2.7 General Practice - The Radiological Features of Pulmonary Oedema. j.a. Beyers

8/13/2019 2.7 General Practice - The Radiological Features of Pulmonary Oedema. j.a. Beyers

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792 enel alPl actice

SA MED I L JOURN L 2 May 979

Radiological eatures of Pulmonary edemaJ. A. BEYERS

SUMMARYA clinical classification embracing most of the causes ofpulmonary oedema is given, as well as a radiologicalclassification, and t he d if fe rent ways in which pulmonaryoedema may present radiologically a re briefl y described.

Air med l 55, 792 1979 .Pulmonary extravascular fluid balance, like extravascularfluid balance anywhere in the body, depends on thefollowing factors: a hydrostatic pressure in the capillariesand i n t he i nt er st it ia l tissue; b osmo tic pressure in thec ap il la ri es a nd in the interstitial tissue; c) permeability ofthe capillaries; d capacity of the ly mph vessels to draini nt er st it ia l fluid. I n a dd it io n, s ur fa ct an t a nd i nt ra -a lv eo la rgas pr es su re i n t he lungs ha ve an influence on extravascularfluid balance.

Pulmonary oedema may develop whenever there is asufficiently severe derangement in any of these mechanisms.The lung has, however, a big reserve, and pulmonarycapillary pressure may increase from the normal of about7 mmHg to 20 - 25 mmHg, and pulmonary lymphaticdrainage may i nc re as e m an yf ol d b ef or e o ve rt p ul mo na ryoedema develops.

Many c ond it ion s c an d era ng e one or more of thesenormal controlling mechanisms to such a degree thatpulmonary o ed ema develop s. In some c ond it io ns t hemechanism of production of p ul mo na ry o ed em a is simple,but in most c on di ti on s it is complex and in some it isill-understood.Whatever the cause or mechanism of pulmonary oedemat he re is a wide v ar ie ty of radiological appearances spanninga wide spectrum. Although there are certain clues andc er ta in a ss oc iat io ns , i n the individual case the cause ormechanism of pulmonary oedema cannot be d ed uc ed f ro mthe radiological appearance.

CLINICAL CLASSIFICATIONBecause of t he c om pl ex it y of t he me ch an is ms of production of pulmonary oedema, the causes of pulmonaryoedema are best ap pr oa ch ed f ro m the clinical point ofview and grouped as follows:Cardiac causes. T he se include lef t ve nt ric ul ar failure,mi tr al valve disease, left atrial myx oma , cor triatriatum

Department of Radiology, Tygerberg Hospital, Parowvallei,CPJ A BEYERS, M.B . CH .B., M .MED. RAD.), M.D. eUN.) , art-time onsultant RadiologistDate received: 6 November 1978.

a nd p ul mo na ry v enous o bs tru cti on, e it he r co ng en it al oracquired. These causes operate mainly by raising thepulmonary venous and p ul mo na ry c ap il la ry p re ssu re .R en al causes. The se i nc lud e a cu te n ep hr it is and chronicren al failure as well as ren al involvement in lupus e ry the matosus, polyarteritis nodosa, Goodpasture syndrome, etc.T hes e causes work mainly through disturbed water andelectrolyte balance, da mag e to the p ul mo nar y capillarymembrane and perhaps alterations in t he p la sm a p ro te in s.Central nervous system causes. These include head injury,i nt ra cr an ia l h aemo rrh ag e, epileptic a tt ac k, and braintumour. These probably work through the adrenergicnervous system with liberation of circulating catecholamineswhich increase pulmonary capillary pressure.Pulmonary causes. These include irritation due to inhalation of ir ri tan t gases s uc h as ozone, n it ro us oxide, woodsmoke, chlorine or phosgene, or aspiration of irritantfluids su ch as gastric c on te nt s Me nd els on sy nd ro me) orwater drowning in salt or f re sh w at er ); o ve rw he lmi ngi nfe ct io ns , especially t ho se d ue t o v iruse s s uc h as i nf lu en zaviruses, but also with bacteria such as Friedlander s bacillus;t ra um a to the chest wit h p ul mo na ry c on tu si on ; p ro lon ge dinhalation of oxygen at h ig h c on ce nt ra ti on c au si ng p ulm on ar y oxygen i nt oxi ca ti on ; p ul mo na ry art eri tis in, forexample, lupus e ryt hema to su s a nd po lya rt er iti s n od os a;asphyxia with damage to the pulmonary capillaries by

