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Chapter 11
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Management ofChronic Constrictive
Pericarditis
Chronic constrictive pericarditis belongs to the category of diseases, which usually
result in cardiac failure with normal ejection fraction. Other entities in this group
which should be differentiated from chronic constrictive pericarditis are restrictive
cardiomyopathy, cardiac amyloidosis, tropical endomyocardial brosis, BuddChiari syndrome, and a few other diseases [1, 2, 8–12, 22–30, 40, 48, 58, 62–64, 82–
85, 88–90, 102, 128, 156–160, 201]
Clinical features suggestive of constrictive pericarditis include presence of congestive cardiac failure with absence of systemic hypertension or myocardial or valvular disease. Claude Beck stressed on the triad of cardiac compression, raised
venous pressure, and ascites along with a quiet small heart. History of tubercular or
bacterial pericardial or pleural effusion, may suggest the underlying etiology [13,
14, 64].
Presence of Kussmaul’s sign although positive is not specic to constrictive pericarditis, since it can also be seen among patients with endomyocardial brosis,
restrictive cardiomyopathy, right ventricular failure and tricuspid stenosis [22–29,
82–85, 102–104]. Among patients of constrictive pericarditis being referred for
pericardiectomy, Ling and associates from the Mayo Clinic found that 19% had
pulsus paradoxus and 21% had Kussmaul’s sign [88, 92, 93].
A completely normal electrocardiogram is rare in constrictive pericarditis.
Although non-specic, it may demonstrate low voltage QRS complex, ST-T abnormalities, p-mitrale, and atrial brillation [1, 22–31, 58–60, 106, 107, 133, 167].
Some clinical features help in differentiating constrictive pericarditis from similar
pathologies. Pulmonary congestion is usually absent in constrictive pericarditis but
present in restrictive cardiomyopathy [1, 9, 15, 22–30]. A low voltage QRS complex
suggests cardiac amyloidosis. Presence of patchy endomyocardial calcication and
cardiomegaly suggest endomyocardial brosis or restrictive cardiomyopathy [31,
108, 122].
It needs to be emphasized that no single approach is conclusive to diagnose all
cases of constrictive pericarditis. Pulsus paradoxus, reduced pulse pressure, reduced
Ltd. 2023
U. K. Chowdhury, L. K. Sankhyan, Surgical Treatment of Chronic Constrictive
Pericarditis, https://doi.org/10.1007/978-981-99-5808-5_11
199© The Author(s), under exclusive license to Springer Nature Singapore Pte
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11 Management ofChronic Constrictive Pericarditis
systolic blood pressure, radiological evidence of diminished cardiac pulsation, pericardial calcication, characteristic haemodynamic changes, electrocardiographic,
echocardiographic, computed-tomographic, magnetic resonance imaging ndings,
endomyocardial biopsy, and inadequate medical response to congestive cardiac failure are some of the ndings to suggest the presence of chronic constrictive pericarditis [1, 8–12, 16, 22–34, 103–108, 120–122, 132, 133, 141–153, 193–197, 202,
208, 215]. Corroborative ndings of at least two investigations are required, namely
computed tomography, echocardiography, magnetic resonance imaging, and/or cardiac catheterization, to conclusively establish the diagnosis of constrictive pericarditis [1, 22–34, 122, 189–192, 202–207]. If constrictive pericarditis is diagnosed
correctly, timely surgical intervention will be curative [9, 22–31, 82, 83, 108, 153].
After establishing the diagnosis, the disease activity should be assessed by the
patient’s clinical condition and erythrocyte sedimentation rate. The medical treatment for symptomatic patients consists of restricted physical activity, minimal
sodium intake, high protein diet, steroids, non-steroidal anti-inammatory agents,
and antibiotics. Although the usefulness of digitalis is controversial, it is the practice
in the author’s institution to digitalize patients with atrial brillation and utter to
prevent perioperative atrial brillation [22–29]. Excessive use of diuretics in the
preoperative period is not desirable, to prevent intravascular volume depletion and
sudden collapse. Slow drainage of large pleural, and pericardial effusions provides
symptomatic relief. It is the practice to insert an indwelling peritoneal drainage cannula and drain intraoperatively in the author’s institution to prevent sudden autotransfusion following pericardiectomy [22, 26, 27]. In cases of tubercular aetiology,
anti-tubercular treatment should be started, although the progression of the disease
process to cardiac constriction does not disappear in majority of cases.
