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Acta Radiologica: Diagnosis
ISSN: 0567-8056 (Print) (Online) Journal homepage: https://www.tandfonline.com/loi/iard19
To cite this article: (1967) Own Investigations, Acta Radiologica: Diagnosis, 6:sup264, 20-64, DOI: 10.1080/05678066709170532
To link to this article: https://doi.org/10.1080/05678066709170532
Published online: 04 Jan 2010.
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P A R T
I.HUMAN MATERIAL Material
The material consisted of the bodies of 58 infants and children who died a t the Children’s Hospital during the period Sept. 8 , 1959-March
4,1960. All age groups from a few hours to 14 years were represented, although the youngest age groups predominated. The time t h a t elapsed between death and autopsy varied between G and 60 hours (one case), the average being 28 1/2 hours. The cases were in no way selected, the series comprising the majority of the patients who died during the period in question. Only occasional cases in which no roent- genographic follow-up studies could be performed were omitted.
When patients die a t the Children’s Hospital the routine procedure is as fol- lows:
When the physician in charge has establislied t h a t the child is dead, the parents are informed. The dead body is kept for Fome hours, as a rule G , in a bed in the ward. Then i t is brought to the mortuary, where it is kept a t a temperature of
about 5°C. As soon as the body has been brought to the mortuary, b u t not be- fore, autopsy is theoretically possible. To perform i t the parents’ permission is necessary. This permission is not asked for until the child has died. In cases of particular medical interest permission may be granted by the County Medical Of- ficer of Health against t h e will of the parents.
Owing to these rules autopsy can never be performed until 6 hours post mor- tern. Occasional cases have to wait as long as GO hours, b u t in the majority of cases autopsy is performed 1 2 4 8 hours post mortem, and always b y a pathologist. Macroscopic investigation is supplemented by microscopic study of most organs. A particular autopsy record is made of both the macroscopic and microscopic findings, and t h e organs and specimens collected are stored for many years.
In this connection it may be mentioned t h a l of all patients who die a t tlie Children’s Hospital more than 90 per cent are examined post mortem.
Within the limitations set by this routine the present study was carried out as follows:
Immediately after the death of a child the roentgenologist was informed. Within one hour (in exceptional cases 2 hours) post mortem chest roentgenograms were taken in four projections (antero-posterior, straight lateral and the two ob- lique projections). This investigation was as a rule repeated 6, 12, 24 and 48 hours post mortem, the last time always immediately preceding autopsy. In 15 cases roentgenograms were also taken 2-3 hours post morteni. A t autopsy the lungs were removed entire, and rriicroscopic sections of all lobes were separately studied. The lung sections were investigated in co-operation with tlie pathologist of the Children’s Hospital (HJELT). In a few instances the above-mentioned time sche- dule could not be followed in all details, b u t chest roentgenograms takeii immedi- ately post mortem and immediately before autopsy, the time of which is indicated, are available in all cases.
Furthermore, bacterial specimens were collected by sterile puncture of the median part , mostly t he middle lobe, of the right lung. The aspirated substrate, usually a tiny drop of fluid, was cultured on blood agar plates a t 37OC for 23 hours. When t he result was positive, a bacteriological analysis was performed a t tlie State Serum Institute. If Staphylococcus aureris was found, a determination of the phage t l p e of the coagulase-positive cocci was performed. The method of the bacteriological analysis has heen described by RANTASALO & €IJELT 19G3.
a. Roentgenographic findings i n the lungs
During t he postmortal follow-up period roentgenographic changes occurred in striking abundance. On the basis of these findings the material was classil’ied in four groups as follows:
1 ) Cases in which no changes were detected during the postmortal period of observation as compared with the condition immediately post mortem. This group comprised 0 bodies. In 2 of these no roentgenograpliic changes were seen throughout the whole period of observation (Fig. 1). In 4 cases opacities were ohserved in the chest roentgenograms immediately post mortem, b ut no further changes occurred during the follow-up period. Detailed information with regard to this group may be found in Table I .
2) A group of 12 cases in which lobar, local opacities were perceived during the postmortal period of observation (Figs. 2, 3, 4 and 5). For details the reader is referred to Table 2.
3 ) '1 large group coinprising 35 cases in which diffuse density developed in lubes which immediately post morteni were clear, or slight opacities became niore marked during the follow-up period. For details, see Table 3. Examples of the roentgenographic changes typical of this group, which comprised the majority of the present rases, are shown in Figs. (i arid 7 .
4 ) -1 group comprising G cases in which the lungs were so opaque immediately post rnortcrn t h a t no changes could be discerned during the postmortal period of o1)servation. Fig. 8 is an example of the findings i n this group. Ilctailed d a t a are given in Table 4.
I n the present study the term opacity is used to describe a limited area in wliicli the absorption of the roentgen rays is increased, irrespective of the cause. The terni increasing density is used to describe a gradual increase in t h e absorli- Lion of t h e roentgen rays, resulting in a diffuse, structureless haziness on the roentgenograms.
b. Microscopic findings in the lungs
Jlicroscopic investigation revealed a great abundance of a variety of patholo- pica1 changes in various lobes in all patients. Both extensive and minute alveolar pneuniunias, infantile septa1 reactions, atelectases of Loth the rnecliariical and the microatelcc.tatic type and various degrees of oedcma in the alveoli occurred.
dctailed report on all the microscopic changes t h a t were noted wonld entail long lists which are of no interest in this connection.
On f lie whole, there seemed to be no correlation between slight rnicrosropic cliaiiqcs and the roentgenographic findings, b u t a comparison of the grave niicro- scopic arid roentgenographic changes is of interest, as appears from Table
c . Comments on the findings
T h e r o e n
tg e n o g r a p h i c f i n d i n g s
]\'it11 rrspect to the patients' ages, clinical diagnoses, and length of the period of observation post mortem, there was no difference between the woentgenograph- ically negative)) cases listed in Table 1 and the ))roentgenographically positive)) cases listed in Tables 2 and 3. In group 4 the roentgenographic opacity ohserved immediately post morteni was so grave that no further changas could be expected. Regarding t h e cause of the fact t h a t a roentgenographically observable increase in density failed to occur in some cases whilst in the majority i t did occur post mortem, no definite conclusions can be drawn from the above-mentioned data. Concerning t h e time when a n increase in density became roentgenographically discernible i t may be mentioned t h a t in those 1:) cases in which roentgenograms
Fig. 1. Case 769/60. (Table 1.) Boy aged 9 days. D i a g n o s i s a n d c I i n i c a 1 c o u r s e : Admitted to t h e Children’s Hospital a t thc age of 8 days with vomiting and dyspnoea. Expircd within one day. Autopsy revealed a n intracranial hacmorrhage h u t nothing pathological in the
a. Chest roentgenogram one hour post mortem.
b. Chest roentgenogram 40 hours post mortem. N o changes or very slight diffuse density in the right upper lobe.
c. Microscopic section of the right upper lobc. Moderate hypostasis, no pncumonia. Slight cel- lular desquamation in some alveoles.
