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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3715_Библиотеки_им_академика_М_И_Перельмана
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15 The Operation: Radical Pericardiectomy via Modied Left Anterolateral…
• Calcic patches, plagues and bars are divided with rongeurs or using a thick
hemostat and are removed piecemeal avoiding injury to the underlying vessels chambers and phrenic nerve. Isolated calcic deposits burrowing deeply
into the ventricular muscle may be safely left in situ (Figs. 15.9a, b, and
15.10a, b).
Fig. 15.9 (a, b) Inferiorly,
the pericardium overlying
the diaphragmatic
pericardium is dissected
from the diaphragmatic
muscle and diaphragmatic
surface of the right
ventricle and excised
in toto
a
b
15.2 Useful Maneuvers to Facilitate Pericardiectomy Via Left Anterolateral…
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263
Fig. 15.10 (a, b)
Intraoperative pictures of
the decorticated heart with
an intact phrenic pedicle
and the excised
pericardium
a
b
15.2 Useful Maneuvers toFacilitate Pericardiectomy Via
Left Anterolateral Thoracotomy
• In individuals with massive pleural effusion and ascites, it is the author’s practice
to place an indwelling peritoneal dialysis catheter in the peritoneal cavity before
thoracotomy. An intercostal chest drain on the right side in patients with massive
right-sided pleural effusion facilitates placement of the patient in left lateral position without compromising ventilation. An indwelling peritoneal dialysis catheter helps in removal of the third space uid after completion of the pericardiectomy.
This minimizes autotransfusion after the procedure is over, thereby preventing
cardiac dilation and low cardiac output in the perioperative period. The general
belief of acute sudden circulatory collapse following sudden decompression of
the third space has been unfounded in our experience.
Two ventricular pacing wires are placed as a routine. Two intercostal drains are
placed, and wound is closed in layers.
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15 The Operation: Radical Pericardiectomy via Modied Left Anterolateral…
References
1. Chowdhury UK, Seth S, Reddy SM.Pericardiectomy for chronic constrictive pericarditis. J
Operative Tech Thorac Cardiovasc Surg. 2008;13:14–25.
2. Chowdhury UK, Narang R, Malhotra P, Choudhury M, Choudhury A, Singh SP.Indications,
timing and techniques of radical pericardiectomy via modied left anterolateral thoracotomy
(UKC’s modication) and total pericardiectomy via median sternotomy (Holman and Willett)
without cardiopulmonary bypass. J Prac Cardiovasc Sci. 2016;2:17–27.
3. Chowdhury UK, George N, Singh S, Sankhyan LK, Sengupta S, Ray R, Vaswani P, etal.
Total pericardiectomy via modied left anterolateral thoracotomy without cardiopulmonary
bypass: a video presentation. Ann Thorac Surg. 2021;112:1483–92. https://doi.org/10.1016/j.
athoracsur.2020.10.045.
4. Chowdhury UK, George N, Sankhyan LK, Singh S, Chauhan A, Gupta A, Chowdhury
P.Radical pericardiectomy via left anterolateral thoracotomy (UKC’s modication): a video
presentation. Int Med. 2019;1(4):246.
5. Sankhyan LK, George N, Sushamagayatri B, Chauhan A, Avneesh S, Jha A, Malik V,
Chowdhury UK.Total pericardiectomy via modied left anterolateral thoracotomy without
cardiopulmonary bypass (UKC’s modication): a video presentation. J Clin Cardiol Cardiovasc
Interv. 2020;3(13) https://doi.org/10.31579/2641- 0419/108.
Chapter 16
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Calcic Constrictive Pericarditis
Chronic calcic constrictive pericarditis is a clinical-haemodynamic syndrome of
multifactorial aetiology. It is the end stage of a long-standing, chronic inammatory
and non-inammatory disease process, causing either localized or circumferential
obstruction to the diastolic lling of the cardiac chambers, leading to cardiac failure
[1–3, 7–10, 22–24, 44–48, 59, 94–97, 101, 102, 112, 127, 139].
The calcied pericardium may be of a ‘ring-like’, ‘patchy block-like’ or circumferential ‘cocoon-like’ conguration. It is usually accompanied by a rigid, nonpliable, pericardial shell encasing the heart, insulating the cardiac chambers from
variations in intrathoracic pressure during the respiratory cycle.
16.1 Incidence
The frequency of calcic constrictive pericarditis varies greatly depending on the
patient population studied, the aetiology of constrictive pericarditis, and the year of
study [1, 22–33, 44–46, 54, 60–62, 94–97, 101, 127, 139].