anoxia; rapid aspiration of pleural fluid or a pneumothorax;a nd p ul mo na ry e mb ol is m, e it he r t hr om bo -e mb ol is m; fa tembolism or amniotic fluid embolism. y p ~ a J b u m i n a e m i a This may be a main cause or acontributing factor in renal disease, hepatic disease, proteinlosing enteropathy or severe malnutrition such as kwashiorkor.Diverse causes. These include shock lung adult respiratory distress syndrome, post-traumatic pulmonary insufficiency); high altitude pulmonary oedema; allergic reactions,f or e xa mp le d ue to n it ro fu ra nt oi n, b us ul ph an or penicillin;ov er do sa ge wi th nar cotics , especially h er oi n; o ve rtr an sfusion with fluid or blood; circulating toxins , for examplealloxan or s na ke v en om or toxins in septic shock and

eclampsia; and can also o ccu r during pr egn anc y or afterconfinement possibly amniotic fluid embolism).Depending on the cause of p ul mo na ry o ed ema , t he remayor may no t be cardiac enlargement and/or evidenceof raised pulmonary venous pressure.

RADIOWGICAL CLASSIFICATIONPathologically and radiologically, pulmonary oedema canbe classified as: i interstitial pulmonary oedema; il intraa lv eo la r p ul mo na ry o ed em a; iii) mixed interstitial andintra-alveolar pulmonary oedema.


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Mei 1979 SA M I S TY SKR I F 793nterstitial Pulmonary Oedema

The radiological features of interstitial pulmonaryo ed ema are as follows: o ed emat ou s i nt er lo bu lar s ept a w it hassociated dilated lymph vessels become radiologicallyrecognizable as Kerley A, Band C lines and Kreel Dlines Fig. 1). Kerley B lines are the best known and aremos t commo nl y seen. They appear as short, thin sharplydefined hairline shadows situated horizontally a nd extending perpendicularly to the pleural surface and theya re m ost n um er ou s in t he lower lung fields, especially inthe costophrenic sulci. They are due to oedematous interlobular septa and dilated lymph vessels in the lung periphery.Kerley A lines are longer, somewhat angular hairlineopacities be st seen in the upper and mid-lung zones andextending towards the hili. They are cau sed b y o ed emat ou sinterlobular and intersegmental septa and d il at ed l ymphvessels s itua te d m or e c ent ra lly in t he lungs. Ke rl ey C linesa re only rarely seen and appear as a fine reticular patternprobably due to superimposition of fine oedematous interlobular septa. Kreel D lines are thicker and longer thanKerley A, B or C lines, being up to 2 mm in width and5 - 7 mm in length. They are o ft en s harp ly ang ul at ed andar e more often seen in the anterior parts of the lungs asviewed on lateral radiographs. They also are due tooedematous interlobular and intersegmental septa.Oedem atous interstitial tissue a djac ent to the visceralpleura and on both sides of the interlobar fissures becomesradiologically visible as so-called thickened pleura,thickened interlobar fissures or lamellar pleural effusions.I nt er st it ial o ed ema ext end in g f ro m t he h il ar regions i nt othe lung fields imparts a slight ground-glass veiling to thehilar regions and obliterates the sharp demarcation of thehilar pulmonary vessels, so that t hese vessels n ow b ecomepoorly defined and blurred in outline. This is the so-calledhilar or perihilar clouding Fig. 2).As the interstitial oedema extends further into the lungfields, the slight ground-glass veiling and the blurring ofthe pulmonary vessels extend further out from the hilarregions producing so-called pulmonary clouding.

The oedematous perivascular and peribronchial sheathscause blurring of vessel outlines and thickening of bronchialwalls; the latter can, however, only be recognized whena b ro nchu s is seen end on.ntra alveolar Pulmonary Oedema

The radiological features of intra-alveolar pulmonaryoedema are as follows: as fluid ac cum ula te s in th e alveolithe hi la r and bas al l ung regions a ss um e a finely g ra nu la rappearance. This soon becomes patchy, giving poorlydefined, irregular, blotchy, coalescent opacities in thelung fields. Together with these opacities the pulmonaryvessels become indistinct or invisible and i f the opacitiesare extensive enough an air bronchogram may becomevisible Fig. 3).Th e pulmonary opa citi es va ry in size f rom tiny noduleswith a fine mil ia ry pattern to big confluent opacities fillingmost of the lung fields. Th e commonest picture is probably

that of medium-sized opacities symmetrically and uniformly distributed throughout both lungs, but sparing the

F ig . 1. I nt er st it ia l pulmonary oedema due to left ventricular failure. Top Kerley B lines are seen as thin,horizontal, hairline opacities at th e lung bases; bottom:Kreel D lines are seen as l on g, a ng ul at ed , s tr an dl ik eopacities in t he anterior lung fields. Note also t he oedematous horizontal and oblique interlobar fissures.


