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Chapter 4
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Aetiological Search
An extensive aetiological PubMed, MEDLINE, Google Scholar, Embase and Cochrane Database for systematic reviews, Cochrane central register of control tri­als, ovid EMBASE (1974 to 31/12/2019) search of hospital admission for all cases of pericardial effusion reveals varying causes of pericarditis; clinicians are required to identify causes that require targeted therapies [7–16, 18–32, 56–59, 65, 88–93,
114–122, 136]. Acute pericarditis of various etiologies may eventually result in con-
strictive pericarditis [7, 8].
Over the past few decades, the aetiological spectrum of chronic constrictive peri­carditis also has changed resulting in diagnostic uncertainties and commensurate change in the indications and complexity of surgical pericardiectomy [17–24, 123–
128, 142, 148]. Certain high risk clinical features are proposed for triage of patients
with pericarditis and for complete aetiologic search and hospital admission [60, 61,
80–83, 129–133].
Imazio and associates in 2007, prospectively studied more than 450 consecutive cases and validated the following major high-risk clinical features indicating pos­sible non-viral, non-idiopathic origins of acute pericarditis which required hospital admission and a full aetiological search: fever more than 38°C (hazard ratio [HR]
3.56), large pericardial effusion (diastolic echo-free space 20mm in width), or car­diac tamponade (HR 2.15), subacute course (symptoms occurring over several days or weeks; HR 3.97), and failure of NSAIDs or aspirin (HR 2.50). During follow-up, increased risk of complications was noted with large pericardial effusion and tam­ponade and aspirin or NSAID failure. In absence of these negative predictors, patients were at a low-risk of complications, and managed on out-patient basis [56–63].
In developing countries, tuberculosis is the leading cause of chronic constrictive pericarditis with an incidence of 38–83% [18–20, 34, 35, 51, 61–63, 88–97, 106,
107, 114–119, 136, 137]. In patients with AIDS, with the emergence of drug-
resistant strains of tuberculosis, the prevalence has become more than 90% [88–93]. Like other aetiologies of chronic constrictive pericarditis, tubercular pericarditis
Ltd. 2023 U. K. Chowdhury, L. K. Sankhyan, Surgical Treatment of Chronic Constrictive Pericarditis, https://doi.org/10.1007/978-981-99-5808-5_4
35© The Author(s), under exclusive license to Springer Nature Singapore Pte
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4 Aetiological Search
also shows dense brosis and calcication without any direct evidence of the pres­ence of tubercle bacilli. Mediastinal radiation and previous open heart surgery are the aetiological causes in developed countries [1, 6, 9, 25–35, 41–45, 47, 57, 59, 61,
69, 87–96, 100, 106, 107, 131, 132]. The specic causes that need to be ruled out
are tubercular pericarditis, auto-immune etiology and neoplastic pericarditis, each having a frequency of around 5% [1, 6, 9, 25–33, 41–45, 47, 57, 59, 61, 69, 93–
96, 100].
Presently, staphylococcal, pneumococcal, streptococcal, hemophillus inuenza, and legionella infections are the causative factors for 20–25% of purulent and adhe­sive pericarditis [10–12, 41–44, 48, 50, 52, 106, 107]. Constrictive pericarditis may occur following incomplete drainage of purulent pericarditis. In remaining ~80% cases, one or more predisposing factors- namely, malignancy, chronic renal failure, recent thoracic surgery, HIV infection and various other immunosuppressive disor­ders are responsible for this disease entity [10–12, 41–44, 48, 52, 106, 107].
With increasing hospital-acquired infections, fungal infections have become quite common (up to 20%) particularly in patients on hyperalimentation, prolonged antibiotic therapy, steroid administration, burns, immunosuppression, malignancy and following cardiac surgery [2, 18–20, 25–30, 59, 61, 64, 91–93, 96, 106, 107,
114–121]. Iatrogenic causes include pacemaker insertion, coronary interventions,
and catheter ablation [122, 130, 132, 133]. The prevalence of idiopathic chronic constrictive pericarditis varies from 24% to 61% in India [3, 12, 36, 79, 82, 106,
107, 114–121].
Various rare and uncommon infectious causes of constrictive pericarditis are Legionella pneumonia, Lassa fever, meningococcal, nocardia asteroids, histoplas­mosis, Whipple’s disease, actinomycosis, amoebic liver abscess, and salmonella infections [20, 26, 37, 70–72, 85, 101–103, 105, 142]. Immunosuppressed patients and children are vulnerable [10, 11]. Pericardium may be inltrated by metastatic deposits from lung and breast cancer and lymphomas [10, 11, 26–48, 84].