Fig. 2. Case 24/60. (Tablc 2 . ) Girl aged 11 years. D i n g n o s i s a n d c 1 i n i c a 1 c o u r s e : Disseminated lupus erytliematosiis was observed a t the age of 8 years. In spite of medical treat- ment t h e s t a t e steadily deteriordtrd and t h e girl died a t the age of 11 years. Autopsy proved t h e clinical diagnosis and evcn showed a frcsh cerebral hactmorrhage. N o pneumonia.
a . Chest roentgcnogram one hour post mortcm. A central opacity is visible in t h e right upper
lobr. A very small a m o u n t of fluid (visible in the oblique projections only) in both pleural cavities.
b. Chest roentgenogram 12 hours post mortern. The opaque area has markedly enlarged post-
mortally. The amount of pleural fluid is unchanged. c. The right hilar region in detail one hour post mortrm.
d. The same area 6 hours post mortem.
e. The same area 12 hours post mortrrn. The onaqur area is clearly larger and a more diffuse density is seen in t h r peripheral parts of the lung.
f. Microscopic section of t h e right upper lobe. hIarkrd oedrma in the central part of the lobe. N o pneumonia.
Fig. 3. Case 50'20/59. (Table 2 . ) Giri aged 1 y r a r and 7 months. D i a g 11 o s i s a n d c I i n i c a 1
c o II r s r : The child suffrrrd for two weeks of encephalitis and pnrumonia and did not respond
to antibiotic treatment. Autopsy verified the clinical diagnosis. The pneurnonias are duc to
a . Chest roentgenogram one hour post mortern. b. Chest roentgrnograrn 2 hours post rnortern. c. Chest roentgenogram 6 hours post rnortern.
e. Microscopic section of the left upper lobe. A large alvrolar pneumonia is seen. Haematoxylin-eosin. x 120.
f. Microscopic section of the right upper lobe. Thick alveolar septa with cellular infiltration are seen, but no alveolar pneumonia.
Fig. 4. Case 5520/59. (Table 2 . ) Girl aged 17 days. D i a g n o s i s a n d c 1 i n i c a 1 c o II r s e : T h r child was born with a perforated myelocele in the lumbar region. An operation was performed b u t the wound was infected. Pneumonia on the right side was later observed. I n spite of anti- biotic treatment the child died. Autopsy revealed intraventricrilar cerebral haemorrhage and alveolar pneumonias in all lobes in both lungs.
a. Chest roentgenogram one hour post mortem. b. Chest roentgenogram 6 hours post mortem. c. Chest roentgenogram 13 hours post mortem.
d. Chest roentgenogram 22 hours post mortem. Increasing density is seen in the right lung and also in the lower area of tho left.
Fig. 5. Case 808/60. (Table 2.) Boy aged 1 year a n d 1 month. D i a g n o s i s a n d c I i 11 i c a 1
c o u r s e: The boy had a cerebellar tumour and obstructive internal hydroczphalus. l i e was
admitted in rather poor condition. Autopsy revealed no pneumonia and only slight ocxdcma in the lungs.
a. Chest roentgenogram taken one hour post mortem. h. Chest roentgenogram taken 6 hours post mortem. c. Chest roentgenogram 12 hours post mortem. d. Chest roentgenogram 44 hours post mortem.
Fig. 6. Case 1658/59. (Table 3 . ) Girl aged 10 years and 5 months. D i a g n o s i s a n d c 1 i n i c- a 1 c o u r s e: When the pnticnt was 10 years old a sarcoma was found in the coecum. A radical operation was performed b u t postoperative radiation treatment was not completed because t h e mother did not bring the child to t h e hospital. Four months later the child died of local re-
currence of the tumour and metastases in t h e liver. Autopsy rcvealed numerous metastases in the abdominal cavity b u t neither metastases nor pneumonias in t h e lungs.
a. Chest roentgenogram one hour post mortcm. b. Chest roentgenogram 21 hours post mortcm.
e. d .
Fig. 7. Chsr Y12/60. (Tatilc 3.) Boy ngrd Y months. D i n g n o s i s :I 11 d c 1 i 11 i c ii I c o I I r s I’ : W h r n thc patient was 3 months old skeletal anomalies and cardiiic insiifficiency wwc olistbrvcbtl. Cardiac fibroelastosis was diagnosed, b u t in spitc of treatment the dySpnOeR grew worsr anti the child died after hnving had pneumonia for two days. Autopsy vrrified t h r diagnosis of fil~rotbl:ts- tosis of the heart and revcalcd pneurnonias in all pulmonary lobrs cxcrpt tht. right ripprr lolie. a. Chest rorntpenograrn one hour post rnortrrn.
b. Chest roentgenogram 6 hours post rnortcrn. c. Chest rorntgcnograrn 10, hours post rnortern. d. Chest roentgenogram 34 hours post mortcrn.
A diffuse density of the right lung developcd 6 hours post rnortcm and increased until autopsy was performed 34 hours post mortcrn.
Fig. 8. Case 744/60. (Table 4.) Girl aged 9 hours. D i a g n o s i s a 11 d c 1 i n i c a I c o u r s e : The child was delivered by caesarean section necessitated by maternal diabetes a n d placenta praevia. Resuscitation was attempted a n d treatment in oxygen tent was given b u t 9 hours after birth heart action ceased. Autopsy revealed polycystic degeneration of both kidneys a n d marked pulmonary atelectasis with hyaline membranes.
a. Chest roentgenogram one hour post mortem. b. Chest roentgenogram 24 hours post mortem.
Both lungs are rather opaque from the beginning, and no change is observable during the follow-up.
33 were takcn both inirncdiately after death and 2 and (i hours post rnorteni, an in- crease in density was observed as soon as 2 hours post morteni in o n l j 3 cases (ell of which exhibited pneiimoiria in the lobe in question). Such a cnsc is shown in Fig. 3 . In the majority of C ~ S C S (38 out of 46) the first signs of increascd dcnsity were not observed until G hours post mortem; in 6 cases they were only observcd 12 hours post rnortem. In all cases the density was found to have increased in the roentgenograms taken 12 hours post mortem. I n only 8 cases was a further increase in density seen in roentgenograms taken between 12 and 24 hours post mortem (Figs. 4 and
5\,and only in one case did the density increase with certainty later than 21 hours post mortem. The occurrence of pneumonia in a lobe seems to be connected with an increase in density developing soon after death. Table 3 shows, however, t h a t even in the presence of a pneumonic focus a slight, diffuse opacity may develop as late as 12 hours post mortem. Consequently the prcsence or ab- scnce of pneumonia is not a decisive factor from the standpoint of a postmortal increase in density of t he lunqs.
