Download Heart Failure Due to a Post-Traumatic Calcified Pericardial Hematoma

Case
Reports
Heart Failure Due to a
Post-Traumatic Calcified
Pericardial Hematoma
Amit H. Manhas, MD
Robert T. Martin, MD, FACC
George J. Reul, MD
Raymond F. Stainback, MD
Chest-wall trauma can produce bleeding into the pericardium and initiate a process of inflammation, calcification, and scarring that may eventually produce pericardial constriction.
Herein, we present an unusual case of a man who experienced chest trauma at age 16
years, and developed heart failure 40 years later secondary to a large, calcified pericardial
hematoma. During its prolonged genesis, the pericardial mass became deeply embedded
in the myocardium and produced evidence of both constrictive and restrictive cardiomyopathy. Despite attempted surgical resection, the lesion could not be completely removed,
nor could its hemodynamic impact be completely resolved. (Tex Heart Inst J 2008;35(3):
345-8)
Key words: Calcinosis/
complications/etiology;
cardiomyopathy, restrictive/
physiopathology/ultrasonography; echocardiography,
Doppler, pulsed; heart
injuries/complications/
pathology; hematoma/
complications/etiology;
pericarditis, constrictive/
diagnosis/etiology/physiopathology/radiography;
pericardium/physiology;
thoracic injuries/complications; time factors
From: Section of Cardiology (Dr. Manhas), Baylor College of Medicine, Houston,
Texas 77030; Ark-La-Tex
Cardiology, APMC (Dr. Martin), Shreveport, Louisiana
71135; and departments of
Cardiovascular Surgery (Dr.
Reul) and Adult Cardiology
(Dr. Stainback), Texas Heart
Institute at St. Luke’s Episcopal Hospital, Houston,
Texas 77030
Address for reprints:
Raymond F. Stainback, MD,
6624 Fannin, Suite 2480,
Houston, TX 77030
E-mail: [email protected]
© 2008 by the Texas Heart ®
Institute, Houston
Texas Heart Institute Journal
oth constrictive pericarditis and restrictive cardiomyopathy can produce heart
failure, often with a preserved left ventricular ejection fraction. In some cases,
constrictive and restrictive physiology may coexist. Differentiating these 2
heart failure mechanisms, although difficult, is important, because surgical intervention can cure constrictive pericardial disease. Therefore, numerous clinical, radiologic, and echocardiographic criteria have been defined to help distinguish between
these conditions.1 In some cases, however, as in constrictive–restrictive cardiomyopathy, classification and treatment planning may be particularly difficult. Herein, we
describe the case of a patient who survived severe chest trauma at age 16 years and developed symptoms of congestive heart failure 40 years later.
Case Report
A 58-year-old man was admitted to the hospital with progressive shortness of breath,
edema, and anorexia. Over 2 years, he had gradually developed symptoms of New
York Heart Association (NYHA) functional class III–IV congestive heart failure.
At age 16 years, he had incurred chest-wall trauma upon being thrown into a dashboard during an automobile accident. Immediately after that accident, he had required
no medical intervention. Later that year, however, he developed volume overload and
failure to thrive. Physical examination revealed massive hepatomegaly, peripheral
edema, and a large right-sided pleural effusion. After a steroid regimen proved unsuccessful, pleural decortication and a pericardiectomy were performed. The right lung
was atelectatic and rubbery. During pericardial stripping, the moderately thickened,
heavily calcified pericardium adhered to the myocardium. Calcium plaques were embedded in the myocardium and could not be completely removed. After surgery, the
patient gradually recovered and had a normal life.
After 40 years of good health, including vigorous exercise, the patient began to show
symptoms of heart failure. He complained of decreasing exercise tolerance, progressive
lower-extremity edema, a persistent dry cough, and decreased appetite. He did not respond to diuretic or asthma medications prescribed by his local physicians. Noninvasive imaging, performed by his cardiologists, showed a large pericardial mass and
possible constrictive pericarditis. When the patient was referred to our institution, he
was in NYHA functional class III–IV and was no longer able to work.
Physical examination revealed a thin man who appeared chronically ill and fatigued. He had a blood pressure of 115/70 mmHg (pulsus paradoxus, 5–10 mmHg),
a heart rate of 98 beats/min, and unlabored respirations at 18 per minute. His jugular
venous pressure was elevated to 6 cm at 30 degrees with a prominent A wave. The apical impulse was visible and easily palpable at the left nipple. The S1 and S2 sounds were
Calcified Pericardial Hematoma
345
normal, without physiologic splitting; there was no precordial knock and no S3 or S4 sound. The right side of
his thorax was slightly smaller than the left. His lungs
were clear to auscultation, and excursion was decreased
on the right side. His abdomen was soft with a slight
fluid wave. The liver span was increased, with obvious
hepatojugular reflux, and the spleen tip was palpable.
