Download Ventricular Septal Defect and Ventricular Aneurysm following

58 1
MEDlASTlNAL AND SUBCUTANEOUS EMPHYSEMA
increased rate of reabsomtion and relieves anv
pressure symptoms caused by ambient air.6 If this
fails to relieve the tension pneumomediastinum,
cervical mediastinotomy should be performed by
making incisions in the supraclavicular fossae posterior to the sternocleidomastoid muscles and in the
suprasternal notch. Tracheostomy under these circumstances has been advocated by some, since it
not only decompresses the mediastinum but also
decreases the intra-alveolar pressure and prevents
further escape of air into the mediastinum.
Although not present in this case, the occurrence
of pneumothorax as an additional complication
during an acute asthmatic attack should be suspected when there is a sudden intensification of dyspnea associated with chest pain, and absence of
breath sounds with hypenesonance to percussion
on physical examination. Clinical signs may be minimal and difficult to interpret because of hyperaeration. Confirmation of the suspected diagnosis by
x-ray is the most reliable method. The treatment
of pneumothorax is initially conservative. Bedrest,
oxygen mist, mild sedation, and specific medication
for the underlying asthma will usually produce a
successful outcome. If the pneumothorax is estimated to be more than 20 percent, or if it progresses,
then we advise closed tube thoracostomy. Careful
observation is required since further increase in
respiratory distress may herald the onset of tension
pneumothorax. The physical findings of pneumothorax coupled with tracheal deviation to the opposite side suggest this lethal development. Closed
tube thoracostomy to improve pulmonary function
should be performed as an emergency procedure.
Tracheostomy may be lifesaving if bronchospasm
cannot be relieved.
L
1 K ~ o r r ,G.A.: On emphysema of the neck caused by
violent coughing, Lancet, 1:16, 1850.
2 G r m s o ~ G.,
, AND ALTMAN,D.H.: Pneumomediastinum
as a complication of acute bronchial asthma, J. Florida
Med Assoc., 52:318, 1965.
K., ROE-IT, K., HAYWOOD,
3 MCGOVERN,J.P., OZKARAGOZ,
T.J., AND HENS=, A.E., JR.: Mediastinal and subcutaneous
emphysema complicating atopic asthma in infants and
children, Pediatrics, 27:951, 1961.
4 PAYNE, T.W., AND GEPPERT,L.J.: Mediastinal and subcutaneous emphysema complicating bronchial asthma in
a nine-year-old male, J. Allerg., 32:135, 1961.
5 JORCENSEN,
J.R., FALLIERS,C.J., AND BUKANTZ, S.C.:
Pneumothorax and mediastinal and subcutaneous emphysema in children with bronchial asthma, Pediatrics, 31:
824, 1963.
6 MACKLIN,M.T., AND M a a m , C.C.: Malignant interstital
emphysema of lungs and mediastinum as an important
occult complication in many respiratory diseases and
other conditions, Medicine, 23:281, 1944.
AND PETERS,
G.A.: Mediastinal emphysema
complicating acute asthma, Minn. Med., 50:341, 1967.
7 DINES,
D.E.,
Reprint requests: Dr. Kirsh, (27175 Outpatient Building,
The University of Michigan Medical Center, Ann Arbor,
Michigan 48104.
Ventricular Septal Defect and
Ventricular Aneurysm following
Myocardial Infarction*
Amuwatra L i m w a n , M.D.,
Bertram A. Glass, M.D.,F.C.C.P., and
Sydnql Jacobs, M.D.,F.C.C.P.
The exact incidence of both interventricular septal perforation and ventricular aneurysm subsequent to myocardial infarclion is little known. In the reviewed Literature there were only six attempts to repair both hterventricular septal perforation and ventricular aneurysm.
The longest survival was 24 months. Presented here is
a case of interventricnlar septal perforation and ventricular aneurysm complicating myocardial infarction
h which the patient has survived for more than two
years following surgical correction.
INTRODUC~ION
upture of the interventricular septum (IVSP)
subsequent to myocardial infarction was h t
observed at autopsy and described by Latham in
1945. Latham's findings are quoted in detail in an
article by Harrison and associates.' The first antemortem diagnosis was by Brum in 1923.2 Septal
infarction is relatively frequent, occurring in about
60 to 70 percent of all myocardial infarctions, but
septal perforation after myocardial infarction is
rare. The incidence of IVSP is reported by various
e ~their
authors, including Edrnondson an2 ~ o w i in
large series, as 1 to 2 percent of all myocardial
infarctions. The time of rupture after infarction
varies from less than 24 hours to 14 days with an
average of seven days. Survival after IVSP is less
than 24 hours to 13 days with an average of five
days. It has been noted that over 50 percent of
those with the lesion die within the first ~ e e k . ~ - ~
The first reported surgical repair of IVSP due to
myocardial infarction was by Cooley and associates
in 1957.7The patient survived 45 days after operation. Since then 17 attempts to close a ventricular
septal defect following myocardial infarction have
been reported, the longest survival being 2.5
years.*p9
R
"From the Departments of Medicine and Surgery, Touro
Infirmary, New Orleans, Louisiana.
