Cough and fever

Robert T. Bramson, MDN. Thorne Griscom, MDRobert H. Cleveland, MD

Published online before print10.1148/radiol.2361041278

Radiology 2005; 236:22–29

1 From the Department of Radiol-ogy, Children’s Hospital, Boston,300 Longwood Ave, Boston, MA02115. Received July 22, 2004; revi-sion requested September 22; revi-sion received November 10; acceptedDecember 10. Address correspon-dence to R.T.B. (e-mail: [email protected]).© RSNA, 2005

Interpretation of ChestRadiographs in Infants withCough and Fever1

An understanding of the appearance of the infant chest radiograph requires anunderstanding of the anatomy and the physiologic, immunologic, and pathologicprocesses in the infant’s chest. The authors describe the features of the infant chestthat most influence the appearance of the chest radiograph in infants with coughand fever. They discuss why confusion sometimes occurs when radiology residentsand general radiologists familiar with adult chest radiographs first evaluate theinfant chest radiograph. The radiographic appearance of acute inflammation doesnot look the same in infants as it does in older children and adults. The hallmark ofinflammatory lung disease in the infant chest is air trapping on the chest radiograph.© RSNA, 2005

EDITOR’S NOTE: Please see the January 2005 From the Editor, where this new feature, Review forResidents, was announced.

Radiology residents have often expressed to us their frustration and confusion whenattempting to interpret chest radiographs of infants. Radiologists not trained in pediatricradiology find terms like air trapping, peribronchial thickening, bronchiolitis, lower re-spiratory tract infection, and peribronchial pneumonia confusing (1). Pediatric radiolo-gists have, in fact, conflicting definitions of these terms and varying opinions about theirmeaning. The authors hope to clarify the relationship between the pathologic changeswithin the infant chest and their radiographic appearance, explaining in pathophysiologicterms why the infant chest looks the way it does in inflammatory airways diseases.

An understanding of the infant chest radiograph requires a review of how embryology,anatomy, physiology, pathology, immunology, and the physics of fluid mechanics influenceits appearance. This knowledge is critical in the interpretation of the infant chest radiograph.

EMBRYOLOGY AND ANATOMY

We will summarize the science that explains the appearance of the infant chest, with thecaveat that universal agreement on the details does not exist. All of the generations of theairways have developed by the time the fetus reaches the 16th week of gestational age.There are about 22 generations of airways, depending on how the last generation iscounted and where the count is performed. Near the lung hila, there may be as few as 10generations of airways before the gas-exchange units—the respiratory bronchioles andalveolar sacs—are reached. In the lung periphery, there may be as many as 25 generationsof airways before the gas-exchange units are reached. As the child grows and becomes anadult, the airways grow in length and diameter but not in number (2–4) (Fig 1).

The alveoli, the gas-exchange units, develop after the airways. They start proliferatingabout the 29th week of gestational age. By the 40th week of gestation, there are approx-imately 20 million alveoli in the newborn lung, although the precise number is debated.The mature lung contains approximately 300 million alveoli; that number is reached atabout 8 years of age (2). The alveoli then increase in size, and their lining gets progressivelythinner as the child becomes an adult. The total alveolar surface area is 70–80 m2 in theadult. In the newborn infant, the total alveolar surface area is only about 3 m2. The ratioof the alveolar surface area to the body surface area is more than three times as great in theadult as in the newborn (5). Thus, the infant is at a distinct disadvantage, compared with

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the adult and older child, in his or herreserve of alveolar surface area for gasexchange. The alveolar walls contain thepulmonary capillaries, which form a gi-ant blood surface area for the exchangeof respiratory gases (4).

The adult lung and that of the olderchild have communications betweenthe alveoli, the pores of Kohn (intraal-veolar pores), and the channels of Lam-bert (bronchoalveolar channels). Theseallow collateral air drift between theairspaces and are far fewer in infants.Their relative absence influences theappearance of radiographs in infantswith lower respiratory infection, as willbe explained later (4).

The structure of the chest wall in theinfant differs from that in the adult. Theinfant’s ribs and adjacent soft tissues aremore elastic and compliant. As the childgrows, the soft tissues and ribs becomestiffer (6). Watching a baby breathemakes this obvious. The infant moves hisor her chest wall in and out more thanthe adult does, particularly when in re-spiratory distress. The more marked com-pliance of the soft tissues of the infantthorax allows retractions of those tissuesbetween the ribs. The lack of stiffness inthe soft tissues requires more work dur-ing breathing. When the infant is in re-spiratory distress, this increased work be-comes more obvious. The sight of a sickinfant struggling to breathe can be fright-ening, and the grunting and retractionsgraphically demonstrate the increasedwork of breathing. In contrast, adultswith pneumonia do not work particu-larly hard moving air in and out of theirlungs unless the pneumonia is extensive.

