An important clue was the presence of a ârelative sinus bradycardiaâ (HR-84/min) at the time of presentation, when the patient was in cardiac pre- tamponade.
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A Patient with Progressive Dyspnoea AK Agarwal*, Sanjeev Miglani**, Sumeet Singla**, Priyanka Vasudeva**, Arun Jain*** A 35-year-old, non-diabetic, non-hypertensive male, was admitted to the medical emergency with a 6 month history of progressively increasing dyspnoea which worsened on exertion. The patient did not have orthopnoea, paroxysmal nocturnal dyspnoea, chest pain, or sweating. He gave a history of dry cough for one month, lethargy and easy fatiguability. He had no history of fever, palpitation, syncope, ischaemic heart disease, or alcohol abuse. Physical examination revealed an overweight tachypnoeic male. He had a heart rate of 84/per minute, anasarca, raised JVP, mild pallor, and dry scaly skin. Chest examination was normal and the cardiovascular system examination revealed 2nd left intercostal space dullness and muffled heart sounds. ECG showed low voltage complexes. Routine blood investigations were normal. The chest Xray of the patient at presentation is shown in Figure 1.
Fig. 1: Chest X-ray at presentation.
Questions Q. 1: What abnormality does the chest X-ray show? The chest X-ray shows a markedly increased cardiac silhouette in the shape of a bag. The lung fields are
clear. This radiological appearance is diagnostic of a large pericardial effusion. This patient had a large pericardial effusion which led to his dyspnoea. Q. 2: What are the important causes of pericardial effusion? Pericardial effusion may occur due to: a.
Infectious causes – viral, tubercular, bacterial, fungal.
b. Non-infectious causes – malignancy (metastatic carcinoma of breast, lungs, and lymphoma), myxoedema, uraemia, trauma to chest, collagen vascular disease, post myocardial infarction, radiation to chest. c.
Idiopathic.
Tuberculosis is the most important cause of pericardial effusion in northern India, followed by malignancy1. However, malignancy remains the commonest cause of a large pericardial effusion in the developed world 2 . The term idiopathic pericardial effusion comprises various undiagnosed aetiologies. In a study from France3, 141 patients considered to have idiopathic pericardial effusion were evaluated using non-invasive diagnostic testing of blood, throat, and stool samples. Systematic testing for Q fever, Mycoplasma pneumoniae, hypothyroidism, antinuclear antibodies, and viral throat cultures resulted in a specific aetiological diagnosis in 44 of the 141 patients (32.1%) studied. Q. 3: What should be the management of this patient? A pericardiocentesis and fluid analysis is an important diagnostic and therapeutic manoeuvre in a case like this, with impending tamponade.
* Consultant in Medicine, Professor and Head, ** Senior Resident, *** Senior Physician, Department of Medicine, Dr. Ram Manohar Lohia Hospital, New Delhi -110 001.
However, it must be preceded and/or accompanied by an echocardiographic confirmation of the diagnosis. In our patient, echocardiography revealed slightly thickened pericardium, a pericardial effusion 1.42 cm anteriorly and 1.76 cm posteriorly, and a swinging motion of the heart. The fluid analysis in this case yielded a yellowish fluid with high protein content (6.6 gm%), but no cells, no bacteria, and no AFB. The vital clues in this case were the history of lethargy, skin changes, weight gain, and a distinct hoarseness of voice (which on deeper enquiry was found to be present since 6 months). An important clue was the presence of a “relative sinus bradycardia” (HR-84/min) at the time of presentation, when the patient was in cardiac pretamponade. Also important was the absence of fever, lymphadenopathy, and evidence of tuberculosis/malignancy elsewhere in the body. Hence, there was a strong clinical suspicion of hypothyroidism. The patient’s total serum cholesterol was 263 mg% and serum triglycerides were 277 mg%. His serum did not have antinuclear antibodies (ANA) or antibodies to Coxsackie’s virus. Thyroid function tests revealed primary hypothyroidism – FT3-0.56 pg/ml, FT4-0.05 ng/dl, TSH-141.12 IU/ml.
levels are restored. Adjustment of levothyroxine dosage is made in 12.5 or 25 g increments if the TSH is high; decrements of the same magnitude should be made if the TSH is suppressed. In the rare case in whom there is no relief with the above measures, a limited or total pericardiectomy can be done. Our patient was started on 100 g/day of levothyroxine and his subsequent chest X-rays showed gradual resolution of the pericardial effusion (Figs. 2, 3), his general condition showed improvement, and his thyroid hormone status became normal over a period of 6 months (FT3 – 4.06 pg/ml, FT4- 1.31 ng/dl, TSH- 0.36 IU/ml ).