Establishing a bacteriological or histological diagnosis of tubercular aetiology is
often difcult [17, 18, 43–46, 82, 95–98, 159–161]. A history suggestive of lymph
node tuberculosis, pulmonary tuberculosis and skeletal tuberculosis may be seen in
varying percentage of patients [21–30, 35]. The variability of detection of tubercle
bacilli ranges from 0 to 42% in different series [10, 11, 41–44, 96–99, 162, 165].
The sensitivity of pericardial biopsy for diagnosis of tuberculosis ranges from 10%
to 81%. A tubercular aetiology is to be considered if excised pericardium on histopathology shows caseation, giant cells, granulomas or when if the uid removed
during surgery tests positive for tuberculosis [21–30, 35]. In tubercular pericardial
effusion, the enlarged mediastinal nodes which are not routinely seen on a chest
radiograph, but can be visualised on computed tomography imaging or magnetic
resonance imaging [34, 35, 104, 109–113, 150, 162].
Presence of pericardial effusion in patients from tubercular endemic areas, particularly those having HIV infection, is considered as tubercular in aetiology in
absence of other alternative causes [112, 113, 129]. Based on histologic or microbiological criteria, about two-thirds of these cases are diagnosed as tuberculosis
[162–165]. In the remaining patients, other supportive evidence for tubercular etiology include an adequate response to antituberculosis therapy. Anti-tubercular treatment should be started for patients residing in non-endemic areas even in the
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absence of a diagnosis of tubercular pericarditis [22–30, 34, 49–51, 64, 65, 109–
113, 134–139, 159–175, 210–214].
The therapeutic strategy in patients with non-calcic constrictive pericarditis
includes a trial of anti-tubercular treatment for 6–8weeks and referring patients
showing no improvement or worsening of pericardial constriction clinically for
pericardiectomy [9, 19, 22–30, 47, 66–68, 109–115, 129, 162–175]. There are no
trials specically addressing the optimal drug regime and duration of treatment for
tuberculous pericarditis. Over three decades, the published literature along with our
observations suggests that there is no justication in advising anti-tubercular drugs
for treatment of tuberculous pericarditis any longer than for extrapulmonary tuberculosis [22–30, 35, 51, 53, 95, 104, 109–113, 135, 138, 160, 162, 168, 176–178,
210–213]. According to the WHO guidelines, an initial two month regimen com-
prising of isoniazid, pyrazinamide, rifampicin, and ethambutol followed by rifampicin and isoniazid for 4months duration (total 6 months of therapy) is given for
tuberculous pericarditis [214] We advocate treatment of tuberculous pericarditis as
per WHO guidelines for treatment of extrapulmonary tuberculosis.
According to WHO guidelines, for new patients with tuberculous pericarditis
(strong/high grade evidence of pulmonary TB) the optimal dosing frequency is
daily throughout the course of drug therapy. For patient who is not living in an HIVprevalent setting or living with HIV, thrice-weekly dosing [2(HRZE)3 4(HR3)] may
be considered as an alternative to the above recommendation, provided that every
dose of drug therapy is directly observed (conditional/high and moderate grade of
evidence). Treating patients for nine months or longer does not give better results
but has the disadvantage of poor compliance and increased cost. Short-course chemotherapy seems to be effective in treating TB in HIV-infected patients [162, 168,
175, 214].
Overall, survival is dramatically increased in tuberculous pericarditis with antituberculosis chemotherapy. Mortality which used to range between 80% to 90% in
the pre-antibiotic era, currently ranges from 17% to 34% in HIV-positive individuals and 8% to 17% in HIV-negative patients [22–29, 36, 49, 50, 64, 65, 104, 109,
113, 125–127, 159–176, 210–213].
Adjunctive oral corticosteroids are recommended for survival benet in patients
of tuberculous pericarditis. The drug choice and its dosage (methylprednisolone,
prednisolone, prednisone) and route of administration (intravenous, oral, intrapericardial) is variable [1, 22–29, 104, 109, 113, 125, 159–169, 174]. However, studies
have not shown any signicant benet pertaining to progression to constrictive pericarditis or reaccumulation of pericardial effusion [1, 3, 22–29, 35, 86, 87, 104,
108–114, 123–127, 136, 138, 162, 165, 174, 179–181]. Rifampicin-containing drug
regimen when used along with corticosteroids results in signicant decrease in mortality as shown by systematic meta-analysis [22–29, 35, 104, 109, 113, 125, 138,
139, 159–165, 174].