During inspiration, the intrathoracicairways increase in cross-sectional area.

During expiration, the airways narrowand the cross-sectional area decreases.This normal variation in luminal size isaccentuated in the infant because thesupport tissues around the airways aremore compliant and allow more narrow-ing during expiration. Compared with anadult, the number of alveoli is relativelylow in the infant, and the proportion ofthe lung involved in air transport (theairways) is relatively high. In the adult,80% of the airways are bigger than 2 mmin diameter. The smaller peripheral air-ways in adults account for less than 20%of the total resistance to the flow of air. Inthe infant lung, the peripheral airwaysare considerably smaller, and the resis-tance to air flow owing to these smallairways is 50% of the total resistance (4)(Fig 2).

PHYSIOLOGY

Growth is proportionately more rapid ininfancy than at any other time of post-natal life. The metabolic requirements forthat growth include large amounts of ox-ygen (6). However, as previously men-tioned, the adult lung has a ratio of sur-face area of the pulmonary capillary bed(gas-exchange area) to body surface areathat is more than three times as large asthat in the newborn infant (5).

The healthy newborn infant breathes40 times per minute. The healthy adultbreathes 16 times per minute. The highdemand for oxygen in the healthy infantplus the relatively small gas-exchangearea per unit of body surface area taxesthe respiratory system much more in theinfant than in the adult. This is one ofthe causes of the relative tachypnea ofhealthy infants. Infants compensate forincreased oxygen demand primarily byincreasing their respiratory rate (4,7).

Resistance to the flow of air throughthe airways is higher in the infant than inthe adult. This is both because the com-pliance of the tissues surrounding the in-fant airways makes it easier for the air-ways to narrow during normal expirationand because of the higher percentage ofsmall airways in the infant lung (4). Theresistance of the flow of air through acylinder, such as an airway, is describedby the Poiseuille law. A quick summaryof this law is that the resistance to theflow of air through the airways varies in-versely with airways radius to the fourthpower (4). Thus, a tiny decrease in thediameter of the airways leads to a markedincrease in resistance to the flow of air. Aspreviously mentioned, the contribution

of the peripheral airways to the resistanceof flow is considerably greater in infantsthan in adults, even in normal circum-stances (4).

When breathing at 16 times perminute, the adult has 3.75 seconds tomove his or her diaphragm through thefull course of inspiration and expiration.When breathing at 40 times per minute,the infant has only 1.5 seconds for thisdiaphragm movement. The infant in-creases oxygen exchange primarily by in-creasing the respiratory rate. When thishappens, the diaphragm must change di-rection more frequently and either movefaster or not move as far during eachexcursion. During periods of respiratorydistress, these all occur.

The level of the diaphragm seen onchest radiographs is determined by sev-eral things. At all ages, the level of thediaphragm depends on how deep an in-spiration the patient has made when theradiograph was obtained. The adult usu-ally takes a deep breath when requested,and the diaphragm level is determinedby voluntary action. The infant does notvoluntarily take a deep breath and hold itfor a chest radiograph. The technologistmust guess and acquire the radiographwhen the infant appears to haveachieved maximum inspiration. If the in-fant diaphragm moves through the en-tire respiratory cycle in only 1.5 seconds,or even less time when the rate reaches60 breaths per minute, the technologisthas little time to make a correct guess.The diaphragm sits at a level determinedby the resistance to flow of air throughthe airways. Figure 3 depicts lung vol-umes and diaphragm movement duringrespiration, first in health and then indisease, when air trapping has led to anincrease in residual volume (8).

Normally, the dome of the right hemi-diaphragm at inspiration is projected atabout the level of the sixth anterior ribon a chest radiograph. A normal lateralchest radiograph will show a domed,rounded configuration of the diaphragm.Figure 4 shows the typical configurationof the diaphragm on anteroposterior andlateral chest images in a healthy smallinfant.

IMMUNOLOGY ANDPATHOLOGY

Growing children are exposed to manyinfectious organisms and need to de-velop immunity to them. The averageadult inhales more than 9000 L of air perday; the infant, much less (4). A multi-

ESSENTIALS● Most respiratory infections are caused

by viruses in infants and childrenyounger than 24 months and lead tothe pathophysiologic changes of airtrapping.

● Hyperinflation may be the only radio-logic clue to illness.