Constrictive pericarditis may occur in 0.1–0.3% patients following cardiac surgi­cal procedure [4, 5, 13, 18–27, 53, 66, 73–78, 80]. In 1989, Cimino traced 158 cases of chronic constrictive pericarditis post cardiac surgery, in the world literature [30]. In 1989, Killiam reported appearance of constrictive pericarditis between 1 and 204months (mean of 24months) following cardiac surgery in 45 patients [74]. In 1986, Schiavone and associates reported 19 patients with constrictive pericarditis following repair of atrial septal defect (1), valve replacement (5), coronary artery bypass grafting (4) and Beck’s procedure (1) [133]. Constrictive pericarditis appears after a period of 3–24months time interval following cardiac surgery, although it may occur as early as 4weeks [14]. Other causative factors implicated in develop­ment of postsurgical constrictive pericarditis are trauma during the surgery, residual blood elements in the pericardial cavity, low-grade infection and irrigation of peri­cardial cavity with povidone iodine solution. Nonpenetrating or penetrating pericar­dial injury like penetrating injury to the pericardium from pacing catheters, may result in constrictive pericarditis [133, 134]. In 1988, Keogh reported a case of trau­matic hemopericardium following self mutilating injury to chest wall using sewing needles leading to constrictive pericarditis [49, 71, 132, 133].
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37
In cardiac transplantation, constrictive pericarditis occurs rarely as a complica­tion with an incidence ranging from 1.4% to 3.9% [15, 54]. The time period from cardiac transplantation to appearance of constrictive pericarditis varies between 3weeks to as long as 11years [15, 20–24, 27, 31, 32, 54, 73–77, 110, 111, 137].
Drugs like hydralazine, methysergide and procainamide may induce lupus ery­thematosus, resulting in recurrent episodes of pericarditis, pericardial adhesions, and constriction [1, 107–109, 112, 126–129, 135, 144, 149]. Radiation therapy for mediastinal tumor, breast carcinoma, and Hodgkin’s disease may cause constrictive pericarditis at varying time intervals [1, 6, 9, 21, 25, 29, 67, 85, 87, 97, 138, 139,
143–147].
“Dialysis pericarditis” is a specic form of pericarditis that develop in patients with end-stage kidney failure who receive dialysis or renal transplantation. It usu­ally develops after 8weeks of initiation of dialysis and may progress to stage of constriction [2]. Patient of Wagner’s granulomatosis in renal failure may develop constrictive pericarditis [133].
Rare and uncommon hereditary causes of constrictive pericarditis like mulibrey nanism have been reported from United States and Finland [138, 141].
The literature documents cases of rheumatoid arthritis, lupus erythematosus, and rheumatic fever causing either effusive-constrictive pericarditis or constrictive peri­carditis [4, 16, 25, 68, 73, 86, 107, 109, 139, 140].
Other rare causes include myocardial infarction with anticoagulant related hae­mopericardium, sarcoidosis, Whipple’s disease, amyloidosis, dermatomyositis, asbestosis, implantable cardioverter debrillator, primary chylopericardium, cox­sackie virus, histoplasmosis, sclerosing mediastinitis, methysergide therapy and fol­lowing cardiac transplantation [38–40, 45, 46, 55, 72, 78, 86, 98, 99, 104, 107–113,
140, 150].
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Chapter 5
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Clinical Challenges andDiagnostic Dilemma ofChronic Constrictive Pericarditis
This condition has posed a diagnostic dilemma since it was rst recognized. All cases of constrictive pericarditis cannot be diagnosed using an isolated criterion. An individualized diagnostic approach is recommended for each patient. In some patients the diagnosis may be made on the basis of history, physical examination and chest radiography. However, in the majority, echocardiography, cardiac cathe­terization and visualization of pericardium may all be required. The most important diagnostic tool is the clinical suspicion of constrictive pericarditis in a patient with signs and symptoms of right-sided cardiac failure that are disproportionate to pul­monary or left-sided heart disease.
Clinically it is necessary to differentiate constrictive pericarditis from other causes of right-sided heart failure such as mitral stenosis, pulmonary hypertension, pulmonary embolism, right ventricular infarction, restrictive cardiomyopathy, Budd-Chiari syndrome and tropical endomyocardial brosis [1, 7, 8, 10–16, 22, 23,
25, 29, 47–50, 53–56, 65, 71–74, 93–96, 103–106, 125, 133, 138–143, 149, 150].
Hepatosplenomegaly occurs early and may lead to an erroneous diagnosis of cir­rhosis of the liver. Kussmaul’s sign may be positive but lacks specicity, as it is seen also in patients with restrictive cardiomyopathy, right ventricular failure, endomyo­cardial brosis and tricuspid stenosis [10–16, 47–50, 71, 72]. Ling and associates from the Mayo Clinic detected the presence of pulsus paradoxus and Kussmaul’s sign in 19% and 21% of patients with constrictive pericarditis referred for pericar­diectomy [54, 55, 66]. Evidence of pulsus paradoxus is found in the majority of patients [124]. The published literature does not document the exact cause of ‘asci­tes precox’ i.e. the appearance of ascites followed by pedal oedema. Disproportionately high right atrial pressures, protein losing enteropathy causing hypoalbuminemia, increased capillary permeability, cardiac cirrhosis, impedance to lymph ow and disproportionately high atrial natriuretic peptide have been vari­ously implicated as causative factors for ascites precox [53, 71, 72, 97, 98, 107]. A diastolic lift (pericardial knock) that coincides with a high-pitched early diastolic sound and sudden inspiratory splitting of second heart sound (Vogelpoel-Beck sign)
Ltd. 2023 U. K. Chowdhury, L. K. Sankhyan, Surgical Treatment of Chronic Constrictive Pericarditis, https://doi.org/10.1007/978-981-99-5808-5_5
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