible for theearly development of the cough.The remaining twenty-six cases presented with

predominantly dysphagic symptoms, although inseveral the onset of the pulmonary disease wasresponsible for their seeing a doctor. In four thelung lesion was symptomless and was discoveredby the radiologist.Freeman (1940), discussing the symptomatology

of achalasia, states that the average length ofhistory is five years and that the predominantsymptoms are dysphagia, pain, and regurgitation.In this series the dysphagia has often been mini-mal or periodical, despite the presence of enormousmega-oesophagus. Regurgitation, which Freemanregards as a late symptom, has been common; ithas often been associated with nocturnal cougband choking, and has been recorded eighteentimes. Plummer and Vinson (1921) mentionregurgitation as occurring in eighty-nine of 301cases of achalasia.Where the length of history of dysphagia in

patients suffering from achalasia and with pharyn-geal diverticula has been given, it has averagedten years prior to the onset of pulmonary symp-toms. Pulmonary lesions may therefore beregarded as a late complication; but aspirationphenomena complicating carcinomata and stric-tures appear more rapidly.

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THE. PULMONARY COMPLICATIONS OF DYSPHAGIA

TABLE IVSUMMARY OF HISTORIES OF PATIENTS SUFFERING FROM BRONCHIECTASIS


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Schrier .. 12 F Achalasia Bronchiectasis Right middle S i I e n t d y s- Productive cough 6and lower phagia yearslobes

Wooler 18 F Achalasia Bronchiectasis Bilateral Minimal dys- Pneumonia, coughphagia 5 years

Weens 28 F Achalasia Bronchiectasis Bilateral lower Mega-oeso- Productive coughlobes phagus 15 years

Reeke 19 F Achalsia Bronchiectasis Bilateral lower Simultaneous Dysphagia and re-lobes onset gurgitation since

infancyChabrol and 46 M Peptic ulcer Bronchiectasis Right lower Coughs 1 year Dysphagia 2 yearsCachin ofoesopha- lobe

gusCase 7 .. 6 F Achalasia Bronchiectasis Right middle S i I en t d y s- Pneumonia

upper lower phagialobes, left lin-gular -_ _ _ _ _ _ _

Two groups appear to be clinically separatefrom the majority of the cases. Those whichhave been associated with bronchiectasis havealmost all occurred in young people (five out ofsix), and in several it was difficult to determinewhether or not the dysphagia, which in three wasalmost silent (Case 7), preceded the bronchiectasis.The average age for onset of symptoms was sixyears and of presentation 20, whereas in theremainder of this series the average age ofpresentation was 43 years. The bronchiectasishad the usual distribution in the lower and middlelobes, and it is possible that aspiration which inadults is liable to produce lung abscess gives riseto bronchiectasis in younger patients. In thesecond group the pulmonary lesions have beenassociated with acid-fast bacilli in the sputum.It is not stated whether or not the three cases ofpulmonary tuberculosis referred to by Plummer andVinson in relation to achalasia were confirmedon culture and guinea-pig inoculation. The firstcase in which acid-fast bacilli were found andwere recognized as being non-tuberculous wasdescribed by Cummins and Williams (1933);since then there have been three more in theliterature. Cases 2 and 5 in this series make thetotal six. All except Case 5 were secondary toachalasia.The bacilli which Cummins and Williams iso-

lated were non-pathogenic to guinea-pigs. InBaldwin's (1942) case the acid-fast bacilli werenon-pathogenic and were found in both vomitand sputum. A "tuberculin" was made from the

organisms to which the patient gave a markedlypositive reaction, but despite this the organismwas considered to be non-pathogenic and wastfiought to be related to the Timothy grass bacillus.Warring and Rilance (1943) described the next case;the clinical and radiological findings were simi-lar to Baldwin's and to Case 2; the "'tuberculin "reaction was positive. The third case was reportedby Rothstein and Pirkle (1946); the patient was" tuberculin " positive, but negative to the stan-dard tuberculin tests. The-radiographs of two ofthe patients in whose sputa acid-fast bacilli werefound showed cavitation; in the other two thefilms were similar to that shown in Plate Illa.The feature which originally led to the suspicion

that the patients were not tuberculous was thepresence of few or occasional " showers " oforganisms, with persistent copious sputum.Where follow-ups are available the pulmonarylesions have either cleared up completely or haveleft residual fibrosis in the mid-zones. The coughand sputum have been considerably relieved by thetreatment of the dysphagia. Case 2, diagnosedat first as suffering from pulmonary tuberculosis,now shows a clear radiograph (Plate IIb), and wascertainly never tuberculous. Case 5 is still doubt-ful; the acid-fast bacilli were found on only oneoccasion and were not cultured. He is almostsymptom-free and is assumed to be non-tuberculous.The acid-fast bacilli are derived from the

oesophagus, possibly from fruit skins; they areaspirated into the bronchial tree and are non-

