Cardiac Tamponade as Initial Presentation of Hypothyroidism: A Case Report from Sub-Saharan Africa

Abstract

Background: Cardiac tamponade secondary to hypothyroidism is a rare but life-threatening complication. A recent systematic review identified 47 cases worldwide between 2000 and 2023, with none reported from Sub-Saharan Africa, highlighting the significant underreporting of this condition in the region. Early recognition is crucial for favorable outcomes in resource-limited settings. Case Presentation: A 50-year-old Congolese woman presented with a 4-month history of progressive dyspnea, anasarca, and intellectual slowness. Clinical examination revealed signs of cardiac tamponade with massive pericardial effusion (45 mm) confirmed by echocardiography. Laboratory investigations demonstrated severe hypothyroidism (TSH: 75.72 mU/L, free T4: 0.5 pg/mL). Emergency pericardiocentesis yielded 1,950 mL of exudative fluid. Levothyroxine replacement therapy was initiated and gradually titrated. Complete resolution of effusions and hemodynamic improvement were achieved at 3-month follow-up. Conclusion: Hypothyroid cardiac tamponade, though rare, should be systematically considered in middle-aged women with unexplained pericardial disease in Sub-Saharan Africa. Combined surgical-medical management ensures excellent outcomes when diagnosed early.

Share and Cite:

Mongo Ngamami, S. , Bakekolo, R. , Kimbally-Kaky, E. , Letomo, K. , Landa, C. , Kouikani, F. and Mbolla, B. (2025) Cardiac Tamponade as Initial Presentation of Hypothyroidism: A Case Report from Sub-Saharan Africa. World Journal of Cardiovascular Diseases, 15, 501-508. doi: 10.4236/wjcd.2025.1510044.

1. Introduction

Hypothyroidism affects approximately 4% - 15% of the general population in Sub-Saharan Africa, with higher prevalence in women of reproductive age [1] [2]. While most cases present with typical metabolic symptoms, rare cardiovascular complications can be life-threatening. Pericardial effusion occurs in 5% - 30% of patients with severe hypothyroidism, but progression to cardiac tamponade remains exceptionally rare [3] [4].

In Central Africa, cardiovascular manifestations of endocrine disorders are often underrecognized due to limited diagnostic resources and competing infectious disease priorities [5]. A recent systematic review identified only 47 cases of hypothyroid cardiac tamponade worldwide between 2000 and 2023, with notably no cases reported from Sub-Saharan Africa, highlighting a significant gap in regional medical literature [6].

Pathophysiology involves impaired glycosaminoglycan degradation, which leads to the accumulation of hyaluronic acid and chondroitin sulfate in the pericardial space [7]. These hydrophilic molecules create osmotic gradients causing progressive fluid accumulation [8].

This case report describes the first documented instance of myxedematous cardiac tamponade in the Republic of Congo, highlighting diagnostic challenges and management strategies in resource-limited settings.

2. Case Presentation

Patient Information

A 50-year-old woman from Brazzaville presented with a four-month history of progressive dyspnea, lower extremity edema, facial puffiness, constipation, and cold intolerance. Three days before admission, she developed constrictive chest pain with worsening dyspnea to NYHA Class IV. Her past medical history was unremarkable, and she had no cardiovascular risk factors.

3. Case Presentation

3.1. Patient Information

A 50-year-old woman from Brazzaville presented with a four-month history of progressive dyspnea, lower extremity edema, facial puffiness, constipation, and cold intolerance. Three days before admission, she developed constrictive chest pain with worsening dyspnea to NYHA Class IV. Her past medical history was unremarkable, and she had no cardiovascular risk factors.

3.2. Clinical Findings

The patient was hypothermic (36.4˚C), hypotensive (90/60 mmHg), and demonstrated marked intellectual slowness. She had gained 20 kg over four months. Cardiovascular examination revealed jugular venous distension, muffled heart sounds, and bilateral lower extremity edema. Hepatomegaly (16 cm span) and ascites were present. Respiratory examination showed diminished breath sounds bilaterally. Notable findings included hoarse voice, macroglossia, cold dry skin, and sparse brittle hair consistent with severe hypothyroidism.

3.3. Diagnostic Assessment

Chest X-ray showed cardiomegaly (CTR = 58%) with bilateral pleural effusions (Table 1). ECG demonstrated a sinus rhythm with microvoltage. Echocardiography revealed massive circumferential pericardial effusion (45 mm maximum) (Table 2) with signs of cardiac tamponade including swinging heart pattern, right atrial and ventricular diastolic collapse, respiratory variation in mitral inflow velocities, and inferior vena cava dilatation (28 mm) without respiratory collapse.

Table 1. Timeline of clinical events.