The clinical presentation of effusive-constrictive pericarditis may be secondary
to pericardial effusion with cardiac tamponade or pericardial constriction causing
impaired diastolic lling [9, 22–29, 69, 70, 114, 129, 161, 171, 173, 176, 183–186].
There is presence of diastolic cardiac constriction and pericardial thickening
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11 Management ofChronic Constrictive Pericarditis
alongwith uid collection between the parietal and visceral pericardium [70–78].
The clinical, radiological, echocardiographic and haemodynamic ndings are often
mixtures of those associated with effusion and constriction [9, 19, 22–29]. The cardiopericardial silhouette may be larger on a chest roentgenogram than in those with
purely chronic constrictive pericarditis.
Usually, the visceral pericardium is maximally involved. An accepted denition
is failure of reduction of right ventricular end-diastolic, right atrial, and pulmonary
capillary wedge pressures by at least 50% to less than 10mmHg when intrapericardial pressure is decreased to almost zero by pericardiocentesis and/or all detectable
uid is removed [169, 186]. Early pericardiectomy may be desirable if pericardiocentesis fails to drain loculated pericardial effusions, in cases of recurrent effusions,
or if echocardiographic/integrated imaging studies are suggestive of effusiveconstrictive disease or early constrictive pericarditis after 4 to 6weeks of antitubercular drug therapy [71–76, 104, 159, 160, 168, 180, 198].
Presence of calcic constrictive pericarditis is an absolute indication of pericardiectomy. Calcic pericardium signies late presentation with myocardial brosis and
myocardial penetration, causing left ventricular dysfunction that may preclude surgery [9, 57, 71–78, 92, 93, 99, 100, 140]. However, we have been able to remove the
calcic spurs in all patients undergoing pericardiectomy in our institution [22–29].
Post-transplant constrictive pericarditis can be misdiagnosed as a rejection episode or restrictive cardiomyopathy. An integration of clinical and multimodality
imaging is essential to establish an early diagnosis of post-transplant constrictive
pericarditis. A subxiphoid pericardiostomy for pericardial effusion followed by a
radical pericardiectomy is recommended for management of these patients [20, 37,
38, 79, 80, 90, 99, 198, 200].
The mainstay of management of chronic constrictive pericarditis is surgical
decortication of the entire pericardium including the pericardium posterior to the
phrenic nerve, diaphragmatic pericardium and visceral epicardial peel, without
causing injury to cardiac chambers, great vessels and coronaries. It is desirable to
minimize cardiac manipulations during surgical decortication to avoid/minimize
myocardial oedema in the perioperative period. Following surgery, there is improved
survival of patients having chronic constrictive pericarditis [21, 22, 26, 82–87, 93,
105]. Pericardiectomy has poor results when myocardium is predominantly involved
and has better results with dominant constrictive element, which may be reliably
assessed by cardiac magnetic resonance and speckle tracking echocardiography
[4–7, 150]. Patients diagnosed with chronic constrictive pericarditis having
increased central venous pressure / with right atrial pressure more than 12mmHg
with or without presence of hepatorenal dysfunction, pleural effusion, and massive
ascites; with decompensated haemodynamics requiring ventilator support and inotropes during preoperative period and with patchy/focal calcic pericarditis were
candidates selected for semi urgent total pericardiectomy by several investigators
across the globe [8, 25–35, 40, 48, 49, 54, 55, 92, 93, 105, 117, 141, 187–189],
Certain features should be considered while deciding approach for surgical pericardiectomy. Patients with calcic pericardial patch compressing mainly the right
ventricular outow tract and right atrium, annular constrictive pericarditis, calcic
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spurs penetrating the ventricular chambers, circumferential “cocoon” calcication
encompassing all cardiac chambers, post mediastinal irradiation constrictive pericarditis, recurrent pericarditis following previous partial pericardiectomy, previous
open heart surgery, a gradient at the superior and/or inferior cavoatrial junction
more than 2mmHg, extracardiac intrapericardial mass are considered contraindications for left anterolateral thoracotomy approach. Median sternotomy is usually preferred in above subset of patients for easy institution of cardiopulmonary bypass for
inadvertent cardiac injury and bleeding and improved surgical exposure [22–29, 92,
93, 109]. Additionally, left anterolateral thoracotomy approach is usually indicated
for patients with effusive and pyogenic pericardial diseases [22–29].
