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MITRAL VALVE DISEASE FROM BLUNT TRAUMA
MITRAL VALVE DISEASE FROM B L U N T Joseph S. McLaughlin, Baltimore,
M.D.* and R Adams Cowley,
Md., and George Smith,
N. A. Matheson,
M.B.,
****
M.B.E.,
Aberdeen,
M.D.,
TRAUMA M.D.,** ***
and
Scotland
B
LUNT trauma to the chest often produces cardiac injury. The magnitude of injury may vary from that represented by minor changes in the electro cardiogram with no clinical symptoms to massive rupture with sudden death. 1 - 2 In the middle of this spectrum are certain intracardiac lesions that are com patible with limited survival. The availability of modern techniques, particularly cardiopulmonary bypass, has made surgical correction possible and a variety of such lesions, including ruptured aortic valves and ruptured intraventricular septa, have been repaired. 3 ' 4 Kecently the authors treated 2 persons with mitral insufficiency due to blunt trauma. One patient survived following operative correction of the lesion which is to our knowledge the first of its kind sur gically repaired. Since this is a rare lesion, the cases and a summary of the literature are presented below. CASE REPORTS CASE 1.—M. M., a 7-year-old schoolboy, was admitted to the University of Maryland Hospital, J u l y 16, 1962, for evaluation of a heart murmur. He had been in good health until lie was struck by an automobile April 22, 1962. Subsequently he had been admitted to Lutheran Hospital in Baltimore, where the following injuries were noted: numerous abrasions and contusions, a large hematoma of the left parietal region, a fractured skull, a fracture of the left femur, fractures of the second to the eighth left ribs posteriorly, the fifth to the seventh left ribs in the axilla, and a left hemopneumothorax. The patient's course had been stormy but he had slowly responded to stabilization of the fractures, thoracotomy drain age, and general supportive care. On May 1, a systolic murmur was noted. Chest roentgenograms revealed that the heart, while normal in size on admission, was gradually enlarging (Fig. 1 ) . He was digitalized and maintained on Lanoxin, 0.25 mg. daily. His general condi tion was improved sufficiently to permit transfer for cardiac catheterization J u l y 16, 1962. Physical examination revealed a thin hypermotile Negro child in no apparent distress
Prom the Department of Surgery, Division of Thoracic Surgery, University of Maryland School of Medicine, Baltimore, Md., and the Department of Surgery, University of Aberdeen, Aberdeen, Scotland. Received for publication Jan. 9, 1964. •Senior Surgeon, National Heart Institute. National Institutes of Health, Bethesda, Md. Formerly Resident in Thoracic Surgery, University of Maryland Hospital, Baltimore, Md. ••Professor of Thoracic Surgery and Head of the Division of Thoracic Surgery, University of Maryland School of Medicine, Baltimore, Md. •••Regius Professor, Department of Surgery, University of Aberdeen, Foresterhill, Aber deen, Scotland. *··'Lecturer in Surgery, University of Aberdeen, Foresterhill, Aberdeen, Scotland. 261
262
MCLAUGHLIN E T AL.
J . Thoracic and Cardiovas. Surg,
Fig. I . - C a s e 1. R o e n t g e n o g r a ^ reveal, ^ ^ s s i v ^ c a r d i a c ^ e n l a r g e r n e n t . A, April 30, 1962.
MITRAL VALVE D I S E A S E FROM BLUNT TRAUMA
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Pig. 2.—Case 1. Electrocardiograms reveal progressive left ventricular and left atrial enlarge ment. A, July 18, 1962. B, October 24, 1962. C, November 28, 1962.
at rest. The temperature was 37° C , respiratory rate 18, blood pressure 120/60 mm. Hg, and pulse rate 60. He was acyanotic. The head and neck were normal except for slight bilateral venous engorgement. No chest deformity was apparent, but a visible thrust was present in the seventh intercostal space, 2 em. to the left of the midclavicular line. The left heart border could be percussed to the left anterior axillary line. The second sound in the pulmonic area was louder than the second sound in the aortic area. A 6/6 systolic murmur was audible over the entire precordium but was loudest at the left sternal border in the fourth intercostal space. One observer heard a soft diastolic murmur in the same area. The lungs were clear. The liver was palpable 2 cm. below the costal margin. There was slight atrophy of the left leg. The white blood cell count was 5,050 with a normal differential. An ASO titer was 166 Todd units and the C reactive protein was negative. Representative electrocardiograms are shown in Fig. 2. Right heart and retrograde left heart catheterizations were performed July 17, 1962. These data are presented in Table I. A cineangiocardiogram revealed mitral insufficiency with marked régurgitation from the left ventricle into a dilated left atrium. Since there
TABLE I. CASE 1. RIGHT HEART CATHETERIZATION CATHETERIZATION
CATHETER
POSITION
PRESSURE
Right atrium (mid) Right ventricle (low) Right ventricle (mid)
a = 10-12 Mean (8)
Main pulmonary artery Right pulmonary artery Pulmonary artery wedge Brachial artery
40-45/20-25 Mean (28)
Ascending aorta Left ventricle
40-48/7-10
100-115/55-60 Mean (70) 100-105/70 Mean (75) 100-120/5-25
AND RETROGRADE L E F T HEART
OXYGEN SATURATION
PER CENT ΚΓ85
74 65 66 66
3%
REMARKS
Respiratory variation in pressure
68
99
Technically not pos sible
264
MCLAUGHLIN E T AL.
