A 63-year-old woman with past medical history of tobacco abuse and hypertension, who was on no home medications and had no medical care for the last 14 years, presented after a mechanical fall. Prior to her fall, her family reported a decline in functional status over 3 months.
Vital signs were 95.8°F, 149/85 mmHg, heart rate (HR) 56 beats per minute (bpm), 97% oxygen saturation on room air. On exam, she exhibited right-sided facial droop, flaccid right upper and lower extremities, and trace bilateral pitting edema overlying bilateral shins. Cardiac rhythm was regular. Thyroid, pulmonary, and abdominal exams were without pertinent positive findings.
Laboratory was remarkable for thyroid-stimulating hormone (TSH) 42 uIU/mL (0.35–4.8), free thyroxine (fT4) 0.28 ng/dL (0.9–1.9), thyroid peroxidase antibody (TPO) 201 IU/mL (0.0–34.9), early morning cortisol 12.8 ug/dL,[6–21] brain natriuretic peptide 725.6 pg/mL (0–100), creatine kinase 1766 U/L (96–140), and troponin 1.9 ng/mL (<0.06).
The patient was admitted to the neurology service for acute basal ganglion ischemia demonstrated on computed tomography. Laboratory testing suggested rhabdomyolysis and hypothyroidism. ECG demonstrated sinus bradycardia with T-wave flattening (Figure 1A). A transthoracic echocardiogram, obtained for work-up of ischemic stroke, showed concentric ventricular hypertrophy, a large pericardial effusion with echocardiographic signs of tamponade including elevated right atrial (RA) pressure, right ventricle (RV) diastolic collapse, and significant respiratory variation in diastolic left ventricular filling. The patient did not demonstrate pulsus paradoxus on clinical exam. Given the patient's stable hemodynamic state pericardiocentesis was deferred and she was treated with 50 mcg of intravenous (IV) levothyroxine; the IV formulation was selected due to dysphagia. Repeat echocardiogram 8 weeks after the initial study demonstrated a significant reduction in the size of pericardial effusion with normalized diastolic filling of all cardiac chambers. The patient was discharged on 150 mcg (2.3mcg/kg) of levothyroxine daily.
Lead II ECG findings on admission demonstrating findings consistent with myxedema heart. 1a (Case 1) demonstrates sinus bradycardia with flattened t waves; 1b (Case 2) and 1c (Case 3) with low voltage and T-wave flattening.
A 61-year-old female with a past medical history of rheumatoid arthritis, polymyositis, interstitial lung disease, and hypothyroidism presented with 3 days of generalized weakness. Over the last several years, the patient had noted dry skin, cold intolerance, and a change in voice quality. She had not seen a physician or taken medications for approximately 1 year.
Vital signs 98.0°F, 150/113 mmHg, HR 83 bpm, and 100% oxygen saturation on room air. She was a chronically ill appearing, cachectic (body mass index 18), but oriented. She had slurred speech, jugular venous distention to the level of the mandible, muffled cardiac sounds, and rales at the base of the right lung but no wheezes. In addition, she had symmetric upper (4/5) and lower (3/5) limb weakness, bilateral no pitting edema overlying the tibia up to her knees, diffusely dry skin with scale on limbs, and delayed relaxation of deep tendon reflexes. Thyroid exam was normal.
Laboratory evaluation was notable for TSH 198.7 uIU/mL (0.35–4.8), fT4 < 0.10ng/dL (0.9–1.9), TPO 20.2 IU/mL (0.0–34.9), random cortisol 8.2 ug/dL,[6–21] and sodium 140 mmol/L (137–147).
Her ECG was notable for low voltage, and T-wave flattening (Figure 1B). TTE showed a large pericardial effusion with pericardial thickening and plethora of the inferior vena cava (IVC) indicating right atrial pressure elevation, along with diastolic collapse of the RA and RV. This patient also did not have pulsus paradoxus on exam.