CHEST, VOL. 57, NO. 6, JUNE 1970
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LIMSUWAN, GLASS AND JACOBS
Aneurysms are said to occur in 10 to 38 percent
of infarcted cases.lO.ll Ventricular aneurysms rarely
rupture; their lethal effects are the result of wasted
cardiac energy from paradoxic motion and comequent diminution of cardiac output.
The first attempt to repair a ventricular aneurysm
was made by Beck in 1944.Is He plicated the
attached pericardium along with a fascia lata graft
and reduced the size of the aneurysm. Unfortunately the patient died a few weeks later from empyema. Since then, excision of cardiac aneurysm
and ventriculoplasty have been successfully carried
out on a small number of patients in this country,
and on two patients in England.18-l6
In the reviewed literature there have been only
six attempts to repair both IVSP and ventricular
aneurysm: one in England, one in Canada, and
four in this c o ~ n t r y . The
~ ~ - longest
~~
time of survival was 24 months.
A 55-year-old white woman was brought to the emergency room of T o m Infirmary on September 7,1967 with
severe chest pains. Because of diffuse arteriosclerosis with
intermittent claudicntion in the left calf, aorticoiliac bifurcation graft and left femoral endarterectomy had been performed on March 21, 1967 and bilateral syrnpathectomy
on June 8,1967.
She was pale and sweating profusely; blood pressure
120/80, pulse 126; the cardiac rhythm was regular but
the apex beat could not be discerned. The heart sounds
were soft; a grade I systolic murmur was audible at the
left sternal edge in the fifth i n d space. The femoral
were clear. The jugular
pulses were normal and the 1venous pressure was slightly elevated. The liver and spleen
ware not palpable, and there was no e l w a d edema. No
abnormal neurologic signs were elidted.
The clinical diagnosis of myocardial infarction was confirmed by the electrocardiogram, which showed changes
due to a recent posterior myocardial infarction, with prominent Q waves in L2, La, and AVF, unusual S-T elevation
and T waves inversion in these leads and L1, V4, V5, V6
(Fig 1).
Blood examination showed hemoglobin 11.5 gm per 100
ml; wbc 10,500 with 51 percent neutrophile, 28 percent
lymphocyte, 20 percent monocyte and 1 percent eosinophile;
the SCOT was 55 units and LDH was 710. Treatment with
heparin was started immediately.
The following morning a grade IV pan-systolic murmur
was heard over the entire precordial area and rales were
heard at both lung bases. The blood pressure dropped to
90/60 mm Hg. A diagnosis of ruptured ventricular septum
following myocardial infarction with possible papillary
muscle infarction was made. Digitalis and m d u r i &
(Mercuhydrin) were administered intramuscularly. Her SCOT
was 210, LDH 870.
During the next few days her condition deteriorated.
On September 16, 1967 she was breathless on slight movement and coughed up blood-stained sputum. Rising pulse
rate, falling blood pressure, and apical gallop rhythm were
also noted, together with diffuse cardiac impulse, suggesting left ventricular aneurysm. The enzymatic test showed
SCOT 1040, LDH 1930. Rotating tourniquets were applied.
On September 29, 1967, right heart catheterization hydrogen inhalation was done via right medial antecubital
vein. The findings are shown in Table 1.
The hydrogen inhalation studies showed a rapid appearance of hydrogen when the catheter tip was in the right
ventricle, indicative of a left-t-right shunt at this level.
This was confirmed by oxygen saturations showing increase
at the level of the right ventricle. The pressure in the pulmonary wedge position was elevated; calculation of this
shunt revealed the pulmonary to systolic flow ratio to be
4:l.
Suspicion of infarction of papillary muscle prompted left
heart catheterization via right brachial artery on October 9,
1967, but the catheter could not be advanced past the
axillary area because of arterial spasm.
On October 25, 1967 supraventricular tachycardia with
ventricular premature beat (WC) occurred and was amtrolled with quinidine and adrenal cortical corticosteroids.
Surgical correction of the shunt was now regarded as the
only measure likely to interrupt the "intractable" congestive
heart failure.