J. Thoracic and Cardiovas. Surg.
was no record of a heart murmur being present on previous physical examinations and no history of rheumatic fever, a traumatic etiology was ascribed to the lesion. The patient was returned to Lutheran Hospital for continued convalescent care. He was readmitted to University Hospital Oct. 23, 1962, and operation was performed Dec. 12, 1962 ( F i g . 3 ) . A right thoracotomy was used and the patient was connected to the pump oxygenator by cannulas in the right atrium and the left femoral artery. P a r t i a l heart-lung bypass was undertaken and he was cooled to 30° C. by the heat exchanger in the line. Subsequently total bypass was begun and the enlarged left atrium was entered by an incision within the interatrial groove. The mitral annulus was dilated. The anterior leaflet of the mitral valve was torn away from the annulus for about one third of its attachment
Pig. 3.—Case 1. Operation performed December 12, 1962. A, Incision in the left atrial wall within the interatrial groove viewed from the right thoracotomy position. B, Mitral valve : the anterior leaflet is torn from the annulus, and the chordae to that portion of the valve are ruptured which precludes primary suture. C, Technique of plicating mitral annulus. D, Repair completed. Since the annulus had dilated, plication did not produce stenosis. medially. The chordae tendineae to this portion of the valve were ruptured. Plication of the annulus was performed with No. 2-0 silk tied over Teflon pledgets. The atriotomy in cision was closed and cardiopulmonary bypass was discontinued. The patient tolerated his new circulatory status well and the operative procedure was terminated. The postoperative course was prolonged and complicated. Respiratory difficulty devel oped late in the first postoperative day. Tracheostomy was performed and respiration was controlled by the Bennett respirator. Bronchial pneumonia ensued and the resultant copious secretion necessitated frequent bronchoscopie aspiration. Bilateral empyema developed and bilateral thoracotomy drainage was performed. Suppurative pericarditis further complicated the course. Bacteriological studies revealed hemolytic Staphylococcus aureus, sensitive to oxacillin. Large doses of oxacillin and chloramphenicol were administered. Following pericardial drainage the course was one of gradual improvement. All drainage tubes were re moved by J a n . 3, 1963. Thereafter the patient was afebrile until his discharge Feb. 5, 1963. A t present he is improved clinically and there is no evidence of infection. A systolic mur mur is audible at the left sternal border in the fourth intercostal space.
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"^
CASE 2.—A male patient, 19 years old, previously in good health, was thrown from his motorcycle onto the road after a collision with an automobile April 4, 1963. After initial treatment at an outlying hospital, he was transferred to the Aberdeen Boyal Infirmary, ar riving 4 hours after the accident. On admission he was conscious; the heart rate was 120 and systolic blood pressure was 70. The following injuries were noted: fracture of the left ramus of the mandible, contusions of the left anterolateral chest wall above the costal margin, and numerous abrasions. A Grade 2 systolic murmur with maximum intensity at the cardiac apex was heard over the precordium. There was rigidity and marked tenderness in the left upper quadrant of the abdomen. X-ray examination of the chest revealed possible broadening of the superior mediastinum and normal lung fields (Fig. 4 ) . Skeletal survey was noncontributory. Catheterization of the bladder revealed gross hematuria. An intravenous pyelogram indicated extravasation of the dye in the region of the left kidney. An electro cardiogram showed a pattern of right bundle branch block and myocardial damage (Fig. 5 ) .
Fig. 4.—Case 2. Roentgenograms reveal progressive mediastinal widening with a con comitant increase in heart size and vascular prominence. A, On admission. B, Twelve hours following admission. An emergency laparotomy was performed. One thousand five hundred cubic centimeters of blood was present within the peritoneal cavity. The spleen and left kidney were ruptured, small lacerations were present in the right lobe of the liver, and contusions of the cardioesophageal junction and both the splenic and hepatic flexures of the colon were present. Splenectomy and, because of continued profuse bleeding, left nephrectomy were carried out. The lacerations of the right lobe of the liver had sealed and drains were inserted into the subphrenic areas. Gastrostomy was performed. He received a total of 3 L. of blood. Following the operative procedure the patient's condition was satisfactory and con tinued so throughout the next 10 hours. His blood pressure then began to fall despite no evidence of renewed blood loss. The neck veins became distended and there was perceptible cyanosis of the face and extremities. X-ray examination of the chest showed broadening
266
MCLAUGHLIN
ET
AL.
J. Thoracic and Cardiovas. Surg.
Fig. 5.—Case 2. A, Electrocardiogram made on admission reveals right bundle branch block and myocardial damage. B, Electrocardiogram made 12 hours following admission reveals a pattern compatible with right heart strain.
Pig. 6.—Case 2. Photograph of heart demonstrates rupture of papillary muscle.
of the mediastinum, mottling of the right lung field and a general increase in the vascular markings of both lungs (Fig. 4 ) . Perieardial t a p yielded no blood. An electrocardiogram was interpreted as showing right heart strain in addition to right bundle branch block and myocardial damage (Fig. 5 ) . Twelve hours after the first operation, while the patient was being anesthetized for thoraeotomy, cardiac arrest occurred. The thorax was immediately entered and cardiac mas sage instituted. All chambers of the heart were dilated and massage was ineffective. Blood could not be expelled from the heart into the aorta but flowed back to distend the left atrium and pulmonary veins, which suggested that mitral insufficiency was present. Besuseitation was unsuccessful and the patient died. Postmortem examination revealed that the anterior papillary muscle had been torn across at its base from the left ventricular wall (Fig. 6 ) . There were contusions of the
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posterior aspect of the right lung and the anterior aspect of the lower lobe of the left lung. Blood was present within the mediastinum but its source was not detected. The intra-abdominal bleeding had been controlled. DISCUSSION
Mitral valve lesions from blunt trauma are rare. A review of autopsy find ings in 546 patients who received nonpenetrating trauma to the heart revealed no instance of isolated mitral valve trauma. 5 The lesion is equally rare in ex perimental animals subjected to hammer blows to the chest wall or myocar dium.6· 7 Rupture or avulsion of the papillary muscle and chordae tendineae is somewhat more common and is responsible for the majority of cases of traumatically produced mitral valve disease. The mechanics of valvular injury have been described by physicians of former generations. 8 ' 9 In essence, rupture of the mitral valve or its attach ments occurs when the heart, filled during diastole, is violently compressed. A more subtle lesion may develop when the valve and the adjacent myocar dium are injured with sufficient force to cause scar formation with resultant contracture and distortion. Although mitral insufficiency is the most common result of injury, mitral stenosis has been reported from the latter circumstances. 10 Reports in the literature of mitral valve injury from blunt trauma are difficult to verify. Frequently follow-up data are absent and autopsy inter pretations are questionable in the light of modern knowledge. A survey of the English literature revealed 18 original cases, 15 of which are summarized in Table II. 1 0 1 9 Two patients with papillary muscle rupture and associated interatrial septal defects, who lived approximately one hour, are not included since clinical data were not given.6 Gibson's case is excluded because the mitral valve injury was immediately fatal. 20 Also not included is Heimann's patient who, although noted in the American literature, was originally reported in the non-English literature. 21 Barie's 3 patients and Adams' 5 patients are ex cluded for the same reason. 8 ' 22 Allbutt's 2 cases, cited through the years as classic examples of mitral stenosis from trauma, have been questioned as to their validity. 23 Perhaps the reports of mitral stenosis from trauma by Barber and Osborn10 and Warberg 14 lend more credence to this claim. The remaining cases appear to be substantiated on pathological or clinical grounds. An analysis of the collected series is as follows. The patients are males. The age range is from the first to the seventh decade, with peak instance dur ing the third and sixth decades. If equestrian accidents from an earlier period are excluded, the usual etiology is an industrial or automobile accident. The initial symptoms are variable, being dependent on associated injuries as well as the magnitude of the cardiac injury; however, a shock-like state with dyspneas cyanosis, and pain is frequently present in the more severe injuries. A murmur is usually, but not invariably, present and, if not specifically sought, may be easily overlooked in the face of associated thoracic injury. The mur mur is usually systolic in time but a late diastolic murmur also may be heard. Congestive heart failure, if not initially present, soon develops. In the collected series, if death did not occur within one hour, the patient
MCLAUGHLIN E T AL.
