4I2

TRAUMATIC INJURY TO THE HEARTDUE TO BLUNT FORCE

With a case reportBy B. S. DHILLON, F.R.C.S. (Edinburgh), F.R.C.S. (England)

Royal Infirmary, Sheffield

Non-penetrating injuries of the chest wall cangive rise to a variety of cardiac lesions. The extentof cardiac damage depends on the intensity of theinjury and on pre-existent disease of the heart. Inthe majority of cases there is a direct blow to theanterior chest wall but serious myocardial damagehas been produced by blows directed against theposterior chest wall and abdomen. The crushingchest accidents account for a large number of re-ported cases but a blow in the precordium withfist, cricket ball, hockey ball, baseball and kick bya powerful animal can produce heart injury. Theremay or may not be an associated fracture of theribs; greater cardiac damage seems to occur inpatients without associated fracture of the ribs.lIt is difficult to assess the exact incidence ofcardiac injury as most patients with minor damagepass unnoticed or there is reluctance to make thediagnosis. The post-mortem incidence of cardiacinvolvement in instances of blunt trauma to thechest is i8 to 26 per cent.2 A frequent cause ofcardiac injury is " steering wheel " accidents.The pericardium and myocardium are most

frequently inijured but valves and their attach-ments have also been torn following blunt traumato the chest wall. Contusion of the pericardiumpasses unnoticed as it rarely produces any signsand symptoms. Myocardial damage may amountto superficial contusion of any chamber of theheart, it may be partial laceration with or withoutinjury to the coronary vessels or it may producecomplete rupture of one or more chambers of theheart with instananeous death. Bright and Beck3have collected 13 cases with perforation of theinterventricular septum and one case of rupture ofthe inter atrial septum. It is quite possible that,in rare instances, the initial tear may involve theendocardium4 only with subsequent developmentof an aneurysm and delayed rupture of the heart.There are well authenticated cases in the medicalliterature of rupture of normal heart valves as aresult of blunt injury to the chest wall. Theaortic valve is most frequently affected and injuryto the mitral valve includes tear of the chordaetendinae more commonly, tear of the valve cuspsitself and occasionally tear of a papillary muscle.6

The anterior aspect of the heart is injured mostfrequently, which is in direct relation to the siteof the mechanical force, but the posterior aspectof the heart may be bruised by squeezing againstthe vertebral column. The sudden increase of theintracardiac pressure produced by mass dis-placement of the blood towards the heart cancause tearing of the valves and their attachments,rupture of the auricles and in rare cases of theventricles.7 The delayed rupture of the heart hasbeen known to occur'and the usual time is 7-I4days after injury. It usually follows deep con-tusion (or infarction) of the wall with subsequentsoftening and rupture.8 The delayed rupture ofthe chordae tendinae has not been reportedbefore, this is especially liable to happen if thepapillary muscles or chordae tendinae have beentraumatised at the time of the original injury andthe onset of rapid auricular fibrillation a few dayslater produces a marked strain on the alreadyweakened valve attachments, leading to theirrupture.The case history of a patient is presented who

sustained injury to the heart following a crushinginjury to the chest.

Case HistoryA male patient aged 30 was admitted to hospital

at 4 p.m. on 25.8.56. He was working in a trench2 ft. deep when a fall of clay and rock trapped him

against the skip, crushing his left chest. Onexamination, he was a well-built man complainingof severe pain in the left chest. Pulse i IO, fairvolume, respiration 30 per minute and B.P. Ioo/55.He had a large haematoma over the anterior endsof the left 3rd and 4th ribs, another haematomabelow the left scapula and surgical emphysema ofthe left chest wall posteriorly. The trachea wascentral, apex beat could be felt in the 5th inter-space in the anterior axillary line, heart soundswere clearly audible and no murmur was detected.The'patient was extremely distressed with pain,morphia, 4 gr., was given intravenously and cir-cular strapping (elastoplast) applied from thelevel of the 2nd ribs to the level of the 9th ribs,with immediate relief of pain. At 4.30 p.m. a

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August 1957 DHILLON: Traumatic Injury to the Heart Due to Blunt Force 413

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FIG. I.-X-ray chest on admission showing small lefthaemothorax.

radiograph of the chest was taken and the patienttransferred to the thoracic surgical ward. B.P.and pulse were recorded every 15 minutes and by5 p.m. B.P. was 80/55 and pulse I20 per minute.

Serial B.P. readings were recorded whichshowed continued fall in the systolic blood pressureand by 8 p.m. it was 60 mm. of Hg. while diastolicblood pressure stayed at a more or less constantlevel (55 mm. of Hg). There was a steady rise inthe pulse rate and by 8 p.m. it was noticed thatthere was a rise in the jugular venous pressure. At8.30 p.m. intravenous blood transfusion wascommenced and two more radiographs of thechest were taken, which showed progressive in-crease in the cardiac size and considerable effusionin the left pleural cavity. The heart sounds weremuffled and by 9 p.m. there was marked distensionof the jugular veins. E.C.G. showed ventriculare trasystoles and inversion of T1. From theabove data it was concluded that the patient hadhalemopericardium which had resulted in cardiactamponade and progressive bleeding in the leftpleural cavity.