Although using cardiopulmonary bypass routinely for achieving total pericardiectomy is a debatable issue, it may be employed in specic circumstances, namely
(i) cardiac surgery or previous partial pericardiectomy; (ii) inadvertent injury to
cardiac chambers or great vessels; (iii) pericardiectomy for post mediastinal irradiation; (iv) coexistent cardiac lesion; and (v) presence of calcic pericardial “cocoon”
encompassing all cardiac chambers [8, 25–35, 40, 48, 49, 92, 93, 141, 189],
Cardiopulmonary bypass facilitates surgical dissection by emptying the ventricular cavities and making appropriate plane of dissection visible and also helps in
managing inadvertent cardiac injury. Therefore, one should not be reluctant to utilize cardiopulmonary bypass if needed to facilitate a complete pericardial resection
that will undoubtedly impact patient outcomes. Additionally, use of cardiopulmonary bypass in patients with massive ascites helps in controlling the uid shifts and
ultraltrating some of this uid off, thus avoiding cardiac distension [22–30, 54, 55,
92, 93, 105, 117, 187, 188].
The following perioperative management protocol is practiced at the author’s
institution:
• For chronic constrictive pericarditis with signicant pleural effusion on right
side undergoing pericardiectomy via left anterolateral thoracotomy approach, a
right-sided intercostal drain is placed prior to positioning the patient to prevent
respiratory and hemodynamic compromise.
• Both pleural cavities are electively opened and drained whenever possible. The
pleural and pericardial cavities are electively washed using normal saline.
• It is the practice to insert an indwelling peritoneal drainage cannula and drain
intraoperatively to prevent sudden autotransfusion following pericardiectomy
[22, 26, 27].
• Inotropes, namely dopamine, dobutamine, and/or adrenaline, are administered
intraoperatively on completion of pericardiectomy.
• It is desirable to electively place two ventricular and two atrial pacing wires in all
patients.
• Electrolyte imbalance should be avoided.
• Intravenous uids should be administered judiciously. It is desirable not to
administer more than 1 ml/kg of intravenous uids to prevent cardiac
overdistension.
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• No bolus intravenous uids/plasma products or blood should be administered
postoperatively to prevent sudden cardiac over-distension and failure of Starling’s
phenomenon.
• Anti-arrhythmic drugs, namely intravenous lignocaine and amiodarone need to
be administered in selected instances of patients with supraventricular and ven-
tricular arrhythmias in the postoperative period.
• Parenteral administration of plasma proteins or albumin may be required in the
postoperative period. There may be transient deterioration of hepatic and renal
function in the postoperative period which needs to be managed on an individu-
alized basis.
• It is the author’s practice not to administer bolus intravenous furosemide at a
high dose to manage low urine output. A combination of intravenous infusion of
furosemide, spironolactone, and/or acetazolamide and manipulation of inotropes
is extremely helpful in the great majority of cases to manage low urine output.
An occasional patient may require peritoneal dialysis or hemodialysis for a vari-
able postoperative period.
• Central venous pressure monitoring being a static preload indicator, may not suf-
ce for haemodynamic assessment when used alone. For haemodynamic moni-
toring of patients presenting with low cardiac output syndrome after
pericardiectomy or pericardiostomy, Vigileo™/FloTrac™ device may be the
investigation of choice [27, 56].
• Electively using inotropes like dobutamine and dopamine immediately after
completion of pericardiectomy is safer than instituting later in the postoperative
period. Trial administration of intravenous uid or blood in these patients may
actually be deleterious.
• For decreasing postoperative myocardial oedema, it is mandatory to do minimal
cardiac manipulation and avoid intermittent prolonged hypotensive episodes
during pericardiectomy.
The majority of patients undergoing radical/total pericardiectomy demonstrate
signs of varying degrees of low cardiac output syndrome within 6–8hours following surgery, thus requiring thoughtful intervention and exquisitely diligent bedside
monitoring. An accepted constellation of physiologic and haemodynamic alterations may alert the cardiac intensivist to the presence of low cardiac output syndrome [22–30, 50, 54, 55, 92, 93, 112, 117–119, 130, 179–183, 187, 188, 199, 216].
