Pulmonary abscess

ROBERT F. EGGERT, D.O.,* Columbus, Ohio

Pulmonary abscess is always a serious condition;it carries with it a high mortality.

Actual mortality statistics seem to vary consider-ably between various sources. According to a ratherextreme estimate as late as 1947, 1 pulmonary ab-scess had the highest mortality rate of any pulmo-nary disease except neoplasms.

Causes and classification

Abscesses may be single or multiple, small or large,with or without associated changes in other partsof the lungs, pleura, or other organs. The diseaseis caused by a variety of agents. 2 The lung may beinvolved by hematogenous implantations of septicemboli from distant foci, or as a result of secondaryinfection following acute inflammation. The mostfrequent cause is aspiration of infected materialfrom the upper air passages, especially duringoperations under general anesthesia or followingtrauma and unconscious states.3

Some authors do not differentiate between putridand nonputrid lung abscess, but a majority seemto recognize pathologic and clinical distinctionsbetween the two. 1 ,4 -6 The following are the mostimportant types of abscess formation:1

1. Embolic lung abscess2. Bronchogenic lung abscesses

a. nonputridb. putridc. chronic

3. Lung abscesses secondary to other pulmonarydiseases ( notably bronchiectasis, infarction, andneoplasm )

4. Lung abscesses secondary to pathologic proc-This paper was submitted in partial fulfillment of the requirementsfor certification by the American Osteopathic Board of Radiology.

°Address, 1087 Dennison Ave.

esses in the thoracic wall, esophagus, mediastinum,spine, and other adjacent organs.

Blood-borne implantations of septic emboli in thelungs occasionally give rise to suppuration and ab-scess formation. The source of the pyemia may bein an osteomyelitic bone, a suppurative appendix,otitis media, infection of the urinary tract, or inbacterial vegetations on the cardiac valves. Throm-bophlebitis may be the primary nidus. Theseabscesses are soft, yellowish, and practically odor-less. The symptoms, aside from moderate cough andchest pain, are those of a generalized sepsis ratherthan a pulmonary disease. Physical examination isusually noncontributory. The roentgenogram of thechest shows sharply defined densities of approxi-mately the same size, more numerous in the middleand lower lung fields. At other times, the pictureis that of a suppurative bronchopneumonia. Largerdensities may show evidence of central rarefaction.The small abscesses may simulate metastatic neo-plasms.

Nonputrid bronchiogenic abscesses are causedby pyogenic organisms such as streptococci, staphy-lococci, and pneumococci. The abscesses are usuallysmall and involve both lungs. Similar but largerabscesses occasionally follow infections of the upperrespiratory tract, operations, or difficult labor. Thenonputrid character of the abscesses is ascribed tothe fact that the mouths of the particular individu-als happen to be free from anaerobic organisms.This explains the comparative rarity of lung ab-scesses in children except after tonsillectomy.3

Nonputrid abscesses may be associated with fewsymptoms or with signs of pneumonia. A rapidlyresolving pneumonia may roentgenographicallysimulate a pulmonary abscess, but whereas pneu-monia takes a few weeks to resolve, pulmonaryabscess usually takes several months. Antibiotictherapy and supportive measures are effective ina vast majority of nonputrid abscesses which arenot complicated by other major diseases. If a large,solitary pulmonary abscess fails to respond to

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specific treatment or shows signs of enlargement,surgical drainage is indicated.3

Pathology and pathogenesis

Putrid abscesses were known to the pathologistsfor many years as lung gangrene. 1 The conditionis caused by aspiration of anaerobic organismsnormally present in the upper air passages of adultsand found in abundance in those with pyorrhea,gingivitis, diseased tonsils, or carious teeth. Theseanaerobic organisms include streptococci, fusiformbacilli, vibrios, spirochetes, and other gram-negativebacilli acting in symbiosis. It is interesting to notethat none of these organisms could produce thedisease when experimentally injected alone." Incombination, they were found to give rise to gas,fetid odor, and greenish pus.