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J. R. BELCHER

TABLE VCAUSES AND CONSEQUENCES OF DYSPHAGIA IN THE PRESENT SERIES

Number Abscess Bronchiectasis Fibrosis Pneumonitis Collapse Lipoid.pneumonia

Achalasia .. .. 34 9 4 10 6 2 3Pharyngeal diverticulum 5 3 - - 1 - ICarcino,wa of oesophagus 3 3 _Various strictures .. 6 3 2 1 _

Total .. .. 48 18 6 10 8 2 4

pathogenic. The pulmonary lesions they produceare similar to those of pneumonitis in which noacid-fast bacilli have been demonstrated, and thefinding of the organism is coincidental. Theassociation of pulmonary tuberculosis with mega-oesophagus is sufficiently uncommon to have beenreported when it has occurred, and it is suggestedthat when aspiration pneumonitis appears thediagnosis of tuberculosis should be confirmed byculture or guinea-pig inoculation. Achalasia andpulmonary tuberrulosis can co-exist as in the caseillustrated (Plate JVb); this man had had six yearsof recurrent pulmonary symptoms prior to anacute onset of achalasia.The causes of dysphagia and their consequences

in this series are shown in Table V.

SUMMARY1. Forty-eight cases of " dysphagia pneumo-

nitis" have been collected. Their incidence,aetiology, clinical presentation, and pathologyhave been discussed.

2. In association with dysphagia, pneumonitis isdue to small sporadic aspirations; pulmonaryabscess to a major spill of oesophageal contents;fibrosis to a prolonged period of small aspirations;and lipoid pneumonia to this type of aetiologywith the addition of a high fat content in theretained oesophageal material.

3. " Silent dysphagia" is a possible cause of pul-monary lesions of obscure origin.

4. Acid-fast bacilli found in the sputum ofpatients with mechanical dysphagia should beregarded as non-pathogenic until proved otherwise.

5. The end result of the syndrome is most fre-quently pulmonary.fibrosis.

My gratitude is due to the members of thehonorary staff of the Brompton Hospital who haveprovided the material for the new cases describedand who have been helpful with their advice andcriticisms.

REFERENCESBaldwin, E. R. (1942). Amer. Rev. Tuberc., 45, 756.Bird-Acosta, I. (1944). Amer. J. Roentgen., 52, 481.Brock, R. C. (1946). "Anatomy of the Bronchial Tree."

London.Camiel, M. R., and Loewe, L. (1941). Ann. int. Med.,

15, 63.Chabrol, E., and Cachin, M. (1933). Bull. Nem. Soc.

Med. Hosp., Paris, 49, 1531.Cummins, S. L., and Williams, E. M. (1933). Tubercie,

15,49.Eley, A. J. (1948). Personal communication.Freeman, E. B. (1940). Rev. Gastroenterol., 7, 385.Hall6, J., and others (1930). Arch. Mid. Enfants, 33, 670.Harrington, S. W. (1945). Surgery, 18, 66.Hawes, L. E., and Soule, A. B. (1945). Amer. J. Roentgen.,

53, 124.Heaton, T. G. (1948). Dis. Chest., 14, 425.Jackson, C., and Jackson, C. L. (1933). Sect. Otolaryn-

gol. A.M.A., p. 197.Keefer, C. S. (1934). Ann. int. Med., 8, 72.Lahey, F. H. (1946). Amer. Surg., 124, 617.Lallemant, M., and Ordioni, P. (1945). Ann. d'otolaryn-

gol., 12, 284.Mallory, T. B. (1938). New Engl. J. Med., 218, 607.Negus, V. E. (1942). Proc. R. Soc. Med., 36, 85.Plummer, H. S., and Vinson, P. P. (1921). Med. Clin.

N. Amer., 5, 355.Pruvost, P., and Leblanc, M. (1935). Arch. med.-chir.

Appar. resp., 10, 242.Reeke, T. (1933). Dtsch. Z. Chirg., 241, 488.Robson, T., and Wilkinson, R. S. (1946). Lancet, 1, 737.Rothstein, E., and Pirkle, H. B. (1946). Dis. Chest., 12,

232.Sampson, D. A. (1938). New Engl. J. Med., 219, 982.Schrier, T. (1938). Lancet, 2, 1225.Sergent, E. (1937). Rev. gen. Clin. Therap. J. Pract., 51,

497.Sergent, E., Poumeau, Delille-G. (1934). Paris Mid.,

1, 154.Tcherthoff, I. (1941). Quart.Bull. Sea View Hosp., 7,334.Thomas, C. Price (1948). Personal communication.Thomas, W. S., and Jewett, C. H. (1936). Clift. med. Bull.,

12, 130.Tucker, G. (1933). Sect. Otolaryngol. A.M.A., p. 197.Turner, G. Grey (1946). "Injuries and Diseases of the

Oesophagus."- London.Vinson, P. P. (1927). Amer. J. Surg., 2, 359.Waffing, F, C., and Rilance-,A. B. (1943). J. Lab. clin.

Med., 28, 1591.Weens, H. S. (1944). Amer. J. Roentgen., 52, 472.Wooler, S. (1948). Thorax, 3, 53.

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