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Pulmonary Interstitial Emphysema in the Newborn InfantPrecursors and Sequelae*A Clinical and Pathologic Study

PAUL A. KIRSCHNER, M.D., AND Lol-FE STRAUSS, M.D.t

New York, New York

INTRODUCTIONP ULMONARY INTERSTITIAL EMPHYSEMAhas been shown by Macklin to be the

precursor of pneumomediastinum (medi-astinal emphysema, pneumothorax andpneumoperitoneum) in a variety of situa-tions. A substantial mortality rate accom-panies these complications in the newborninfant. While the clinical manifestations inthe neonate have been amply described,reports of underlying morbid anatomY arefew.58 Most of our understanding has beenextrapolated from observations in adultsand animalsL?sO and then applied to thenewborn lung.4

Our purpose is to present the precursorsand sequelae of pulmonary interstitial em-physema in the newborn infant and to cor-relate the pathologic with the clinical find-ings.

MATERIAL

Four hundred ninety-seven necropsicsperformed on live-born infants dying with-in seven days of birth during the period1952-1960 inclusive were reviewed. Forty-seven of these (9.5 per cent) showed evi-dence of pulmonary interstitial emphysemawith or without its sequelae. The longestsurvivor of these lived four days. Onlyseven had clinically detectable pneumo-thorax. An additional four infants withpneumothorax survived. Thirteen of the 47necropsied cases had severe congenital an-omalies incompatible with survival and will

*From the Departments of Surgery and Pathol-

ogy (Division of Pediatric Pathology), TheMount Sinai Hospital.

#{149}*Associate Attending Surgeon for Thoracic Sur-gery, Mount Sinai Hospital, N. Y.

tAssociate Attending Pathologist in charge ofDivision of Pediatric Pathology, Mount SinaiHospital, N. Y.

be considered separately leaving 34 post-mortem examinations and four clinical sur-vivors to form the main body of this report.

NECROPSY FINDINGS

The necropsy should be conducted so asnot to overlook pneumothorax or pneumo-peritoneum. Prior clinical information ishelpful. Upon preliminary inspection, bulg-ing of one or both sides of the chest orlow-lying abdominal viscera (if the abdo-men is opened first) are highly suggestive.The body cavities should be opened underwater, bubbles indicating abnormal air col-lections. Pneumomediastinum or mediastin-al emphysema is easily diagnosed by theblebs of air in the areolar tissue of theanterior mediastinum (Fig. 1). At timesthey may elevate the thymus gland. Acollar of air vesicles will be noted surround-ing the roots of the lungs in the hilar areas.The prosector should look for dissection ofair up into the neck (Fig. 2) or downretroperitoneally. Subpleural blebs on thesurface of the lungs are recognized withease (Fig. 3). They tend to be groupedalong interlobular septa like strings ofbeads.

Fixation of the uncut lungs is necessaryto preserve the spaces produced by inter-stitial collections of air. Examination of thecut surface with a hand lens will revealthese clefts in the bronchovascular rays.Vascular compression may be seen (Fig.4). We have never observed the intrapul-monary point of alveolar rupture, but onoccasion have noted the torn subpleuralbleb responsible for the pneumothorax.

Table 1 indicates the distribution of ab-normal collections of air. Lack of absolute

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418

TABLE 1-DISTRIBUTION OF ABNORMAL COLLECTIONS OF AIR: 34 CASES

I.Pulmonary interstitial emphysema: 34 Cases

Bilateral 17Unilateral 10 (L 7 R 3)Focal 6 (microscopic only)Location not stated 1

2. Pneumothorax: II Cases

a. with pneuiiomediastinum or mediastinal emphysema: 7 casesBilateral pneumothorax: 5 Bilateral pulmonary Unilateral pulmonary

interstitial emphysema: 4 interstitial emphysema:Unilateral pneumothorax: 2 Bilateral pulmonary Unilateral pulmonary

interstitial emphysema: 2 interstitial emphysema: 0b. without pneumomediastinum or mediastinal emphysema: 4 cases

Bilateral pneumothorax: 0 Bilateral pulmonary Unilateral pulmonaryinterstitial emphysema: 0 interstitial emphysema: 0

Unilateral pneumothorax: 4 Bilateral pulmonary Unilateral pulmonaryinterstitial emphysema: 3 interstitial emphysema: 0

3. Pneumomediastinum or mediastinal emphysema: 11 Cases

a. with pneumothorax: 7 Unilateral Bilateralpneumothorax: 2 pneumothorax: 5

b. without pneumothorax: 4 Unilateral Bilateralpneumothorax: 0 pneumothorax: 0

FIGURE 1: Severe anterior pneumomediastinum ormediastinal emphysema and bilateral pneumotho-rax. Note elevation of thymus by emphysematousblebs, and dilatation of right ventricle. Pulmonaryinterstitial emphysema of both lower lobes notwell seen, (Premature infant, case R.S.; weight2250 gm.; no resuscitation; delayed onset of res-piratory distress; survived 42 hours.)