Fig. 2: Chest X-ray after three weeks of therapy
Q. 4: What are the further treatment options for this patient? The therapeutic options for this patient are thyroid hormone replacement with or without therapeutic pericardiocentesis. Adult patients who are under 60 and without any evidence of heart disease may be started on 50 to 100 g levothyroxine (T4) daily. The dose is adjusted on the basis of TSH levels, with the goal of treatment being a normal TSH, ideally in the lower half of the reference range. TSH responses are gradual and should be measured about 2 months after instituting treatment or after any subsequent change in levothyroxine dosage. The clinical effects of levothyroxine replacement are often slow to appear. Patients may not experience full relief from symptoms until 3 to 6 months after normal TSH
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Fig. 3: Chest X-ray after three months of therapy.
Discussion Both hypothyroidism and hyperthyroidism are associated
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with clinically significant cardiovascular involvement. In hypothyroidism, the cardiovascular derangements include pericardial effusion, congestive heart failure, hypertension, hyperlipidaemia, coronary artery disease, and primary pulmonary hypertension. Pericardial effusion was reported in early studies in 30 80% of subjects with hypothyroidism. However, these earlier studies were conducted when the diagnosis of hypothyroidism was made by classic clinical features. In contrast, the diagnosis has recently been established in the early mild stage or in an asymptomatic stage because of the frequent use of highly sensitive thyroid function tests. Thus, the subjects in the older studies were severely hypothyroid at the time of diagnosis and may not be representative of the present hypothyroid population. A recent echocardiography based study has estimated the prevalence of pericardial effusion to be 3 - 6% in hypothyroid pateints4. Moreover, the occurrence of pericardial effusion in hypothyroidism appears to be dependent on the severity of the disease. Thus, a large pericardial effusion may be a frequent manifestation in myxoedema, but a rare association of hypothyroidism, an early mild stage. As a corollary, concomitant pathologies like viral pericarditis, tubercular pericarditis, and malignancy must be ruled out in hypothyroid patients with large pericardial effusion or cardiac tamponade. The pathophysiological basis of pericardial effusion in hypothyroidism is increased capillary permeability leading to exudation of proteins into the pericardial cavity, increased accumulation of hygroscopic mucopolysaccharides, and the distinct entity of cholesterol pericarditis5 (characterised by the typical ‘gold paint’ appearance of myxoedematous pericardial fluid, due to the presence of shimmering cholesterol crystals). Once the diagnosis of a pericardial effusion has been made, a decision must be taken on whether the patient
Journal, Indian Academy of Clinical Medicine
requires emergency pericardiocentesis or not. Only after that, must we proceed to treat with thyroxine. Adequate thyroid replacement reverses all of the cardiovascular derangements of hypothyroidism. Final diagnosis: Large pericardial effusion due to hypothyroidism.
Learning points 1. Pericardial effusion is seen in 3 - 6% of hypothyroid patients. 2. The size of pericardial effusion is related to the severity of hypothyroidism. 3. Cardiac tamponade in myxoedema is a rarity because of the slow accumulation of fluid in the pericardial cavity. 4. Other co-existing causes of pericardial effusion, viz., viral, tubercular, malignancy must be excluded in a case of hypothyroidism with large pericardial effusion or cardiac tamponade.
References 1.
Jain S, Sharma N, Varma S et al. Profile of cardiac tamponade in the medical emergency ward of a North Indian hospital. Can J Cardiol 1999; 15 (6): 671-5.
2.
Gibbs CR, Watson RD, Singh SP, Lip GY. Management of pericardial effusion by drainage: a survey of 10 years’ experience in a city centre general hospital serving a multiracial population. Postgrad Med J 2000; 76 (902): 809-13.
3.
Levy PY, Corey R, Berger P et al. Aetiologic diagnosis of 204 pericardial effusions. Medicine (Baltimore) 2003; 82 (6): 385-91.
4.
Kabadi UM, Kumar SP. Pericardial effusion in primary hypothyroidism. Am Heart J 1990; 120 (6): 1393-5.
5.
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Jimenez EA, Montes OPM, Vallejo YV et al. Cholesterol crystals pericarditis. Rev Esp Cardiol 2001; 54 (9): 1119-20.
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