The operation took place on November 2, 1967. The
heart-lung machine used in this case was bubble-oxygenated
system "De Wall type." Intracardiac heparin (75 mg) was
followed by cannulization of the right femoral artery and
attachment to a disposable oxygenator. Venous catheters
were then passed into the superior vena cava, inferior vena
Table 1-Hemodynamic
Data
-- -
OXYGEN
% Saturation
FIGURE
1. Electmcardiogram on admission showing recent
extensive posterior myocardial infarction.
Superior Vena Cava
&.A. (mid)
R.V. out
R.V. in
Pulmonary artery
Rt. pulm&ry artery
Lt. radial artew
53.0
52.5
83.7
76.5
83.9
84.1
93.3
RessGre
nun Hg
18/7 (13)
65/13-18
59/18
63/26 (wedge)
108/69
CHEST, VOL. 57, NO. 6, JUNE 1970
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VENTRICULAR SEPTAL DEFECT AND ANEURYSM
cava, and into the right auricle appendage through a stab
wound. The cavae were encircled with umbilical tapes to
be used to divert venous blood into the catheters, which
were in turn connected to the venous inlet of the oxygenator.
Then total cardiopulmonary bypass was started.
A right ventriculotomy was performed and a defect inferiorly and posteriorly measuring approximately 2 cm in
diameter was seen in the muscular portion of the interventricular septum. An area of infarcted muscle of the
posterior wall of the left ventricle adjacent to the ventricular
septum was seen to be exhibiting paradoxical motions. Its
width was 2 x 2.5 cm; its thickness was 0.5 cm as contrasted with 1.5 cm thickness of other portions of the
ventricular myocardium.
When the aneurysm on the posterior wall of the left
ventricle was incised, the septal defect was more clearly
visible and easier to repair through this opening than it was
through the right ventriculotomy. Heavy No. 1 cardiwascular silk was used to close the septal defect by passing
mattress sutures through the ventricular septum and then
through the wall of the ventricle so as to draw the septum
up against the ventricular wall and effectively close the
defect.
The left ventricle was closed in layers using a continuous
mattress suture No. 2 cardiovascular silk buttressed with
T d o n felt pledgets on either side of the closure. The
right ventriculotomy was closed using continuous 3-0 black
silk sutures reinforcing the suture line with two pledgets
of Teflon felt.
Following incision of the infarction and closure of both
left and right ventriculotomies, complete heart block occurred; two pacemaker wires were sutured into the lateral
aspect of the left ventricular myocardium and brought out
through the chest wall to be connected to an external
pacemaker. Regular rhythm at a rate of 80 to 90 beats per
minute and adequate blood pressure were maintained,
after which the use of the pump oxygenator was discontinued.
The chest was closed with 2 drains, placed into the
pericardium. Recovery proceeded uneventfully. Isoproterenol
(Isuprel) (0.2 mg in 100 rnl infusion) and assisted respiration with the Bird apparatus were needed in the immediate
postoperative period.
On the second postoperative day tracheostomy was done
to facilitate respiratory assistance. By the third day after
operation she had normal sinus rhythm without the aid of
the pacemaker and normal blood pressure without need
for Isuprel; the second chest tube was removed on this day;
the acem maker wires were removed the next day. On the
7th postoperative day, the tracheostomy tube was expelled
by cough and was not replaced. Thoracentesis was performed once; 1050 ml of straw-colored fluid was removed
from the left hemithorax. By the 20th postoperative day
she was ambulatory; and became an outpatient 27 days
after operation. She was last seen in our Clinic in March,
1969 when her condition was good.
DISCIJS~ION
Post-infarction perforation of the interventricular
septum occurs in about 1 to 2 percent of cases,
usually in the period 4 to 12 days post-infarction.
It should be suspected when a patient worsens
suddenly and is found to have a loud systolic
cardiac murmur. There may be acute pulmonary
edema, tachycardia, evidence of pulmonary hypertension, raised venous pressure, and gallop rhythm.
Harrison et all pointed out that the murmur is pansystolic and maximal between the left sternal edge
and the apex, unlike the murmur of congenital
ventricular septal defect, which is normally localized to the lower left sternal edge. The diagnosis
should be confirmed by cardiac catheterization because of the grave import of such a perforation; 50
percent of patients live no longer than seven day^.^-^
Barnard and Kemedy21 in 1965 concluded that
the optimal time for open heart closure of perforation was 3.5 to 6 months after infarction and rupture. However, Allen and WoodwarkO reported
15-month survival where repair of the defect was
performed on the 10th post-infarction day and 12
hours after rupture. They classified patients into
Group I (successful return to cardiac compensation
with medical treatment); Group I1 (significant improvement with medical therapy permitting elective
surgical repair at two to three months after rupture), and Group I11 (requiring immediate surgical
repair). Our case has some of the attributes of
Groups I1 and I11 and illustrates the value of
surgical repair optimally timed.