FIGURE 2: Interstitial emphysema of neck struc-tures extending from pneumomediastinum or medi-astinal emphysema. (Full-term infant, weight 3459gm.; with intrauterine fetal distress; required re-suscitation; survived one and one-half hours.)

KIRSCHNER AND STRAUSS Diseases ofthe Chest

correlation between pneumomediastinum ormediastinal emphysema and pneumothoraxindicates that rupture of subpleural blebsdirectly into the pleural space is a signifi-

cant cause of pneumothorax in addition tothe classic circuitous route via the medias-tinum as emphasized by Macklin. Only onecase had unilateral pulmonary interstitialemphysema, pneumomediastinum or mcdi-astinal emphysema and bilateral pneumo-thorax. Four of the 11 cases of pneumo-

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Volume 46, No. 4October 1964

FIGURE 3: Thoracic situs showing severe bilateral pulmonary interstitial emphysema and subpleural blebs.A few blebs are seen also on the surface of the thymus. (Full-term infant, weight 3040 gin., with intra-uterine fetal distress; required resuscitation; survived less than one hour.)

FIGURE 4: Pulmonary interstitial emphysema;perivascular collections of air compressing and de-forming a medium-sized artery. (Hematoxylin-eosin, x45) (Full-term infant, weight 3459 gin.,with intrauterine fetal distress; required resuscita-tion; survived one and one-half hours.)

Male Female TotalOver 3500 gm. 3 3 63000-3499 gm. 5 4 92500-2999 gin. 4 1 52000-2499 gm. 3 3 6Under 2000 gm. 6 2 8Fetal Distress 18 cases (5 unstated)Resuscitative Measures 19 cases (3 unstated)

PULMONARY INTERSTITIAL EMPHYSEMA IN NEWBORN 419

thorax did not have pneumomediastinumor mediastinal emphysema.

Table 2 indicates a male predominanceof almost 2: 1. Twenty-six of the 34 in-fants weighed 2000 grams or more at birth.This suggests that prematurity is not animportant predisposing factor. Fetal dis-tress during delivery and the employmentof resuscitative measures occurred in slight-ly more than half of the entire group.

The most significant pulmonary findingsare summarized in Table 3. All but one

case showed substantial lung pathology.This exception had subdural hemorrhageand required vigorous resuscitation.

In a general sort of way, pulmonary in-volvement was patchy, with zones of aer-ated or overexpanded lung alternating withareas of unexpanded parenchyma. Thiswas due to aspiration, pneumonia, hemor-rhage and edema occurring alone or invarious combinations.

Aspirated material was found in thedeeper ramifications of the bronchial tree,since that in the trachea and larger bronchiusually had been removed prior to deathby endotracheal suction during resuscita-tion. It only remained when it was tooinspissated to permit complete removal. Itconsisted of mucus, vernix caseosa and

TABLE 2-GENERAL CLINICAL INFORMATION34 CASES

Sex: Male 21Female 13

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420 KIRSCHNER AND STRAUSS

FIGURE 5: Uneven aeration of lung. Patchy ob-structive emphysema (left), adjacent to non-aerat-ed lung with aspirated amniotic sac contents inbronchi and alveoli. (Hematoxylin and eosin, x45)(Full-term infant, weight 3700 gm.; Cesarean sec-tion; meconium-stained amniotic fluid; requiredresuscitation; survived nine hours.)

TABLE 3-NECROPSY FINDINGS-34 CASES

Pulmonary Pathology-33 casesAspiration 16Pneumonia 16 (2 focal)Atelectasis 28 (1 focal)Hyaline membranes 11 (3 without other pathology)Hemorrhage 14 (Focal)Cardiac Dilatation-17 observed

2 not present

15 not stated

Central Nervous System Hemorrhage-i 7 observedSubdural 7Subarachnoid 14Cerebral 4

sometimes meconium. Distribution deep inthe lung was of a patchy nature with areasof focal obstructive emphysema due to par-tial bronchial obstruction alternating withcomplete obstruction and atelectasis (Fig.5). Pneumonia occurred in over half of thecases and was confined to the obstructedareas.

When pneumonia predominated, it alsooccurred in a scattered type of distributionwith the inflammatory alveolar exudateacting as the obstructing mechanism. Againthe alternating pattern of obstructive em-physema and non-aerated lung was appar-ent. Some lungs were more diffusely infil-trated with exudate and showed only min-imal patchy aeration. In a few lungs withpredominantly interstitial inflammation, abizarre pattern of over-expansion of the

Diseases ofthe Chest

terminal bronchioles and atelectatic alveoliwas found producing a Swiss cheese ap-pearance (Fig. 6).

