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MEDICINE
Primary Hypothyroidism Leading to Massive PericardialEffusion and Diastolic Right Ventricular Compression: a Case Report
Saeide Bahrani1 & Sayed Ali Emami1,2 &Mehrbod Vakhshoori3 &Mansour Siavash4& Keivan Kiani4 & Farhad Mahmoudi1
Accepted: 10 July 2019# Springer Nature Switzerland AG 2019
AbstractAlthough hypothyroidism with primary etiology could cause small pericardial effusion, massive one leading to cardiactamponade and ventricular diastolic compression is rare and less reported in the literature. Here we described a patient withsevere primary hypothyroidism leading to pericardial effusion and right ventricular compression. A 56-year-old diabetic manreferred to the emergency department complaining of dyspnea worsening over the prior month. Further evaluations includingelectrocardiography, chest X-ray, and echocardiography plus laboratory data were requested. Para-clinic data revealed massivepericardial effusion in the presence of primary hypothyroidism. Pericardiocentesis was performed due to his severe symptomswhich symptoms improvement were considerably achieved. Despite its rareness, hypothyroidism should be kept in mindwhenever evaluating patients with massive pericardial effusion, especially after exclusion of other more common etiologies.
Keywords Hypothyroidism . Pericardial effusion . Levothyroxine . Pericardiocentesis
Introduction
Although cardiac manifestations of hypothyroidism, includ-ing bradycardia and pericardial effusion (PE) are common,massive pericardial effusion or pericardial tamponade is rarelyreported [1]. Hypothyroidism is infrequently presented pri-marily by pericardial effusion, but the most common cardiacmanifestation which could happen in patients suffering fromsevere hypothyroidism would be bradycardia and pericardialeffusion [2]. Cardiac tamponade leading to right ventricular(RV) and right atrial (RA) compression happens extremelyrare [1]. Here, in this paper, we described a patient with right
ventricular (RV) collapse as the first presentation of severeprimary hypothyroidism.
Case Presentations
A 56-year-old Iranian male presented to our emergency depart-ment with worsening of dyspnea associated with weakness, fa-tigue, slow speech, and periorbital edema since last month beforehis admission. He also complained of orthopnea. His medicalhistory was unremarkable except for smoking one packet ofcigarette daily for 10 years (10 packs/year) and type two diabetesmellitus diagnosed 10 years earlier.
This article is part of the Topical Collection on Medicine
* Sayed Ali [email protected]
Saeide [email protected]
Mehrbod [email protected]
Mansour [email protected]
Keivan [email protected]
Farhad [email protected]
1 Cardiac Rehabilitation Center, Isfahan Cardiovascular ResearchInstitute, Isfahan University of Medical Sciences, Isfahan, Iran
2 School of medicine, Isfahan University of Medical Sciences,Isfahan, Iran
3 Heart Failure Research Center, Isfahan Cardiovascular ResearchInstitute, Isfahan University of Medical Sciences, Isfahan, Iran
4 Isfahan University of Medical Sciences, Isfahan, Iran
https://doi.org/10.1007/s42399-019-00110-4SN Comprehensive Clinical Medicine (2019) 1:924–927
/Published online: 6 September 2019
On physical examination, he was stable without any signsand symptoms of respiratory difficulty. Blood pressure was100/70 mmHg, pulse, and respiratory rate were 74 and 20per minute, respectively. Head and neck examinations re-vealed a raised jugular venous pressure (JVP), periorbitalpuffiness, and dry and cold skin. The only positive findingon heart auscultation was the presence of muffled heartsounds. Pulsus paradoxus was not detected. Other
examinations did not reveal any positive findings except de-creased deep tendon reflexes and severe non-pitting pretibialedema. Requested CXR and ECG showed huge cardiomegaly(increased cardio-thoracic ratio) with globular pattern andlow-voltage QRS complexes, respectively (Fig. 1a, b). Intransthoracic echocardiography (TTE), severe PE with RAcollapse during diastole was reported (Fig. 2). Left ventricularand RV systolic function were normal, and there was evidence
Fig. 1 aCXR, cardiomegaly witha globular pattern. b low-voltageECG
Fig. 2 Echocardiography ofapical four chamber viewsshowing pericardial effusion ofthickness by 296 mm
SN Compr. Clin. Med. (2019) 1:924–927 925
of tamponade. Due to the persistence of his symptoms,pericardiocentesis was performed, and about 400 ml of serousfluid was drained and sent for laboratory and culture analysis.Concurrently, his blood sample was taken, and positive find-ings were in agreement with the diagnosis of primary hypo-thyroidism (thyroid stimulating hormone 100 mIU/ml, freeT4:0.870 mg/dl, and T3 < 3 nmol/L). The pericardial fluidanalysis was unremarkable for the presence of any malignan-cies or infections. After fluid drainage, patient’s symptomswere relieved and para-clinic examinations returned approxi-mately back to normal ranges. Thyroxin replacement therapy(25 mcg/day of levothyroxine) was initiated. The patient wasdischarged in a healthy physical condition; and on the nextfollow-up, within 6 months after the attack, all laboratoryparameters had been normalized, and no PE was detected onTTE.
