Early repair of traumatic ventricular septal defect

Early repair of traumatic ventricular septal defect Traumatic ventricular septal defect may present as an isolated injury following blunt chest trauma. Medical therapy is indicated in small defects. Defects 2 em. or larger usually lead to death or marked cardiac disability. Surgical repair can usually be done as an elective procedure with good results and a low mortality rate. However, with some patients early repair is necessary as a lifesaving measure. By using the approach through the apex of the heart, a better exposure and more secure repair is obtained without compromising a large portion of myocardium.

Thomas A. Clark, M.D.,* Francis H. Corcoran, M.D.,** William P. Baker, Ph.D., M.D., *** and Mitchell Mills, M.D., **** Bethesda, Md.

Bunt cardiac injury is a common problem. Approximately 150,000 cardiac injuries occur each year from automobile accidents alone. 1 Myocardial contusion is the most common of these injuries and is usually well tolerated, especially when primarily the right ventricle is involved. Rupture of the ventricle is almost always fatal. Rupture of the atrium, the ventricular septum, and various components of the valve mechanism may all result from blunt trauma and all have been successfully repaired." Fortunately, patients who live to reach the hospital will usually survive for a sufficient period to permit definitive diagnostic studies and a routine operative procedure. On occasion, the hemodynamic handicap of such injuries requires urgent diagnosis and immediate surgical intervention. From the Thoracic and Cardiovascular Surgery Service, Naval Hospital, National Naval Medical Center, Bethesda, Md. 20014. The opinions or assertions contained herein do not necessarily reflect the views of the Bureau of Medicine and Surgery of the Navy Department or the Naval Service at large. Received for publication June 25, 1973. 'Resident, Thoracic and Cardiovascular Surgery. "Director, Cardiac Catheterization Laboratory. ••• Head, Cardiovascular Division, Department of Internal Medicine. ····Chief, Thoracic and Cardiovascular Surgery.

One of the earliest case reports of traumatic ventricular septal defect was published 15 years ago when a 21-year-old sailor was brought to the National Naval Medical Center in severe cardiogenic shock following blunt chest trauma." He died 52 hours after admission in spite of intensive medical therapy. At autopsy, he had an isolated ventricular septal defect measuring 5.5 em. The purpose of our report is to present a similar patient who was recently operated upon successfully within 24 hours of injury. Case report An IS-year-old sailor sustained blunt anterior chest trauma in an automobile accident 12 hours prior to admission on Nov. 2, 1972. The patient was asymptomatic immediately after the accident but was admitted to a local hospital for observation. The physical examination at that time was within normal limits, with no evidence of fractured ribs or other injuries except for a small contusion on the left anterior chest wall over the apex of the heart and a soft Grade 2/6 holosystolic murmur heard along the left sternal border. On previous enlistment examinations no cardiac murmur was heard. During the following 12 hours of observation the patient began to have progressive respiratory insufficiency associated with hemoptysis, hypotension, and tachycardia. At that time he was transferred to Bethesda Naval Hospital in a state of severe pulmonary edema.

121

The Journal of

122

Clark et al.

Thoracic and Card iovascular Surgery

I

I

•

4'"

I

~

.. - .. .. .... ... ~

::::

I

....

L

,

.:

,

i~

'!i " .:

l:

, :1,;1"':g:

.,,,::, .

'Iii;;

"

, · ·" i "·

,

I:

v. ..

'II

'WilJI

".

I :;

:1 '!'1 I· .. ..

..

, Iii' .i', Yo

;; :!j:

, iV

...

" :;;

H

;;;

,

YO

,"

"

, ,

IA.

"

,,,

... , .. .. ..

.. .. " .

.t .

-t

:

,

. "... ....-..

-':1

I

.--

.,

'I '

., ii; I: i: i t: ,

J:

,, ,.

.

-

"

.-.... ...-

.:il

... I'

I,

,,"

IU

Yo'

I

K

.. "

<,;;

..

,

,

,

-

"

F

H!~ 'OJ .. .. I;E .. i!",',M i;' ;..IV

t:

,I,'

l

, ! ., .. '" - :h: II: .. ...,:

' I'

-

... .:i .. :;1

..

..

I· I

:1: ..

r,

,.;:

,"

..

L .. I

f-

'.

..

,

;j

--

I

...

I

;If:

-

III

I

\J

-

I

I

,

I

I

.:

"'"

I :

i

l ..