Only three of 11 infants had hyalinemembranes without pneumonia or definiteevidence of intra-uterine aspiration. Henceit is our feeling that the hyaline membranesyndrome per se does not predispose to thedevelopment of pulmonary interstitial em-physema. This is in agreement with theobservations of ourselves and others thatpulmonary interstitial emphysema usuallyaffects the larger newborn and hyalinemembrane the more premature.

Intrapulmonary hemorrhage, when asso-ciated with pulmonary interstitial emphy-sema also occurs in a patchy fashion. Itcannot be stated whether hemorrhage aloneis a factor or whether an alteration in pul-monary circulation or some other poorlyunderstood mechanism is operative. On theother hand congenital heart disease whichoften affects pulmonary blood flow wasconspicuously absent.

The common occurrence of cardiac dila-tation, particularly affecting the right heart(17 cases) suggests that obstruction to pul-monary blood flow is present. We feel it isdue to compression of pulmonary vessels bythe interstitial air.

Central nervous system hemorrhage wasfound in a substantial number of cases.

FIGURE 6: Swiss cheese pattern of lung due tooverdistention of terminal bronchioles and atelec-tasis of distal portions of lung, associated withinterstitial inflammation of lungs. (Hematoxylinand eosin, x45) (Full-term infant, weight 3460gm.; delayed onset of respiratory distress; survivedthree days.)

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This may have been secondary, due to theanoxia of respiratory distress at birth, orprimary, and responsible for inefficient res-piratory drive resulting in aspiration andthe need for resuscitative measures.

Thirteen other cases of the total of 47had severe anomalies incompatible withlife. Eight of them had hypoplastic lungs.Frequently such infants had been resusci-tated because of failure to breathe spon-taneously with rather dramatic emphyse-matous effects on the lungs and loosemesenchymal tissues of the chest and ab-domen. While such cases have no clinicalsignificance, they further indicate that lungsunable to expand uniformly and fully areprone to internal rupture.

DISCUSSION

When pulmonary interstitial emphysemaoccurs, air passes into the perivascular andperibronchial connective tissue sheaths andthe interlobular septa. From these locations,dissection of air may be centripetal or cen-trifugal. In the former instance, air travelsinto the mediastinum causing mediastinalemphsema. From here it may breakthrough the thin mediastinal pleura intoone or both pleural cavities to cause pneu-mothorax. Upward dissection from themediastinum into the anatomically con-tinuous fascial planes of the neck producesso-called subcutaneous emphysema.Downward tracking from the mediastinumleads to pneumoperitoneum. Centrifugaldissection of air along the bronchovascularrays and interlobular septa to the lung sur-face is manifested by subpleural blebs. Rup-ture of such blebs is the second cause ofpneumothorax in pulmonary interstitial em-physema.

Review of necropsy material indicatesthat pulmonary interstitial emphysema inthe newborn usually develops in diseasedor abnormal lungs. Normal, uniformlyaerated lungs are nQt prone to internalrupture unless subjected to extremely highintra-alveolar pressure far exceeding phys-iological limits. Pressures required to cx-

pand the normal infant lung vary from 20to 30 cm. H20, sufficient to rupture thelung.

In lungs in which aeration is patchy andincomplete due to the conditions found atnecropsy, high pressure zones may well de-velop due to alterations of pressure-volumerelationships, and alveolar rupture can

easily occur in these areas. It is not neces-sary to invoke excessive artificial ventilationand over-vigorous resuscitative techniquesto account for all cases of rupture. Spon-taneous respiratory efforts are sufficient.8Even adherence to acceptable limits can beharmful.24

Hypoplastic lungs are particularly proneto develop pulmonary interstitial emphy-sema. It appears again that the previouslymentioned volumetric disproportion be-tween bronchial and alveolar beds is re-sponsible. The clinical importance of hypo-plastic lungs is trivial as this condition isassociated with a high incidence of otherserious developmental anomalies incompat-ible with survival.

The role of prematurity in the causationof pulmonary interstitial emphysema is notentirely clear. Emery6 has shown that lusty,full-term infants are more prone to developpulmonary interstitial emphysema than pre-matures. Our findings confirm this (morethan half weighed over 3000 gm.). On theother hand, Landing and Lubchenko4 im-plicate prematurity as a common pre-exist-ing state.