● Bacterial pneumonia can have thesame appearance in adults and in-fants.

● The radiographic appearance reflectsthe pathologic process occurring in therespiratory system.

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tude of organisms enter the airwaysalong with this inspired air. The organ-isms that infect the respiratory tract ininfancy are usually viral. The most severediseases in the lower respiratory tract arecaused by the parainfluenza viruses andthe respiratory syncytial virus (9,10).These are also among the most commonorganisms to infect the infant’s respira-tory tract (9–11). Adults have some im-munity to most of these organisms be-cause they were exposed to them aschildren and developed an immunity. Al-though adults may be infected and trans-mit these viruses to others, they usuallybecome no more than mildly ill. Infantshave not yet developed substantial im-munity to these viruses and often get sickbecause of them, especially the parainflu-enza and respiratory syncytial viruses.

The terminology for lower respiratorytract infections in infants is confusing.For example the definition of bronchioli-tis varies with local pediatric usage. Somephysicians limit the term bronchiolitis torespiratory syncytial virus infection inchildren. Affected children may have re-tractions, tachypnea, air hunger, and ex-treme respiratory distress. Other childrenof a similar age may have the same clin-ical findings, but respiratory syncytial vi-rus cannot be cultured; some pediatri-cians also call this bronchiolitis. Otherphysicians may call all these clinical find-ings pneumonia, but still others are un-comfortable with that term because, tothem, pneumonia means airspace con-solidation on a chest radiograph. Some-times the term peribronchial pneumonia orinterstitial pneumonia is used to differen-tiate this airways infection from airspacepneumonia. Some individuals simply call

all of these lower respiratory tract infectionsin the attempt to avoid the confusion interminology.

Radiologists should be aware that thenomenclature is confusing. Heated de-bates may occur between physicianswho use different definitions for theseterms. We suggest that radiologists usethe terms and definitions generally em-ployed by the referring clinicians andbe alert to the problem of confusion.

During these respiratory viral infec-tions, the airways react in several ways,most notably with bronchoconstrictionand increased secretion of mucus (12).These two factors have the effect of nar-rowing the cross-sectional area of theairways—particularly the small airways(12th generation airways or smaller) (Fig5). These airways, which already contrib-ute 50% of the total airways resistance,suddenly have a marked decrease in av-erage radius. Since resistance is inverselyproportional to the fourth power of theradius, this has the effect of greatly in-creasing the total resistance to air flowthrough the airways.

RADIOLOGIC FINDINGS

As was mentioned earlier, the primaryway for the infant to increase ventila-tion is to increase his or her respiratoryrate. Infants in respiratory distress dueto viral infection often breathe 60–80times per minute. Their air hunger canbe recognized by the use of the acces-sory respiratory muscles. The increasedwork of breathing is largely caused bythe increased resistance to the flow ofair through the small airways. Their air

hunger causes retractions and gruntingas they work to overcome this resis-tance.

Infants breathing at 60 or more timesper minute have less time to move thediaphragm through its inspiratory-expi-ratory cycle. They have only 1 second,sometimes less, for each breath. The dia-phragm tends to move in a narrow rangebecause of the resistance to the flow of airthrough their small airways (Fig 3).

The dead space in the upper airwayscannot be reduced and remains constant.However, it gets more difficult to propelthe dead-space air back up and out of themouth because of the increased resis-tance in the peripheral airways. As therising diaphragm pushes the air out ofthe lungs, it must almost immediatelycontract to start inspiration. The inspira-tion starts before the usual volume of airhas been expelled. Because of the diffi-culty of pushing all the air out duringexpiration, the lungs are at a more ex-panded state when inspiration startsagain—that is, there is an increase in re-sidual volume, and there is air trapping(Fig 3). The lungs are at a high volumeeven at the end of expiration. On a radio-graph, the diaphragm is projected at alevel lower than the sixth anterior rib (Fig6), and the diaphragm leaves are flat-tened. The radiologist will notice thatthere is an increase in the transverse di-ameter of the chest and a flattened dia-phragm on an anteroposterior projec-tion. On a lateral image, there is flatten-ing of the diaphragm, and the sternummay be bowed upward and outward (Fig7). Some radiologists gauge hyperaera-tion by counting posterior ribs, particu-larly if the radiograph is obtained withthe patient in an apical lordotic position.Those who use posterior ribs in this situ-ation usually believe the diaphragm islocated at the level of the eighth poste-rior rib during normal inspiration (8).