268
J. Thoracic and Cardiovas. Surg. TABLE
AUTHOR AND YEAR
SEX AND AGE
SOURCE OP TRAUMA
INITIAL FINDINGS
1. Allbutt 1873
M, 14
Violently kicked
Became faint and sick
Presystolie murmur
2. Allbutt 1873 3. Glendy and White 1936 4. Barber and Osborn 1937 5. Payne and Hardy 1937
M, 16
Blow of cricket ball
M, 24
Run over by truck
Stunned, prolonged syncope Shock, board-like abdomen
"Thrill of mitral contraction" None present; sounds of good quality
M, 20
Buried by shell ex plosion
Systolic murmur
Developed presystolie thrill and bruit
M, 51
6. Warberg 1938 (Case 178) 7. Anderson 1940
M, 20
Shock, cyanosis, Probably struck in None, but sounds chest by stick used lungs clear faint to reapply machine belt Pressed against wall Shocked, faint heart Presystolie mitral by mad bull bruit noted 3 years sounds, systolic murmur after injury Stepped on by horse "Winded," systolic Same, but less in tense a year later bruit and thrill
8. Cameron 1942 9. Van Eaalte 1946
M, 35
Fell from scaffold
M, 20
Struck by 5 gallon can of gasoline
10. Arenberg 1943 (Case 12)
M, 54
Struck in chest by swinging draft of castor beans 500 lbs. in weight
Not definitely stated Blowing systolic and late diastolie at apex
11. Arenberg 1943 (Case 24)
M, 53
Fell 28 feet into hold of ship
12. Arenberg 1943 (Case 25)
M, 60
Struck in chest by 100 lb. bag of coffee
Fractured ribs ; sev Systolic eral hours follow ing injury devel oped dyspnea, cya nosis, and auricular fibrillation Blowing systolic Resumed work murmur heard over entire chest
13. Rodriguez and Nido 1961
M, 40
Telephone pole fell on chest
Shock ( B P 70/50), Grade I I I systolic murmur
Same
14. Case 1 1963
M, 7
Struck by automobile
Shock, unconscious ness, multiple rib fractures, hemopneumothorax
Blowing systolic and late diastolie
15. Case 2 1963
M, 19
Motorcycle collision with automobile
Shock; rigid abdo men; systolic mur-
Systolic at apex
M, 30
Congestive failure noted at 10 days Drove to hospital on bicycle carrying can; short of breath, developed frank congestive failure
and thrill (18 months later)
Loud systolic bruit in mitral area High pitched systolic and soft presystolie at apex
Vol. 48, No. 2 August, 1964
MITRAL VALVE D I S E A S E FROM BLUNT TRAUMA
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II
Fractured rib
DIAGNOSIS
COURSE
MS
18 mo. later, progressive deteriora tion
MS
1 yr. later did desk work
Ruptured spleen MS
Lived 22 yr. Autopsy : scar in ven tricular wall extending into valve
—
Died % hr. after reaching the hos pital, 1 hr. after injury. Autopsy : ruptured papillary muscle
MS and M I
Improved to where he could under take light work 3 years later
Enlarging heart size
Indefinite
Enlarged heart at 10 days
Myocardial injury M I or rupt. I V S simulating coronary thrombosis — MI
— Increased heart size
"Compatible with mitral vitium"
Died 26 hr. later. Autopsy: rup tured papillary muscle
MI
Improved to where he eould take light exercise a year later Improved 3 yr. later, murmur still present but less intense Improved and doing sedentary work a year later
Enlarged heart noted Auricular at 10 weeks after injury
fibrillation
MI
Poorly compensated on digitalis one year later
Auricular
fibrillation
MI
Poorly compensated on digitalis one year later
"Negative"
High voltage, slur ring QRS complexes and marked left axis (6 months after injury)
MI
Unable to work day following in jury, developed progressive dysp nea, not able to work 6 months later
Fractured ribs
LBBB 1st degree A-V block 1st Acute ant. 2nd MI Developed L V H and L A H pattern
MI
Improved at 4 weeks on digitalis; follow-up not given
MI
Improved on digitalis; defect re paired utilizing cardiopulmonary bypass. P a t h . : valve torn from annulus Cardiac arrest during anesthesia induction. Autopsy: ruptured papillary muscle
Enlarging heart
Enlarging heart and increased vascular markings
Right heart strain MI pattern developed Ruptured spleen and kidney over 10 hour period
270
MCLAUGHLIN
E T AL.
