56 Ng, Thomson, Dear

cular steroid has little influence on its immuno-suppressive effect. Dexamethasone, which is oneof the most potent corticosteroids, has compara-tively little immunosuppressive property.6The results of our study show that the use of

dexamethasone in the treatment of broncho-pulmonary dysplasia is not associated with anappreciable increase in the incidence of infec-tion, although the possibility of a Type II errorprevents us from ruling out a small effect.Steroids should not be withheld for fear ofpredisposing to infection.

1 Mukwaya G. Immunosuppressive effects and infections asso-ciated with corticosteroid therapy. Pediatr Infect Dis J1988; 7:499-504.

2 Lepper MH. Prophylaxis in patients receiving adrenal steroidtherapy. J Chronic Dis 1962;15:691-71 1.

3 Kwong FK, Sue MA, Klaustermeyer WB. Corticosteroidcomplications in respiratory disease. Ann Allergy 1989;58:326-30.

4 Anderson R, Malmwall BE, Bengtsson BA. Long term corti-costeroid treatment in giant cell arteritis. Acta Med Scand1986;220:465-9.

5 Fitzhardinge PM, Eisen A, Leitenyi C, Metrakos K, RamsayM. Sequelae of early steroid administration to the newborninfant. Pediatrics 1974;53:877-83.

6 Langhoff E, Ladefoged J. Relative immunosuppressivepotency of various corticosteroids measured in vitro. EurJ Clin Pharmacol 1983;25:454-62.

Neonatal pneumomediastinum with isolated mitralobstruction

C L Case, P Oslizlok, D Fyfe, P C Gillette

South CarolinaChildren's Heart Center,Medical University ofSouth CarolinaC CaseP OslizlokD FyfeP C GilletteCorrespondence to:-Dr C L Case,South CarolinaChildren's Heart Center,Medical University ofSouth Carolina,171 Ashley Avenue,Charleston, SC 29425,USA.Accepted 7 September 1989

AbstractWhile mediastinal air accumulation in theventilated newborn is usually a benign entity,tension pneumomediastinum can embarrassboth respiratory and cardiac function. A caseof isolated left ventricular inflow obstruc-tion caused by a pneumomediastinum in apremature infant is described that resolvedwith high frequency ventilation. The develop-ment of pneumomediastinum and haemo-dynamic compromise in a premature infantwarrants echocardiographic examination.

Intrathoracic air accumulation is a commoncomplication of mechanical ventilation in thenewborn intensive care unit. The clinicalconsequences of pneumomediastinum andpulmonary interstitial emphysema in thepremature infant have been well described.' 2Pneumomediastinum is a less commonlyencountered result of barotrauma, often havingminimal pulmonary or cardiac consequences.We here describe a case of pneumomediastinumin a low birthweight premature infant thatcaused haemodynamic compromise secondaryto isolated left ventricular inflow obstruction.High frequency ventilation was successfullyused to decompress the mediastinum andrestore normal cardiac function.

Case reportA boy, weighing 750 g, was born vaginally at 25weeks' gestation to a 23 year old woman(gravida 4, para 3) with an uncomplicatedprenatal course. Labour was spontaneous andApgar scores were 4 at 1 minute and 5 at5 minutes with immediate intubation in thedelivery room. During the first 12 hours of life,the patient required increasing ventilator ratesand pressures secondary to severe hyalinemembrane disease. A small patent arterial ductwas diagnosed by echocardiography at 12 hours

of age and indomethacin treatment wasinstituted.

During the next 12 hours, the ventilatorypeak pressures and rates were modestly weaned.The infant's chest radiograph, however, showedsigns of worsening disease with the appearanceof interstitial emphysema. During the secondday of life there were increasing ventilatorrequirements. Peak ventilatory pressures of30 cm H20 (mean airway pressure of 17 cmH20) and rates of 70 breaths/minute and 100%oxygen were needed to maintain a pH of 7-24, acarbon dioxide arterial pressure of 7-8 kPa andan oxygen arterial pressure of 7-8 kPa.On day three of life, the patient continued to

require maximal respiratory support. A chestradiograph showed free air in the mediastinumand increasing opacity of the lung fields (fig la).Subcutaneous emphysema was also noted.Repeat echocardiography was performed toassess the efficacy of the indomethacin treat-ment. Pulsed Doppler examination confirmedthat the arterial duct had closed. The fourchamber view, however, showed a large masslike effect superior and posterior to the leftatrium (fig lb). Pulsed Doppler examinationshowed evidence of inflow obstruction at themitral valve with turbulent flow and a peakinflow velocity of 100 cm/second (fig Ic). Simul-taneous tricuspid inflow was laminar with apeak inflow velocity of 20 cm/second (fig Id).Postulating that a tension pneumomediastinumwas compromising mitral inflow and possiblycontributing to pulmonary oedema, strategies todecompress the mediastinum were considered.In view of the infant's precarious condition,surgical decompression was thought to be toorisky. High frequency jet ventilation at a rate of420 breaths/minute was instituted and a reduc-tion of mean airway pressure from 17 to 8 cm/H2O was effected.Over the next 12 hours, the infant's chest

radiograph showed resolution of mediastinal air(fig 2a) with concurrent improvement in arterial