ACKNOWLEDGMENTS: W e wish to extend sincere appreciation to Dr. M e n Myer, Director of Cardiac Studies at
Touro Infirmary, to Dr. Paul Bagalman, Fellow in Cardiology
at Touro Infirmary, and to Dr. Dennis Rosenberg (Touro
Infirmary Thoracic Sur ery Service) for their help in saving
this patient's life and for making it possible to report this
case.
1 HARRISON,R.J., SWILLINGFORD,
J.P., ALL, G.T. AND
TEARE,D.: Perforation of the interventricular septum
after myocardial infarction, Brit. Med. J., 1:1066, 1961.
, Zur Diagnostik der erworbenon Rupture der
2 B R ~F.:
Kammer Scheidewand der Herzens, Wien. Arch. Int.
Med., 6:533, 1923.
3 EDMONSON,H.A. AND HONIE, H.J.: Hypertension and
cardiac rupture, Amer. Heurt J., 24719, 1942.
4 BOND,V.F., WELFARE,C.R., LIDE, T.N. AND MCMILLAN,
R.L.: Perforation of the interventricular septum following myocardial infarction, Ann. Int. Med., 38:706, 1952.
5 SW~UNBANK,
J.M.: Perforation of the interventricular
septum in myocardial infarction, Brit. Heart I., 21:562,
1959.
6 SANDERS,R.J., KERN, W.H. AND BLOUNT, S.G., JR.:
Perforation of the interventricular septum complicating
myocardial infarction, AM. Heart J., 51:736, 1956.
D.A.,
Y , BELMONTE,B.A., ZEIS, L.B. AND SCHNUR,
7 C~~LE
S.: Surgical repair of ruptured interventricular septum
following acute myocardial infarction, Surgery, 41:930,
1957.
8 PADHI, R.K., FLETCHER,
A.G., JR., DIM, F. SERVID,
L.M., MWALIK, G.S. AND MODY, S.M.S.: Closure of
ventricular septal defect following myocardial infarction,
Arch. Surg., 94:188, 1967.
9 ALLEN,P. AND WOODWARK,
G.: Surgical management of
post infarction ventricular septal defect, 1. Thorac.
CHEST, VOL. 57, NO. 6, JUNE 1970
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GOLDBERG AND MORl
Cardwu. Surg., 51:346, 1966.
10 BETACH,W.F.: Cardiac aneurysm with spontaneous rupture, A m . H e m I., 30:567, 1945.
11 SHRIKMAN,
M.D., FIELD, J. AND PEARCE,M.L.: Repair
of ruptured interventricular septum complicating acute
myocardial infarction, Arch. Int. Med., 103:140, 1959.
12 BECK, C.S.: Operation for aneurysm of the heart, Ann.
Surg., 120:34, 1946.
13 BAILEY,C.P., BOLTON,H.E., NICHOJS, H. AND GILMAN,
R.A.: Ventriculoplasty for cardiac aneurysm, 1. Thorac.
Surg., 3537, 1958.
14 COOLEY,D.A., HENLEY,W.S., AMAD, K.H. AND CHAPMAN,D.W.: Ventricular aneurysm following myocardial
infarction. Result of surgical treatment, Ann. Surg., 150:
595, 1959.
15 TELLING, M., AND WOOLER, G.H.: Excision of cardiac
aneurysm, Lancet,2:181, 1961.
16 COLLIS,J.L., RAISON,J.C.A., MACKINNON,
J. AND WHITTAKEFI, S.R.I.: Repair of acquired interventricular septal
defect following myocardial infarction, Lancet, 2:172,
1962.
17 TAYLOR,F.H., CITRON,D.S., ROBICSEK,
F. AND SANGER,
P.W.: Simultaneous repair of ventricular septal defect
and left ventricular aneurysm following myocardial infarction, Ann. Thorac. Surg., 1:72, 1965.
18 GREEN,L., OAJCLEY,
C.M., DAVIES,D.M. AND CLELAND,
W.P.: Successful repair of left ventricular aneurysm and
ventricular septal defect after indirect injury, Lancet,
2:984, 1965.
19 HEIMBECKER,R.O., CHEN, C., HAMILTON, N. AND
MURRAY,D.W.G.: Surgery for massive myocardial infarction: An experimental study of emergency infarctectomy, Surgety, 61:51, 1967.