In early reports from the US, calcication was observed in approximately 50%
of cases of constrictive pericarditis [23–25, 60–63, 113, 139–142]. When the cause
was predominantly tuberculous, calcied disease occurred in as many as 76% of
cases [2]. In a Mayo Clinic study of 231 patients from 1936 through 1982, in which
idiopathic constriction accounted for 73% of cases, the incidence of calcic disease
was 40% [94, 95]. In a 1959 study, Gimlette and associates documented pericardial
calcication in 90% of all cases [53].
In a series of 106 patients with idiopathic or post irradiation constrictive pericarditis, Cameron and colleagues reported 5% incidence of calcic pericarditis [25]. In
a more recent European cohort, Rienmuller and colleagues reported 53% incidence
of calcic constrictive pericarditis, in which idiopathic constrictive pericarditis
accounted for 50% of cases [121, 122].
Ltd. 2023
U. K. Chowdhury, L. K. Sankhyan, Surgical Treatment of Chronic Constrictive
Pericarditis, https://doi.org/10.1007/978-981-99-5808-5_16
265© The Author(s), under exclusive license to Springer Nature Singapore Pte
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The incidence of pericardial calcication in tubercular constrictive pericarditis
ranges from 5% to 76% [3, 7, 22–39, 81, 82, 94–97, 101–106, 112, 127–131, 139–
147]. In two different studies, the overall incidence of pericardial calcication
detected on chest roentgenogram ranged between 5% and 27% [25, 94, 95]. Bozbuga
and associates found pericardial calcication in 44% of patients with tuberculous
pericarditis [7]. In the series reported by Ghavidel and associates, pericardial calcication was detected on chest roentgenogram in 20% of all patients, and in 30% of
patients with tubercular pericarditis [54].
In the cumulative series of 547 patients from All India Institute of Medical
Sciences, New Delhi, 37% of patients had radiologically and intraoperatively
demonstrable calcication [27–33, 39]. This is comparable to 39% in 9 previous
studies among a total of 803 patients [3, 8, 102, 108–111, 127, 136, 137].
16 Calcic Constrictive Pericarditis
16.2 Pathogenesis andDisease Progression
The exact pathogenesis of calcic pericarditis is not clearly understood. The presence of pericardial calcication, regardless of the degree of pericardial thickening,
frequently implicates constriction as the cause of symptoms in the appropriate clinical setting. Pericardial calcication is associated with a longer duration of the constrictive process but not with a specic aetiology. An absence of calcication does
not exclude constrictive pericarditis [3, 8, 27, 33, 39, 102, 109–111, 127, 136, 137].
In the Western series, pericardial calcication was more commonly associated
with idiopathic constrictive pericarditis, while in developing countries a majority of
patients of calcic pericarditis exhibited evidence of tuberculosis [3, 8, 27, 33, 39,
102, 109–111, 127, 136, 137].
In patients with idiopathic constrictive pericarditis, the paradox of the relative
frequency of calcic pericarditis and the rarity of proven tubercular infection may
also reect longer duration of symptoms, the chronicity of the disease, and tissue
brosis; dystrophic calcication may obliterate evidence of previous infection [53,
60, 139, 140].
As observed by other investigators including ourselves, maximal pericardial calcication occurs predominantly over the right atrium and right ventricle, diaphragmatic surface, and atrioventricular grooves [27–33, 39, 60–62, 94, 95, 104, 119].
Fluid displaced by vigorous contractions of the left ventricle during resorption of
the primary pericardial effusion preferentially gravitates towards the transverse
sinus, the diaphragmatic recesses, and the right side of the heart, where calcium and
even bone are slowly deposited in the inspissated uid [24]. Although MacGregor
and colleagues found apical left ventricle calcication to be rare, we as well as the
Mayo clinic group, however, encountered it in almost 20–25% of our patients [27–
33, 39, 94, 95, 104, 107].
The association of pericardial calcication with larger echocardiographic atrial
dimension and volume was documented in the Mayo clinic study. The larger atria
seen in patients with calcied disease could be due to atrial arrhythmia (which was
16.2 Pathogenesis andDisease Progression
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267
frequently coexistent in our patients) or to a greater degree of myocardial restrictive
disease [59, 94, 95].
In accordance with a previous study, we found that calcication was uncommon
in patients who developed constriction after cardiac surgery [26–33]. This is probably related to the relatively brief duration of the pathologic process in this setting.
In a Cleveland Clinic series of 19 patients with constrictive pericarditis, 11 of whom
had had previous open heart surgery, the presence of pericardial calcication was
independent of the cause of constriction [127]. Rienmuller and colleagues, however,
reported calcication to be “common” in patients who had previous cardiothoracic
surgery [121, 122].
Myocardial involvement may occur as part of the primary lesion, causing myopericarditis or atrophy secondary to long-standing encasement. Penetration of the
myocardium by calcium spurs has also been reported by several investigators
including ourselves [27–33, 39–42].