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Neonatal pneumomediastinum with isolated mitral obstruction

Figure la, Infants chest radiograph showing mediastinal and subcutaneous air accumulation as well as opacified lungfields.lb, Echocardiogram (four chamber view) showing large mass effect (m) superior to the left atrium. Asterisk indicates area ofmitral valve commissural opening; ra, right atrium; rv, nrght ventricle; lv, left ventricle; s, supenror; and 1, left. Ic, PulsedDoppler examination ofmitral inflow before high frequency jet ventilation treatment. Note turbulentflow as well as abnormal100 cmlsecond peak inflow velocity. Id, Pulsed Doppler examination of tricuspid inflow before high frequency jet ventilationshowing normal laminarflow and peak inflow velocity of20 cm/second.

I

I

Figure 2a, Infant's chest radiograph after high frequency jet ventilation showing resolution ofmediastinal air. 2b, Repeatechocardiogram (four chamber view) after high frequency jet ventilation showing resolution ofmass effect on left atrium;ra, right atrium; rv, rght ventricle; lv, left ventricle; la, left atrium.

blood gases. Repeat echocardiography showedresolution of the mass effect impinging on theleft atrium (fig 2b) and normal mitral inflow.

DiscussionThe clinical consequences of intrathoracic airaccumulation in the neonate secondary to

mechanical ventilation have been welldescribed.' 2 Air trapped in the pleura, lungparenchyma, or mediastinum, especially ifunder tension, can embarrass respiratory andcardiac function.A tension pneumomediastinum can interfere

with the normal intrathoracic pressure associa-tions, compromising normal venous return

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58 Case, Oslizlok, Fyfe, Gallette

patterns to the right and left sides of the heart.3This may be reflected in low right and leftventricular inflow velocities on pulsed Dopplerexamination. Most cases of pneumomedia-stinum in the neonate result in anterior airaccumulation with negligible cardiac or respira-tory sequelae. A large isolated posteriormediastinal air accumulation is much lesscommon, but may also lead to respiratorydecompensation as has recently beendescribed.4The above case illustrates a previously

undescribed cardiac side effect of pneu-momediastinum in the neonate. The echocar-diogram showed an air filled mass compressingthe superior, posterior left atrial wall impingingupon the mitral valve. In contrast with the lowvelocity signal that would have been obtainedhad the systemic or pulmonary veins beenobstructed, the pulsed Doppler patternconfirmed obstruction at the mitral valve level.Venous return through the tricuspid valve,however, as evidenced by Doppler flow, wasnormal. This localised cardiac effect is postu-lated to have resulted from the regional differ-ences of air accumulation in the posteriormediastinum.The physiological consequences of acute

mitral valve obstruction are varied dependingon the severity. Both pulmonary oedema andlow cardiac output are possible sequelae. In ourcase, the increased opacity of the lung fields onthe chest radiograph paralleled the development

of mitral obstruction. It is not clear, however,whether the change in the chest radiographreflected pulmonary oedema, worsening lungdisease, or both. Similarly, although cardiacoutput was compromised during this time, therelative contribution of mitral obstruction isdifficult to quantify. Clinical improvementrapidly followed resolution of the pneumo-mediastinum.

Surgical decompression has been describedas the treatment of choice for tensionpneumomediastinum.' ' High frequency venti-lation, however, has been recently utilised inthe neonate to treat life threatening pulmonaryair leaks5; this was effectively employed todecrease the air leakage and decompress themediastinum in our patient. Normal left ventri-cular venous inflow was demonstrated afterresolution of the mediastinal air.

1 Yu VYH, Wong PY, Bajuk B, Szymonowicz W. Pulmonaryair leak in extremely low birthweight infants. Arch l)isChild 1986;61:239-41.

2 Thibeault DW, Lachman RS, Laul VR, et al. Pulmonaryinterstitial emphysema, pneumomediastinum and pneumo-thorax. Am7 Dis Child 1973;126:611-4.

3 Jewett TC, Adler RH, Taheri SA. Tension pneumomedia-stinum in the newborn. 7 ?Ihorac Cardiovasc Surg1962;43:540-7.

4 Purohit DM, Lorenzo RL, Smith CD, Bradford BF. Casereports: bronchial laceration in a newborn with persistentposterior pneumomediastinum. 1Pediair Surg 1985;20:82-5.

5 Mammel MC, Boros SJ. High frequency ventilation. In:Goldsmith JP, Karotkin EH, eds. Assisted ventilation oJ'theneonate. Philadelphia: WB Saunders, 1988:190-9.

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