The relationship of altered pulmonarycirculation to pulmonary interstitial emphy-sema is less well understood. Neonates withcongenital heart disease causing pulmonarycongestion and edema are not likely to de-velop pulmonary interstitial emphysema.Contrariwise, infants with intracranialhemorrhage and anoxia develop pulmo-nary hemorrhage, edema and alteration ofrespiratory activity to the extent that pul-monary interstitial emphysema developsspontaneously or follows on the heels ofexpert resuscitation.

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422 KIRSCHNER AND STRAUSS

CLINICAL MANIFESTATIONS

AND DIAGNOSIS

In all the 51 cases, symptoms appearedwithin 27 hours of birth. Two major cate-gories could be distinguished: (a) thosewith immediate onset of respiratory distressor initial apnea; and (b) those with de-layed onset after a variable period of ap-parently normal respiration.

Immediate Onset Group: Resuscitativemeasures are always required as there areno spontaneous respiratory efforts or merelyineffectual gasps. Many of these cases havebeen heralded by signs of fetal distress dur-ing labor, evidenced by meconium-stainedamniotic fluid.

Signs of difficulty are frequently notedjust following the first spontaneous breathsor upon the heels of resuscitative measures.Breathing is labored, irregular and shallowwith intercostal retractions and progressiveanterior ballooning of the chest and stern-um. Tachycardia is uniformly present. Cy-anosis, especially circumoral, is common inroom air, but may disappear in a highoxygen atmosphere. Tracheal suction oftenyields tenacious mucus, vernix or meconi-um. Bloody fluid is sometimes obtained,due either to aspiration during delivery oras a result of massive pulmonary hemor-rhage. A weak high-pitched cry hints ofintracranial hemorrhage of traumatic oranoxic origin.

Tracheal shift and cardiac displacementmay be present in unilateral pneumothorax,but may be difficult to detect in the smallneonate. Breath sounds are diminished orabsent on the side of the pneumothorax.and tympany may be noted on percussion.Auscultatory signs of pneumonia may notbe detectable. Bilateral pneumothorax maybe even more difficult to diagnose, but ifit is extensive, a ballooned configuration ofthe chest will be apparent.

Hepatomegaly due to progressive rightheart failure is often present, but the truesize of the liver may be exaggerated by alow diaphragm.

An abnormal appearance (facies, skeletaldeformities) as seen in renal agenesis or

Diseases ofthe Chest

dysgenesis calls the attention of the exam-iner to the frequent concomitant pulmonaryhypoplasia. Sometimes the renal malforma-tion may present as an abdominal mass.

Delayed Onset Group: Following a vari-able initial period of apparent well-being,respiratory distress develops and at a some-what slower rate. More deliberate assess-ment is therefore possible since resuscitativemeasures are less urgent, and radiologicstudy can be employed. The degree ofdyspnea is often out of proportion to thesize of the pneumothorax probably becauseit is due to pulmonary interstitial emphy-sema and pneumomediastinum or medias-tinal emphysema as well. Cardiac failureand hepatic enlargement are more commonbecause of longer duration of symptoms.

Radiologic Diagnosis: Pneumothoraxand pneumomediastinum or mediastinalemphysema are the only features discern-ible on x-ray examination. The forerunner,pulmonary interstitial emphysema, cannotbe seen due to the lack of contrasting den-sities within the lung. Pulmonary collapseis usually partial, rarely complete. At times,multiple oblique views are necessary to de-tect a mantle pneumothorax. Wideningand bulging of the intercostal spaces, some-times noted clinically, are readily seen onthe film. Pneumomediastinum or medias-tinal emphysema is best visualized in thelateral projection and is manifested by an-terior bulging of the sternum with retro-sternal lucency. In the posteroanterior view,the thymus may appear elevated and wid-ened. Pulmonary infiltrations can representpneumonia, hyaline membranes, atelectasisor congestion. Cardiac dilatation and evenhepatic enlargement may be seen. Pleuraleffusions have not occurred. It is importantto distinguish the shadows cast by axillaryand pectoral skin folds from pneumothorax.

PROPHYLAXIS AND TREATMENT

The goal of treatment is efficient pulmo-nary and cardiac function. Initially theairway should be cleared of foreign materialby gentle suction. In the absence of spon-taneous or effective respiratory efforts, arti-

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ficial support including positive-pressure de-vices and mouth-to-mouth breathing mustbe employed. That such measures may ag-gravate pre-existent pulmonary interstitialemphysema in some babies or actually pro-duce it in others with the correspondingpathologic substrate is recognized. Some-times extensive pneumothorax may be pro-duced during these maneuvers (case M.O.).Antibiotics should be administered routine-ly on the sound premise that pulmonaryinfection is frequently present. Digitalis isindicated in cardiac failure and should begiven promptly. Oxygen is given as well.