Accordingly, to dene low output syndrome, a combination of relevant clinical,
bedside echocardiographic and laboratory criteria is used. The various diagnostic
criteria used are: decreased toe temperature, cold extremities, absent pedal pulses,
reduced systolic pressure, metabolic acidosis, increased serum lactate levels
(≥2.0mmol/L, ≥2hours), impaired renal function and oliguria (<1.0mL.kg−1.h−1),
low mixed venous oxygen saturation (≤50%), and blunt sensorium [22–30, 50, 54,
55, 92, 93, 112, 117–119, 130, 179–183, 187, 188, 199, 216]. In addition, low car-
diac output syndrome is diagnosed when patient requires inotropic support namely
dobutamine at 5–10μg/[kg·min], dopamine at 4–10μg/[kg·min], milrinone (50μg/
kg intravenous bolus followed by 0.375–0.75 μg.kg−1.min−1), epinephrine at
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0.01–0.1μg/[kg·min], either alone or in combination during surgery or in intensive
care unit, for maintaining stable haemodynamic parameters in the absence of residual structural lesions such as signicant valvular lesions and mechanical external
compression, residual mechanical cardiac constriction, after correcting blood gas or
electrolyte abnormalities and after adjusting preload to its optimal value. Another
diagnostic criteria for low-output syndrome is an escalating requirement of the
above-mentioned inotropes with or without use of intra-aortic balloon counterpulsation along with reduction of afterload with sodium nitroprusside. Patients who need
renal dose of dopamine (less than 4μg/kg/min) are not considered to be in low
cardiac output state [22–30, 50, 54, 55, 92, 93, 112, 117–119, 130, 179–183, 187,
188, 199, 216].
In patients with massive pericardial effusion, gradual pericardiocentesis helps
gradual myocardial adaptation. After stable hemodynamics is achieved, complete
pericardial decompression is safe.
Hemodynamically, impaired ventricular diastolic compliance is the hallmark for
chronic constrictive pericarditis. Massive uid shifts occur from the extravascular to
intravascular space following a successful pericardiectomy. This autotransfusion
causes failure of Frank-Starling mechanism, resulting in acute cardiac dilation thus
mimicking acute left ventricular dysfunction from volume overload [22, 92, 109].
Acute stretching of the annuli may cause worsening of valve function resulting in
functional regurgitation. Inserting a peritoneal dialysis catheter intraoperatively and
draining ascitic uid during pericardiectomy followed by peritoneal drainage for
the next 24–48hours helps in preventing sudden auto-transfusion, increase in preload, and failure of Frank Sterling mechanism following surgery.
During the process of pericardial mobilization, repeated mechanical compression results in myocardial oedema, which usually subsides over time [22, 23, 26, 92,
109]. It is difcult to ascertain a specic factor responsible for low cardiac output
syndrome post pericardiectomy. Although atrial brillation and high right atrial
pressure are associated with poor outcomes, addressing tricuspid regurgitation or
atrial brillation aggressively at the time of pericardiectomy is not advocated. If
attempts to sustain cardiac output by the currently available medical treatment fails,
then mechanical circulatory assistance may be the considered.
The use of intra-aortic balloon counterpulsation in patients undergoing pericardiectomy for chronic constrictive pericarditis remains sporadic. Use of intra- aortic
balloon counterpulsation facilitates recovery of left ventricular function by decreasing the left atrial and left ventricular end-diastolic pressure, thus helping the systemic ventricle and indirectly the pulmonary ventricle by the phenomenon of
ventricular interdependence [28, 29, 56, 131]. The ease of application makes intraaortic balloon counterpulsation preferred choice over left atrial-aortic assist devices
[28, 29, 56, 131]. Since its use as an absolute “last resort” decreases its success rate
and thus making the timing of initiation of support a difcult decision. Other assist
device like veno-arterial extracorporeal membrane oxygenation and axial ow
pumps can be used as salvage procedure [28, 29, 56, 91]. Use of intra-aortic balloon
counterpulsation is limited in children due to technical difculties in inserting
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11 Management ofChronic Constrictive Pericarditis
balloons, alongwith sparse availability and difculty in tracking rapid heart rates
and narrow pulse pressures of children presenting in shock. Additionally, risk of
complications like mesenteric ischaemia, renal failure and limb ischaemia is higher
in children because of inappropriate balloon length [131].
An exhaustive search must be made for adequacy of pericardiectomy, and excluding any surgically correctable cause(s) like signicant coronary artery disease, signicant tricuspid and/or mitral regurgitation, or other correctable surgical lesions.
For patients with left or right ventricular failure undergoing pericardiectomy leading to biventricular failure, use of intra-aortic balloon counterpulsation may be successful. Finally, an early recognition of perioperative low cardiac output syndrome
and judicious and timely manipulation of inotropes and/or mechanical counterpulsation is the key to a successful outcome.
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11 Management ofChronic Constrictive Pericarditis
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