The clinical picture in these infections variesfrom simple bronchitis to fulminating gangrene,bronchiectasis, and putrid abscess formation. Pre-existing pneumonitis, bronchial asthma, pulmonaryarteriosclerosis, infarction, advanced age, diabetes,alcoholism, and a generalized pulmonary constitu-tional inadequacy are among the conditions favor-ing massive putrefaction. There is reason to believethat in the presence of carious teeth and poor oralhygiene, aspiration infection may arise spontane-ously during sleep or under the effects of soporificsand alcohol. Putrid abscess may follow diabeticcoma, insulin shock, cardiospasm, or aspiration ofvomitus from one cause or another.'

Atelectasis is a prerequisite to the formation ofputrid lung abscess; it has been shown experi-mentally that the presence of anaerobic bacteriawithout atelectasis fails to produce the disease.5Once the organisms become implanted in atelec-tatic lung there is rapid necrosis of the tissue withthe liberation of compounds such as indole andskatole, which facilitate the process of decomposi-tion.

Putrid lung abscesses arise most often in a su-perior segment of a lower lobe or in the basalsegment of an upper lobe, chiefly of the rightlung. These locations have been shown experi-mentally to be the favorite sites in aspiration in-fections when the individual is on his back, aswould occur during anesthesia or some other un-conscious state. 3 The more direct course of thebronchi in the right lung is responsible for thegreater vulnerability of this organ to aspirationinfection.

Inasmuch as impaction of an infected particleis most likely to occur in the lumen of a smallbronchus or bronchiole, the disease almost invari-ably begins in a peripheral portion of the lung.The subpleural location of these lesions causes anearly reaction between the lung and the chest wall,between adjoining lobes, or between the lung andthe diaphragm, or wherever the infected materialhappens to lodge. The zone of inflammation extendsto the pleura in every case, resulting in a localizedpleurisy with adhesions early in the disease process.

It perforation occurs before a protective pleuritishas been formed, a putrid empyema is the result.In such a case it is often difficult to ascertain theprimary site of the disease. Lung abscesses usuallycommunicate with a bronchus; so perforationthrough the pleura can produce a pyopneumothorax.In a case where perforation occurs early and aprotective pleuritis has not formed, a total pyo-pneumothorax is possible, and such a complicationhas been stated to be almost always fatal.'

With abscess formation, the major part of theaffected bronchopulmonary segment undergoesliquefaction and the contents are eventually ex-pelled through the bronchi. A cavity forms, thewall of which is soft and easily collapsible, con-taining a variable amount of greenish-gray, foul-smelling debris. The surrounding lung tissue is con-gested and edematous.

Later stages are characterized by thickening ofthe cavity wall which becomes hard and smooth,the formation of additional necrotic foci, and thedevelopment of fibrosis and bronchiectasis in theadjoining lung tissue. Specimens obtained at lobec-tomy may show considerable fibrosis and bronchiec-tasis in patients whose abscesses are of fairly recentdevelopment, a point to be remembered when theproblem of surgical drainage or lobectomy is underconsideration.

Diagnosis

The symptoms of putrid lung abscess vary consider-ably in intensity and duration. At one extreme onemay encounter a relatively benign inflammationwith rapid healing; at the other, a fulminatinggangrene with a fatal outcome.

The initial manifestations are those of an acutepneumonia with irregular fever, cough, chest pain,chills, sweats, tachycardia, and dyspnea. Foulbloody expectoration soon dramatizes the disease.The foul sputum is a distinguishing feature ofanaerobic lung infection. 5 Sudden stoppage of ex-pectoration, usually caused by block in the drain-ing bronchi, is likely to be followed by an exacer-bation of symptoms. Once free expectoration isestablished, it is customary to find temporary reliefof symptoms. Chest pain is also a prominent symp-tom and usually appears early. The pain maydisappear when the visceral and parietal layers ofthe pleura become fused.

When physical signs are elicited they point moreto pneumonia than to an abscess. More revealingare the history, foul-smelling expectoration, chestpain, and digital clubbing. The last often comeson fairly rapidly. ? There is usually a variable degreeof anemia and leukocytosis.