In most cases, we feel that pneumo-thorax should be treated aggressively bymeans of closed thoracotomy with under-water drainage (case C.G.). While successhas been reported with needle aspiration,we do not advise its routine use as it can-not control a continuing air leak, and itmay cause further trauma to the lung. Ifthe infants condition is not desperate, aperiod of careful observation may be util-ized during which time spontaneous absorp-tion of the pneumothorax may occur (caseD.H.). On the other hand, when adequatedeflation of the pleural space has been ac-complished without concomitant clinicalimprovement, one can assume that the un-derlying pulmonary disease itself is respon-sible for the symptoms (case R.S.).

Prophylaxis lies in good prenatal careand constantly improving obstetric prac-tices designed to obviate the developmentof fetal distress or intrauterine infection.Resuscitation must always be careful andgentle with constant awareness that themorbid conditions of the lungs responsiblefor spontaneously developing pulmonaryinterstitial emphysema may also provokeits precipitation by artificial means.

CASE REPORTS

CASE 1

D.H. This 3260 gm., full-term, boy was deliv-ered October 17, 1955, by low-flap repeat Cesar-ean section. There was no sign of maternal orfetal distress. Breathing and crying were spon-taneous and occurred immediately, and no re-suscitation was carried out.

He did well for 15 hours, when suddenly hedeveloped cyanosis, grunting respiration and acry of distress. Breath sounds were almost absenton the right side and diminished on the left.There was marked retraction of both diaphragms,and the abdomen was distended. Marked tachy-cardia and an enlarged liver developed within afew hours.

A clinical diagnosis of right pneumothorax orbronchostenosis was made. X-ray film of thechest showed a right pneumothorax, with shiftof the mediastinum to the left. In addition, amarginal left pneumothorax could not be ex-cluded,

Treatment consisted of oxygen, vapor, penicil-lin, tetracycline and digitalis. Substantial im-provement occurred within 14 hours of startingdigitalis. Aspiration of the pneumothorax wasconsidered, but was not carried out. The pneu-mothorax resorbed within five days, and com-plete recovery ensued.

Comment: This is an example of de-layed spontaneous appearance of pneumo-thorax in a vigorous, full-term infant, with-out antecedent distress or resuscitation. Sec-ondary right heart failure was a prominentclinical feature and responded quickly todigitalis. Aspiration of the pneumothoraxwas not carried out because of the vigorand relatively good condition of the infantand its rapid response to the rest of thetherapeutic regimen, particularly digitalis.

CASE 2

R.S.: This boy, weighing 2250 gm., was bornone month prematurely by vertex presentationafter spontaneous onset of labor. He breathedand cried immediately. Slight circumoral cyanosiswas present at birth, but no resuscitation wasemployed. In the nursery, the baby was vigorousand active, with a good Moro reflex and grasp.

At 15 hours of age, dusky cyanosis appeared,followed by high-pitched cry, rapid grunting res-pirations, retractions and visible ballooning of thechest. Breath sounds became distant posteriorlywith occasional rales at the right base.

X-ray film revealed bilateral pneumothoraxand increased density of the right upper lobe.Oxygen, penicillin and chloromycetin were ad-ministered, Twenty hours after birth, the leftpleural cavity was aspirated of 50 ml. of air,without improvement. Polyethylene tubes wereinserted bilaterally for underwater drainage.There was continuous bubbling from the righttube, indicating a continuous air leak. There wassome temporary improvement in breath soundsbut the infants condition deteriorated rapidlyand steadily, and it ceased 30 hours after birth.

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4q24 KIRSCHNER AND STRAUSS

Necropsy: Bilateral pneumothorax and pneu-momediastinum or mediastinal emphysema werepresent. The right heart was dilated (Fig. 3).The lungs were almost airless. Subpleural blebsoccupied both lower lobes, which were firm andhyperemic. The major air passages were unob-structed. Microscopically extensive atelectasis andobstruction of potential air spaces by precipitatedprotein or exudate occasionally mixed with redblood cells was seen. Many alveolar ducts con-tained hyaline membranes. in the lower lobesterminal bronchioles were plugged by a mixtureof exudate and basophilic debris. Surroundinglung parenchyma showed acute bronchopneu-monia. Pulmonary interstitial emphysema wassparse and scattered. Culture of the lung yieldedenterococcus.

Comment: This case included practicallyall the features which we feel to be theclassic manifestations of the pathogenesis,etiology and morbid anatomy underlyingpulmonary interstitial emphysema in thenewborn. Therapy can only be supportivein such a situation unless some way can bedeveloped to overcome the bronchiolar ob-struction.