20 DAICOFF, G. AND RHODES, M.L.: Surgical repair of
ventricular septal rupture and ventricular aneurysm,
JAMA, 203:457,1968.
21 BARNARD,P.M., AND KENNEDY,J.H.: Post-infarction
32:276, 1985.
ventricular septal defect, Cir-n,
Re rint requests: Dr. Lirnsuwan, Departments of Medicine
an8 Hygiene, Tulane University School of Medicine, New
Orleans, Louisiana 70112.
Multiple Myeloma with Isolated
Visceral (Epicardial) Involvement and
Cardiac Tamponade*
Emanuel Goldberg, M.D., F.C.C.P. and Ken Mori, M.D.
A case of multiple myeloma with isolated visceral involvement of the epicardium associated with pericardial
effusion and tamponade is reported. No simfiar cases
are found in the literature. The pathogenesis of multiple
myeloma in general and isolated visceral involvement
in particular, remains obscure.
M u l t i p l e myeloma is known to present with
various clinical manifestations and many
modes of organ involvement. Although there are
'From the Departments of Medicine (Dr. Goldberg) and
Patholo (Dr. Mori) Beth Israel Medical Center, New York,
New YO%.
sporadic case reports of cardiac involvement, no
one was associated with s i g d c a n t clinical cardiovascular manifestations. In the patient presented,
pericardial effusion and tamponade were prominent
findings and myelomatous involvement of the epicardium was an unexpected finding at autopsy.
The only extraskeletal myelomatous involvement
in this case was the epicardial lesion.
A 66-year-old Negro woman was admitted for the first
time on January 7, 1967, with severe dyspnea, anemia, and
an enlarged right hilurn on chest x-ray of three weeks' duration. Her past history included "asthma" for 15 years and
a hospital admission 2% years previously for bilateral deep
venous thrombophlebitis of the lower extremities and joint
effusions of both knees. Symptoms at that time responded
to bed rest and anticoagulation. Total protein on the
previous hospitalization was normal and the RAI uptake
was 19 percent. There was no history of heart disease or
hypertension.
Physical examination on January 7, 1967, disclosed a blood
pressure of 150/74, pulse 92 beats per minute, temperature
98 F, respiration 22 per minute. The lungs were clear, but
the neck veins were distended. A grade II/VI systolic
murmur was heard at the apex. No abdominal organs or
masses were palpable and no adenopathy was noted. The
thyroid was unremarkable.
Venous pressure was 220 mm of water. No endpoint was
obtainable for the circulation time. The electrocardiogram
demonstrated a peaked P wave in leads 11, 111, and AVF,
and nonspecific ST and T wave changes. The white blood
cell count was 7,50O/mm3 with a shift to the left. Hemoglobin was 8.0 gm/100 rnl., hernatocrit 22 percent, and
platelets 50,000 per mm3. Urine was negative except for
2+ albumin. No Bence Jones protein was detected in the
urine. The total protein was 12.6 grn/100 ml, albumin 2.9
gm/100 ml. Other admission chemistries were normal (fasting blood sugar, blood urea nitrogen, calcium, phosphorous,
alkaline phosphatase, and serum bilirubin). A sickle preparation was negative and a sputum culture showed Sheptococcus oiridans. On the chest x-ray examination there was
generalized cardiac enlargement, a prominent right hilum
and clear lung fields.
The patient was treated for congestive heart failure with
salt restriction, oxygen and diuretics. A bone marrow
examination on January 12, 1987, confirmed the diagnosis
of multiple myeloma and skull films were suggestive of
myelomatous involvement. On January 15, 1967, a ten day
course of melphalan (Alkeran) was started, packed red cell
transfusions were given and digitalis was administered.
The blood urea nitrogen increased to 58 mg/100 ml,
then to 84 mg/100 ml and serum calcium increased to
11.7 mg/100 ml. The protein bound iodine was found
to be 2.2 pg/100 ml. The PaCO, was 57 mm Hg, the
PaO, was 55 mm Hg, the pH 7.51 and the oxyhemoglobin
saturation 87 percent. The patient became stuporous on
January 15, 1967, and comatose on January 17, 1967.
Serum electrolytes on the 17th were C 0 2 content 34 mEq/
liter, chlorides 92 mEq/liter, sodium 137 rnEq/liter and
postassium 3.8 mEq/liter. Optic fundi exhibited papilledema
and spinal fluid opening pressure was 430 mrn Hg, closing
pressure 240 mm Hg. Spinal fluid glucose and protein were
normal and the results of microscopic examination was
CHEST, VOL. 57, NO. 6, JUNE 1970
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