1059LEADING ARTICLES

Apical Localisation of PulmonaryTuberculosis

THE LANCETLONDON : : SATURDAY, NOV. 20, 1954

PROBABLY we have all wondered why in pulmonarytuberculosis the lesion is nearly always close to theapex. DAVID T. SMITH and his colleagues 1 at DukeUniversity, North Carolina, suggest a hypothesiswhich will interest workers both in tuberculosis andin cardiology. This hypothesis assumes a " streamflow" through the heart by which blood from thesuperior vena cava and blood from the inferior venacava pass through the right auricle and rightventricle in layers without mixing fully. Most of theblood from the superior vena cava goes to the superiorbranches of the pulmonary artery and thence to theupper lobes of the lungs ; while most of the blood fromthe inferior vena cava goes to the lower part of thepulmonary artery and thence to the lower lobes.

Consequently tuberculous material, spreading alonglymphatics to the thoracic duct and thence to thesuperior vena cava, is carried along in the streamflow to the upper lobes as microscopic or macroscopicemboli, whereas most pulmonary infarcts (from emboliarising in pelvic or leg veins) are in the lower lobes.SMITH et al. describe experiments in rabbits which

showed that particulate matter (lycopodium spores andtuberculous pus) injected intravenously caused pulmonaryemboli whose distribution depended on the site ofintravenous injection and on the posture of the animal.Thus, with the rabbits in their normal posture theinfarcts were predominantly (80 %) in the lower lobesafter injection into an ear vein, but 52 % were in theupper lobes after injections into the femoral vein ;while with rabbits in the vertical position there was astatistically significant difference in the position ofinfarcts (only 60 % in lower lobes fter injection intoan ear vein and 30 % in upper lobes after injection intothe femoral vein). SMITH et al. remark that in therabbit the heart, large blood-vessels, and mediastinumare very flexible, and when the posture is changedfrom horizontal to vertical the angle at which blood fromthe superior and inferior venae cavse enters is also changed,so altering the stream flow and the sites of emboli.Coloured plastic material was next injected into the

right auricle of dogs through the superior and inferiorvenae cavse. The heart action ceased before the colouredplastics were injected. In 10 dogs injected in the supineposition and in 5 out of 8 injected in the upright positionthe main mass of the coloured plastic went to the appro-priate lobes. In a further series of an unspecified numberof dogs fixed in the vertical position, green plastic wasinjected into the left subclavian vein and red plasticsimultaneously into the inferior vena cava and the rightsubclavian vein. The green plastic was distributedto both upper lobes as the predominant colour and isillustrated, in a drawing of a branch of the main pul-monary artery, as a distinct layer on top of the red andgoing to the superior branches while the red goes to theinferior branches.1. Smith, D. T., Abernathy, R. S., Smith, G. B. jun., Bondurant, S.

Amer. Rev. Tuberc. 1954, 70, 547 ; Abernathy, R. S., Smith,G. B. jun., Smith, D. T. Ibid, p. 557; Bondurant, S., Smith,D. T. Ibid, p. 570.

It is unfortunate that this novel hypothesis hasbeen advanced without fully convincing experi-mental evidence. The analogy with the double streamof blood in the portal vein 2 is obvious ; but theportal vein is a straight tube where the simple hydro-dynamic principle ’’ that fluids of the same viscositymay flow side by side for a considerable distancewith a minimum of admixture " certainly operates.Does this principle also operate in a passage with twowide cavities, two sets of valves closing at least everysecond, an angle of almost 180°, and a T-junction of180° before the individual branches are reached ?Is it possible for layering of the blood-stream to

persist through this ? The experiments with colouredplastic injected after the dog’s heart had ceased tobeat do not answer these questions. Possibly observa-tions with radioactive material-such as those 3

cited by SMITH et al. themselves as proof of the layer-ing in the portal vein-may yield further evidence.The experiments with lycopodium spores and tuber-culous pus certainly show a relative increase ofembolism in the upper lobes when the animal isheld upright and the ear is injected ; but this increasenever amounted to more than 50% and, even if therewere a direct analogy, this still would not explainthe great preponderance of lesions of the upperthird of the lung in man. Nevertheless this " stream-flow " hypothesis, though not yet proved, is certainlynot disproved.Most recent experimental evidence supports the