T h e m i c r o s c o p i c f i n d i n g s
Pizerirnonic infillrations in lobes which remained clear during the follow-up period were found in group 1 in only one case. In this case the pneunronic infiltra- tions were punctulate. On the other hand, larger pneumonic infiltrations occurred in 8 cases o u t of 11 in group 2 in lobes exhibiting lobar opacities which developed
or enlarged post mortem. The possibility t h a t t h e pnedmonic infiltrations enlarged post mortem cannot confidently be either proved or eliminated. Since pneumonic infiltrations occurred in only 18 cases out of 35, however, in the group showing diffuse increased density in all lobes post mortem, i t appears t h a t the occurrence of such densities is not contingent on the presence of pneumonic infiltrations. The G cases in group 4 in which the entire lungs were markedly opaque throughout th e time of observation cannot be evaluated from this standpoint.
Marked ateleclasis occurred in only one case out of 6 in which the lungs remained unaltered post mortem, and in 3 cases ou t of 11 in which the lungs showed local opaque areas in the postmortal roentgenograms. I n group 3, which exhibited diffuse increasing density post mortem, marked atelectasis was observed in 10
o u t of 15 children who had died during their first week of life, b u t only in 3 chil- dren who had died later, i.e. in a total of 13 in this group of 35. In cases showing extensive pneumonic changes it is difficult to estimate the degree of atelectasis with certainty as marked or slight. Hence i t is possible t h a t in some cases another investigator would have defined the degree of atelectasis differently. However,
it is very unlikely t h a t atelectasis was responsible for the diffuse density develop- ing post mortern.
.llarlwd oedenia in the alveoli did not occur a t all in those lungs which remained roentgenographically unaltered post mortem. In groups 2 and 3 , which exhibited local opaque areas or diffuse increasing density post mortem, marked oedema was observed in only 17 o u t of 4G cases, b u t on detailed study of Tables 2 and 3 it is seen t h a t marked oedema was present in precisely those cases which esliibited no pneumonic infiltrations. Since pneumonic infiltrations are as a rule associated with fluid in the alveoli i t seems justifiable to conclude t h a t the presence of oe- dernatous fluid in t h e alveoli constitilted the main cause of the roentgenographic opacity occurring post mortem. In one case only (case 5760/;39 in Table 3 ) were neither pneumonic infiltratioris, niarked atelectasis nor ninrked oedema ohserv- able o n microscopic investigation. I t seems possible t h a t in this case the presence of intrapleural fluid accounts for the opacity.
d. Occurrence of intrapleural fluid
In a total of 11 cases free fluid was observed a t the last examination before autopsy, and the finding was verified a t autopsy. The cases and the relevant data are presented in Table 0.
I t is seen in Table G t h a t the amount of fluid increased post mortem in 7 pleural cavities of 4 bodies. An increase is clearly discernible in Figs. 9 and 10. Roentgeno- graphically the amount of fluid remained the same in 7 pleural cavities of (i bodies.
It was interesting to observe t h a t in
5pleural cavities of 4 bodies no fluid was discernible a t the first roentgenographic investigation immediately after death, b u t during the postmortal follow-up period a small amount of fluid developed. Examples of this phenomenon are given in Figs. 11 and 12. In this connecticn
it may be emphasized t h a t a t each investigation roentgenograms were taken in both oblique projections, as well as in the antero-posterior projection. Thus the findings could be verified. Only the necessary miriimuni of pictures have been reproduced. In all cases in which fluid developed post mortem i t was clear and translucent by inspection. Hence, i t probably was comparable to the oedeniatous fluid which often enters t he alveoli post mortem. In none of those cases ill which th e fluid seemed to have developed entirely post mortem could fibrinous layers on t h e pleura be demonstrated. This argues against th e assumption t h a t the fluid in these cases was due to a postmortal inflammatory. process in the pleura. In the cases shown in Figs. 10 and 1'2 no pneumonia was present, eilher, but, the patients had suffered from diseases predisposing to the development of oedema. No che- mical or microscopic investigation of the pleural fluid was performed.
I t may thus be regarded as proved t h a t free fluid can develop after death and t h a t fluid t h a t has developed in the pleural cavities during life can increase post mortern. I t seems probahlc t h a t this fluid is comparable to oedernatous fluid.
Fig. 9. Case 1372/60. (Table 6.) Girl aged 1 year and 1 month. D i a g n o s i s a n d c 1 i n i c a 1
c o u r s e: The child had suffered from heart disease since birth and was admitted to the Child- ren’s Hospital in poor condition, showing cardiac insufficiency and pneumonia two days before she died. Autopsy revealed cardiac fibroelastosis and myocarditis. Bilateral pneumonia8 were detected in the lungs a n d a thin fibrinous layer was seen on the surface of the lungs.
a. Chest. roentgenogram one hour post mortem. Fluid is clearly present in both pleural cavities. b. Chest roentgenogram 6 hours post mortem. The intrapleural fluid has clearly increased post
Fig. 10. Case 6108/59. (l'able 6 . ) Girl aged 14 yrars and 3 months. D i a g n o s i s a n d c 1 i- n i c a 1 c o u r s e: The girl suffered from a collagen distwsr, Hartnup's disease, with liver cirr- hosis a n d nephrocalcinosis. Profuse blerdings from the gastrointestinal t r a c t a n d increasing car- diac insufficiency were complicating factors. Finally, pulmonary oedema occurred. A t autopsy t h e above-mentioned findings were verified and myocardial infection was observed. The lungs were markedly oedematous.
a. Chest roentgenogram 2 hours post mortem.
b. Chest roentgenogram 12 hours post mortem. The a m o u n t of intraplcural fluid has consider- ably increased post mortem.
Fig. 11. Casr 1013/60. (Table 6.) Boy agcd 4 months. D I a g n o s i s a 11 d c 1 i n I c a 1 c o II r s r:
A purulent mrningitis provrd fatal i n spitr of treatment. Autopsy revealed meningitis and bi- lateral pneumonia. Microscopically no fibrinous la) ers werr seen on the pulmonary surface.
a. Chest roentgenogram in the anteropostcrior projection one hour post mortcm.
b. Chest roentgenogram in the right oblique projection one hour post mortem.
c. Chest roentgenogram in the same oblique projection 12 hours post rnortem. Within the plru-
Fig. 13. Case 3845/59. (Table 6 . ) Girl aged 14 years and 8 months. D i a g n o s i s a n d c 1 i- n i c a 1 c o u r s e: Aplasia of the left kidney and hydronephrosis and insufficiency of the right kidney. Death in uraemia. Autopsy revealed no changes in the lungs except marked oedema.
a. Chest roentgenogram 1/2 hour a n t e mortem.