Cardiovas. Surg. J. Thoracic and
was usually able to compensate for his injury; thereafter, the course was one of valvular heart disease. This is in marked contrast to cases of papillary mus cle rupture occurring in association with myocardial infarction where pro gressive deterioration and early death is the rule. 24 An explanation may be found in the lack of ischémie myocardial damage in the former, but one may speculate that the extent of injury in the presented series may be significantly less than in the cases associated with infarction and that, when comparable damage is present, rapid deterioration and death will occur. This was the situation in Case 2. X-ray examinations are valuable for comparison of initial to later heart size and for graphically demonstrating pulmonary vascular congestion and edema. Electrocardiograms are invariably abnormal but the pattern is non specific. The ultimate treatment is surgical repair of the defect. Frequently such treatment may be carried out as an elective procedure, the patient's cardiac status being maintained with digitalis and other measures while he recovers from his other injuries. Emergency cardiopulmonary bypass is within the realm of possibility and should be utilized in those circumstances where it may be life saving.
SUMMARY
The eases of 2 patients with mitral valve disease from blunt trauma are pre sented. Cardiac catheterization and cineangiocardiography were performed in one and the defect was corrected with the use of cardiopulmonary bypass. The second patient died 12 hours following his injury during induction of anesthesia for exploratory thoracotomy. The English literature is surveyed and a total of 18 cases of mitral valve disease from trauma are noted. An analysis of the col lected series is made. We are indebted to Drs. Leonard Scherlis and Eobert Singleton of the Department of Medicine, Section of Cardiology, University of Maryland School of Medicine, and Dr. Elliott Michaelson, Thoracic Surgeon Attending Lutheran Hospital, Baltimore, Md. REFERENCES 1. Watson, J . H., and Bartholomae, W. M. : Cardiac Injury Due to Nonpenetrating Chest Trauma, Ann. I n t . Med. 52: 871, 1960. 2. Sigler, L. H . : Traumatic Injury of the Heart. Incidence of I t s Occurrence in Forty-two Cases of Severe Accidental Bodily Injury, Am. Heart J . 30: 459, 1945. 3. Campbell, G. S., Vernier, B., and Lillehei, C. W . : Traumatic Ventricular Septal Defect: Beport of Two Cases, J . THORACIC SUKG. 37: 496, 1959.
4. Spurny, O. M., and Hara, M. : Bupture of the Aortic Valve Due to Strain, Am. J . Cardiol. 8: 125, 1961. 5. Parmley, L. F., Manion, W. C , and Mattingly, T. W. : Nonpenetrating Traumatic Injury of the Heart, Circulation 18: 371, 1958. 6. Kissane, B. W., Tidier, B. S., and Koons, B. A . : Electrocardiographic Changes Follow ing External Chest Injury to Dogs, Ann. I n t . Med. 1 1 : 907, 1937. 7. Bright, E . F . , and Beck, C. S.: Nonpenetrating Wounds of the H e a r t : A Clinical and Experimental Study, Am. Heart J . 10: 293, 1935. 8. Barie, E. : Becherches sur les ruptures valvulares du coeur, Bev. de Med. 1: 132, 1881. 9. Howard, C. P . : Aortic Insufficiency Due to Bupture by Strain of a Normal Aortic Valve, Canad. M. A. J . 19: 12, 1928.
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August, 1964
MITRAL VALVE DISEASE FROM BLUNT TRAUMA
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10. Barber, H., and Osborn, G. R. : A Case of Mitral Stenosis, the Result of Trauma, Guy's Hosp. Rep. 87: 510, 1937. 11. Allbutt, C. : On Overwork and Strain of the Heart and Aorta, Tr. Clin. Soc. London 6: 101, 1873. 12. Glendy, R. E., and White, P . D. : Nonpenetrating Wound of Heart. Rupture of Papil lary Muscle and Contusion of Heart Resulting From External Violence. Case Re port, Am. Heart J . 1 1 : 366, 1936. 13. Payne, W. C , and Hardy, H. H., J r . : Traumatic Rupture of the Papillary Muscles of the Mitral Valve, New Orleans M. & S. J . 89: 373, 1937. 14. Warberg, E.: Subacute and Chronic Pericardial and Myocardial Lesions Due to Nonpenetrating Traumatic Injuries: A Clinical Study, edited by Humphrey Milford, London, 1938, Oxford University Press. 15. Anderson, R. G. : Nonpenetrating Injuries of the Heart, Brit. H. J . 2: 307, 1940. 16. Cameron, R. A. (Cited by Barber, H.) : The Effects of Trauma, Direct and Indirect, on the Heart, Quart. J . Med. 13: 137, 1944. 17. Van Raalte, H. G. S.: Traumatic Rupture of Cardiac Valve, Indust. Med. 15: 436, 1946. 18. Arenberg, H . : Traumatic Heart Disease: Clinical Study of 250 Cases of Nonpenetrating Chest Injuries and Their Relation to Cardiac Disability, Ann. Int. Med. 19: 326, 1943. 19. Rodriguez, R. C , and Nido, R. C.: Traumatic Rupture of the Mitral Valve: Report of a Case, Bol. asoc. med. Puerto Rico 5 3 : 16, 1961. 20. Gibson, G. A.: System of Medicine, edited by Allbutt and Rolleston, 6: 381, 1909. 21. Heimann, M.: Ueber einen Fall von Endocarditis Mitralis Traumatica, Inaug. Dissert., Berlin, J u n e 5, 1896. Cited by Warneld, L. M. : Injuries to the Heart and Aorta, Wisconsin M. J . 32: 688, 1933. 22. Adams, A. (Cited by White) : Ueber die Traumatischen Veränderungen gesunder Klappen des Herzens, Ztschr. f. Kreislaufforsch. 19: 313, 1927. 23. White, P. D., and Glendy, R. E. : Trauma and Disease, edited by L. Brahdy and S. Kahn, Philadelphia, Pa., 1937, Lea & Febiger. 24. Craddock, W. L., and Mahe, G. A.: Rupture of Papillary Muscle of Heart Following Myocardial Infarction, J . A. M. A. 151: 884, 1953.