To diagnose air trapping, the dia-phragm needs to be flattened on bothanteroposterior and lateral projections. Ifthe lung volume is high on one radio-graph and normal on the other, then thehigh-volume projection happened to beexposed at a moment of an unusuallydeep breath. If the diaphragm is welldomed on the other view, then the infantis able to move air out of his or her lungsduring expiration and there is no air trap-ping.

To summarize, these sick infantsbreathe faster and work harder tobreathe, their airways narrow during ex-piration, and the greatly increased air-ways resistance severely impedes the flow

Figure 1. Diagram shows gas exchange that occurs in the respiratorybronchiole and alveolar sac. In the lung periphery there may be asmany as 25 generations of airways before the respiratory bronchiole isreached or as few as 10 (near the hila), depending on where the countis performed. Inset shows how a distal bronchiole may become nar-rowed with edema and mucus during inflammation.

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of air. The air trapping revealed by theincrease in lung volume on the chest ra-diograph is the best available indicator ofinflammatory lung disease in infancy.Hyperinflation may be the only radio-logic clue to illness in these children. Thealveoli are usually clear, and there isnone of the airspace consolidation asso-ciated with classic bacterial pneumoniain adults.

The radiologist should not becomewedded to the relationship of the dia-phragm to the sixth anterior rib, but thisfinding does serve as a useful rule ofthumb. An experienced pediatric radiol-ogist quickly recognizes hyperaeration ata glance without counting ribs. A lessexperienced observer will find the sixthanterior rib to be a helpful landmark.

There are often additional signs of in-flammatory disease of the small airways.Edema and mucus in these airways cancause peripheral atelectasis. Small plugsin many small airways produce manysmall patches of atelectasis. If enough ofthese small patches accumulate in oneregion, a patch of atelectasis shows up ona chest radiograph (Fig 8). The abnormalappearance is often difficult to define, ex-

cept that the interstitial lung tissues lookprominent. Some observers call this peri-

bronchial cuffing or peribronchial thickeningor bronchial wall thickening. Sometimes

Figure 2. (a) Diagram shows that during normal inspiration and expiration, there is dilation and collapse of the airways.This is most obvious in distal airways. Collapse in infant airways is greater than that in adult airways because cartilaginoussoft tissues supporting the airways are more compliant in children. This is illustrated on (b) a lateral chest radiograph of aninfant obtained near the end of normal expiration. The trachea (arrows) collapses to a much smaller diameter during normalexpiration.

Figure 3. Graph depicts lung volumes at inspiration and expiration.Line on the left shows lung volume at expiration (A) and inspiration(B), as well as maximum expiration (C) and inspiration (D) duringnormal quiet respiratory cycles. The line on the right shows thatwhen peripheral small-airways resistance is high (a, b), then residualvolume (RV) is increased. This is the air trapping depicted on radio-graphs of infants with small-airways disease. c � Maximum expira-tion, d � maximum inspiration, ERV � expiratory reserve volume,IRV � inspiratory reserve volume, TLC � total lung capacity, TV �tidal volume, VC � vital capacity. (Reprinted, with permission, fromreference 7.)


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the radiologist looks at the airways endon. If the radiologist thinks the wallsof these airways (usually of the third,fourth, or fifth generation) look thicker,he or she will use the term peribronchialthickening or bronchial wall thickening. Inreality, thickening of the smaller air-ways (12th generation or higher) has afar more deleterious effect on gas ex-

change than does thickening of the air-ways that are identifiable on a radio-graph. The patches of peripheral atelecta-sis may shift when the infant coughs anddislodges small mucus plugs. Therefore,the radiographic appearance may changefrom image to image. Hyperinflation, how-ever, remains the major clue to inflamma-tory small-airways disease (12).

As the infant improves, interestingthings happen. The diaphragm returns toa more normal level, but the radiographmay show increasing patches of atelecta-sis. This can confuse pediatricians andradiologists alike. Perhaps as the hyper-expansion of the lung decreases, somealveoli kept open by the air trapping nowsuccumb and collapse, leading to an ap-pearance of increased atelectasis. In real-ity, the child is improving even thoughthe radiograph may look mildly worse.

CAVEATS

The changes we have described are themost common ones in lower-airways in-flammatory disease in infancy. Most re-spiratory infections in this age group arecaused by viruses and lead to the patho-physiologic changes described. Yet, justlike adults, infants can also get bacterialinfections. In those cases, the radio-graphic appearance mimics that seen ona chest radiograph in an adult with bac-terial pneumonia. Air bronchograms,consolidation, and some volume loss inthe consolidated segment usually do notconfuse radiology residents and generalradiologists, even when seen in infants.Pneumonia looks the same in adults,and, when bacterial, it can look that wayin infants too. Infants with bacterialpneumonia can have pleural effusionsand adenopathy. Children are not im-mune to the types of pulmonary infec-

Figure 4. (a) Anteroposterior radiograph of normal chest in a 4-month-old child referred because of a possible fracturedclavicle. (b) Lateral radiograph in the same infant shows rounded configuration of the diaphragm (arrows).