11. Chest roentgenogram 12 hours post mortern.
c. Chest roentgenogram 21 hours post mortem. Intraplcural fluid which has developed post mortem is visible in t h e first a n d second intercostal spaces on the left.
P A R T 11.
A total of 90 rabbits, varying in weight between 1300 and 2G00 g, were used in tlie experiments. ,111 seemed to be clinically healthy. Prior to the experiments chest roentgenograms were taken of all aninials; their lungs were found to be normal.
I n order to produce experinieiital pneumcnia the animals were inoculated with l~acteria by direct puncture of the right lung after sterilization of tlie skin as siig- gested by WADSWORTH (1904) and
KIANE& WINTERNITZ (1915). ‘Thus tlie whole amount of bacteria mas injected into one lung. Nevertheless the aninials developed general sepsis and bilateral pneumonia in the first experiments. The remaining animals were therefore inoculated with a mixture of 0.3 nil of bacterial emulsion $0.3 nil of a G per cent mucin solution. This mixture has been shown by GLASER & WOOD (1931) to fix the inoculated bacteria better to the inoculated lung. The total volume of fluid injected was thus 0.6 nil.
Virulent strains of Staphylococcus artreus, phage type 80, and Klebsiella pneu- moriiae were used for inoculation. These bacterial strains were chosen because they had proved to be the most common cause of severe pneumonic processes in the autopsy series (RANTASALO & IIJELT 19G3). The bacteria were obtained in pure cultures in broth tubes from the State Serum Institute. Prior to inoculation the bacteria were incubated for one hour a t 37°C. No quantitative analysis of the amount of bacteria injected was attempted. Thirty-five animals were inoculated with Staphylococcus aureus and 34 with Klebsiella pneumotiiae. As far as possible, equal numbers of animals were inoculated with each kind of bacterium in every experimental group.
The first 9 animals were inoculated intra vita m with bacterial suspension alone
(Group I). After inoculation chest roentgenograms were taken every second hour until pneumonia was observed. Then the animals were killed by clubbing on the head. Breathing ceased immediately, whilst cardiac activity sonietiines continued for a minute or two. The subsequent 10 animals (Group 11) were likewise inoculated intra vitam, b u t with bacterial eniulsion + m u c h solution. When pneumonia had been detected roentgenographically, the animals were killed as described above. Forty animals (Group 111) were first sacrificed and then inoculated within 10 mi- nutes with bacteria + m u c h . Ten animals (Group IV) were inoculated with bac- teria + m u c h 30 and GO minutes, respectively, post mortem. A further 10 animals (Group V) were injected with sterile broth +mu& within 10 niinutes post mortem. Eleven animals (Group V I ) used as contruls were sacrificed without being injected in a n y way.
The dead animals were stored for a maximum of 48 hours. Autopsy was per- formed immediately after sacrifice in 4 cases, 2 hours later in (; cases, G hours post
mortem in 8 cases, 10-12 hours poet mortem in 8 cases and 24 hours post mortem in 8 cases, whilst 56 rabbits were kept under observation for 48 hours before au- topsy was performed.
For the first G hours the cadavers were kept a t room temperature (about 20°C)
and subsequently a t about 5--10°C. The purpose of this arrangement was to attain postmortal thermal conditions as similar as pos5iiLle to those prevailing ill the treatment of the human material. The body teniperature was checked by rectal measurement in 3 rabbits. It was 18
&1 "C: 12 hours post mortem and 10
&1 "C 21 hours post mortem.
During storage the animals were examined G, I f ? , 24 and 48 hours after death. A t each of these times chest roentgenograms were taken in three different projec- tions wiitli t he animals suspended upriglit. Simultaneously, specimens for bacterial analysis were obtained by sterile puncture of the right lung, i.e. the same lung which was inoculated except in th e controls. On 9 animals this investigation was also performed 2 hours post mortem.
The specimens obtained by aspiration were cultured on blood agar plates which were incubated for one hour a t 37°C. When growth of bacteria was observed, further bacteriological analysis was performed a t the State Serum Institute under the supervision of Professor ( a t t h a t time Assistant Professor) Ilari RANTASALO, h1.D. For details of t he method the reader is referred to r 3 A " r A s A L o L L I ~ J E L T
1963. When growth of Staph!ylococcirs aureiis was observed, the phage type was also determined.
Those cadavers, totalling 86, which were stored for some time before being dissected were ke pt in various positions in order to permit evaluation of the effect of the postmortal position. Thirty rabbits were kept suspended with their heads
up, Ci lying on the right side and 9 on the left. F o u r rahbits were stored in the prone position and 37 supine. The reason for keeping such a large number of animals supine was t h a t all the dead bodies of the human material were kept lying in this position. The effect of the postmortal position is analysed in Table 21.
A t autopsy t he lungs were removed and each lobe was separately examined microscopically. The sections were stained with haematoxylin-eosin. In addition, some sections were aleo stained b y Laidlaw's method in order to make the inter- stitial tissue fibrils clearly visible. In doubtful rases the results of th e microscopic analysis were checked b y Assistant Professor HJELT, RI.D., pathologist of the Children's Hospital.
The various sizes of the pneumonic infiltrations whirh ocrurred in some cases in group I1 were approximately assessed on the slides and the infiltrations were classified in three groups: 1) punctulate, in which the truly pneurnonic area did not exceed 1 m m in diameter, 2 ) medium size, i.e. pneunionic areas larger than 1 mm
in diameter though n o t exceeding one-third of t h e area o l the section, and 3) large pneumonias, exceeding one-third of the area of t h e section. I t goes with- o u t saying t h a t such a classification is subjective and t h e results cannot he indi- cated with scientific accuracy.
I .Animals inoculated solely with bacterial suspension intra vitam The group comprised 9 rabbits. Five animals were inoculatcd with S f a p h y l -
The results are shown in Table 7.
Coniriierifs. The frequency of cases showing fluid in t h e pleural cavities is st rik- ing. In 3 animals hydrothorax was already observed on either or both sides intra v i t a m , b u t t h e amount of fluid seemed to increase post rnortem. I n 3 animals, in which no fluid had been observed intra vitarn, bilateral hydrotlioras developed within t h e first G hours after death. In one case t he roentgenogram showvl a
markedly enlarged heart, wliirli was found a t autopsy to be due t o massive intra- perdicardial thickenings. I t seems probable t h a t in this case inoculation had I ~ c e n made b y too deep puncture, willi the result t h a t a large proportion of the baclcrial suspension had been injected intrapericardially and only a minor proportioil into the lung. In one case only (rabhit 7) could a pneunionic infiltration which \ \ a s al-
ready visible intra vitani be followed up for 48 hours without intrapleimil fliiid interlering. This infiltration appeared to increase somewliat in size post niorteni,
wliilst dilluse increasing density became noticeable in oilier parts of tlie liings o n tlie roentgrnograms taken G hours after death and later.