M.D.* and R Adams Cowley,
Md., and George Smith,
N. A. Matheson,
M.B.,
****
M.B.E.,
Aberdeen,
M.D.,
TRAUMA M.D.,** ***
and
Scotland
B
LUNT trauma to the chest often produces cardiac injury. The magnitude of injury may vary from that represented by minor changes in the electro cardiogram with no clinical symptoms to massive rupture with sudden death. 1 - 2 In the middle of this spectrum are certain intracardiac lesions that are com patible with limited survival. The availability of modern techniques, particularly cardiopulmonary bypass, has made surgical correction possible and a variety of such lesions, including ruptured aortic valves and ruptured intraventricular septa, have been repaired. 3 ' 4 Kecently the authors treated 2 persons with mitral insufficiency due to blunt trauma. One patient survived following operative correction of the lesion which is to our knowledge the first of its kind sur gically repaired. Since this is a rare lesion, the cases and a summary of the literature are presented below. CASE REPORTS CASE 1.—M. M., a 7-year-old schoolboy, was admitted to the University of Maryland Hospital, J u l y 16, 1962, for evaluation of a heart murmur. He had been in good health until lie was struck by an automobile April 22, 1962. Subsequently he had been admitted to Lutheran Hospital in Baltimore, where the following injuries were noted: numerous abrasions and contusions, a large hematoma of the left parietal region, a fractured skull, a fracture of the left femur, fractures of the second to the eighth left ribs posteriorly, the fifth to the seventh left ribs in the axilla, and a left hemopneumothorax. The patient's course had been stormy but he had slowly responded to stabilization of the fractures, thoracotomy drain age, and general supportive care. On May 1, a systolic murmur was noted. Chest roentgenograms revealed that the heart, while normal in size on admission, was gradually enlarging (Fig. 1 ) . He was digitalized and maintained on Lanoxin, 0.25 mg. daily. His general condi tion was improved sufficiently to permit transfer for cardiac catheterization J u l y 16, 1962. Physical examination revealed a thin hypermotile Negro child in no apparent distress
Prom the Department of Surgery, Division of Thoracic Surgery, University of Maryland School of Medicine, Baltimore, Md., and the Department of Surgery, University of Aberdeen, Aberdeen, Scotland. Received for publication Jan. 9, 1964. •Senior Surgeon, National Heart Institute. National Institutes of Health, Bethesda, Md. Formerly Resident in Thoracic Surgery, University of Maryland Hospital, Baltimore, Md. ••Professor of Thoracic Surgery and Head of the Division of Thoracic Surgery, University of Maryland School of Medicine, Baltimore, Md. •••Regius Professor, Department of Surgery, University of Aberdeen, Foresterhill, Aber deen, Scotland. *··'Lecturer in Surgery, University of Aberdeen, Foresterhill, Aberdeen, Scotland. 261
262
MCLAUGHLIN E T AL.
J . Thoracic and Cardiovas. Surg,
Fig. I . - C a s e 1. R o e n t g e n o g r a ^ reveal, ^ ^ s s i v ^ c a r d i a c ^ e n l a r g e r n e n t . A, April 30, 1962.
MITRAL VALVE D I S E A S E FROM BLUNT TRAUMA
Vol. 48, No. 2 August, 1964
263
Pig. 2.—Case 1. Electrocardiograms reveal progressive left ventricular and left atrial enlarge ment. A, July 18, 1962. B, October 24, 1962. C, November 28, 1962.
at rest. The temperature was 37° C , respiratory rate 18, blood pressure 120/60 mm. Hg, and pulse rate 60. He was acyanotic. The head and neck were normal except for slight bilateral venous engorgement. No chest deformity was apparent, but a visible thrust was present in the seventh intercostal space, 2 em. to the left of the midclavicular line. The left heart border could be percussed to the left anterior axillary line. The second sound in the pulmonic area was louder than the second sound in the aortic area. A 6/6 systolic murmur was audible over the entire precordium but was loudest at the left sternal border in the fourth intercostal space. One observer heard a soft diastolic murmur in the same area. The lungs were clear. The liver was palpable 2 cm. below the costal margin. There was slight atrophy of the left leg. The white blood cell count was 5,050 with a normal differential. An ASO titer was 166 Todd units and the C reactive protein was negative. Representative electrocardiograms are shown in Fig. 2. Right heart and retrograde left heart catheterizations were performed July 17, 1962. These data are presented in Table I. A cineangiocardiogram revealed mitral insufficiency with marked régurgitation from the left ventricle into a dilated left atrium. Since there
TABLE I. CASE 1. RIGHT HEART CATHETERIZATION CATHETERIZATION
CATHETER
POSITION
PRESSURE
Right atrium (mid) Right ventricle (low) Right ventricle (mid)
a = 10-12 Mean (8)
Main pulmonary artery Right pulmonary artery Pulmonary artery wedge Brachial artery
40-45/20-25 Mean (28)
Ascending aorta Left ventricle
40-48/7-10
100-115/55-60 Mean (70) 100-105/70 Mean (75) 100-120/5-25
AND RETROGRADE L E F T HEART
OXYGEN SATURATION
PER CENT ΚΓ85
74 65 66 66
3%
REMARKS
Respiratory variation in pressure
68
99
Technically not pos sible
264
MCLAUGHLIN E T AL.
