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N Jain, P Dutta, A Dutta, R Sharma, A Bhansali, Panhypopituitarism: a rare cause of cardiac tamponade, QJM: An International Journal of Medicine, Volume 111, Issue 10, October 2018, Pages 731–732, https://doi.org/10.1093/qjmed/hcy127
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Case presentation
A 48-year-old farmer, father of three children, presented with exertional dyspnoea and pleuritic chest pain for 10 days and altered behaviour for 3 days. Past history revealed low blood pressure records, postural dizziness and loss of body and facial hair over the last 2 years. He was hemodynamically unstable (systolic blood pressure <80 mm Hg, heart rate 92/min); however, jugular venous pressure was not raised nor was pulsus paradoxus noted. In view of low voltage complexes on electrocardiogram and ‘money bag appearance’ of heart on chest roentgenogram (Figure 1), echocardiography was done which showed massive pericardial effusion (PE) with right atrial and right ventricular collapse suggestive of cardiac tamponade (CT). Pericardiocentesis was immediately performed and pericardial fluid analysis revealed exudative effusion with lymphocytic pleocytosis. Adenosine deaminase and polymerase chain reaction for mycobacterium tuberculosis were negative, as were cultures for bacterial infections. On consultation, we noted hoarseness of voice, puffy face, wrinkles around the eyes, madarosis, dry and coarse skin, delayed relaxation of deep tendon reflexes, absent axillary and pubic hair, minimal body and facial hair. Investigations were notable for severe hyponatremia (serum sodium- 110 mEq/l), low T3 (0.24 ng/ml, N-0.8-2), low T4 (1.34 μg/dl, N-4.8-12.7), with inappropriately elevated thyroid stimulating hormone (TSH) (14.53 mIU/ml, N-0.27-4.2), and positive anti-thyroid peroxidase antibody (36.14 IU/ml, N-<34). Serum cortisol (252.7 nmol/l, during stress N->550) and DHEAS (0.47 μg/dl, N-44.3-331) levels were suppressed with undetectable adrenocorticotropic hormone (ACTH) (<1 pg/ml, N-5-60). Serum testosterone levels were also low (2.62 nmol/l, N-9.9-27.8), with inappropriately low FSH (4.05 mIU/ml, N-1.5-12.4) and LH (5.35 mIU/ml, N-1.7-8.6). Serum prolactin (6.88 ng/ml, N-5-15.2) and insulin-like growth factor-1 (IGF-1) levels were in low normal reference range. Other autoimmune workup was non-contributory. Magnetic resonance imaging (MRI) brain revealed empty sella with normal stalk (Figure 1), probably suggestive of resolved lymphocytic hypophysitis. Ultrasonography neck confirmed atrophic thyroid gland. A diagnosis of panhypopituitarism, consequent to lymphocytic hypophysitis was made and the patient was initiated on hydrocortisone followed by levothyroxine replacement in incremental doses. Patient exhibited rapid improvement with correction of hyponatremia, reversal of circulatory shock and resolution of PE on treatment.