9 p.m. Pericardial tap via the xiphi-sternalroute was performed and I 5 c.c. of blood aspiratedfrom the pericardium, following which there wasmarked diminution in the size of the distendedjugular veins, and some improvement in thegeneral condition of the patient. At 9.30 p.m.t he B.P. was 60/55 and it was decided to carry outthoracotomy to control the bleeding points.

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FIm. I i.-X-ray chest two hours after admission showingincrease in the left haemothorax and increase inthe cardiac size.

I0.30 p.m. Left Thoracotomy (B.S.D.) underG.A. The patient was placed in the right lateralposition and a postero-lateral incision was made.After the skin and muscles were incised it wasnoticed that the intercostal muscles of the left 6thinterspace had been completely torn by theinjury and the lung was presenting through thisextensive gap in the 6th interspace, there wasfracture of the anterior ends of the 2nd, 3rd and4th ribs and a double fracture involving the 5th,6th and 7th ribs. There were nearly 3 pints ofblood inside the pleural cavity, which was rapidlysucked out and the bleeding appeared to be comingfrom three sources. (i) From the ruptured inter-costal vessels of the 3rd and 4th spaces. The tornends of these vessels were freely hanging in thepleural cavity. (2) From the torn intercostalmuscles of the 6th interspace. (3) From a tear inthe left lower lobe near the inferior pulmonaryvein.

Bleeding from the intercostal vessels and thelung was rapidly controlled. There was a largehaematoma along the phrenic nerve, which com-pletely covered the upper half of the pericardiumand the ascending, transverse and descending partof the arch of aorta was surrounded by suffusedblood. The pericardium was tense and full ofblood, and it was noticed that the wall of the leftauricle was contused and this contusion extendedalong the atrio venticular groove on to the wall of

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414 POSTGRADUATE MEDICAL JOURNAL August 1957

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FIG. 3.-25.8.56. Preoperative E.C.G. showing ventricular extrasystoles andinverted T1. 26.8.56. Postoperative E.C.G. showing sinus rhythm.

the left ventricle for about 2 in. The coronaryarteries and veins were intact. The blood in thepericardium appeared to be coming from thisextensive contusion of the wall of the left auricleand left ventricle which was more of the nature ofgeneralized oozing than a specific bleeding point.A hole in the pericardium was left for drainage intothe pleural cavity. The fractured ends of the ribswere trimmed and an appreciable gap left betweenthe rib ends to reduce the post-operative pain.The pleural cavity was drained-an intercostal

catheter connected to underwater seal. He wastransfused with I,8oo c.c. of blood during theoperation.

Post-operative ProgressOn return to the ward the pulse was 8o, regular,

good volume, B.P. i20/80 and no cardiac murmurwas detected except for a pericardial rub, which isnot unusual after the pericardium has beenopened.

26.8.56--4p.m. The patient was listless, tonguewas dry, pulse I30, poor volume, extremities werecold and B.P. I05/70. There was no obviousloss of fluid to account for this circulatory collapse,examination of the abdomen revealed slight dis-tension in the epigastric region, marked tym-panitic note on percussion and a portable radio-graph of the abdomen revealed acute dilatation ofthe stomach. A Ryles tube was passed intothe stomach and i,450 c.c. of dark-brown fluidaspirated from the stomach. An adequate electro-lyte and fluid replacement was carried out withimprovement in the general condition of thepatient.

27.8.56. The routine post-operative examina-tion of the cardiovascular system revealed noabnormality.

28.8.56. The patient maintained satisfactoryimprovement but at i p.m. there was sudden onset

of auricular fibrillation with apex rate of i6o andB.P. ioo/6o, the extremities were cold and thepulse was irregular and weak in volume (rate?).The auricular fibrillation was paroxysmal first butsoon became fully established. The patient wasdigitalized with digoxin i.5 mg. followed bydigoxin I mg. at 6-hourly intervals for two dosesand maintained on digoxin 0o.25 mg. t.i.d.

29.8.56. There was rise in the jugular venouspressure with crepitations at the right base andsacral oedema. A systolic thrill could be palpatedin the mitral areas and a harsh systolic murmurGrade III, conducted to the axillae was heard inthe mitral area. The congestive cardiac failureresponded to restricted fluid intake, salt-free dietand Mersalyl injections. His further post-operative progress was smooth.On I.Io.56 examination of the heart revealed

apex beat in the 6th space in the anterior axillaryline.

Mitral Area. A systolic thrill was still palpable,the first sound was normal, there was a loud, harshsystolic murmur (Grade III) conducted to theaxilla. Fluoroscopic examination of the heart re-vealed enlargement of the left auricle and leftventricle. He was discharged home with in-structions to attend the follow-up clinic.

DiscussionThis case presents several interesting features.