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794 SA MEDI L JOURN L 12 May 1979

Fig. 2. Interstitial pulmonary oedema due to l ef t v en tr icular failure. Top: the hilar regions show ground-glassveiling and the sharp demarcation of the pulmonaryvessels is obl iterated; bot tom: the pulmonary oedema hascleared up the hiJar regions ar e normally translucent andth e pulmonary vessels are sharply demarcated. Note alsohow the engorged upper lobe vessels have returned tonormal and how the h eart has decreased in size.e xt re me p ul mo na ry apic es and e xt re me lung p er ip he ry .When these opacities are concentrated mainly around theh il ar areas, a so-called b at win g appearance is produced.The opacities are not always symmetrical or widespreadand they may be confined to one lung or even one lobe.These opacities o ft en c ha nge ra pid ly in a pp ea ran ce, sizeand distribution an d with treatment they may clear in24 - 48 hours. The speed with which this change occursis often the mos t important or only way to differentiatepulmonary o ed em a f ro m p ul mo na ry in fec ti on.Mixed Intraalveolar and Interstitial Oedema

I nt ra -a lv eo la r a nd interstitia l p ul mo na ry o ed em a o ft en

Fig. 3. Intra alveolar pulmonary oedema in mitra l stenosis.Note the poorly defined coalescent opacities which obscurethe pulmonary blood vessels.

occur together and then the changes of intra-alveolaroe dema m as k or completely obliterate the changes ofinterstitial oedema.Unusual distributions of pulmonary oe dema can occu rwh en c er ta in factors e it he r p re ve nt or precipitate oedemain a certain part of the lung. Unilateral pulmonary oedemama y o ccu r in the dep enden t lung in unconscious or venti

late d p ati en ts who lie for a long time on one side; whengastric contents are aspirated into one lung; whenpulmonary contusion or veno-occlusive disease affects onelung only; after rapid aspiration of a large pleural effusionor p ne um ot ho ra x Fig. 4); when t he re is h yp op la si a of onepulmonary artery or a big u nilateral pulmonary embolus;or when one lung is . severely u nd er pe rf us ed as inMacleod s syndrome Fig. 5 or i n t he s ci mi ta r s yn dr om e.

Pulmonary oedema from whatever cause diminishespulmonary compliance an d this in turn causes elevationof both domes of the diaphragm. Together with pulmonaryoedema, especially if of long standing, tnere may beunilateral or bilateral pleural effusions.

CONCLUSIONSNo specific pattern of pulmonary oedema can be attributedto any specific cause, but certain clues and certaingeneralizations can be made:

1 Di la ted u pp er l ob e vessels or so-called u ppe r lobeblood diversion will indicate raised pulmonary venouspressure most likely due to a mitral valve lesion or toleft ventricular failure.2 An enlarged heart shadow will probably indic ate acardiac or renal cause.


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12 Mei 1979 SA M I S TY SKR I F 795

Fig 4. Top: a big left-sided pneumothorax; bottom:pulmonary oedema involving the left lung after aspirationof the pneumothorax

Slowly increasing pulmonary capillary pressure tendst o pro duce pr edo min an t interstitial p ul mo na ry oedemaand this is well seen in mitral valve lesions and left

Fig S Top: interstitial pulmonary oedema involving thenorma l l ef t l ung in a patient with a Macleod syndromeof the right lung; bottom: the pulmonary oedema haslar gely cleared from the left lung. Note that the hyper-lucent underperiused abnormal right lung remains un-changed.

ventricular failure when -the latter develops slowly.4 Acute incidents ten d t o pr odu ce p red om in an t intraalveolar p ulmon ar y oedema as seen in cor onar y thrombosis acute left ventricular failure or acute glomerulonephritis.5 The batwing type of p ul mo na ry o ed ema t en ds tooccur in renal failure acute left ventricular failure lupuserythematosus and polyarteritis nodosa.An awareness of t he n ume ro us causes and the widespectrum of radiological appearances of pulmonaryo ed ema will hel p in the diagnosis of obscure pulmonaryopacities.

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2.7 General Practice - The Radiological Features of Pulmonary Oedema. j.a. Beyers