CASE 3

M.O.: This baby boy, weighing 2580 gm., wasborn after 40 weeks gestation on September 12,1959, after a seven and one-half hour spontaneouslabor, vertex presentation and mid-forceps de-livery. His mother, aged 42, received a total of250 mg. meperidine (Demerol), 1.0 mg. scopola-mine and 50 mg. promethazine (Phenergan) dur-ing a three and one-half hour period. Ten mg.of nalorphine (Nalline) was given just beforedelivery.

The infant was born limp, covered with me-conium. He was apneic for ten minutes. Trachealintubation was accomplished, meconium was suc-tioned, and mouth-to-tube artificial respirationwas carried out until the baby made spontaneousgasps. At this time, bulging of the chest wasnoted, and a clinical diagnosis of bilateral pneu-mothorax was made. The left chest was aspiratedtwice, yielding 100 ml. of air each time. Seventyml. of air was aspirated from the right hemi-thorax. Underwater drainage of both sides of thechest was established through bilateral tubes.Rapid improvement ensued. A temporary setbackwas caused by plugging of the left tube. Othertherapy included vapor, 02, penicillin, chloro-mycetin and tetracycline. The baby was dis-charged home on the 11th day with a normalchest x-ray film.

Comment: This exemplifies the imme-diate-onset group. In this instance, fetal

Diseases ofthe Chest

distress was a prominent feature. It mayhave been caused by heavy sedation ofthe mother during labor. Artificial mouth-to-tube respiration was necessary becauseof apnea. The ballooning of the chest didnot appear until spontaneous respiratoryactivity developed. This suggests that therequired resuscitative measures alone maynot have been responsible for the develop-ment of pneumothorax. A prompt thera-peutic effect was obtained by continuousdeflation of both chests by tubes after inter-mittent aspiration had failed.

CAsE 4

C.G.: On July 25, 1960, a 2430 gm. girl wasdelivered of a diabetic mother by Cesarean sec-tion under spinal anesthesia, after 37 weeks ges-tation. She breathed and cried immediately andvigorously. Except for slight circumoral cyanosis,she was noted to have good color, good lungaeration and no intercostal retractions.

Within one-half hour, respirations became ir-regular, and intercostal retraction and expiratorygrunt appeared. Three hours later the chest wasnoted to be in a position of expansion, and res-pirations became shallower. The liver was en-larged, and tachycardia was marked. The infantscondition deteriorated over the next 24 hours,despite supportive measures, including digitalis,penicillin, chloromycetin, vapor and oxygen. Theclinical diagnosis was hyaline membrane syn-drome.

X-ray film of the chest revealed left pneumo-thorax with 40 per cent collapse of the lung anda shift of the heart and mediastinum to the right.A left thoracentesis yielded an inexhaustible sup-ply of air, and accordingly tube thoracostomywith underwater drainage and mild controlledsuction was established. There was continuousbubbling for a few days. The left lung expandedpromptly. Recovery was complete within a week.

Comment: Respiratory distress developedspontaneously within one-half hour of birthin this 37-week, 2430 gm. child of a dia-betic mother. The downhill course waspromptly reversed by effective managementof a left pneumothorax by means of tubethoracostomy and continuous underwaterdrainage of air from a patent fistula.

SUMMARY AND CONCLUSIONS

The precursors and sequelae of pulmo-nary interstitial emphysema in the new-born infant have been described based up-

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on observations in 47 necropsies and fourclinical cases of pneumothorax.

Pulmonary interstitial emphysema occurs

in a diseased lung (pneumonia, aspiration,hemorrhage, atelectasis) or an abnormallydeveloped lung (hypoplasia). Patchy in-volvement with alternating areas of hyper-inflation and collapse appears to be the pre-requisite.

While resuscitative forces often cause in-trapulmonary rupture, spontaneous respira-tory efforts of an infant in distress are suf-ficient.

Clinically, the cases fall into two mainsubgroups based upon time of onset ofsymptoms: (a) immediately at birth andfrequently on the heels of resuscitation, and(b) after a variable symptom-free period,usually spontaneously.

The gravity of this condition is empha-sized by the death of seven of 11 infantswith clinically detectable pneumothorax.

An outline of therapy with emphasisupon tube thoracotomy for pneumothoraxhas been presented.

AODENDUM: Aballi, A. J., Moreno, 0., Bel-tran, 0. S., Fontao, J. A., Boudet, L. and DonVarona, A.: Mediastinal Emphysema in the New-born, Rev. Cubana de Pediat., 26:629, 1954(Abst. in Radiology, 66:131, 1956). Ten cases arereported. There were six fatalities, all of whichshowed aspiration of amniotic fluid at necropsy.

RESUMEN

Se han descrito las caracterIsticas precursoras ylas secuelas del enfisema pulmonar intersticial enel reci#{233}n nacido, bas#{225}ndose en las observacionesde 47 autopSias y de 4 casos clinicos de neumo-t#{243}rax.