Summarizing t h e results in Group I , it may be stated t h n t fluid can develop in t h e pleural cavities post mortem, and t h a t fluid already present can increase post rnortem. No definite difterence was discernible between t h e animals inoculated with S/aph!y/ococcus arir’eris and those inoculated with Klebsie//a ptierinioiiia?. ‘rhe
s t u d y of pneunionic infiltrations and otlier intrar~ulinonary processes was fre-
quently lianipered by the occurrence of fluid in t h e pleural cavities.
ococcus aureus and 4 with Klebsiella pneurnotiiae.
II.Animals inoculated intra vitam with bacteria+ mucin The group comprised 10 rabbits. Five animals were inoculated with Sfaphylo-
T h e results are shown in Table 8.
Comnicrifs. Microscopically, definite alveolar pneumonia was obserk ed in 25 lobes and septa1 reaction in a further G lobes. Thus, pneunionic changes were seen cocrus aiir‘eiis and
5with Klebsiella pneunioniae.
in 31 lobes o u t of GO. No animal was unaffected. lnoculation with Staphylococcus aureus produced pneumonia or septal reaction in a total of 20 lohes, i.e. 14 lobes of t h e right, lung and G lobes of the left lung, whilst Klehsiclla pneumoniae caused changes in 11 lobes, i.e. 9 lobes of the right lung and 2 lobes of the left. N o animal showed signs of general sepsis such as were seen in group
T.I t appears, thcrcfore, t h a t the addition of mricin conduced to fixing the inoculated bacteria to the lungs, and in particular t o the inoculated lung. The possibility t h a t on injection
apro- portion of the bacterial emulsion entered the bronchi and thus found its wa y to the left lung cannot he eliminated. The two bacterial strains used and the techni- que of inoculation appeared to be suitable for continued experiments.
Roentgenographically, increasing opacity was observed in the lungs during the postmortal period (Table 9). The change consisted of a rather diffuse increase in density, observable in most cases as early as G hours post mortem. There was a slow accentuation of this density until autopsy was performed 48 hours after death. I n occasional cases only did a n increase in roentgenographic density set in later than ci hours post mortem. Only 2 lobes in the whole group exhibited no definite changes during t he whole time of observation. An increase in roentgenographic density was observed not only in lobes with pneumonic changes h u t also in other lobes.
Furthermore, Table 9 shows t h a t fluid was found in one or both pleural cavities in 4 animals, i.e. in one animal on both sides and in 3 animals on one side only. I t is noteworthy t h a t this fluid developed or increased only during the postmortal period; of those
5pleural cavities which contained fluid a t the roentgenographic investigation 48 hours post mortem, only one had shown such changes intra vitam.
In all cases with fluid in the pleural cavities the lungs exhibited signs of fibrinous layers and/or marked inflammatory processes in the marginal zone, which argues in favour of the assumption t h a t the secretion of fluid had already hegun intra vitam. The amount of fluid increased definitely post mortem, however, though a t a decreased rate, u p to 48 hours after death. I n one case fluid in th e pleural cavity was only discernible 48 hours post mortem. In all cases in which fluid was roent- genographically observable, the finding could be verified a t autopsy. Of the 4 animals which exhibited fluid in a pleural cavity, 3 had been inoculated with Klebsiella pneunioniae and one v ith Slaphylococcus aureus. No chemical or micro- scopic investigation of the pleural fluid was performed.
As ma y be seen in Table 9, 18 lobes with microscopically demonstrated alveolar pneumonias or septal pneumonic reactions showed no signs of any pathological changes on roentgenograms taken intra vitam. On the other hand, a t th e postmor- tal follow-up investigation local opacities were seen on the roentgenograms of these lobes. An attempt was made to clarify this phenomenon by approximative estimation of the extent of the pneumonic changes in the microscopic section, as previously described. A classification o n this basis is given in Table 10.
43 As was to b e expected, th e ))large)) infiltrations were usually visible already on roentgenograms taken intra vitam. I t is striking t h a t 3 infiltrations classified as ))large)) and 10 classified as ,medium)) were not roentgenographically observable until G hours post mortem, and one ))punctulate)) pneumonia was only detected 48 hours post mortem. This lesion, in particular, was surrounded by an extensive area showing no inflammatory changes, b u t an abundance of fluid in the alveoli. Those pneumonic infiltrations which became visible on roentgenograms only 6
hours post mortem were mostly surrounded b y a larger oedeniatous area than the pneumonias seen in animals on which autopsy was performed immediately after death. An example of the former kind is shown in Fig. 13. Parallel to the postmortal development of local opacities in those pneumonic lobes which intra vitam had been roentgenographically clear, increased density also developed in 10 lobes without pneumonic infiltrations, as may be seen in Tables 9 and 10. These lobes also showed a relative abundance of oedematous fluid.
Furthermore, it may be mentioned t h a t the time that, elapsed between inorula- tion with bacteria + m u c h and the appearance of an opacity in the roentgenogram varied between 4 and 8 hours in those
5cases in which Staphylococcus aiiriws was used, whilst it varied between G and 9 hours in th e 5 rabbits inoculated with Klebsiella ptzeumoniae. I t was then only the inoculated lobe t h a t showed an opa- city. Nonetheless, a t autopsy all rabbits except one also exhibited pneumonias in other lobes, which had been roentgenographically clear intra vitam. Hnbljit lfi (Fig. 14) is a typical example. Although the question of how soon a pneurnonic process becomes roentgenographically visible is a n interesting one, this fell out- side the scope of the present study, and therefore experiments were not continued to elucidate it.
Fig. 13. Rabbit 11. Inoculnted with Staphylococcus aureus intra vitam. Stored in supine position for 48 hours post mortem.
a. Chest roentgcnograrn intra vitam 4 hours after inoculation. A pneumonia is seen in the right lower lobe. The animal was sacrificrd immediately after t h e roentgenogram was taken. b. Chest roentgenogram 6 hours post mortem. The right lower lohe is denser t h a n intra vitam.
c. Chest roentgenogram 12 hours post mortrm. lncrrased drnsity is s r r n over t h r whole of the right lung. The left. lung, too, shows a diffuse density.
d . Chest roentgenogram 48 hours post mortern. The state has remained unchanged since 1’2 hours post mortem.
e. Microscopic section of the right lowcr lobe. Alveolar pneumonia is seen. Haernatoxylin-cosin. x 1’20.
Autopsy also revealed pneumonias in the right upper and left lower lobes. No sigiis of fluid within t h e pleural cavity.