The lower extremities had 3+ pitting edema bilaterally
to the knees.
Echocardiography (Figs. 1A and 1B) showed a large
intrapericardial mass centered in the left atrioventricular
groove, mild biatrial enlargement, a small left ventricle
with an end-diastolic diameter of 2.4 cm, and normal
overall systolic function (left ventricular ejection fraction, 0.50). The intrapericardial mass produced a notable systolic and diastolic deformity of the adjacent
ventricle, and a pronounced ventricular diastolic septal bounce was noted. The mitral inflow pattern, illustrated by pulsed-wave Doppler methods, was restrictive
(Fig. 1C) and showed no significant respiratory variation (Fig. 1D). Cardiac magnetic resonance imaging
(MRI) (Fig. 2) confirmed the presence of a large (14 ×
10 × 9-cm), complex, crescent-shaped intrapericardial mass inferolateral to the left ventricle. The mass appeared to be extensively calcified, with both soft-tissue
and proteinaceous-fluid components. Left- and rightsided heart catheterization showed normal coronary arteries and only minimal ventricular discordance of peak
systolic pressures during respiration (Fig. 3). Moderate
pulmonary hypertension was accompanied by a severely elevated right atrial pressure and equalized diastolic
pressures (in mmHg): right atrial, 19; right ventricular, 46/19; pulmonary artery, 47/18; pulmonary capillary wedge, 22; left ventricular systolic, 103; and left
ventricular end-diastolic, 22. The extensive, complex,
partially calcified intrapericardial mass invaded the adjacent epicardium, producing a mixed constrictive–restrictive physiology.
Although we thought that restrictive cardiomyopathy
was playing a substantial role in the patient’s condition,
we believed that excision of the large mass might lead
to palliation by relieving the pericardial constriction.
A
B
C
D
Fig. 1 A) Apical 4-chamber echocardiographic view shows the pericardial mass deforming and restricting the left ventricle. B) Parasternal long-axis echocardiographic view shows the pericardial mass impinging on the posterior lateral wall of the left ventricle. C) Pulsedwave Doppler studies suggest a severely restrictive filling pattern, due to the early-to-late diastolic filling ratio of >2 and the reduced
deceleration time. D) Pulsed-wave Doppler studies failed to show the respiratory variation in flow across the mitral valve that is typically
seen in constrictive pericarditis.
Real-time
motion
are available
at texasheart.org/journal.
Click here
forimages
real-time
motion
image: Fig. 1A.
346
Calcified Pericardial Hematoma
Click here for real-time motion image: Fig. 1B.
Volume 35, Number 3, 2008
Fig. 2 Cardiac magnetic resonance imaging reveals a complex
retrocardiac mass with components of fluid and soft-tissue
density.
Real-time
image ismotion
available
at texasheart.org/journal.
Click heremotion
for real-time
image:
Fig. 2.
In the operating room, the mass appeared to be an old
calcified hematoma that was adhering to the myocardium (Figs. 4A and 4B). After resecting the mass, we attempted to dissect the adherent debris and calcification
from the epicardium. Much of the calcium was deeply embedded in the muscle, however, and could not be
completely excised. Pathologic examination of the mass
revealed benign soft tissue with xanthogranulomatous
inflammation, sclerosis, and associated old hemorrhage
and focal calcification.
After surgery, the patient continued to experience volume overload and minimally improved cardiac hemodynamics. Repeat echocardiography and MRI revealed
a persistent hollow shell or potential space in the area
of the previous mass. Repeat echocardiography of the
heart continued to show a prominent diastolic deformity where the mass had been located. The patient experienced persistent respiratory insufficiency and, after a
3-month hospitalization, died of multiorgan failure related to low cardiac output.
Discussion
Fig. 3 Pressure-tracing from the right and left ventricles shows a
slight discordance with respiration. This pattern is typically seen
in constrictive pericarditis, because the diminished pulmonary
capillary wedge pressure-to-left atrial pressure gradient results in
preferential right-sided filling during inspiration.