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was no record of a heart murmur being present on previous physical examinations and no history of rheumatic fever, a traumatic etiology was ascribed to the lesion. The patient was returned to Lutheran Hospital for continued convalescent care. He was readmitted to University Hospital Oct. 23, 1962, and operation was performed Dec. 12, 1962 ( F i g . 3 ) . A right thoracotomy was used and the patient was connected to the pump oxygenator by cannulas in the right atrium and the left femoral artery. P a r t i a l heart-lung bypass was undertaken and he was cooled to 30° C. by the heat exchanger in the line. Subsequently total bypass was begun and the enlarged left atrium was entered by an incision within the interatrial groove. The mitral annulus was dilated. The anterior leaflet of the mitral valve was torn away from the annulus for about one third of its attachment
Pig. 3.—Case 1. Operation performed December 12, 1962. A, Incision in the left atrial wall within the interatrial groove viewed from the right thoracotomy position. B, Mitral valve : the anterior leaflet is torn from the annulus, and the chordae to that portion of the valve are ruptured which precludes primary suture. C, Technique of plicating mitral annulus. D, Repair completed. Since the annulus had dilated, plication did not produce stenosis. medially. The chordae tendineae to this portion of the valve were ruptured. Plication of the annulus was performed with No. 2-0 silk tied over Teflon pledgets. The atriotomy in cision was closed and cardiopulmonary bypass was discontinued. The patient tolerated his new circulatory status well and the operative procedure was terminated. The postoperative course was prolonged and complicated. Respiratory difficulty devel oped late in the first postoperative day. Tracheostomy was performed and respiration was controlled by the Bennett respirator. Bronchial pneumonia ensued and the resultant copious secretion necessitated frequent bronchoscopie aspiration. Bilateral empyema developed and bilateral thoracotomy drainage was performed. Suppurative pericarditis further complicated the course. Bacteriological studies revealed hemolytic Staphylococcus aureus, sensitive to oxacillin. Large doses of oxacillin and chloramphenicol were administered. Following pericardial drainage the course was one of gradual improvement. All drainage tubes were re moved by J a n . 3, 1963. Thereafter the patient was afebrile until his discharge Feb. 5, 1963. A t present he is improved clinically and there is no evidence of infection. A systolic mur mur is audible at the left sternal border in the fourth intercostal space.
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CASE 2.—A male patient, 19 years old, previously in good health, was thrown from his motorcycle onto the road after a collision with an automobile April 4, 1963. After initial treatment at an outlying hospital, he was transferred to the Aberdeen Boyal Infirmary, ar riving 4 hours after the accident. On admission he was conscious; the heart rate was 120 and systolic blood pressure was 70. The following injuries were noted: fracture of the left ramus of the mandible, contusions of the left anterolateral chest wall above the costal margin, and numerous abrasions. A Grade 2 systolic murmur with maximum intensity at the cardiac apex was heard over the precordium. There was rigidity and marked tenderness in the left upper quadrant of the abdomen. X-ray examination of the chest revealed possible broadening of the superior mediastinum and normal lung fields (Fig. 4 ) . Skeletal survey was noncontributory. Catheterization of the bladder revealed gross hematuria. An intravenous pyelogram indicated extravasation of the dye in the region of the left kidney. An electro cardiogram showed a pattern of right bundle branch block and myocardial damage (Fig. 5 ) .
Fig. 4.—Case 2. Roentgenograms reveal progressive mediastinal widening with a con comitant increase in heart size and vascular prominence. A, On admission. B, Twelve hours following admission. An emergency laparotomy was performed. One thousand five hundred cubic centimeters of blood was present within the peritoneal cavity. The spleen and left kidney were ruptured, small lacerations were present in the right lobe of the liver, and contusions of the cardioesophageal junction and both the splenic and hepatic flexures of the colon were present. Splenectomy and, because of continued profuse bleeding, left nephrectomy were carried out. The lacerations of the right lobe of the liver had sealed and drains were inserted into the subphrenic areas. Gastrostomy was performed. He received a total of 3 L. of blood. Following the operative procedure the patient's condition was satisfactory and con tinued so throughout the next 10 hours. His blood pressure then began to fall despite no evidence of renewed blood loss. The neck veins became distended and there was perceptible cyanosis of the face and extremities. X-ray examination of the chest showed broadening
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Fig. 5.—Case 2. A, Electrocardiogram made on admission reveals right bundle branch block and myocardial damage. B, Electrocardiogram made 12 hours following admission reveals a pattern compatible with right heart strain.
Pig. 6.—Case 2. Photograph of heart demonstrates rupture of papillary muscle.
of the mediastinum, mottling of the right lung field and a general increase in the vascular markings of both lungs (Fig. 4 ) . Perieardial t a p yielded no blood. An electrocardiogram was interpreted as showing right heart strain in addition to right bundle branch block and myocardial damage (Fig. 5 ) . Twelve hours after the first operation, while the patient was being anesthetized for thoraeotomy, cardiac arrest occurred. The thorax was immediately entered and cardiac mas sage instituted. All chambers of the heart were dilated and massage was ineffective. Blood could not be expelled from the heart into the aorta but flowed back to distend the left atrium and pulmonary veins, which suggested that mitral insufficiency was present. Besuseitation was unsuccessful and the patient died. Postmortem examination revealed that the anterior papillary muscle had been torn across at its base from the left ventricular wall (Fig. 6 ) . There were contusions of the
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posterior aspect of the right lung and the anterior aspect of the lower lobe of the left lung. Blood was present within the mediastinum but its source was not detected. The intra-abdominal bleeding had been controlled. DISCUSSION