It is a good practice to examine the sputum foracid-fast organisms, as pulmonary suppuration maycoexist with fibrotic pulmonary tuberculosis, espe-cially in older patients. Rubin' has written of sev-eral cases of lung abscess which came under hisobservation where there was reason to believe thatthe suppuration sloughed out a dormant tuberculous

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process, which was evidenced by short periodsduring which the sputum contained acid-fastorganisms.

At its onset, a bronchogenic lung abscess, whetherputrid or nonputrid, appears roentgenographicallyas an area of undifferentiated density such as oneencounters in pneumonia. With liquefaction andexpulsion of the contents, one or more areas ofcavitation are noted. At this stage the inflammatoryreaction surrounding the abscess is still quite pro-nounced.

Later, the surrounding inflammation subsidesand one notes an irregular faint line of increaseddensity, often with a fluid level at the base. Afluid line may be the most conspicuous part of theabscess, because at this stage the wall is not dis-tinctly formed; its margin merges imperceptiblywith that of the surrounding parenchyma. Thecavity may be delineated better in films taken inseveral projections. Fluid levels shift with changesin position; so the use of fluoroscopy is extremelyvaluable in this point of differentiation and diag-nosis.8

The x-ray occasionally fails to reveal a distinctcavity. In such instances, overexposed or body-section films are often diagnostic. At times, thepleural reaction may obscure the lung detail tosuch an extent that the nature of the disease maynot be known with certainty until a thoracotomyis performed.

Complications

The chief complications of pulmonary abscess re-sult from spread of the disease within the lung tothe pleura, or to distant organs, particularly thebrain, spleen, liver, and kidneys.

Cerebral involvement is a serious complicationof lung abscess. For many years it was difficult toexplain the relatively frequent occurrence of cere-bral abscess as a complication of pulmonary sup-puration, bronchiectasis, or pulmonary neoplasm.This was clarified in 1940 when Batson drew at-tention to a collateral circulation existing betweenthe veins of the chest, abdominal wall, and thevertebral column.' The pressure in this venoussystem is so low that with every compression ofthe trunk during strain or cough the pressure israised sufficiently to shunt the blood flow from theazygous channels to the vertebral system. Thepresence of this collateral circulation serves to ex-plain the high incidence of intracranial metastasessecondary to neoplastic or suppurative diseases ofthe lung.

There is no specific criterion which designatesthe time when an acute abscess has become chronic.In an arbitrary division, however, an abscess isacute if less than 6 weeks old, subacute from theseventh to the twelfth weeks, and chronic afterthe twelfth week. With chronicity, the soft necroticmembrane which limits the process in its earlystages becomes converted into an unyielding thickwall eventually covered by epithelium ingrown

from neighboring bronchi. The original abscess maybe partly collapsed and obscured by indurativetissue. Secondary abscesses are quite common; theymay be more pronounced than the primary disease.Other changes consist of interstitial fibrosis, vascu-lar thrombosis, and bronchiectasis. Variable degreesof emphysema, pleuritis, mediastinitis, and intra-thoracic displacements are usually present.

Treatment

The treatment of pulmonary abscess, including thepromotion of healing and the prevention of chron-icity and complications, requires close cooperationbetween internist, roentgenologist, bronchoscopist,and surgeon. Any part of the history or of theclinical course that may suggest the possibility ofan abscess should be supplied to the diagnosticteam when the consultations are requested. Fre-quently, however, the diagnosis is not establishednor the roentgenograms even requested until lique-faction has occurred and the abscess has alreadyopened into a bronchus.

The roentgenogram is invaluable in followingthe course of this disease. In deciding on theproper course to take in treatment, it is well tokeep in mind that healing, if it will occur, willdo so early and will be revealed in successivex-ray films.

Any tendency for the abscess to become chronicor to enlarge calls for operation. Spontaneous cureis unusual after a lapse of 3 or 4 months, andchances from then on decrease rapidly.

All patients with suspected lung abscess shouldhave the advantage of bronchoscopic examinationfollowed by bronchography. 9 In some cases of longstanding, the abscess has cleared and disappearedafter establishment of adequate intrabronchialdrainage.3 If an abscess is allowed to becomechronic, the results of surgical drainage are poorand lobectomy or pneumonectomy becomes neces-sary. Intensive specific antibiotic therapy probablyheals twice as many cases of lung abscess as doessurgical intervention.