,

Fig. 1. Electrocardiogram 13 hours after the injury shows an extensive anterior myocardial infarction. Phy sical exam ination on admission revealed an alert but extremely pale , diaphoretic man in acute respiratory distre ss. His blood pressure was 90/60 mm. Hg in both arms with a heart rate of 150 beats per minute. Pertinent physical findings in addition to those already mentioned were limited to examination of the lung s and cardiovascula r sys tem. Aus cultation of the lungs revealed diffuse, wet rale s. Examination of the heart revealed the point of maximum impulse to be in the fifth intercostal space, in the midcl avicular line. A thrill was palpated over the left sterna l border in the third a nd fourth intercostal space s. The heart sounds were not audible due to a loud Grade 4/6 holosystolic murmur heard best a long the left stern al border, ra diating to the apex a nd to the ba se of the heart. Laboratory dat a were as follows on admission : The hematocrit value was 52 per cent; th e whi le blood count was 21,900 with a norm al differenti al ; electrolytes and urinalysis were with in normal limits; on 100 per cent o xygen and a volume respirator, Po , was 88 mm . Hg, Pco, was 35 mm. Hg , and pH was 7.36 with a 96 per cent saturation. An electrocardiogram (Fig. 1) showed an anterior mycardial infarction. A che st x-ray film on admiss ion revealed diffuse bilateral pulmonary infiltrates compatible with acute pulmonary edema. There was no cardiomegaly by x-ray study. On admission, the impression was that the patient had a tr aumatic ventricular septal defect with pulmonary edema. A trial of intensive medical therapy was sta rted, including digoxin, Isuprel,

diuretics, and respiratory control with a volume respirator. In spite of these measures, the patient's condition continued to deteriorate. Within 16 hours of the injury the blood pressure was 70/40 mm . Hg and the Po, on 100 per cent oxygen was 60 mm. Hg , Cardiac catheterization confirmed the initial impression of a large, low ventricular septal defect with a step-up in oxygen satura tion from the right atrium to the right ventricle (T able I) and a 4 : 1 ratio of pulmonary to system ic flow. The cardiac inde x was 2 L. per minute per square meter. Left ventricular function was poor, and an area of paradoxical motion was present at the apex. Six hours after admission , as a lifesaving measure, an exploratory lap arotomy was performed to rule out any intra-abdominal injury. The incision was e xtended into a medi an sternotomy, cardiopulmonary bypass was instituted, and a 6 em. laceration of the muscular interventricular septum was repaired with a Dacron patch. On entering the pericardium, we found 60 c.c. of fre sh blood without any evidence of rupture of the heart. The defect in the septum was appro ached through an apical incision which exposed both ventricular cavities and the laceration of the septum ( F ig. 2) . The Dacron patch was placed on the left ventricular side and the interrupted Teflon pledget sutures were brought out on the righ t ventricular side, incorporating the inferior septal repair with repair of the apical ventriculotomy incision. The patient tolerated the procedure without complication, and his post-

Volume 67

Traumatic ventricular septal defect

Number 1

12 3

January, 1974

Fig. 2. Operative exposure as seen through the apical incision with the arrow pointing to the traumatic ventricular septal defect.

Table. I. Cardiac catheterization data

I

Before operation " Oxygen saturation (% )

Aorta Left ventricle Pulmonary artery Right ventricle

96 96 88 93

Right atrium

64

Superior vena cava Systemic flow index (L./min./sq. M.) Pulmonary flow index (L. /min./sq. M .) Qp/Qs Hydrogen inhalation

65

Pressure (mm . Hg )

80/60 (70) 80/12 EDP 38/20 (30 ) 38/8 EDP a-8 v-6 (4)

Two months after operation Ox ygen saturation (%)

I

Pressure (mm. Hg )

90/65 (75) 90/18 EDP 20/8 (13 ) 20/5 EDP a-5 (3) v-4

99 79 78 81 73

2.0

4.2

8.0 4/1 Not done

4.2 1/ 1 9 sec. appearance time in pulmonary artery

Legend : EDP . End-d iastolic pressure. QpJQs. Pulmonary-systemi c flow ratio . Mean values are in parenth eses. ·On volume-limited respiratory assistance .

operative course was characterized by rapid improvement of cardiac and respiratory function with discontinuance of all supportive measures within 48 hours of operation. Two months postoperatively, the patient had resumed regular activities without limitation and was taking no medications. Follow-up cardiac catheterization (Table I) showed no residual ventricular septal defect. There was a smaIl area of akinesia at the apex and a left ventricular enddiastolic pressure of 18 mm, Hg. The coronary arteries were normal. Chest x-ray films showed

a slight increase in cardiac size, and electrocardiograms continued to show evidence of an anterior myocardial infarction.