Fig. 14. I<ahbit 16. Inoculated with Klebsiella pneumoniae intra vitam. On the site of inocula- tion a pnrumonia was roentgenographically visible 8 hours after inoculation. The animal was immediately sacrificed. I t was stored for 48 hours in supine position.
a. Chest roentgenogram intra vitam 8 hours after inoculation. A small pneumonic infiltration is seen on the right side in t h r right middle lobe.
b. Chest roentgenogram 6 hours post mortem. The lower lobe is also opaque.
c. Chest roentgenogram 12 hours post mortem. The opacity has intensified on both sides. The
left lower lobe is clear.
d. Chest roentgenogram 48 hours post mortem. The state has remained unchanged since 12 hours post mortern.
Autopsy revealed large alveolar pneumonias in all lobes except t h e left lower lobe. The pnerr- monias in both upper lobes and in the right lower lobe had t h u s been woentgenographically invisible)) intra vitam and changed t o rroentgenographically visibler as late as 6 - 12 hours post mortem.
I I I .Animals inoculated with bacteria+mucin
immediately post mortem
This group comprised 40 rabbits. Half the number were inoculated with The results are shown in Table 11.
Comments. As regards experimental technique it may be stated t h a t positive results were obtained with both t h e bacterial strains used, and t h a t the results made possible t he interpretation of many factors.
Roentgenographically the development of increasing density post morteni was observed in almost onc-third of all lobes examined. The relationship between the roentgenographic and microscopic findings is shown in Table 11. The occurrcnce of oedematous fluid in the alveoli shows a better correlation with the roentgeno- graphic changes than the otlier factors recorded. Table 12 shows the effect of the length of time t h a t elapsed before autopsy. The frequency of cases showing oede- matous fluid in t he alveoli clearly increased u p to 48 hours post mortem. The roentgenographically observable increase in density exhibited a change in the same direction. I t is difficult, however, to draw any clear-cut conclusions from the results. I t therefore appears t h a t the density of the lungs must be influenced by some other factor, apart from oedematous fluid. Th e position of the diaphragm may constitute such a factor.
Microscopically the most striking discovery was the presence of punctulate pneumonic reactions in a total of 24 lobes. Among these,
5exhibited obvioiis al- veolar pneumonia with abundant leukocytes in some alveoli. A t the samc time abundant white blood cells occurred in the alveolar septa outside the capillaries, and even giant cells were observed (Fig. 15, h ) . Nineteen lobes exhibited a septal reaction, i.e. similar changes in the septa b u t no appreciable nunibers of white blood cells in the alveoli (Fig. 1 G ) . I t was difficult to distinguish between this kind of reaction and thickened septa resulting from microatelectasis. Diagnosis was facilitated b y Laidlaw staining, which makes the elastic fibrils clearly visible (Fig. 15, g ) . l h e fact t h a t no pneumonic changes were observed in the group of animals on which autopsy was performed as soon as 2 hours post mortein, although such changes were seen in all other groups, is very puzzling. Against the background of later experiments i t does not seem probable t h a t pneumonia progresses more than 2 hours post mortem. The longer a n animal was stored before autopsy, the more the alveolar oedematom fluid increased. Iiypostasis and atelectasis however did not show any obvious changes as time went on. On the other hand there was a clear correlation between increased alveolar desquamation and postmortal time. Intrapleural free fluid was observed in 3 animals, in all cases bilaterally. Two of them exhibited a mediastinal haematoma, probably due to trauma on sacrifice. In t he third animal a punctulate septal reaction was seen in one lobe, b u t micro-
Fig. 15 e .
Fig. 15. Rabbit 28. Inoculated with Klebsiella pneumoniae immediately after death. Stored in supine position for 48 hours.
a. Chest roentgenogram intra vitam.
b. Chest roentgenogram immediately after inoculation.
c. Chest roentgenogram 6 hours post mortem. A diffuse density has developed over the area of both lungs.
Fig. 15 f .
d. Chest roentgenogram 12 hours post mortem. The lower parts of both lungs show heavy d m - sity.
e. Chest roentgenogram 24. hours post mortem. The state has remained unchanged.
f. Microscopic section of the right lower lobe. Leukocytes are seen within several alveoli, indi- cating a postmortal alveolar pneumonia.
Haematoxylin-eosin. x 300. (Fig. 15 is continued on p. 50)
Fig. 15 h.
g. Microscopic section of the right lower lobe. The intra-alveolar position of the leukocytes is clearly visible as the interstitial fibrils are stained.
Laidlaw. x 300.
Haematoxylin-eosin. x 120.
Autopsy revealed septa1 reactions in all other lobes. No fluid was present in the pleural cavity on either side.
scopically i t did not reach the surface of the lobe. Hence, it did not seem to be a likeiy cause of the fluid in the pleural cavity. In all these 3 animals the fluid in the pleural cavities was first observed a t examination G hours post rnortem and thereafter appeared to increase in volume.
I n Table 13, the results obtained with the two bacterial strains used are com- pared.
Klebsiella pneumoniae appeared to be somewhat more pathogenic to the strain of rabbits used in the experiments than did Staphylococcus aureus.
IV.Animals inoculated with bacteria
+mucin 30-60 minutes post mortem
This group comprised 10 rabbits, 5 of which were inoculated with Staphylo- The results are shown in Table 14.
Cornmenis. N o pneumonic changes were observed, nor any fluid in the pleural cavities. Otherwise, the roentgenographic and microscopic findings did not differ from those made in Group 111. Against the background of the results obtained in the present group i t seems improbable t h a t bacteria present in the lungs a t the time of death are capable of causing any pneumonic reaction as much as 30 mi- nutes post mortem. Hence, i t may be assumed t h a t the punctulate small pneu- monias which were observed in the animals inoculated immediately post mortem (Group 111) had developed during the first few minutes after inoculation.
coccus aureus and
5with Klebsiella pneumoniae.
V.Animals inoculated with sterile solution
Five rabbits were inoculated intra vitam with 0.3 ml of sterile broth+0.3 ml m u c h and subsequently sacrificed. Five animals were similarly injected imme- diately post mortem.
The results are shown in Table 15.
Commenis. None of the animals inoculated intra vitam exhibited any changes on the roentgenograms taken immediately after inoculation, nor did any of the animals inoculated immediately post mortem show any roentgenographic changes. During the postmortal follow-up period increasing density occurred on the roent- genograms in the same proportion, broadly speaking, as in the previous groups. In one animal fluid developed in one pleural cavity, probably owing to a mediastinal haematoma. The latter probably developed in connection with the trauma on sacrifice.
Fig. 16 a. Fig. 16 b.
Fig. 16. I(ab1)it 77. lnoculatrd with Klebsiella pneurnoniae immediately after death. Stored hang- ing upright for 12 hours.
a . Chest roentgenogram immediately after inoculation.
IJ. Chest roentgenogram 12 hours post mortem. A slight diffuse density has developed over the
right middle lobe a n d the left lower lobe.