Differential diagnosis

Eight differential considerations in pulmonary ab-scess are as follows:

1. False cavities due to emphysema. These havethin walls and are characterized by rapid and com-plete disappearance.

2. Cavity of abscess formation from broncho-genic carcinoma. In this case, there is no responseto treatment. There are positive cell studies bybronchial washings and biopsy.

3. Bronchiectasis. There is usually a prolongedhistory in this disorder. The diagnostic measure isbronchography.

4. Lung cyst with secondary infection. Cystshave sharp external outlines and thin walls. Biopsyof the cystic wall does not show the thick zone ofcellulitis seen in abscess.

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5. Interlobar empyema. Sharper margins and aninterlobar position distinguish this condition.

6. Acute primary fungous infection (for ex-ample, coccidioidomycosis ). A less toxic coursemarks these infections. There will be a history ofexposure. Skin tests and bacteriologic assays areavailable for differentiation.

7. Rare Echinococcus cyst. There will be ahistory of contact with a dog. Eosinophilia, liverinvolvement, and a positive Casoni skin test confirmthat diagnosis.

8. Tubercular abscess. Nontubercular abscessesare more likely to occur in lower lung segments,and also to have a thicker and more irregular cap-sule and usually more fluid. An upper-lobe non-putrid abscess may simulate tuberculosis. The ab-sence of tubercle bacilli in the sputum, and thecomparatively quick resolution of the abscess com-pared to that characterizing tuberculous cavitation,serve to rule out tuberculosis. Of course, a pul-monary abscess may complicate tuberculosis.

A ninth consideration might be the unusuallesion described by Sullivan and Bailey l° in 1951.A series of four cases was presented. The initialfilm studies showed evidence of segmental pneu-monia with a diffuse homogenous density. Thepattern cleared under intensive antibiotic therapy,but a residual abscess cavity with air and fluidpersisted. Surgical intervention recovered Enta-mocha histolytica as the etiologic agent. All subse-quent cases responded to emetine.

It might be well to emphasize here that therecognition of a cavity on an x-ray film dependson contained air. A cavity filled with fluid orexudate cannot be differentiated from infiltrationalone.11

Case report

A 21-year-old asthenic white woman was admittedto the medical service of Doctors Hospital on June19, 1956, with a chief complaint of hemoptysis.There was a history of a childhood emotionalproblem for which she had been hospitalized atage 14 and received shock therapy. X-rays at thattime had been negative for pulmonary tubercu-losis. The first episode of hemoptysis had been inNovember 1955, after years of repeated colds andinfluenza] attacks. Hemoptysis had then appearedintermittently in varying degrees of severity until,approximately 6 months prior to her hospital ad-mission, frank pulmonary hemorrhage had occurredafter a bout of influenza. It is not established whattreatment was utilized at that time, if any. Thebasis for the present admission was the onset ofpulmonary hemorrhage following an episode ofsevere coughing, with dyspnea and left chest pain.

On admission, a survey of the eyes, ears, nose,and throat was essentially noncontributory. Therewas apparent inhibition of thoracic excursions. Onauscultation, a grade 2 mitral systolic murmur waselicited. The right lung was clear; in the left lung,

breath sounds were absent in the base, and therewas dullness to percussion. The abdomen revealedno masses, tenderness, or any other irregularity.There was rather marked clubbing of the fingersand toes with moderate cyanosis. The temperaturewas 102.6 F; the pulse rate was 100 and regular;and the respirations were 32 per minute.

Laboratory examination showed the urine tocontain hemoglobin and occasional erythrocytesand leukocytes. The erythrocyte count was 3,750,000,and the leukocyte count was 12,250, with a differ-ential count of 77 per cent polymorphonuclearneutrophils, 20 per cent lymphocytes, 1 per centhasophils, and 2 per cent juvenile forms. The Kahntest was negative. The sputum was negative foracid-fast organisms, but it was positive for strep-tococcus and staphylococcus. Purified-protein de-rivative tests 1 and 2 were both negative. Theprothrombin time was 100 per cent; the plateletcount was 504,000. The sedimentation rate was 42mm. per hour. Blood cultures were negative. Therewere nonspecific T-wave changes on the electro-cardiogram suggestive of electrolyte imbalance andischemia.

