Sudden death of a rugby international after a test game

Clinical SUDDEN

DEATH

Reports

OF A RUGBY TEST

INTERNATIONAL

AND

JOHBNNESBURG.

A

FTER having played a strenuous 39 years of age, captain of the and died.

A

GAME

E. H. CLUVER, M.D.,’

CASE

AFTER

SOUTH

E.

Jam, M.D. t AFRIU

REPORT

game at Johannesburg Transvaal Representative

Autopsy.-The body was that of an adult, European muscular. Weight was 169 pounds; height, 6 feet. So gross of the face, neck, shoulders, and fingernails. nervous system were detected. There were congestion of marked engorgement of the veins on the surface.

in July, Rugby

1940, Team,

S. C. I,., collapsed

male, and was well built and There was marked cyanosis abnormalities of the central tlrc vessels of the brain an11

Significant pathologic changes were found in the cirr~ulatory system. The heart was generally hypertrophied, and weighed 482 Gm. ( 17 ounces). The hypertrophy was most apparent in the left ventricle, the wall of which measured 0.7 cm. in thitzkness. There was dilatation of all of the cavities of the heart, especially of the right The ventricle, which also showed hypertrophy. Its wall was 0.7 cm. thick. papillary muscles were markedly thickened and prominent. Macroscopically, the myocnrdium appeared firm. However, numerous fibrotic patches were irregularly distributed in the left ventricle. The aortic valve was nompet,ent, although the cusps were slightly thickened. The mitral valve, whirl1 was also competent, admitted On the surface of the mitral valve there was a large athrromatous two fingers. patch. The left coronary artery showed numerous atheromatous areas which had caused One of these atheromatous areas marked narrowing of the lumen at three places. was located at the orifice of the left coronary artery, and another at a point about htheromatous patches were also midway along the anterior descending branch. present in the right coronary artery. The diameter of the ascending aorta and the aortic arch was normal, but the wall was extraordinarily soft and thin. The descending aorta measured a little over half an inch in diameter, which is less than half There were many atheromatoua patches in various parts of the the normal size. intima. There was congestion bronchi contained thick showed some edema and siderably enlarged.

of the thoracie and abdominal The lungs were mucopus. a slight excess of pigmentation.

organs. The trachea slightly emphysematous The hilar nodes were

The liver was congested, but otherwise normal; There was considerable congestion of the spleen, it showed a marked excess of Gm. ) ; on section

it weighed 2,495 Gm. and it was enlarged lymphoid tissue.

Received for publication Sept. 26, 1940. *Director, South African Institute for Medical tHead of Department of Physical Education, Johannesburg, South Africa.

Research. Witwatersrand

405

and and ron-

(3% pounds). (weight, 434

Technical

College.

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AMERICAIS

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The left kidney was very small (weight, and was the scaat of advnm?d 6 2 Gm.), hydronephrosis. The parenchyma was stretched and thinned, and the pelvis was much dilated. The left ureter was skarply kinked about one imh above the bladder. The right kidney was greatly kypertrophied (weight, 350 Cm.). There was a persistent thymus gland which weighed 26 Cm. (normal weight at this age, 15 Cm., according to Wolf1 and Cowrlry~). The genital organs were conspicuously small. microscopic %aminafion.-There were several areas of fibrosis in the keart nlu?cle. The papillary muscles and the base of the left ventricle were especially aft’ected. Areas of narrowing of the coronary arteries showed marked atheromatous thickening. The intima was greatly distorted. Xtlmromatous c:hanges were also found in the aorta. The thymus gland contained scattered foci of entirely normal tliymus tissue embedded in fatty tissue; there mere areas of considerable infiltration and several Numerous Hassall’s corpuscles of large size vjere large collections of lymphocytes. The entire picture was t1mt observed. The blood supply of the glxnd was abundant. structure wliich one would expect of an active gland, rather than the involutionary at the age of 32 years (hschoff~). Sections of the left kidney revealed normal tissue, alt,liougli there was extreme congestion. The right kidney showed chronic pyelitis, fibrous thickening of the capsule, patchy fibrosis, a,nd infiltration of the parenchpma with small round cells. All lympboid structures were lryperplnstic, including those of the throat, nasopharynx, intestinal canal, and the lymph nodes. Prehous History.-1~. had been one of the most prominent South African rugby players of the preceding decade. He was known as “ the iron man of rugby. ” He had represented his country on the playing fields of South Africa, Britain, Australia, and New Zealand. His identical twin brother J. also died during exertion at the age of 30 years. J. was bathing in the water at the coast when he suddenly collapsed and was swept away. The following information was kindly supplied by Major Danie Craven, captain of the Hpringbok team:

(L I have known I,. since 1931, and played on the same t-am with him on numerDuring 1937 and 1958, I traveled with kim to Australia and New ous occasions. Zealand, and roomed with him at various places. I alvvays regarded L. as a very ill This man. He used to complain of severe pain in the lower portion of his h:Lllr. On many occasions I had to massage his pain he thought was due to kidney trouhle. He also suffered from boils. After every football hack because of these pains. match he felt sick. He used to put his finger into his throat until he vomited, after which he felt better. He could not take any alcokolic drinks because they also made him sirk. His stamina was exceptionally good. However, in the course of tke Australia-New Zealand tour, two years prior to his death, his efficiency deteriorated During the last matches of the tour liis performance was very IJOO~. His greatly. strength was outstanding, and on the boat he performed wrestling matches with the strongest of his teammates. He always had a husky voice, and suffered from chronic hronckitis. When he n-as tired, as, for example, after a game, he breathed heavily and noisily. He smoked at least thirty cigsrettcs a day. ( ‘His twin brother J., wkom 1 also knew very well, was apparently an identical twin. J. looked the same as L., had the same kusky voice, and played the same type of game as his brother. In 1937, J. went swimming at Port Elizabeth inside It was a quiet day and the water looked like a the fenced portion of the beach. After a few minutes of bathing, J. suddenly collapsed and sank. His body lake. was never found. ” Verv little information is available concerning L. ‘s condition immediately prior It could be ascertained, however, that, between February and July, to his death. 1910, he lost more than 20 pounds in weight. This may have indicated failing health. A roentgenogram of his chest which was tnken a few months before he

CLUVER

died (anteroposlerior; hypertrophy as was was made.

distance, present at

AND

,JOKL:

5 feet; autopsy.

SUDDEN

standing) does Unfortunately.

DEATH

-207

not show as much eardi:tr no lateral romtgenogrnm

DI,SCUSSIOX

This is a case in which a congenital developmental abnormality caused a fatal circulatory crisis in a first-class athlet,e. There are man)- remarkable features. First of all, the deceased’s twin brother had died two -cars before, also during exertion. ITnfortunately, post-mortem examin+ tion in this instance was not possible; otherwise it is more than lilrcl> that an attempt could have been made to prevent the second catastrophe. ,Second, stlldy of this case emphasizes the truth of the statement made 011 previous occasions47 i that even an extraordinarily high standard of physical efficiency is not at all a reliable indicator of t,he state ot’ health of the athlete concerned. The outst,anding performances of 1~. WC’IY! possible in spite of a grossly abnormal cir~nlator~ system. The probable development of the disease and mcchnnism of death INI> hc as follows: Drr~702~~eat of Discnse.-Persistenrc of the thymes gland arrestetl 111c normal puhert;r- and postpuberty development of the circula.tory sysf cm. Tflis arrest of growth, which also affected the urogenital system, ciluse~l the dcsccnding aorta to remain in an infantile state. Conseynentl~, t hc heart was compelled to pump against a greatly increased resistance. It may be assumed that the arterial blood pressure was high. Hypertropb?: and dilatation of the heart followed. The lymphatic tissue throughout the body was more actire than usual and the spleen was arcall>- (wlarged. Thv early development of atheromatosis can be interpreted as a w sulf of the extraordinary h-drodynamic st.rain upon blood vessel walls. a strain which, under the pathologic circtunstancq was aggravated b>strenuous physical activities. The heart had to work under most unfavorable conditions, and the multiple fibrotic patches in the myocardium hear witness to the deficiencies of blood supply. It is remarkable that, with such a circulatory system, the man had been capable of s~zch outstanding physical performances. As similar observations hare heen communicated by ot~e of us ( Jok14, “) on several previous occasions, it map now be accepted as an established fact, that there is no strict relationship between heart disease and even an outstandingly high exercise tolerance. Xednlzisvz of D&h.-The mechanism of death in this case seems clear. The deceased had taken part in a strenuous game. The oxygen requirements of his heart were thus greatly increased. After the game he took a hot bath. This must have shifted large amounts of blood from the intestinal circulation into the skin. In combination with the physiologic fall of blood pressure after the exercise, this must have added to the existing deficiency of blood supply to the roronary artery. The