V I .Controls
This group comprised 11 animals. N o injections were given. The results are shown in Table 1 6 .
Comments. The findings in this group did not differ from the findings in those cases in the preceding groups in which no pneumonias were detected. In 2 rabbits fluid was observed in both pleural cavities. Since no signs of haematoma or in- flammation of the lungs or mediastinum were observed a t autopsy, the cause of th e pleural fluid remains obscure.
Free f l u i d i n one or both pleural cavities
I n t he experimental material a total of 16 animals exhibited free fluid in the pleural cavities a t autopsy. I n 10 cases the animal had been inoculated intra vitam, b u t only in 3 of these animals was a n y free fluid observed in the pleural cavities a t roentgenographic investigation intra vitam. I n the remaining 7 cases fluid was only observed o n t he roentgenograms taken G , 12, 24 or
48hours post niortem
Fig. 16 d.
c. Microscopic section of the right middle lobe. A septal reaction is seen with very thick alveolar septa rich in cells.
Haematoxylin-eosin.' x 300.
interalveolar septa are clearly visible as the septal fibrils are stained. Laidlaw. x 300.
A t autopsy the other lobes were found to be normal, except that rather marked oedema was present in the left lower lobe.
(Figs. 17 and 18). Rlicroscopically, inflamniatory changes were observed in the peripheral parts of t he lungs of lhese animals. Hence i t seems more than likely t h a t the fluid was due t o inflammation.
Moreover, fluid was observed in a further G animals, in one animal only in the right, in 5 animals in both pleural cavities. On microscopic investigation one ani- mal (rabbit 71) exhibited a septic reaction, b u t in this case the cause of the fluid in the pleural cavities seems t o have been a mediastinal haematoma, which prob- ably developed as a result of the trauma on sacrifice. A further 2 animals, which had no inflammatory changes, likewise exhibited mediastinal haematoma, and these animals, too, showed fluid in both pleural cavities. Furthermore, free fluid occurred in t he pleural cavities of 3 animals, i.e. 2 controls and one animal inocu- lated with bacteria without any pneumonic changes resulting. I n none of these cases could any definite aetiological factors be demonstrated. I n all these cases
it was striking t h a t no fluid was observed on the roentgenograms taken intra vitam or immediately post mortem; i t was only detected G or 12 hours post mortem. A survey of t he animals showing free fluid in the pleural cavities is given in Table 17.
The results show t h a t the amount of free fluid observed in one or both pleural cavities a t autopsy 48 hours post mortem was larger tha n the amount present intra vitam or immediately post mortem. I n most cases the fluid was visible on roentgenograms taken G hours post mortem, b u t in one case i t could no t be de- monstrated until 48 hours post mortem. Between the first and last observations
no definite increase in fluid was found, b u t this may have been due to th e fact tha t relatively small volumes were involved.
The pooled experimental material
I n order to reach t he best possible understanding of the interesting relation- ship between t he roentgenographic and microscopic findings the results obtained from the different experimental groups were pooled. Since pneumonic infiltrations and fluid in t h e pleural cavities interfered with th e evaluation of other findings, all animals showing pneumonic infiltrations, septa1 reactions or fluid in the pleu- ral cavities were discarded. Of th e total of
90rabbits used in this study, 46 remained as pooled material.
Effect of.the lenglh of time elapsing between death and aulopsy
The first factor analysed was the effect of the length of time t h a t elapsed be- tween sacrifice of the animals and autopsy. The results of this analysis are shown in Table 18.
Fig. 17. Rabbit 23. Inoculated immediately after d e a t h with Staphylococcus ourcus. Stored in supine position for 48 hours.
a. Chest roentgenogram immediately after inoculation.
b. Chest roentgenogram 6 hours post mortem. Marked opacity over both lungs.
c. Chest roentgenogram 24 hours post mortem. Fluid probably present in t h e right pleural ca- vity. Oblique project.ions revealed the presence of a small a m o u n t of fluid within both pleural cavities.
d. Chest roentgenogram 4 8 hours post mortem. Fluid is clearly visible (arrow) on the right side. Oblique projections showed a small amount of fluid on t h e left side, too, which is not clearly visible in anteroposterior projection.
Autopsy revealed no pneumonia nor fibrinous layers on t h e pleura on either side b u t clear non-haemorrhagic fluid in t h e pleural cavity on both sides.
Fig. 18. Rabbit 40. Inoculated with sterile solution immediately after death. Stored on left side
for 48 hours.
a. Chest roentgenogram immediately after inoculation.
b. Chest roentgenogram 6 hours post mortem. Fluid is clearly visible in the right pleural cavity. c. Chest roentgenogram 12 hours post mortem. The intrathoracal s t a t e is unchanged. ( A sub- cutaneous emphysema has developed on t h e right side, probably due to the sterile puncture of the right lung by which bacterial specimens were obtained. K O other rabbit showed a si- milar subcutaneous emphysema).
d. Chest roentgenogram 48 hours post mortem. The intrathoracal s t a t e has remained unchanged since 6 hours post mortem.
Autopsy revealed clear non-haemorrhagic fluid in the right pleural cavity b u t not in the left.
N o pneumonias were observed b u t marked alveolar oedema was present in both lungs. N o
57 Comments. The following facts emerge from a s t u d y of Table 18:
1) Roentgenographic density, mostly diffuse, occurred in over one-third of all lobes
48hours after death. This feature was sometimes discernible even 2 hours post mortem. Six hours after death diffuse density was seen on the roentgenograms in about half or nearly half of all cases, and this ratio between clear and opaque lobes was maintained for u p
to48 hours post mortem, even though the density of individual lobes showed some increase.
2 ) Alveolar cellular desquamation was t h e microscopic finding most clearly related to t he time factor. Desquamation was hardly observed a t all until 12 hours post mortern, after which it showed a marked increase. Forty-eight hours post mortem this microscopic finding was made in over one-third of all lung lobes examined.
3) The ratio between lobes with oedema in the alveoli and lobes without oedema also showed a clear change connected with time. A relationship between the roent- genographic changes and th e presence of alveolar oedema seems possible.
4) The occurrence of lobes without atelectasis and lobes with either mechanical atelectasis or microatelectasis were not affected by the time factor.
5) The occurrence and degree of hypostasis was not appreciably changed by
the time factor.
Relationship between the roenlgenographic and microscopic findings
Table 19 was made in order to enable a comparison to be made between the roentgenographic and microscopic findings.
Comments. The microscopic finding showing the best correlation with the roent-
genographic finding is t he occurrence of oedeniatous fluid in the alveoli. In no other microscopic finding, be i t atelectasis, hypostasis or alveolar cellular desqua- mation, could any definite relat.ionship with the roentgenographic finding be de- monstrated. Fig. 19 shows a microscopic section of a lung exhibiting mechanical atelectasis. Despite the atelectasis the lung lobe remained roentgenographically clear throughout the time of observation.
