‘“I
FIG. 1. Chest X-ray film prior to penicardial window shows marked cardiac enlargment with globular configuration suggesting large penicardial effusion. Note the absence of the
vascular engorgelnent in the lung fields.
amenable
to preparation
than
is that
of the
long-haired dog. The tuberculin syringe is more readilyavailable
to
the
clinician
than
is
a
laboratory
blood-collecting
tube.
Finally,
the
minimum
steps
required
with
the
syringe
method
would
reduce
sampling errors.MAJ
PAULB.
JENNINGS,VC,
USA
CPT
ROBERT S. DIxON,VC,
USA
MARY
K.
MCCARTHY,M.Sc.
PAMELA
R.
METTLERMadigan Army Medical Center
Tacoma, Washington
Supported by the Clinical Research Service, Madigan
Army Medical Center, Tacoma, Washington.
ADDRESS FOR REPRINTS: (P.B.J.) Clinical Research Service, Box 99, Madigan Army Medical Center, Tacoma, Washington 98431.
REFERENCES
1. Fischer GW, Crumrine MH, Jennings PB: Experimental
Esclzcrichia co!i sepsis in rabbits.
J
Pediatr 85:117, 1974.2. Jennings PB, Crumrine MH, Fischer GW, Cunningham TC: Small-sample blood culture method for identi-fication of bacteria in central arterial and pen-pheral blood. Appi Microbiol 27:297, 1974.
ACKNOWLEDGMENT
The authors wish to thank Nancy Whitten for her editorial assistance in manuscript preparation.
CASE REPORT
L. B. (UWH No. 684 090) had Ebstein’s anomaly
confirmed at age 6 weeks by cardiac catheterization. Because of progressive cyanosis and exercise intolerance, at the age of 13 years she underwent total repair of tricuspid valvulopasty and closure of atrial septal defect. Ten days after surgery, chest X-ray film and echocardiography showed moderate amount of penicardial effusion. Because she was asymptomatic she was discharged on the 18th postoperative
day without specific therapy. On subsequent outpatient visits, chest X-ray films showed progressive enlargement of the cardiac silhouette with clear lung fields (Fig. 1) and echocardiograms showed increasing penicardial effusion (Fig. 2).
Fourteen weeks after surgery she was readmitted to the hospital because of signs of cardiac tamponade. She denied any symptoms. Blood pressure at that time was 110/90 mm
Hg with 10 mm Hg paradox, respirations were 18 breaths per minute, and pulse 80 beats per minute. The skin was dusky. Lungs were clear to auscultation. Heart sounds were distant and there was a grade 2/6 pansystolic murmur at the lower left sternal border. The jugular veins were distended with
hepatojugular reflux. The liver was firm and palpable 5 cm below the right costal margin. There was moderate ascites. No peripheral edema was noted. Serosanguineous fluid
(
3,000 ml) was removed from the pericardial space and a window was made between the pericardial and the left pleural space because of the possibility of reaccumulation.The postoperative period was uneventful until four hours after the procedure when she developed a sinus tachycardia with a rate of 150 beats per minute and a blood pressure of
70/50 mm Hg. Temperature was 38.3 C. There was no
response to fluid replacement and the central venous pres-sure measured 31 cm HO.
Pericardial
Window
Complicated
by Acute
Congestive
Heart
Failure
in a Patient
With
Chronic
Pericardial
Effusion
Pericardial
effusion,
as part
of the
post-pericar-diotomy syndrome, appears in the early postoper-ative period and is generally benign andself-m’
Recently, a patient developed chronic pericar-dial effusion with cardiac tamponade after repair
of
Ebstein’s
anomaly.
Surgical
drainage
of
the
pericardial effusion resulted in acute cardiacfailure
and
death.
968
PERICARDIAL
WINDOW
FIG. 2. Echocardiogram from this patient before the pericardial window. It shows a wide echo-free space behind the left ventricular wall representing large amounts of pericardial fluid (rig/it).
Also there is a moderate amount of pericardial effusion anteriorly (left). AW, anterior wall;
Endo, endocardium; Epi, epicardium; PE, pericardial effusion.
Eleven hours postoperatively, she was again taken to surgery for an exploratory thoracotomy for possible hernia-tion of the heart through the window but no herniation was found. She was put on cardiopulmonary bypass to enable visualization of the tricuspid valve as a possible contributing source of cardiac failure. The valve ring was dilated with a degree of insufficiency not estimated to be severe. A
Carpen-tier ring was inserted to eliminate the tricuspid insufficiency.
Postoperatively she was maintained on cardiopulmonary
bypass because of poor cardiac function, but she died after two days.
An autopsy revealed niarkedly thickened pericardium (8 mni). The heart chambers were enlarged and the myocar-dium was flabby and pale. On microscopic examination, the pericardium showed dense, hyalinzed fibrous tissue with extensive zones of recent hemorrhage, chronic inflammatory cells, and granulation tissue (Fig. 3, top). Throughout the myocardium there were focal zones of fibrosis and diminu-tion in the size of the myocardial fibers (Fig. 3, bottom)
consistent with the changes seen in compression atrophy due to long-standing pericardial effusion and chronic constrictive
pericarditis.2
DISCUSSION
Post-pericardiotomy
syndrome
is a
well-recog-nized
complication
of
open
heart
surgery.