An admission 72-inch frontal projection of thechest showed major left heart enlargement withobliteration of the left diaphragm by a densitywhich extended up and out to the third rib anteri-orly and was suggestive of effusion, both interseptaland parietal in distribution (Fig. 1).

Fig. I. This 72-inch frontal film taken on admission shows markedcardiomegaly and decreased illumination in the lower left lung.

Nothing was recovered by thoracentesis at-tempted at the sight of effusion. Fluoroscopicstudies of the patient on the second hospital dayincluded the use of oral opaque contrast media.The left heart enlargement and mitral configuration

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were evident but not as prominent as 24 hoursearlier (Fig. 2 ). No abnormal tracheal variationwas noted. The density in the lower left pulmonaryfield was essentially that seen on earlier films. Nofluid shift or evidence of cavitation was identified.

Fig. 2. Prominent decrease in heart size following whole bloodtransfusion. Decreased illumination in the lower left lung persists.

The over-all treatment program might be summedup to include the specific antibiotic therapy ( Chlo-romycetin, 6.0 grams, and streptomycin, 6.0 grams ),symptomatic treatment for pain which includednarcotics, digitalization to augment cardiac reserve,coagulants in the form of Mephyton, and multipletransfusions of whole blood.

The erythrocyte count of this patient fluctuatedfrom a low of 2,600,000 to a high point of 3,800,000.The bouts of hemoptysis and frank pulmonaryhemorrhage showed no true evidence of remissionat any time, and the potential of actual exsanguina-tion appeared on several occasions. The possibilityof congenital heart disease accounting for thecardiornegaly seen on the admission chest film wasconsidered. Subsequent films, however, showedmarked diminution in heart size within 72 hoursfollowing the initial blood transfusion. The mech-anism involved could well have been that of cardiaccompensation for the debit of circulating oxyhemo-globin.

Bronchoscopy was extremely difficult because ofheavy discharge of necrotic material from the leftbronchial tree. However, bronchograms were ob-tained and the area of involvement was reasonablywell delineated. These films showed the tertiarybronchi supplying the left upper lobe to be un-impaired. Some of the Dionosil used in this exami-nation was seen to gravitate to a very minor extentinto the proximal portion of the bronchial system

Fig. 3. Bronchogram shows a bizarre pattern in the lower leftlobe, with one of the abscessed bronchiectatic cavities partiallyfilled with opaque medium.

of the lower left lobe. The pattern was extremelybizarre and definitely suggestive of major paren-chymal damage (Fig. 3 ).

Successive roentgenograms pointed to a develop-ing chronic status and the case was subsequentlydeemed refractive after 26 days of conservativemedical management. The patient was transferredto a surgical service and the chest was opened.The area of the lower left lobe of the lung wasoccupied by a necrotic mass of tissue from whichexuded multicolored pus and fluid upon the slight-est pressure. The foul odor was pronounced. Lowerleft lobectomy was performed without any promi-nent surgical complications. The patient receivedsix pints of blood during the surgical procedure.

The pathologist's transsection of the specimendemonstrated an exudate-filled cavity approxi-mately 6 x 4 x 3 cm. located in the posterior andsuperior portion of the lobe. Microscopic examina-tion showed diffuse inflammatory, fibrotic, andbronchiectatic changes.

The postoperative course was uncomplicated andthe patient was discharged in a satisfactory condi-tion, to be followed up by her physician. A dis-missal chest film showed the left chest to be almostentirely filled with the normal re-expanded upperleft lobe.

Summary

A classification of the most significant pulmonaryabscesses has been amplified by some discussionof etiologic factors, symptomatology, diagnosticconsiderations, and brief comments in regard totreatment. Putrid suppurative bronchogenic lungabscess has received the most attention in order to

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make the presentation of such a case more corn-prehensive. The case presented has served well todemonstrate the over-all management required inan extensive putrid abscess formation.