hypothesis, put forward by ORTH,4 VOLLAND, andJACOBy,6 that the apical localisation of lung lesionsresults from relative anaemia due to the erect posture.MEDLAR and SASANO 7 showed that the number andextent of pulmonary lesions in the upper lobes ofrabbits was increased by keeping the animals uprightfor ten hours each day. ROTHLIN and UNDRITZ 8

produced lesions in the uppermost parts of the lungsin the flying fox when hanging by its feet, its usualposition. On the basis of established figures forintracardiac pressure (obtained by catheterisationof the right heart), DOCK 9 has pointed out that thepulmonary-arterial pressure in the upper 5 cm. ofthe lung, even in systole, can rarely be more than10 mm. Hg : since nearly 15 mm. Hg pressure is

required to overcome the difference in colloidalosmotic pressure between the plasma and the pul-monary tissue-fluid, no tissue-fluid or lymph willbe formed in the upper parts of the lungs of mostadults while they are erect ; with decreased blood-flow there will be very slight gas exchange, leaving ahigh oxygen tension as in the trachea. Thus thetubercle bacillus is encouraged to grow, few macro-phages or antibodies are brought to the area, removalof bacteria and their products is almost nil, and alesion develops. This conforms with the well-knownfact 10 that apical tuberculosis is rarely found withmitral stenosis. Recent opinion about the source of2. McIndoe, A. H., Counsellor, V. S. Arch. Surg. 1927, 15, 589;

Copher, G. H., Dick, B.M. Ibid, 1928, 17, 408.3. Hahn, P. F., Donald, W. D., Grier, R. C. jun. Amer. J. Physiol.

1945, 143, 105.4. Orth, J. Ætiologisches und Anatomisches über Lungen-

schwindsucht, Berlin, 1887; p. 20; Die Behandlung derLungenschwindsucht in Hochgebirge, Leipzig, 1889 ; p. 23.

5. Volland, A. Dtsch. med. Z. 1889. p. 702.6. Jacoby, E. Münch, med. Wschr. 1897, 44, 197, 232.7. Medlar, E. M., Sasano, K. T. Amer. Rev. Tuberc. 1936, 34, 456.8. Rothlin, E., Undritz, E. Schweiz. Z. allg. Path. 1952, 15, 690.9. Dock, W. Amer. Rev. Tuberc. 1946, 34, 456.

10. Cappell, D. F. In Muir’s Textbook of Pathology. London,1951; p. 433.

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these apical infections is crystallised in FLOREY’S 1statement : " Infection occurring in adults is dueeither to activation of an infection that started inchildhood or, probably more commonly, to - a new

infection " ; and RicH 12 agrees that reinfection maybe exogenous or endogenous. Thus any compre-hensive hypothesis of the reason for the localisationof these lesions must allow for airborne or blood-borne infection. DOCK’S explanation of the influenceof posture does allow for any method of infection andgives an excellent reason for advocating, in treatment,recumbency for some time each day rather thansimple restriction to bed. SMITH’S stream-flow hypo-thesis may apply to some cases of endogenousreinfection of the apices, but not to all apical lesions.

11. Florey, H. W. Lectures on General Pathology. London, 1954;p. 662.

12. Rich, A. R. The Pathogenesis of Tuberculosis. Springfield,Ill., 1951; chap. 19.

13. Sigurdsson, B., Sigurjonsson, J., Sigurdsson, J., Thorbelsson, J.,Gudmunsson, K. R. Amer. J. Hyg. 1950, 52, 222.

14. Pellew, R. A. A. Med. J. Aust. 1951 i, 944.

Not PoliomyelitisIN the past few years a number of puzzling out-

breaks of illnesses rather like poliomyelitis have beendescribed. All of them were at first attributed to

poliomyelitis, but the aberrant features grew morestriking as time wore on. Five outbreaks which have

recently been reported have some interesting featuresin common.The first was at Akureyri, in Iceland, in the 1948-49

winter.13 It began in November, 1948, and during thefollowing three months there were 465 cases in thetown, no less than 6-7% of the population beingaffected. Spread apparently was by personal contactand the incubation period was estimated at five toeight days. Prominent features of the illness includedlow-grade fever, pains in the nape of the neck and inthe back, muscle tenderness, flaccid paresis of one ormore muscle groups, and disturbances of sensation.Most cases would probably have been diagnosedindividually as poliomyelitis, but the group as a