Discussion

In 1847 Hewett - first described the pathological diagnosis of traumatic ventricular septal defect in a 5-year-old boy who died shortly after being run over by a horse carriage. In 1959, Campbell" reported the first successful repair of a traumatic ventricular

The Journal of

124

Clark et al.

Thoracic and Cardiovascular Surgery

septal defect, with a dog's lungs used for an oxygenator. Since that time there have been reports of 12 patients, including this one, who have had repair of a traumatic ventricular septal defect; 5 of them had persistent intracardiac shunts after operation. 1 There are only two previous reports of repair within 2 weeks of injury, both patients having persistent left-to-right shunts postoperatively.' The symptoms of this lesion cover a spectrum from minimal exertional dyspnea to severe, progressive shock and pulmonary edema leading to early death. Two thirds of patients have no evidence of rib or sternal fracture on chest x-ray." In many cases, the x-ray films do show evidence of pulmonary congestion and cardiomegaly. The electrocardiogram may be an important indicator of myocardial injury. Such findings usually consist of changes in voltage, some shift of the electrial axis, and S-T changes consistent with a myocardial infarction.' Atrial and ventricular arrhythmias are infrequent and conduction defects are rare since the lower muscular septum is principally involved. S The typical holosystolic murmur along the left sternal border is an important clue to diagnosis of ventricular septal defect but may not appear for days or even months after injury." Cardiac catheterization is necessary for definitive diagnosis. The therapy selected depends primarily on how well the patient tolerates the insult. Medical therapy will frequently relieve symptoms of congestive failure. A period of observation is of value since there have been reports of spontaneous closure of traumatic ventricular septal defects months after injury." Kay" showed in animals' that defects less than 12 mm. often close spontaneously. However, in a series of 10 patients who were treated medically, 5 died, all of whom had defects larger than 2 em.' Surgical repair is indicated in any patient who presents with progressive heart failure or pulmonary hypertension. The surgical approach used in this case

has been previously reported by Crosby." It allowed excellent exposure of the defect and both ventricular chambers without compromising a large portion of the myocardium. By placing the Dacron patch on the left side of the septum and tying the interrupted pledget sutures on the right ventricular side, we protected the repair from disruption by the higher left ventricular pressures. The apical approach should be used only for the emergency operation and not for the elective repair of more fibrous chronic ventricular septal defects. REFERENCES

2

3

4 5

6

7

8

9

10

Scheinman, J. I., Kelminson, L. L., Vogel, J. H. K., and Rosenkrantz, 1. G.: Early Repair of Ventricular Septal Defect Due to Nonpenetrating Trauma, 1. Pediatr. 74: 406, 1969. Borgedain, W., Carpathios, 1., Van Suu, D., and Moots, M. F.: Traumatic Rupture of the Myocardium: Successful Surgical Repair. J. A M. A 197: 1102, 1966. Cary, F. H., Hurst, J. W., and Arentzen, W. R.: Acquired Interventricular Septal Defect Secondary to Trauma, N. Eng!. J. Med. 258: 355, 1958. Hewett, P.: Rupture of the Septum Ventriculorum, London Med. 4: 870, 1847. Campbell, G. S., Vernier, R., Varco, R. L., and Lillehei, C. W.: Traumatic VSD: Report of Two Cases, 1. THORAC. CARDIOVASC. SURG. 37: 496, 1959. Pierce, E. C., Dabbs, C. H., and Rawson, F.: Isolated Rupture of the Ventricular Septum Due to Nonpenetrating Trauma, Arch. Surg. 77: 87, 1958. Miller, D. R., Crockett, J. E., and Potter, C. A: Traumatic Interventricular Septal Defect: A Review and Report of Two Cases, Ann. Surg. 55: 72, 1962. Rosenthal, A., Parisi, L. F., and Nador, A. S.: Isolated Interventricular Septal Defect Due to Nonpenetrating Trauma, N. Eng!. J. Med. 283: 338, 1970. Kay, 1. R., Thomas, V., and Blalock, A.: The Experimental Production of High Interventricular Septal Defects, Surg. Gyneco!. Obstet. 96: 529, 1953. Crosby, I. K., Pugh, D., and Reed, W. A: Early Resection of Massive Infarct and Replacement of Interventricular Septum, J. THORAC. CARDIOVASC. SURG. 64: 629, 1972.