The patient was admitted to the cardiac intensive care unit (ICU) where she underwent pericardiocentesis with placement of pericardial drain for determination of etiology of the pericardial effusion in the setting of her concurrent rheumatologic disease and cachexia, in addition to severe hypothyroidism. The pericardiocentesis removed 1.45 L of straw-yellow pericardial fluid, which contained 50 red blood cells/mm3 23 white blood cells (WBC)/mm3 (<499 WBC/mm3) that were 77% neutrophils (<24%), 12% lymphocytes, and 7% monocytes. Microbiologic studies including mycobacterium fluid cultures were negative for infection, and fluid cytology for malignancy were negative. Thus, the etiology of effusion was felt to be hypothyroidism.
The patient was treated with intravenous levothyroxine, initial dose of 25 mcg IV daily. The pericardial drain continued to drain 100 to 200 mL daily. On hospital day 20 the patient developed a low-grade fever and her pericardial drainage grew Proteus and Enterococcus. She was then treated with ampicillin 3 g—sulbactam every 6 h for 7days then transitioned to amoxicillin 875 mg—clavulanate 125 mg every 12 h to complete a 14-day treatment. The patient's generalized weakness improved, and she transitioned to oral levothyroxine 125mcg (2.8 mcg/kg) prior to discharge.
A 66-year-old Bangladeshi female with a medical history of hypothyroidism presented with cough, lethargy, and dyspnea. The patient's husband reported the wife's facial swelling and dry skin over the last several months and a decline in her independent function over the several preceding weeks. Two weeks prior to presentation she began to experience dyspnea, which became progressively severe associated with cough productive of white, frothy sputum unresponsive to antibiotics. He also reported she was noncompliant with her home medications of levothyroxine and omeprazole.
On presentation, vital signs were 97.3°F, 162/90 mmHg, HR 89 bpm, 97% oxygen saturation on 2 L O2 via nasal cannula. On examination, the patient was lethargic but oriented. She had swollen facial features, most prominent at the circumference of ocular orbits, distant cardiac sounds, diffuse expiratory wheeze without rales, diffusely dry skin, delayed relaxation of deep tendon reflexes, and no thyromegaly.
Chest X-ray demonstrated enlargement of the cardiac silhouette and congestion of the pulmonary vessels. ECG demonstrated T-wave flattening (Figure 1C). Transthoracic echocardiogram was notable for a large pericardial effusion with features concerning for tamponade (Figure 2). Findings included IVC plethora, RA/RV diastolic collapse, and significant respiratory variation in diastolic left ventricular filling across the mitral valve. Recurrent measurements for pulsus paradoxus were normal.
Case 3 transthoracic echocardiogram, subxiphoid view, demonstrating large pericardial effusion with RV collapse during diastole.
Laboratory exam included TSH 87.47 ulU/mL (0.35–4.8), fT4 0.35 ng/dL (0.9–1.9), free triiodothyronine 1.2 pg/mL (2.3–4.2), TPO 3305 lU/mL (0.0–34.9), morning cortisol 12.0 ug/dL (6–21), sodium 136 mmol/L (137–147). Arterial blood gas was pH 7.3 (7.35–7.45), partial pressure of carbon dioxide 75.4 mmHg (35–45), O2 94.5 mmHg (80–100) on 2 L of nasal oxygen.
The patient was admitted to medical ICU for acute hypoxic hypercapnic respiratory failure requiring continuous positive airway pressure. She was treated for severe hypothyroidism with intravenous levothyroxine, initial bolus of 200 mcg, followed by 75 mcg daily. Her alertness rapidly improved, however, her respiratory status failed to recover. A contrast computed tomography chest showed compression of the left main stem bronchus and resultant atelectasis due to the large pericardial effusion (Figure 3). Pericardial drainage was performed and 1.1 L of serosanguinous fluid was removed, followed by marked improvement in her respiratory status over the 24 h following her procedure. She was weaned off supplemental oxygen within 72 h postprocedure. The pericardial fluid had 4100 red blood cells/mm3, 102 WBC/mm3 (<499 WBC/mm3), 3% neutrophils (<24%), 80% lymphocytes, and 1% monocytes. Microbiology cultures and cytology were negative. She was discharged on oral levothyroxine 112 mcg (1.5 mcg/kg) daily.
J Endo Soc. 2021;5(1) © 2021 Endocrine Society