Mitral valve lesions from blunt trauma are rare. A review of autopsy find ings in 546 patients who received nonpenetrating trauma to the heart revealed no instance of isolated mitral valve trauma. 5 The lesion is equally rare in ex perimental animals subjected to hammer blows to the chest wall or myocar dium.6· 7 Rupture or avulsion of the papillary muscle and chordae tendineae is somewhat more common and is responsible for the majority of cases of traumatically produced mitral valve disease. The mechanics of valvular injury have been described by physicians of former generations. 8 ' 9 In essence, rupture of the mitral valve or its attach ments occurs when the heart, filled during diastole, is violently compressed. A more subtle lesion may develop when the valve and the adjacent myocar dium are injured with sufficient force to cause scar formation with resultant contracture and distortion. Although mitral insufficiency is the most common result of injury, mitral stenosis has been reported from the latter circumstances. 10 Reports in the literature of mitral valve injury from blunt trauma are difficult to verify. Frequently follow-up data are absent and autopsy inter pretations are questionable in the light of modern knowledge. A survey of the English literature revealed 18 original cases, 15 of which are summarized in Table II. 1 0 1 9 Two patients with papillary muscle rupture and associated interatrial septal defects, who lived approximately one hour, are not included since clinical data were not given.6 Gibson's case is excluded because the mitral valve injury was immediately fatal. 20 Also not included is Heimann's patient who, although noted in the American literature, was originally reported in the non-English literature. 21 Barie's 3 patients and Adams' 5 patients are ex cluded for the same reason. 8 ' 22 Allbutt's 2 cases, cited through the years as classic examples of mitral stenosis from trauma, have been questioned as to their validity. 23 Perhaps the reports of mitral stenosis from trauma by Barber and Osborn10 and Warberg 14 lend more credence to this claim. The remaining cases appear to be substantiated on pathological or clinical grounds. An analysis of the collected series is as follows. The patients are males. The age range is from the first to the seventh decade, with peak instance dur ing the third and sixth decades. If equestrian accidents from an earlier period are excluded, the usual etiology is an industrial or automobile accident. The initial symptoms are variable, being dependent on associated injuries as well as the magnitude of the cardiac injury; however, a shock-like state with dyspneas cyanosis, and pain is frequently present in the more severe injuries. A murmur is usually, but not invariably, present and, if not specifically sought, may be easily overlooked in the face of associated thoracic injury. The mur mur is usually systolic in time but a late diastolic murmur also may be heard. Congestive heart failure, if not initially present, soon develops. In the collected series, if death did not occur within one hour, the patient
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J. Thoracic and Cardiovas. Surg. TABLE
AUTHOR AND YEAR
SEX AND AGE
SOURCE OP TRAUMA
INITIAL FINDINGS
1. Allbutt 1873
M, 14
Violently kicked
Became faint and sick
Presystolie murmur
2. Allbutt 1873 3. Glendy and White 1936 4. Barber and Osborn 1937 5. Payne and Hardy 1937
M, 16
Blow of cricket ball
M, 24
Run over by truck
Stunned, prolonged syncope Shock, board-like abdomen
"Thrill of mitral contraction" None present; sounds of good quality
M, 20
Buried by shell ex plosion
Systolic murmur
Developed presystolie thrill and bruit
M, 51
6. Warberg 1938 (Case 178) 7. Anderson 1940
M, 20
Shock, cyanosis, Probably struck in None, but sounds chest by stick used lungs clear faint to reapply machine belt Pressed against wall Shocked, faint heart Presystolie mitral by mad bull bruit noted 3 years sounds, systolic murmur after injury Stepped on by horse "Winded," systolic Same, but less in tense a year later bruit and thrill
8. Cameron 1942 9. Van Eaalte 1946
M, 35
Fell from scaffold
M, 20
Struck by 5 gallon can of gasoline
10. Arenberg 1943 (Case 12)
M, 54
Struck in chest by swinging draft of castor beans 500 lbs. in weight
Not definitely stated Blowing systolic and late diastolie at apex
11. Arenberg 1943 (Case 24)
M, 53
Fell 28 feet into hold of ship
12. Arenberg 1943 (Case 25)
M, 60
Struck in chest by 100 lb. bag of coffee
Fractured ribs ; sev Systolic eral hours follow ing injury devel oped dyspnea, cya nosis, and auricular fibrillation Blowing systolic Resumed work murmur heard over entire chest
13. Rodriguez and Nido 1961
M, 40
Telephone pole fell on chest
Shock ( B P 70/50), Grade I I I systolic murmur
Same
14. Case 1 1963
M, 7
Struck by automobile
Shock, unconscious ness, multiple rib fractures, hemopneumothorax
Blowing systolic and late diastolie
15. Case 2 1963
M, 19
Motorcycle collision with automobile
Shock; rigid abdo men; systolic mur-
Systolic at apex
M, 30
Congestive failure noted at 10 days Drove to hospital on bicycle carrying can; short of breath, developed frank congestive failure
and thrill (18 months later)
Loud systolic bruit in mitral area High pitched systolic and soft presystolie at apex
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II
Fractured rib
DIAGNOSIS
COURSE
MS
18 mo. later, progressive deteriora tion
MS
1 yr. later did desk work
Ruptured spleen MS
Lived 22 yr. Autopsy : scar in ven tricular wall extending into valve
—
Died % hr. after reaching the hos pital, 1 hr. after injury. Autopsy : ruptured papillary muscle
MS and M I
Improved to where he could under take light work 3 years later
Enlarging heart size
Indefinite
Enlarged heart at 10 days
Myocardial injury M I or rupt. I V S simulating coronary thrombosis — MI
— Increased heart size
"Compatible with mitral vitium"
Died 26 hr. later. Autopsy: rup tured papillary muscle
MI
Improved to where he eould take light exercise a year later Improved 3 yr. later, murmur still present but less intense Improved and doing sedentary work a year later
Enlarged heart noted Auricular at 10 weeks after injury
fibrillation
MI
Poorly compensated on digitalis one year later
Auricular
fibrillation
MI
Poorly compensated on digitalis one year later
"Negative"
High voltage, slur ring QRS complexes and marked left axis (6 months after injury)
MI
Unable to work day following in jury, developed progressive dysp nea, not able to work 6 months later
Fractured ribs
LBBB 1st degree A-V block 1st Acute ant. 2nd MI Developed L V H and L A H pattern
MI
Improved at 4 weeks on digitalis; follow-up not given
MI
Improved on digitalis; defect re paired utilizing cardiopulmonary bypass. P a t h . : valve torn from annulus Cardiac arrest during anesthesia induction. Autopsy: ruptured papillary muscle
Enlarging heart
Enlarging heart and increased vascular markings
Right heart strain MI pattern developed Ruptured spleen and kidney over 10 hour period
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was usually able to compensate for his injury; thereafter, the course was one of valvular heart disease. This is in marked contrast to cases of papillary mus cle rupture occurring in association with myocardial infarction where pro gressive deterioration and early death is the rule. 24 An explanation may be found in the lack of ischémie myocardial damage in the former, but one may speculate that the extent of injury in the presented series may be significantly less than in the cases associated with infarction and that, when comparable damage is present, rapid deterioration and death will occur. This was the situation in Case 2. X-ray examinations are valuable for comparison of initial to later heart size and for graphically demonstrating pulmonary vascular congestion and edema. Electrocardiograms are invariably abnormal but the pattern is non specific. The ultimate treatment is surgical repair of the defect. Frequently such treatment may be carried out as an elective procedure, the patient's cardiac status being maintained with digitalis and other measures while he recovers from his other injuries. Emergency cardiopulmonary bypass is within the realm of possibility and should be utilized in those circumstances where it may be life saving.