El enfisema pulmonar intersticial se presentaen un pulm#{243}n enfermo (neumonia, aspiraci#{243}n,hemorragia, atelectasia) o en on pulm#{243}n condesarrollo an#{243}malo (hipoplasia). Parece que esrequisito para esa condici#{243}n el compromiso deltejido en areas parchadas, con areas alternantesde inflaci#{243}n exagerada y de colapso.

Los esfuerzos de Ia respiraci#{243}n espont#{225}nea enel infante en dificultades respiratorias general-mente bastan en tanto que las fuerzas empleadasen las maniobras de resucitaci#{243}n a menudo caus-an rupturas intrapulmonares.

Clinicamente los casos entran en dos subgruposprincipales, bas#{225}ndose esto en ci tiempo de prin-cipio de los sIntomas: (a) inmediatamente alnacimiento y despu#{233}sde Ia resucitaci#{243}n, y (b)

despu#{233}sde un peslodo variable libre de sIntomas,generalmente de manera espont#{225}nea.

La gravedad de esta afecci#{243}n se destaca por Iamuerte de 7 de 11 infantes con neumot#{243}rax clini-camente discutible. Un plan de tratamiento conCnfasis sobre el uso de Ia toracotomia por en-tubado en el neumot#{243}rax se describe.

REsuME

Lauteur d#{233}crit les facteurs pr#{233}curseurs et less#{233}quelles de lemphysCme pulmonaire interstitieldu nouveau-ne, dapr#{232}s des observations faites sur47 autopsies et 4 cas cliniques de pneumothorax.

Lemphys#{232}me pulmonaire interstitiel survientsur un poumon malade (pneumonic, aspiration,h#{233}morragie, at#{233}lectasie) ou sur un poumon anor-malement d#{233}velopp#{233}(hypoplasie). Une atteinteen mosaIque avec en alternance des zones dhy-perinflation et de collapsus semble #{234}treLa condi-tion n#{233}cessaire.

Alors que les forces utilis#{233}es pour Ia rCanima-lion provoquent souvent a rupture intrapulmo-naire, les efforts respiratoires spontan#{233}s dun nou-veau-n#{233} en d#{233}tresse sont suffisants.

Cliniquement, les cas se divisent en deux sous-groupes principaux, bases sur Ic temps dappari-don des sympt#{244}mes: (a) imm#{233}diatement apr#{232}sIa naissance, et fr#{233}quemment apr#{234}s reanimation,et (b) apr#{232}s one p#{233}riode variable indemne desympt#{244}mes, apparition g#{233}n#{233}ralement spontan#{233}e.

La gravit#{233}de cet #{233}tatest accentu#{233}epar Lamort de 7 nouveaux-n#{233}s sur 11 qui furent atteintsde pneumothorax cliniquement detectable.

Lauteur pr#{233}sente une esquisse de traitement,en mettant laccent sur Ia sonde apr#{234}s thoraco-tomie pour Ic pneumothorax.

ZUSAMMENFASSUNG

Die Anfangsstadien und Folgezustande einespulmonalen interstitiellen Emphysems beim Neu-geborenen werden beschrieben und zwar aufgrundvon Beobachtungen an 57 Sketionen und 4 kIm-ischen Fallen von Pneumothorax. Das pulmonaleinterstitielle Emphysem kommt in einer erkrank-ten Lunge (Pneumonic, Aspiration, H#{228}morrhagie,Atelektase) odcr in ciner krankhaft cntwickeltenLunge (Hypoplasie) vor. Fleckf#{246}rmige Affektio-nen alternicred mit Bezirken mit Ubcrblahungoder mit Kollaps d#{252}rften die Vorauassetzungenseth. W#{228}hrendBem#{252}hungen zur Wicderbelebungoft zu einer intrapulmonalen Ruptur f#{252}hren,reicht bei einem in Not befindlichen Kind oft diespontane respiratorische Anstrengung aus.

Klinisch lassen sich die F#{228}lle in zwei Haupt-gruppen formen, ausgehend von dem Zeitpunkt,zu dem die Symptome beginnen: (a) unmittelbarbei der Geburt und h#{228}ufig den Wiederbelebungs-vcrsuch aus den F#{252}!3en folgend, (b) nach einerverschieden langen symptomenfreien Zeitspanne,gew#{246}hnlichspontan. Die Schwere dieser Erkrank-

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INTRAVENOUS ADMINISTRATION OF VIOMYCIN IN THETREATMENT OF PULMONARY TUBERCULOSIS

426 KIRSCHNER AND STRAUSS Diseases ofthe Chest

ung wird beleuchtet durch den Tod von 7 von11 S#{228}uglingcn mit klinisch festgestelltcn Pncu-mothorax. Umril3artige Darstellung der Therapie

mit Hervorhebung der Thorakotomie mit Saug-drainage wegen Pneumothorax.