whole had unusual characteristics. The high mor-bidity-rate (mainly among school-children in the15-19 age-group), the winter incidence, the mildnessof the illness, the lack of fatalities, and the longduration, combined to make the diagnosis of poho-myelitis unlikely. Convalescence was usually slow,and only 6 out of the 57 more serious cases werecompletely free from symptoms seven to ten monthsafterwards. There were complaints of recurrent pain,fever, and pareses, and of nervousness, palpitation,and sweating. The cerebrospinal fluid, examined ina few cases, showed pleocytosis and increased protein ;but attempts at virus isolation and serological investi-gation yielded no evidence of infection by polio-myelitis, Coxsackie, or arthropod-borne encephalitisviruses.The second outbreak was in Adelaide during the

Australian 1949 winter. a Early in the winter there hadbeen quite a serious poliomyelitis epidemic, but inAugust a number of patients were noted to have normalprotein content and cell-counts in their cerebrospinalfluids. During the period August, 1949, to April,1951, 1350 cases were admitted to hospital, of which800 had fewer than 10 cells per ml. in the cerebrospinalfluid-a much higher proportion of normal findingsthan is usual in poliomyelitis. Symptoms appeared

suddenly or gradually, the illness starting as a rulewith a stiff neck and back, and a bursting headache.Diffuse mild muscle weakness was common, butmuscle recovery was excellent. Fever was short-livedand there were no deaths. Yet, as in the Icelandepidemic, there were complaints of pain in variousmuscles during the following six months, and muscleweakness often came on three months after the mainillness. Depression and difficulty in mental concentra.tion were other common sequelse. PELLEw 14 draws aninteresting contrast. One patient, a typical case ofpoliomyelitis with severe loss of muscle power and nomuscle recovery, was nevertheless the most cheerfulpatient in the ward. Another patient with a polio.myelitis-like infection had completely regained all hismuscle power but was extremely irritable and almostmelancholic. No virus investigations were under.taken.The third outbreak occurred in the northern part

of New York State during the late summer of 1950.WHITE and BURTOH 15 think it so similar to thatdescribed by SIGURDSSON et al.13 that they name theinfection Iceland fever. Once again the cases wereat first regarded as atypical poliomyelitis infections,but the chief symptoms were muscle aching and ten.derness with overlying hyperaesthesia, especiallyround the shoulder girdles, and weakness of the limbmuscles without muscle wasting. Complaints of

paraesthesiae and numbness were frequent. 8 patientsseen fifteen-months after their illness all had muscleaches and 7 said they were easily upset and depressed.In 9 out of 11 patients tested the cerebrospinal fluidwas normal, but in the 2 cases examined earliest inthe disease slight pleocytosis was found. The urinarycreatine excretion was high in some of the patients,and WHITE and BunTCil infer from this that muscle

wasting or dysfunction was an important factor in thedisease. Limited virological investigations revealedno evidence of poliomyelitis or Coxsackie virusinfections.The other two outbreaks were both seen in nurses’

homes. One was in Coventry during the late summerand autumn of 1953.16 The nurses were working inwards to which patients with poliomyelitis were beingadmitted, and again the nurses were at first thoughtto have become infected with poliomyelitis. 13 of 65nurses, aged 18 to 46, took ill within a period of twomonths. The onset was insidious, with headache,backache, chills, and lethargy, and it was followed bvdiffuse paresis associated with muscle tenderness.

parsesthesise, and unsteadiness in response to effort.

Except in 1 case, recovery was substantially completewithin two months, but during convalescence therewere complaints of inability to concentrate, andaching and fatigue in the affected limbs after exerciseIn all these cases the cerebrospinal fluid was normal.Virus investigations yielded no evidence of polio-myelitis or Coxsackie virus infection, and some otherneurotropic virus infections were also excluded. The

Coventry, Iceland, New York State, and Australianoutbreaks have many features in common with onein the nurses’ home of the Middlesex Hospital whichis reported by Dr. AcHESON in our present issue. Heretoo, the illness was usually mild, with a surprisingabsence of serious paralytic sequelse but with a db-15. White, D. N., Burtch, R. B. Neurology, 1954, 7, 506.16. Macrae, A. D., Galpine, J. F. Lancet, Aug. 21, 1954. p. 350.