The culprit pathological mechanism or mechanisms of conjoint involvement of
the epicardium and myocardium by the disease process remain conjectural. Based
on the experimental observations the following mechanisms have been proposed.
(i) Subepicardial penetration of a primary pericardial inammatory pro-
cess: There is no rigid barrier at the epicardial membrane to prevent the intramyocardial extension of a bacterial or fungal infective process arising
immediately subjacent to the pericardial lesion. Several investigators have proposed the above mechanism as the plausible mechanism of subepicardial penetration [7, 9, 42, 84, 138].
(ii) Simultaneous involvement of myocardium and pericardium by the same
pathologic process: Irradiation, rheumatoid arthritis, periarteritis nodosa, and
disseminated lupus erythematosus may induce concurrent inltration of both
pericardium and myocardium [10, 11, 37, 64–66, 86, 87, 117–120, 148].
(iii) Impairment of coronary blood ow: Explicit description of the gross and
microscopic anatomy of the coronary arteries and arterioles in the setting of
constrictive pericarditis has been lacking in the literature. Several investigators
have speculated on the following mechanisms for alterations of blood ow: (a)
low blood pressure, (b) direct or indirect effects of compression on the larger
blood vessels, (c) unusual intramural pressure affecting the smaller intramural
coronary arteries, (d) entanglement of the surface coronary arteries in the pericardial disease process by superjacent or adjacent scar tissue, (e) intrinsic
involvement of the vessel walls or lumen of the vessels by the same pathologic
process causing stenosis of the vessels, (f) decient irrigation of the subendocardial blood supply due to a combination of hypotension, shock, low pulse
pressure, obliterative disease of the coronary arteries, increased intraventricular pressure, and rigidity of the pericardial eschar depriving the coronary vasculature of its normal compliance [10, 12–14, 55, 81, 96–99, 130].
(iv) Independent constrictive pericarditis and concomitant coronary artery
disease: The view that concomitant atherosclerotic coronary artery disease
accounts for myocardial brosis, though reasonable, is thus hardly supported
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by the experience described either in this study or in the pertinent literature.
This discordant experience even suggests the diametrically opposite possibility
that somehow constrictive pericarditis has a sparing effect upon the coronary
arteries. Such a position would be conjectural. Whatever the mechanism or
mechanisms of conjoint involvement of epicardium and myocardium, it has
commonly been considered that atrophy of heart muscle bres, or replacement
of the latter by brous connective tissue, explains myocardial impairment persisting after pericardiectomy − atrophy explaining delayed improvement, and
brosis accounting, at times, for incomplete long-term effectiveness of surgery
[13–15, 25, 65, 82, 87, 88, 97, 113, 130, 131].
16 Calcic Constrictive Pericarditis
16.3 Diagnosis
Tubercular pericarditis is usually symptomatic. Untreated cases usually have an
unfavourable course [15, 66, 136]. The presence of pericardial ‘egg shell calcication’, ‘cocoon calcication’, or ‘amorphous calcication’ on chest roentgenogram
strongly suggests constrictive pericarditis in patients with cardiac failure [60–62,
94, 95, 131–133]. It is best seen from a lateral view, and is predominantly located
over the right atrium, right ventricular and diaphragmatic surfaces of the heart as
well as atrioventricular grooves, and (if present) suggest tuberculosis [41].
Although calcication may support the clinical suspicion of chronic constrictive
pericarditis, its presence is not always specic because it may occur without cardiac
compression [104]. As stated by Lorell, “A calcied pericardium is not necessarily
a constricted one” [96, 97].
Ling and associates reported radiological signs of pericardial calcication in 36
out of 135 patients undergoing pericardiectomy for chronic constrictive pericarditis.
In their study, calcication was found over the inferior/diaphragmatic surface of the
heart in 97% of patients, on the anterior surface of the heart over the right ventricle
in 76% of patients, and over the atrioventricular groove in 62% of cases [94, 95].
In our cumulative experience on 547 patients undergoing pericardiectomy for
chronic constrictive pericarditis, chest roentgenograms revealed pericardial calcication in 37%, pleural effusion in 40%, and pulmonary inltrates in 16.6% of
patients. The calcication was distributed over the anterior and inferior surfaces of
the heart in 22.2% of patients, around the atrioventricular groove in 10%, and all
around the heart like a ‘cocoon’ in 14.8% of patients (Fig.16.1). None had mitral
annular calcication [26–33, 39].
Detection of cocoon calcication and predominant distribution of calcication
over right ventricular outow tract and right atrium on chest x-ray is helpful in planning a surgical approach for pericardiectomy and the possibility of requirement of
cardiopulmonary bypass [2, 3, 7, 8, 25, 27–33, 39, 103, 111, 137].