I t seems probable, therefore, t h a t the increase in roentgenographic density was due mainly, although not entirely, to fluid diffusing o u t of the vascular system and entering t he alveoli, from which a corresponding amount of air was expelled.
Relationship between alveolar oedema and other microscopic and roentgenographic findings
The relationship between th e presence of oedeniatous fluid in the alveoli and th e occurrence of other microscopic and roentgenographic findings is analysed in Table 20.
Fig. 19. Rabbit 79. Inoculated with Klebsiella pneurnoniae immediately after death. Stored hang- ing upright for 6 hours. Roentgenographically both lungs remained clear throughout.
Microscopic section of the right middle lobe. Marked mechanical atelectasis but no other changes. Haematoxylin-eosin. x 120.
Cornmenls. A fairly obvious correlation between the occurrence of oedema and the increase in roentgenographic density emerges from this analysis, too.
On t he other hand, there does not seem to be any obvious relationship between the presence of oedema and the occurrence of mechanical atelectasis or micro- atelectasis. Since some lobes exhibited both mechanical atelectasis and micro- atelectasis, t he number of lobes in the group showing atelectasis is larger than the total number of lobes.
The presence of oedema in the alveoli shows a somewhat clearer correlation with hypostasis t han with atelectatic changes. This is due to t h e fact t h a t a large number of lobes exhibited obvious hypostasis in a small, sharply limited area. In this area oedematous fluid was often, though not invariably, present in the al- veoli. When the area was small and no oedematous fluid was observable in the remainder of t he lobe, t he lobe was classified as showing definite hypostasis b u t no appreciable amount of alveolar oedema.
N o clear correlation is observable between alveolar oedema and alveolar cel- lular desquamation. Both phenomena are obviously influenced b y the length of time elapsing between death and autopsy, as was shown in Table 18.
The question of why alveolar oedema sometimes develops and sometimes does not remains obscure. I n Fig. 20 an animal is shown which was stored for 24 hours
before autopsy without even t h e lowest lung lobes exhibiting a n y kind of either roentgenographic or microscopic changes. Occasionally entirely normal lobes were also observed in animals stored for 48 hours. I t is quite obvious, therefore, t h a t some factor or factors other than time influence the development of alveolar oedema.
Influence of postmorlal posilioning
I n order to s t u d y t h e influence of position o n the development of changes, th e experimental animals were stored in different positions during the time be- tween death and autopsy. I n the groups stored lying on the right or left side or suspended head-up, the right middle lobe was omitted from the analysis. This was done because i t was thought appropriate to have an equal number of right and left lobes, and upper and lower lobes, when the groups were compared. These groups thus comprised only one upper lobe and one lower lobe on each side in each ani- mal.
The results are shown in Table 21.
Comments.The groups ))supine)) and ))prone)) did not differ appreciably from each other, b u t with regard to th e other positions a marked difference was observed between t he lobes t h a t had been situated low and those t h a t had been situated high.
With respect to the changes in roentgenographic density i t is clearly seen t h a t lung lobes situated low exhibited a more marked increase in density than those situated high. T h a t the opposite also could be true is shown in Fig. 21.
Oedematous fluid occurred more frequently and in larger amounts in the lobes situated low t han in those situated high. The total amount of fluid in the chest can hardly be thought to increase or decrease post mortem. The uneven distribution over the lobes of the lung in the different positions may be accounted for, a t least in pa rt , b y t he fact t h a t the blood present in large pulmonary vessels immediately after death, following the law of grvaitation, makes its way towards the lower portions of the lung. Considering, however, t h a t an appreciable number of lobes situated high also exhibited oedema (Fig. 21), even to a marked degree, this explanation cannot alone account for the distribution of the oedematous fluid. I n Table 21 t he correlation between the increase in roentgenographic den- sity and t he occurrence of oedematous fluid in the alveoli is not as obvious as the correlation emerging from Table 18, which was based on the length of time t h a t elapsed between death and autopsy.
On t he other hand, the occurrence and distribution of hypostasis was clearly dependent on positioning. The number of red blood cells in all vessels including the capillaries was definitely larger in the parts of the lung situated low. Within most individual lobes, too, marked hypostasis was present in some portions whilst others showed slight hypostasis or none, depending on the position. These changes
C. d .
Fig. 20. Rabbit 64. Inoculated with Staphylococcus aureus immediately after death. Stored hang- ing upright for 24 hours.
a. Chest roentgenogram 6 hours post mortem. No changes visible.
b. Chest roentgenogram 12 hours' post mortem. Still no changes discernible. c. Chest roentgenogram 24 hours post mortem. No changes visible. d. Microscopic section of t h e right lower lobe. Normal lung tissue.
Haematoxylin-eosin. x 120.
Autopsy showed t h a t all lobes were normal with no pneumonias, oedema, atelectasis or hy- postasis.
C. d .
Fig. 21. Rabbit 41. Non-inoculated control. Stored on left side for 48 hours.
a. Chest roentgenogram immediately after death.
b. Chest roentgenogram 6 hours post mortem. Slight diffuse density developing on both sides.
c. Chest roentgenogram 12 hours post mortem. The diffuse density has increasrd equally on
d. Chest roentgenogram 24 hours post mortem. The diffuse density is more marked on the right side t h a n on t h e lower left side.
Fig. 21 e.
e. Microscopic section of the right lower lobe. Rather marked oederna is seen but no other changes. Haernatoxylin-eosin. x 120.
Autopsy revealed rather marked oedema in the right lung but not in the left lung which was almost clear.
were very clearly discernible even in the animals examined 2 hours post mortem. Hence, the cpnclusion may be drawn t h a t hypostasis mainly developed during the first 2 hours after death. So attempt was made to alter the position after the first 2 postmortal hours.
The occurrence of various types of aieleciasis, mechanical atelectasis in parti- cular, was strikingly little influenced by the position. I n a large proportion of lobes the air content was very uneven. Whilst part of a lobe exhibited a normal air content, slight atelectasis could be present in another part. As a rule, the ate- lectasis was of the mechanical type, although microatelectasis also occurred. The term slobe with mechanical atelectasis)) does not refer to the volume of the lobe as compared with other lobes, i t only implies t h a t mechanical atelectasis was microscopically demonstrated in p a r t of the lobe. The same applies to the occur- rence of microatelectasis. On the basis of the experimental material i t is impos- sible to draw any definite conclusions regarding the occurrence of atelectasis and the implications of this phenomenon. It is possible t h a t a n investigation, prefer- ably performed on a bigger animal than the rabbit, in which the total lobe volume was taken into account would yield valuable information in this respect.
To sum up, it may be stated t h a t the investigation concerning the part played by position revealed a greater increase in roentgenographic density in lung lobes