Discussion
Here, we presented a patient suffering from massive pericar-dial effusion leading to cardiac tamponade due to severe pri-mary hypothyroidism confirmed by clinical and laboratoryfindings.
The prevalence of this condition in patients with severe andmild hypothyroidism was estimated to be 20–30% and 3–6%,respectively [2]. PE and cardiac tamponade are among two ofthe rarest manifestations of hypothyroidism [3]. Parving et al.believed that it is caused by a combination of albumin extrav-asation and slow lymphatic drainage [4]. In another study, themolecular mechanism of the effect of triiodothyronine (T3) incardiac cells was responsible. After binding T3 to its nuclearreceptors, expression of some genes including alpha-myosinheavy chain, beta-1 adrenergic receptor, voltage-gated potas-sium channels, and sarcoplasmic reticulum calcium ATPasewould be changed. Many cardiac manifestations are consid-ered to be related to those gene expression alterations [5].Diagnosis of cardiac tamponade in hypothyroidism is difficultand almost mistaken for heart failure because of several non-specific symptoms including tachypnea, lower limb edema,and increased venous pressure [6]. Beck’s triad components,including increased jugular venous pressure, hypotension, anddiminished heart sounds, define cardiac tamponade. Fromnon-invasive para-clinic tools, the gold standard way to con-firm the diagnosis is TTE, which is optimal for assessing theseverity of effusion and compressive effects on the heartchamber [7]. ECG findings include low-voltage QRS com-plexes, ST segment deviation, PR segment depression, and Twave changes [8]. In patients suffering uremia or hypothy-roidism, bradycardia may be the only cardiac manifestation[9]. Even if the definite diagnosis of hypothyroidism wasmade, other etiologies must be kept in mind because this re-lationship is commonly rare and other pathophysiological
mechanisms need more aggressive and different managementstrategies [10].
While some scientists prefer immediate surgical ap-proaches to make pericardial window initially to preventsymptom recurrence, others believe in the individualizationof therapy. For instance, in case of mild hemodynamic alter-ation, conservative management including close monitoring,performing serial ECGs and avoidance of volume depletionshould have been done. In patients with pulsus paradoxus orrecurrent PE, pericardiocentesis or pericardial window, re-spectively, would be the right management strategies [11].
The base of hypothyroidism treatment is thyroxin replace-ment therapy. It is usually started with low dose thyroxin(25 mcg/day), especially in older people to prevent complica-tions like atrial fibrillation and worsening coronary heart dis-eases and will gradually increase to higher dosages [12]. Afterinitiation of therapy, pericardial effusion will resolve gradual-ly, and as patients gain euthyroid level, effusion would beentirely resolved. Our patient, because of poor compliancewith drug usage, returned to the hospital with massive peri-cardial effusion within few months [2].
In conclusion, it is reasonable that on a routine evaluationof massive pericardial effusion after excluding commoncauses such as malignancies, infections, and connective tissuedisorders, hypothyroidism should be kept in mind and appro-priate diagnostic and therapeutic management must have beenperformed.
Compliance with Ethical Standards
Conflict of Interest The authors declare that they have no conflict ofinterest.
Ethical Approval All procedures performed in studies involving humanparticipants were in accordance with the ethical standards of the institu-tional and/or national research committee and with the 1964 Helsinkideclaration and its later amendments or comparable ethical standards.
Informed Consent Written informed consent was obtained from thepatient for publication of this case report and accompanying images.
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