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significance of such physiologic phases in the causation of t,he final collapse of a diseased circulation has recently been demonstrated by Blnmgart, Schlesinger, and Davis.’ Furthermore, we have evidence that there were accumulation and stasis of inflammatory exudate in the hydronephrotic right kidney, which caused contractions of the smooth muscle of the renal pelvis and ureter. It is probable that unphysiologic tension in intestinal cavities elicits, by means of a reflex, spastic contraction of the coronary arteries. This has been proved conclusively for the stomach.8 The autopsy also revealed signs of infection of the respiratory tract. This must have caused a further impairment of the functional efficiency of the heart. In 1844, Rokitansky” drew attention to the simultaneous occurrence in adults of an infantile aorta, hypertrophy of the heart,, and underdevelopment of the genital system. Although it has been assumed for a long time that the thymus gland exerts a direct influence on puberty and postpuberty development, it is only now that a more detailed picture can be drawn. We are especially indebted to Timme,lO whose studies made possible a full understanding of the condition known as status thymicolymphaticus. Timme showed that the effects of persistence of the thymus gland, leading to arrest of development, mostly at puberty, are often compensated by hyperfunction of other glands in the body. The primary abnormalities caused by thymic persistence are lymphoid hyperplasia, gonadal and adrenal deficiency, a low blood sugar level, low blood pressure, and hypoplasia of the heart and vessels. In most cases, marked compensatory effort,s of the organism lead after some time to a profound change in the picture. The suprarenal cortex and the pituitary are strongly stimulated. We have asked ourselves whether the high standard of physical efficiency of this rugby player could perhaps be explained partly by a special compensatory effort of the suprarenal cortex. The changes in the heart were clearly the result of an attempt on the part of the circulatory system to overcome the obstacle created by the underdevelopment of the descending aorta. Wolf1 states that one of the three possible causes of death in cases of status thymicolymphaticus is weakness of the muscular coat of the arteries which renders them incapable of withstanding sudden changes in blood pressure. This would apply in our case. In view of the circumstances under which the sudden death of L. and his twin brother occurred, Wolf’s suggestion that swimming and bathing should be forbidden to people suffering from status thymicolymphaticus appears to be well founded., SUMMARY

Summarizing, it appears that death occurred because of sudden coronary insufficiency. There was narrowing of the coronary artery

CLUVER

AND

.JOKL:

STDDEN

DEATH

409

caused by atheromatosis. There was the physiologic fall of blood pressure after the exercise. Large amounts of blood were shifted into the skin as a result of taking a hot bath. The oxygen requirements of the heart muscle were greatly increased after the exercise, It is probable that reflex spasm of the coronary artery was caused by the frustrated efforts of the diseased right kidney to expel its inflammatory contents. I.1 may be assumed that permeability of the myocardial cell membranes was adversely affected by the concurrent infection of the respiratory system. This observation allows a detailed analysis of a case of status thymicolymphaticus, a term which has in the pasl- often been used in a rather general way. We can t,race the history of the patient back to the per’sistence of the thymus gland after puberty. We can t,hus understand the arresti,ng, effect of this primary developmentSal disturbance upon 1hc maturation of the descending aorta. This latter anatomic deficiency (xplains the secondary pathologic reactions which created the above described extraordinary situation and caused death. REFERENCES

1. Wolf, IV. : Endocrinology in Modern Practice, Phil:ulelphia and London, 3939. 2. Cow-dry, E. v.: Problems of Ageing. Biologiczl and Medical Aspects, London, 1939. (:owdry, E. V.: Textbook of Histology, London, 19:X8. ::. Aschoff, L.: Pathologische Anat,omie, Jrna, 1923, F’ol. II, p. 1733 (H. Ychritl