REFERENCES

1 MACKLIN, M. T. AND MACKLIN, C. C.: Ma-lignant Interstitial Emphysema of the Lungsand Mediastinum, Medicine, 23:281, 1944.

2 DECOSTA, E. J.: Spontaneous Pneumothoraxof the Newborn Infant, Am. J. Obs. and Gyn.,39:578, 1940.

3 Howm, V. M. AND WEED, A. S.: SpontaneousPneumothorax in the First Ten Days of Life,/. Ped., 50:6, 1957.

4 LUBCHENCO, L. 0.: Recognition of Spon-taneous Pneumothorax in Premature Infants,Pediatrics, 24:996, 1959.

5 SALMON, G. W., FORBES, G. B. AND DAVEN-PORT, H.: Airblock in the Newborn Infant,/. Ped., 30:260, 1947.

6 EMERY, J. L.: Interstitial Emphysema, Pneu-mothorax and Airblock in the Newborn,Lancet, 270:405, 1956.

7 KELMAN, S. R.: Experimental Emphysema,Arch. mt. Med., 24:332, 1919.

8 HAMMAN, L.: Mediastinal Emphysema,J.A.M.A., 128:1, 1945.

9 JOANNIDES, M. AND TsouLoS, G.: The Eti-ology of Interstitial and Mediastinal Emphy-sema, Arch. Surg., 21:333, 1930.

10 VAN ALLEN, C. M., LINDSKOG, G. E. ANDRICHTER, H. G.: Collateral Respiration.Transfer of Air Collaterally Between Pulmo-nary Lobules, J. Clin. Invest., 10:559, 1931.

11 GRUENWALD, P.: Respiratory Difficulties inNewborn Infants, (Special Committee on In-fant Mortality, Panel Discussion), ABRAMSON,H., Ed., N. Y. State J. Med., 58:372, 1958.

12 SMITH, C. A. AND CHISHOLM, T. C.: Intra-pulmonary Pressures in Newborn Infant, J.Ped., 20:338, 1942.

13 DAY, R., GOODFELLOW, A. M., APGAR, V. ANDBECK, G.: Pressure-Time Relations in the SafeCorrection of Atelectasis in Animal Lungs,Pediatrics, 10:593, 1953.

14 WILSON, J. L.: Factors Involved in the Pro-duction of Alveolar Rupture with MechanicalAids to Respiration, Pediatrics, 13:146, 1954.

15 GRUENWALD, P.: Hypoplasia of the Lungs,J. Mt. Sinai Hosp., 24:913, 1957.

16 LANDING, B. H.: Pathologic Features of Res-piratory Distress Syndromes in Newborn In-fants, Am. J. Roentgenol., 74:796, 1955.

For reprints, please write Dr. Kirschner, 2 East92nd Street, New York City.

HYPERTROPHIC OBSTRUCTIVE CARDIOMYOPATHY

Previous experience of obstructive cardiomyopathyhas been reviewed and amplified in the light offurther hemodynamie and angiographic Investiga-tions in 29 patients. Since obstruction is variableand hypertrophy constant, the term hypertrophichas been added to the definition. Hypertrophic ob-structive cardiomyopathy is a generalized disorderof heart muscle in which massive hypertrophy ofthe ventricular septum and of the free wails of theventricles frequently results in outflow tract obstruc-tion. This obstruction to outflow is partly mechan-ical and partly due to abnormal behavior of the

The author reports that it is possible to get higherblood levels of viomycin by administering it intra-venously. In his series of 21 problem cases treatedby this method, he obtained good results. In 19patients. the viomycin was given in conjunction withPAS in an injectable solution, and in the other two

outflow pathways. Impaired function of ventricularmuscle leads to restriction of inflow, and mitralregurgitation occurs in almost half the patients.There is a significant familial incidence suggestinga possible genetic basis. Patients may present withsymptoms and signs of either outflow obstructionor restriction of effective diastolic filling. Treatmenthas been discussed briefly.

COHEN, J.. EFFAT, H., GOODWIN, J. F., OAKLEY, C. M.AND STEINE5, R. E.: Hypertrophic Obstructive Cardio.myopathy, Belt. Heart J., 26:16. 1964.

cases it was given in conjunction with INH andTh1314 by mouth and rectum. In only one case wasit necessary to stop treatment because of a severereaction to viomycin.POZZETTE, H.: La Vyomycine par Vioe Endoveineuse,Le Poumon et Ic Coeur, 19:443. 1963.

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