The development of haemopericardium followingclosed injury of the chest is definite evidence ofmyocardial damage or injury to the coronaryvessels. It may be several hours before there isevidence of cardiac tamponade, if the bleeding isslow and moderate as in this case. The increasedintrapericardial pressure interferes with normalfilling of the auricles from the venous side, itreduces the cardiac output which produces a fall inblood pressure, narrowing of the pulse pressure

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August I957 DHILLON: Traumatic Injury to the Heart Due to Blunt Force 4X5

and rise in the venous pressure. The pulse issmall and its paradoxical nature can be moreeasily elicited' with sphygmomanometer than bypalpation. Cardiac tamponade can be the causeof continued shock and there may be no objectiveevidence of distended neck veins but manometricestimation of the venous pressure always shows arise above the normal value. It is hardly possibleto conduct fluoroscopic examination in a seriously-ill patient but repeated portable radiographs of thechest can yield useful information if the cardiacsilhouette is progressively enlarging. Pericardialaspiration via the xiphisternal route is a com-paratively easy procedure which helps to establishthe diagnosis and in some cases repeated aspirationof the pericardium may be all that is necessary torelieve the acute cardiac tamponade. However,if the patient's condition remains unchanged ordeteriorates after improvement, operative inter-ference with repair of the wound should be carriedout. It is clear from the operative findings in thiscase that repeated aspiration of the pericardiumwould have been sufficient to relieve the cardiactamponade but progressive bleeding from theintercostal vessels and " bursting " of the left 6thintercostal space with herniation of the lung,though the skin and chest wall muscles were intact,were the main reasons for carrying out leftthoracotomy. It is easy to miss the traumaticrupture of the parietal pleura and the intercostalmuscles, the patient usually comes back severalweeks later with bulging and pain due to herniationof the lung. If recognized early it should be re-paired as soon as the patient is fit enough to standthe operation.The most notable feature about this case was the

development of- a systolic thrill and harsh systolicmurmur in the mitral area following sudden onsetof auricular fibrillation three days after injury.This is very suggestive of delayed rupture of thechordae tendinae of the mitral valve, resulting inpure mitral incompetence. There was no detect-able cardiac murmur at the time of his admissionand no murmur was detected on the first orsecond day following injury when the apex ratewas between 80 to 90 per minute. The previoushistory of the patient was, singularly, negative.

It is unlikely that he sustained rupture of a papil-lary muscle of the mitral valve, as the subsequentprogress would have been rapidly downhill.The fluoroscopic examination of the heart at the

time of the patient's discharge from the hospital(five weeks after injury) showed enlargement ofthe left auricle and left ventricle (supported byE.C.G.).The onset of auricular fibrillation is not unusual

following cardiac trauma due to non-penetratinginjury of the chest.8 In this patient there wasspontaneous reversion to normal rhythm aboutthree weeks after the onset of auricular fibrillation.

Acute dilatation of the stomach and intestinalileus may supervene with dramatic rapidity afterchest injury. Cameron et al.9 have reportedan incidence of i6.5 per cent. following severeinjury to the chest. The acute dilatation of thestomach is liable to be missed in the initial stagesif this possibility is not kept in mind. Thepatient is usually listless and there is general de-terioration in the cardio-respiratory status, fol-lowed by anorexia and epigastric fullness; copiousvomiting takes some time to develop. A gastrictube can produce dramatic relief.

SummaryI. The case history of a patient is reproduced

who sustained contusion of the left auricle, theleft ventricle and the pericardium following a non-penetrating injury to the chest. These injuries tothe heart produced extravasation of blood insidethe pericardium, resulting in cardiac tamponade.

2. He also sustained complete disruption of theintercostal muscles of the left sixth interspace andprogressive bleeding from the intercostal arteries.

3. On the first post-operative day he developedacute dilatation of the stomach which presentedwith symptoms of dehydration and circulatorycollapse.

4. Nearly 63 hours after operation -there wassudden onset of auricular fibrillation with apexrate of I6o per minute. Following this a harshsystolic murmur Grade III was heard in the mitralarea for the first time. It is assumed that onset ofrapid auricular fibrillation produced rupture of thechordae tendinae, which must have been trau-matized and weakened at the time of originalinjury.Acknowledgments

I wish to thank Mr. A. W. Fawcett for per-mission to publish this paper.

REFERENCESx. ARENBURG, H. (I943), Ann. intern. Med., 19, 326.2. MESSEN, H. (1955), Arch. klin. Chir., 282, 288.3. BRIGHT, E, F., and BECK, C. S. (1935), Amer. Heart .,

10, 293.4. BARBER, H. (1940), Brit. med. J., 520.5. KISSANE, R. W., FIDLER, R. S., and KOONS, R. A. (I937),

Ann. intern. Med., II, 907.6. GLENDY, R. E., and WHITE, P. D. (1936), Amer. Heart. Y.,

Ix, 366.7. GROSSE BROCKHOFF, F. (I955), Arch: klin. Chir., 282, 300.8. WARBURG, E. (I940), Brit. Heart J., ii, 27.9. CAMERON, D. A., O'ROURKE, P. V., and BURT; C. W,

(I949), Amer. 7. $Sg., 78, 688.

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reportcaseDue to Blunt Force: With a

Traumatic Injury to the Heart

B. S. Dhillon

doi: 10.1136/pgmj.33.382.4121957 33: 412-415 Postgrad Med J

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