1. Rubin, E. H.: Diseases of chest, with emphasis on x-ray diag-nosis. W. B. Saunders Co., Philadelphia, 1947.

2. Coodley, E. L.: Pulmonary abscess as complication of hiatalhernia. Dis. Chest 17:102-113, Jan. 1950.

3. Metras, H., and Charpin, J.: Lung abscess and bronchialcatheterization. J. Thoracic Surg. 27:157-172, Feb. 1954.

4. Ackerman, L. B.: Surgical pathology. C. V. Mosby Co., St.Louis, 1953.

5. Myers, J. A., and McKinley, C. A.: Chest and heart. CharlesC Thomas, Springfield, Ill., 1948, vol. 1.

6. Bigler, L. G.: Chest—handbook of roentgen diagnosis. Year-book Publishers, Chicago, 1946.

7. Pillmore, G. U., ed.: Clinical radiology; correlation of clinicaland roentgenological findings. F. A. Davis Co., Philadelphia, 1946,vol. 1.

8. Storch, C. B.: Fundamentals of clinical fluoroscopy, with es-sentials of roentgen interpretation. Grune & Stratton, New York, 1951.

9. Overholt, R. H.: Foreword, in Radiologic exploration of bron-chus, by S. diRienzo. Charles C Thomas, Springfield, Ill., 1949.

10. Sullivan, B. H., Jr., and Bailey, F. N.: Amoebic lung abscess.Dis. Chest 20:84-96, July 1951.

11. deLorimier, A. A., Moehring, H. G., and Hannan, J. R.:Clinical roentgenology; vol. 3, lungs and cardiovascular system,emphasizing differential considerations. Charles C Thomas, Spring-field, 1955.

Analysis of exchange transfusions at thePhiladelphia College of Osteopathy,August 1959 through January 1961

JOHN C. LESNIEWSKI, B.S., 13.0.,* Erie, Penn-sylvania

The two major criteria for exchange transfusionsare anemia that may be severe enough to result incardiac failure, and the prevention of kernicterus.These two conditions can be alleviated by adequateremoval of sensitized erythrocytes and proper re-placement with nonsensitized cells.

Bilirubin and antibodies must not only be re-moved from the vascular compartment but mustalso be taken from the extramuscular compartment.Therefore, exchange transfusions are now univer-sally recognized as a treatment for hyperbiliru-binemia, anemia, sepsis,L2 drug intoxications, 3 andother conditions.

The purpose of this paper is to report experiencesat the Hospitals of the Philadelphia College ofOsteopathy as to the criteria and methods em-ployed in 32 cases of newborns receiving exchangetransfusions.

During the period of August 1959 through Janu-ary 1961, 1,758 viable births were recorded at theSubmitted to the faculty of the Philadelphia College of Osteopathyin partial fulfillment of the requirements for the degree of Master ofScience (Pediatrics), Philadelphia, Pennsylvania, May 1, 1981.

•Address, 5728 Wattsburg Rd.

Hospitals of the Philadelphia College of Osteop-athy. Of these, there were 32 cases (1.8 per cent)in which exchange transfusions were performed.Cases included in this report were those in whichthere was hyperbilirubinemia.

Infants treated by exchange transfusion gen-erally had a maternal history of a rise or drop inantibody titer, a history of previous siblings havinghad exchange transfusions, blood group incompati-bilities, and other conditions noted later in thisreport. Eight of the babies demonstrated a strongor weak positive result in the Coombs' test on cordblood, and 5 had elevated values of bilirubin in theindirect test on cord blood.

Babies with an unfavorable history and evidenceof progressive hemolytic process were treated byexchange tranfusion soon after birth. In a majorityof instances in which the hemolytic process wasslower, the magic number of 20 mg. per 100 m1.4of indirect bilirubin in the blood was used as thecriterion for exchange in mature infants. In pre-mature infants, 17 mg. per 100 ml. of serum bili-rubin was considered the "transfusion level."

The total number of exchange transfusions per-formed was 51, of which 35 were performed onmature infants (5 pounds 8 ounces or over) and13 on premature infants. Seventeen babies receivedthe benefit of one exchange transfusion; 11 received

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