Computed tomography and cardiac magnetic resonance imaging are superior to
echocardiography for detection of pericardial calcication, loculated pericardial
effusion, pericardial mass, and asymmetric pericardial thickening. Computed
16.3 Diagnosis
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Fig. 16.1 Lateral chest
radiograph reveals
extensive circumferential
pericardial calcication.
(Indicated by white
arrows)
269
tomography with predominant use of an “ultrafast” scanner detected pericardial
calcication in 20% patients who did not have calcication on plain radiographs
(Figs.16.2 and 16.3) [11, 21, 23, 43, 55, 56, 67–71, 73, 85, 88, 129, 143–145]
Cardiac magnetic resonance imaging has the ability to dene both morphological and functional changes including myocardial atrophy/brosis [4–6, 16–21, 49–
52, 54, 57, 67–80, 89–93, 113–115, 121–125]. The results of pericardiectomy are
poor with dominant myocardial involvement (Fig.16.4) [121, 122].
The greater sensitivity of computed tomography compared with chest radiography or magnetic resonance imaging does confer a clinical advantage in establishment of diagnosis and the asymmetric degree of pericardial thickening or
calcication which may be important in determining the optimal surgical approach
for pericardial resection [27–33, 37, 121, 122, 126, 144]. In addition, these techniques, particularly cardiac magnetic resonance can dene the typical morphologic
characteristics and the presence of myocardial atrophy or brosis which can
adversely affect outcome after pericardiectomy [98, 99].
In patients with tubercular pericarditis, the calcication is mostly a sequela of the
disease process rather than disease chronicity [59, 94, 95]. The larger atria seen
sometimes in patients with calcied disease could be due to atrial arrhythmia or to
a greater degree of myocardial restrictive disease [53, 94, 95, 139, 140]. Several
investigators including ourselves have observed that the myocardial involvement
may occur as a part of the primary lesion causing myopericarditis or atrophy
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16 Calcic Constrictive Pericarditis
a
d
Fig. 16.2 Frontal chest radiograph (a) shows plaque-like calcication along the diaphragmatic
(white arrowhead) and left border (black arrowhead) areas of the heart. Note is made of right pleural effusion. Four-chamber (b), two-chamber (c) and short axis (d) reconstructions of CT angiography and volume rendered images (e and f) show extensive pericardial calcication along the
diaphragmatic surface and free walls of both ventricles. Note is made of biatrial dilation and tubular ventricles. (LA left atrium, LV left ventricle, RA: right atrium, RV right ventricle)
b
e
c
f
secondary to long standing encasement. Additionally, penetration of the myocardium by calcic spurs have also been reported [27, 33, 37, 40].
Calcic constrictive pericarditis whenever detected is an absolute indication for
pericardiectomy. Calcic pericardium signies late presentation and can penetrate
the myocardium, causing left ventricular dysfunction and that may preclude surgical options [79].
Analysis of the published literature including ourselves substantiate that patients
with (i) annular constrictive pericarditis, (ii) calcic pericardial patch compressing
predominantly the right atrium and right ventricular outow tract, (iii) circumferential “cocoon” calcication encompassing all cardiac chambers, and d) calcic spurs,
spicules penetrating the myocardium would preferably undergo total pericardiectomy via median sternotomy for improved surgical exposure and easy institution of
cardiopulmonary bypass, if required for intraoperative acute hemodynamic decompensation and inadvertent cardiac injury and massive intraoperative bleeding
[30–39].
The surgical details for removal of the calcic pericardium have been dealt with
in Chaps. 24 and 25. In general, placement of an external debrillator paddle is
helpful for inadvertent intraoperative ventricular brillation. The author would preferably start with an incision over the soft and uncalcied pericardium using a cautery, setting between 8 and 10 mv. Whenever possible, we target to develop a plane
of cleavage above and below the calcied plaque. The circumferential patch of calcied pericardium is crushed with a thick hemostat and/or bone cutter/bone nibbler
16.3 Diagnosis
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271
a
c
Fig. 16.3 Volume rendered images (a–c) show extensive pericardial calcication predominantly
along the free wall and diaphragmatic surface of bilateral ventricles and the atrioventricular
groove. Volume rendered image (d) shows thick calcic spurs inltrating into the right ventricular
myocardium. (LA left atrium, LV left ventricle, RA right atrium, RV right ventricle)
b
d
a
Fig. 16.4 Four chamber MRI cine image (a) shows tubular ventricles with indentation (thick
white arrow) along the free wall of the left ventricle (LV). Short axis cine image (b) shows thin
pericardial collection with thickened pericardium (arrow heads) adherent along the inferolateral
wall of LV.Short-axis image from tagged cine sequence (c) shows adherence and immobility of the
pericardial-myocardial interface
b
c
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