Figure 5. Diagram shows that during viral infection, airways secreteincreased amounts of mucus and become edematous, particularly insmaller peripheral airways. This narrows the airways, and that nar-rowing is accentuated during attempts at expiration.


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tions that older children and adults con-tract. Nevertheless, viruses are the mostcommon cause of respiratory infectionsin infants (10).

Bacterial pneumonia in infancy can

sometimes produce an unusual and dis-concerting appearance because of the an-atomic features mentioned earlier. Theinfant does not have a well-developedsystem of collateral ventilation—there

are fewer pores of Kohn and channels ofLambert. Therefore, exudate that accu-mulates in the alveoli does not spread toadjacent alveoli as easily as in the adult.The limits of the inflammatory process

Figure 6. (a) Anteroposterior radiograph shows hyperinflated lungs with suggestion that peribronchial markings are tooprominent. (b) Lateral radiograph shows flat slope to the diaphragm, with none of the rounded configuration seen in Figure4b. The diaphragm now has a straight-line slope rather than a rounded configuration.

Figure 7. (a) Anteroposterior radiograph of infant chest shows hyperinflated appearance characteristic of infant inflamma-tory airways disease. Hemidiaphragm domes are projected at level of the seventh anterior rib or lower. (b) Lateral radiographof hyperinflated chest shows diaphragm has a straight (not domed) slope.


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are difficult to define in adults unlessthey border on a pleural surface. In in-fants and younger children, however, theexudate tends to be trapped in the alve-oli, unable to spread through the pores ofKohn. Sometimes, because of the lack ofcollateral air drift openings, the exudate

takes the appearance of a spherical con-solidation—a “round pneumonia”. Theinflammatory cells are confined under amild degree of pressure, and these infantsoften have a high fever; 104°F or 105°F(40°C or 41°C) is typical. The radio-graphic appearance can be alarming be-

cause a round pneumonia can look like aneoplasm (13). Several children havebeen referred to us with the suspicion ofa primary or metastatic neoplasm, butthey really had pneumonia with an un-usual spherical appearance (Fig 9).

Other disease processes can produce airtrapping and hyperaeration of the lungs.Increased fluid in the interstitial spacescan compress the small airways and causean increase in small-airways resistance.Enlarged heart chambers and pulmonaryvessels can also compress airways. There-fore, severe cardiac disease and increasedfluid load can lead to radiographs thatshow air trapping. Older infants can anddo aspirate foreign bodies into their air-ways; this may cause focal air trappingor atelectasis. Reactive airways disease,which does occur in infants, can cause airtrapping at any age. Certain chronic lungdiseases such as cystic fibrosis and bron-chopulmonary dysplasia demonstrateair trapping on radiographs. Tachypneafrom a variety of other causes, such asacidosis, fever, and sometimes even fear,will produce the appearance of air trap-ping secondary to the mechanism ofrapid breathing (4).

Nevertheless, most infants who acutelydevelop respiratory distress have a viralillness. The appearance of the radiographreflects the pathologic process occurringin the respiratory system. An understand-

Figure 8. Respiratory syncytial virus infection in a child. (a) Anteroposterior radiograph shows prominent peribronchialmarkings. (b) Patches of atelectasis (arrow) are best seen on lateral projection of the hyperinflated lungs. Scattered patches ofatelectasis tend to follow peribronchial and perivascular structures in a child with respiratory syncytial virus infection.

Figure 9. Anteroposterior chest radiograph displays roundpneumonia (arrow). Child had a fever of 104°F (40°C), abdom-inal pain, and a cough.


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ing of the appearance of the infant chestradiograph requires an understanding ofthe underlying pathologic process. Hyper-aeration of the lungs is often the earliest,and sometimes the only, radiographicsign that the infant has a viral infectioninvolving the lower airways.

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7. Lawson E. Respiratory control after birth.In: Chernick V, Mellin R, eds. Basic mech-anisms of pediatric respiratory disease: cel-lular and integrative. Philadelphia, Pa:Decker, 1991; 288–302.

8. Griscom NT, Wohl M, Kirkpatrick J. Lowerrespiratory infections: how infants differfrom adults. Radiol Clin North Am 1978;16:367–387.

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Cough and fever

Education

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