The
etiology is uncertain but an autioimmune theory has been strongly suggested. In theasympto-matic
individual,
treatment
is
not
usually
required. However, when the pericardial effusioninterferes
with
cardiac
function,
pericardiocen-tesis
should
be
performed.
Recently,
chronic
pericardial
effusion
with
cardiac
tamponade
was
described after open heart surgery and
pericar-diectomy
was
required
for
its successful
manage-ment.5
Dramatic
improvement
can
be
expected
following drainage, but occasionallyreaccumula-tion
occurs.
For
this
reason
pericardial
window
may be indicated.” Acute cardiac failure hasfollowed
pericardiectomy
in
patients
with
chronic
constrictive
pericarditis.7
‘It
has
been
suggested that chronic compression of the heart causes myocardial damage, and in some patientsirreversible
myocardial
changes
have
devel-oped.”’ In the study by Das et al., there was a10%
mortality
rate
immediately
following
pen-cardiectomy due to inadequate myocandialfunc-tion.
‘ ‘McPhail
et al.advocated
cardiac
catheter-ization
prior
to
surgery
for
selection
of patients
according
to
their
myocardial
function.’#{176} There
have
been
only
two
patients
reported
with
chronic
penicardial
effusion
who
have
demon-strated myocardial damage.2 In these two patientsthere
was
microscopic
evidence
of
myocardial
atrophy,
similar
to that
seen
in constrictive
pen-carditis,
but
in both
cases
the
penicardial
effusion
had
been
present
for
at least
ten
months.
In
oun
patient,
although
the
chest
X-ray
film
and
echocardiogram
showed
a large
amount
of
pericardial fluid, intervention was delayed because of the absence of clinical symptoms.Rapid
removal
of the
fluid
caused
acute
dilatation
of the
heart
which
had
already
undergone
at Viet Nam:AAP Sponsored on September 8, 2020
www.aappublications.org/news
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.--- -.
-FI;. 3. lop, Microscopic examination of the pericardiuni showing a zone of dense fibrosis
surrounded l)%’ granulation tissue with chronic inflanimatory cell infiltration and foci of recent hemorrhage (hematoxylin-eosin, X 250). Bottom, Microscopic section of the nlyOcardiulll
showing ilitense fiischinorrhagia indicating ischenuic damage of the myocardial fibers. Also mvocardial fibers are disrupted (heniatoxylin-basic fuschin )icric acid, X 400).
eration due to chronic compression over a
3#{189}-month
period.
Compression
myocardial
damage
was confirmed by postmortem examination.
Small chronic pericardial effusion does not
970 PERICARDIAL WINDOW
such
patients,
the
fluid
should
be
removed
without
delay
even
in
the
absence
of
clinical
symptoms and signs.Echocardiognam
is the
best
modality
to detect
penicardial
fluid.
By serial
postoperative
echocar-diographic examination, the amount ofpenicar-dial
effusion
can
easily
be
monitored
for
proper
management.
MadLion, Wisconsin
DAVID
B.
HERZOG, M.D.ENID
M.
GILBERT,M.B.B.S.
JAY
M.
LEVY, M.D.KYUNG
J.
CHUNG, M.D.Department
of Pediatrics,
University of Wisconsin
Medical
School
Supported in part by grant 133-3479 from the Research Committee Fund, University of Wisconsin Medical School. ADDRESS FOR REPRINTS: (K.J.C.) Department of Pedi-atrics, University of Wisconsin Hospitals, Center for Health Sciences, 1300 University Avenue, Madison, Wisconsin 53706.
REFERENCES
1. Drusin LM, Engle MA, Halstroin JWC, Schwartz MS:
The post pericardiotomy syndrome. N EngI
J
Med 272:597, 1965.2. Dines DE, Edwards JE, Burchell HB: Myocardial atrophy in constrictive pericarditis. Staff Meet Mayo Clin 33:93, 1958.
3. Roberst JT, Beck CS: The effect of chronic cardiac compression on the size of the heart muscle fibers. Am Heart
J
22:314, 1941.4. Engle MA, McCabie JC, Ebert PA, Zabriskie
J:
The postpericardiotomy syndrome and antiheart antibodies.
Circulation 49:401, 1974.
5. McCabie JC, Engle MA, Ebert PA: Chronic pericardial effusion requiring pericardiectomy in the post pen-candiotomy syndrome.
J
Thorac Cardiovasc Sung 67:814, 1974.6. Fredriksen RT, Cohen LS, Mullins CB: Penicandial windows or penicardiocentesis for penicardial
effu-sions. Am Heart
J
82:158, 1971.7. Viola AR: The influence of penicardiectoniy On the
hemodynamics of chronic constrictive penicarditis. Circulation 48:1038, 1973.
8. Simcha A, Taylor JFN: Constrictive penicarditis in childhood. Arch Dis Child 46:515, 1971.
9. Chambliss JR, Jaruszewski EJ, Brofman BL, et a!:
Chronic cardiac compression (chronic constrictive
penicarditis). Circulation 4:816, 1951.
10. McPhail JL, Sukumar IP, Vytilingam KI, et a!: Surgical
nianagement of constrictive penicarditis. J Thorac
Cardiovasc Sung 53:360, 1967.
11. Das PB, Gupta RP, Sukuniar IP, et a!: Pericardiectomy.