A
Chest trauma frequently causes bleeding into the pericardium. Researchers have found that blood injected
into the pericardium of experimental animals generally resolves without consequences. After trauma, however, the fibrinolytic and absorptive functions of the
pericardium are impaired, and adhesions may form between the pericardial layers.2 Fibrosis and calcification
of the pericardium may produce constrictive pericarditis, which is a well-known complication of blunt chest
trauma.3,4
Our patient had a large, organized pericardial hematoma due to such trauma. Although he underwent partial pericardial stripping 1 year after his initial injury,
the disease process was not arrested. This may be because he already had significant epicardial involvement,
and complete resection of the diseased tissue could not
be achieved. Given the duration of the disease process
B
Fig. 4 A) At surgery, the pericardium was found to be heavily calcified and closely adherent to the myocardium. B) Large, calcified
debris was removed from the pericardial space.
Texas Heart Institute Journal
Calcified Pericardial Hematoma
347
and the extent of epicardial involvement, he probably
experienced a self-perpetuating cycle of injury, bleeding,
and fibrocalcific reaction.
Post-traumatic formation of a large, organized, calcified hematoma is rare, but a few such lesions have been
described in the medical literature.5-11 In those patients,
the time from the initial injury to the clinical manifestation of constriction was sometimes prolonged. In
a literature review presented by Brown and Ivey,5 the
time from injury to surgery ranged from 3 to 20 years.
Remarkably, our patient had a 40-year period of clinical stability before his health deteriorated. This long latent period highlights the persistent, insidious nature of
the disease, which had progressed considerably before it
produced any clinical warning signs.
Our patient had a complex lesion with characteristics of both constrictive and restrictive disease.12,13 The
constrictive elements were equalization of diastolic pressures in all chambers, a pronounced septal bounce, and
a slight discordance of ventricular pressures during respiration. Restrictive elements included biatrial enlargement, elevated systolic pulmonary artery pressure, a
restrictive mitral inflow pattern, and minimal respiratory variation in mitral inflow. These findings portended the combined pericardial–myocardial nature of
this lesion, which was verified during surgery. Although
the bulk of the offending mass was removed, almost no
improvement was seen in the patient’s hemodynamic
performance. Therefore, patients with findings of both
constrictive and restrictive disease during the preoperative evaluation of pericardial-mass lesions may have an
incomplete clinical response to surgical resection. In
such patients, the prognosis seems especially grim, and
treatment options may be limited to palliation or cardiac transplantation.
348
Calcified Pericardial Hematoma
References
1. Asher CR, Klein AL. Diastolic heart failure: restrictive cardiomyopathy, constrictive pericarditis, and cardiac tamponade: clinical and echocardiographic evaluation. Cardiol Rev
2002;10(4):218-29.
2. Sbokos CG, Karayannacos PE, Kontaxis A, Kambylafkas J,
Skalkeas GD. Traumatic hemopericardium and chronic constrictive pericarditis. Ann Thorac Surg 1977;23(3):225-9.
3. Goldstein S, Yu PN. Constrictive pericarditis after blunt chest
trauma. Am Heart J 1965;69:544-50.
4. Gothman B, Johansson L, Silander T. Post-traumatic constrictive pericarditis. Acta Chir Scand 1963;125:77-80.
5. Brown DL, Ivey TD. Giant organized pericardial hematoma
producing constrictive pericarditis: a case report and review of
the literature. J Trauma 1996;41(3):558-60.
6. Campbell PG, De Belder MA, Hartley R. Pericardial constriction secondary to calcified intrapericardial haematoma.
Heart 2001;86(2):160.
7. Dunlap TE, Sorkin RP, Mori KW, Popat KD. Massive organized intrapericardial hematoma mimicking constrictive
pericarditis. Am Heart J 1982;104(6):1373-5.
8. Hartl WH, Kreuzer E, Reuschel-Janetschek E, Schmidt D,
Reichart B. Pericardial mass mimicking constrictive pericarditis. Ann Thorac Surg 1991;52(3):557-9.
9. Isaacs D, Stark P, Nichols C, Antevil J, Shabetai R. Post-traumatic pericardial calcification. J Thorac Imaging 2003;18(4):
250-3.
10. Leslie SJ, Brackenbury E, Spratt JC. Calcified mediastinal
haematoma: a rare case of cardiac constriction. Heart 2004;
90(8):846.
11. Taylor MW, Garber JC, Boswell WC, Boyd CR. Delayed
hemopericardium and associated pericardial mass after blunt
chest trauma. Am Surg 2003;69(4):343-5.
12. Goldstein JA. Cardiac tamponade, constrictive pericarditis,
and restrictive cardiomyopathy. Curr Probl Cardiol 2004;29
(9):503-67.
13. Hatle LK, Appleton CP, Popp RL. Differentiation of constrictive pericarditis and restrictive cardiomyopathy by Doppler
echocardiography. Circulation 1989;79(2):357-70.
Volume 35, Number 3, 2008