SUMMARY
The eases of 2 patients with mitral valve disease from blunt trauma are pre sented. Cardiac catheterization and cineangiocardiography were performed in one and the defect was corrected with the use of cardiopulmonary bypass. The second patient died 12 hours following his injury during induction of anesthesia for exploratory thoracotomy. The English literature is surveyed and a total of 18 cases of mitral valve disease from trauma are noted. An analysis of the col lected series is made. We are indebted to Drs. Leonard Scherlis and Eobert Singleton of the Department of Medicine, Section of Cardiology, University of Maryland School of Medicine, and Dr. Elliott Michaelson, Thoracic Surgeon Attending Lutheran Hospital, Baltimore, Md. REFERENCES 1. Watson, J . H., and Bartholomae, W. M. : Cardiac Injury Due to Nonpenetrating Chest Trauma, Ann. I n t . Med. 52: 871, 1960. 2. Sigler, L. H . : Traumatic Injury of the Heart. Incidence of I t s Occurrence in Forty-two Cases of Severe Accidental Bodily Injury, Am. Heart J . 30: 459, 1945. 3. Campbell, G. S., Vernier, B., and Lillehei, C. W . : Traumatic Ventricular Septal Defect: Beport of Two Cases, J . THORACIC SUKG. 37: 496, 1959.
4. Spurny, O. M., and Hara, M. : Bupture of the Aortic Valve Due to Strain, Am. J . Cardiol. 8: 125, 1961. 5. Parmley, L. F., Manion, W. C , and Mattingly, T. W. : Nonpenetrating Traumatic Injury of the Heart, Circulation 18: 371, 1958. 6. Kissane, B. W., Tidier, B. S., and Koons, B. A . : Electrocardiographic Changes Follow ing External Chest Injury to Dogs, Ann. I n t . Med. 1 1 : 907, 1937. 7. Bright, E . F . , and Beck, C. S.: Nonpenetrating Wounds of the H e a r t : A Clinical and Experimental Study, Am. Heart J . 10: 293, 1935. 8. Barie, E. : Becherches sur les ruptures valvulares du coeur, Bev. de Med. 1: 132, 1881. 9. Howard, C. P . : Aortic Insufficiency Due to Bupture by Strain of a Normal Aortic Valve, Canad. M. A. J . 19: 12, 1928.
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10. Barber, H., and Osborn, G. R. : A Case of Mitral Stenosis, the Result of Trauma, Guy's Hosp. Rep. 87: 510, 1937. 11. Allbutt, C. : On Overwork and Strain of the Heart and Aorta, Tr. Clin. Soc. London 6: 101, 1873. 12. Glendy, R. E., and White, P . D. : Nonpenetrating Wound of Heart. Rupture of Papil lary Muscle and Contusion of Heart Resulting From External Violence. Case Re port, Am. Heart J . 1 1 : 366, 1936. 13. Payne, W. C , and Hardy, H. H., J r . : Traumatic Rupture of the Papillary Muscles of the Mitral Valve, New Orleans M. & S. J . 89: 373, 1937. 14. Warberg, E.: Subacute and Chronic Pericardial and Myocardial Lesions Due to Nonpenetrating Traumatic Injuries: A Clinical Study, edited by Humphrey Milford, London, 1938, Oxford University Press. 15. Anderson, R. G. : Nonpenetrating Injuries of the Heart, Brit. H. J . 2: 307, 1940. 16. Cameron, R. A. (Cited by Barber, H.) : The Effects of Trauma, Direct and Indirect, on the Heart, Quart. J . Med. 13: 137, 1944. 17. Van Raalte, H. G. S.: Traumatic Rupture of Cardiac Valve, Indust. Med. 15: 436, 1946. 18. Arenberg, H . : Traumatic Heart Disease: Clinical Study of 250 Cases of Nonpenetrating Chest Injuries and Their Relation to Cardiac Disability, Ann. Int. Med. 19: 326, 1943. 19. Rodriguez, R. C , and Nido, R. C.: Traumatic Rupture of the Mitral Valve: Report of a Case, Bol. asoc. med. Puerto Rico 5 3 : 16, 1961. 20. Gibson, G. A.: System of Medicine, edited by Allbutt and Rolleston, 6: 381, 1909. 21. Heimann, M.: Ueber einen Fall von Endocarditis Mitralis Traumatica, Inaug. Dissert., Berlin, J u n e 5, 1896. Cited by Warneld, L. M. : Injuries to the Heart and Aorta, Wisconsin M. J . 32: 688, 1933. 22. Adams, A. (Cited by White) : Ueber die Traumatischen Veränderungen gesunder Klappen des Herzens, Ztschr. f. Kreislaufforsch. 19: 313, 1927. 23. White, P. D., and Glendy, R. E. : Trauma and Disease, edited by L. Brahdy and S. Kahn, Philadelphia, Pa., 1937, Lea & Febiger. 24. Craddock, W. L., and Mahe, G. A.: Rupture of Papillary Muscle of Heart Following Myocardial Infarction, J . A. M. A. 151: 884, 1953.