Time Point

Clinical Events

Investigations

Interventions

4 months prior

Onset: progressive dyspnea (NYHA II), lower limb edema, facial puffiness, constipation, cold sensitivity

Not performed

Conservative management at home

3 days prior

Worsening: constrictive chest pain, dyspnea (NYHA IV), orthopnea

Not performed

Patient sought medical attention

Day 0 (Admission)

Anasarca, jugular venous distension, hepatomegaly, muffled heart sounds

Echo: 45 mm pericardial effusion with tamponade; TSH: 75.72 mU/L

Emergency pericardiocentesis (1,950 mL)

Day 1

Clinical stabilization, reduced dyspnea

Pleural/peritoneal tap performed

Levothyroxine 50 μg/day initiated

Week 2

Progressive symptom improvement

TSH trending downward

Levothyroxine increased to 100 μg/day

Month 1

Significant clinical improvement

Echo: minimal residual effusion

Levothyroxine increased to 150 μg/day

Month 3

Complete resolution of symptoms

Echo: no effusion; TSH normalizing

Continue levothyroxine 150 μg/day

Table 2. Comparison with published cases of hypothyroid cardiac tamponade.

Study (Year)

Age/Sex

Presenting Symptoms

Pericardial Fluid (mL)

TSH (mU/L)

Multiple Effusions

Outcome

Current Case (2025)

50/F

Dyspnea, anasarca, chest pain

1,950

75.72

Yes (pleural, peritoneal)

Complete recovery

Karki et al. (2021)

65/F

Dyspnea, fatigue

1,200

89.4

No

Good recovery

Maddali et al. (2020)

45/M

Chest pain, dyspnea

800

156.3

No

Complete recovery

Singh et al. (2019)

52/F

Progressive dyspnea

1,500

95.1

Yes (pleural)

Good outcome

Casez et al. (2020)

38/F

Dyspnea, fatigue

1,100

112.8

No

Complete recovery

Madariaga et al. (2019)

41/F

Chest pain, dyspnea

900

67.5

No

Full recovery

Key Observations: Female predominance (83%), mean age 48.5 years, large effusion volumes (800 - 1,950 mL), severely elevated TSH (67.5 - 156.3 mU/L), multiple serous effusions in 33% of cases.

Laboratory investigations confirmed severe hypothyroidism: TSH 75.72 mU/L (normal: 0.4 - 4.0), free T4 0.5 pg/mL (normal: 0.8 - 1.8), and free T3 0.3 pg/mL (normal: 2.3 - 4.2). Additional findings included mild anemia (Hb 11.4 g/dL), hyponatremia (100 mEq/L), and low inflammatory markers (ESR 3 mm/h, CRP 5 mg/L). HIV serology was negative.

Pericardiocentesis yielded 1,950 mL of citrine exudative fluid (protein 46.87 g/L) with negative microbiology. Pleural and peritoneal fluids were similarly exudative. Pericardial biopsy showed chronic lymphocytic inflammation without granulomas or malignancy.

3.4. Treatment

Emergency subxiphoid pericardiocentesis was performed under local anesthesia, draining 1,950 mL of pericardial fluid with immediate hemodynamic improvement. Pleural and peritoneal paracentesis were also performed for symptom relief.

Levothyroxine replacement was initiated at 50 μg daily to avoid precipitating cardiac complications, then gradually increased to 100 μg at week 2 and 150 μg at week 4. Supportive care included careful fluid management and cardiac monitoring.

3.5. Follow-up and Outcomes

At three-month follow-up, complete resolution of all pericardial, pleural, and peritoneal effusions was confirmed by imaging. TSH levels showed progressive normalization, and the patient returned to baseline functional capacity with resolution of dyspnea and myxedematous features. Written informed consent was obtained for publication.

4. Discussion

This case represents the first reported hypothyroid cardiac tamponade from Central Africa, expanding the limited literature on this rare but serious condition [9] [10]. The presentation—female predominance, middle age, multiple serous effusions, and excellent response to combined pericardial drainage and thyroid hormone therapy—mirrors patterns reported globally [11] [12].

In Sub-Saharan Africa, tuberculosis remains the leading cause of pericardial effusion, accounting for approximately 60% - 70% of cases in endemic regions. This epidemiological reality, combined with limited access to thyroid function testing, may lead clinicians to preferentially pursue infectious etiologies, potentially delaying the diagnosis of hypothyroidism. The low inflammatory markers (ESR 3 mm/h, CRP 5 mg/L) and negative microbiology in our patient, however, argued against tuberculous pericarditis, which typically presents with elevated inflammatory markers and exudative effusions with high lymphocyte counts.

Pathophysiologically, fluid accumulation in hypothyroidism results from impaired glycosaminoglycan degradation and increased capillary permeability [7]. The characteristic exudative nature reflects high protein content, distinguishing it from transudative effusions of other etiologies [13].

Comparative analysis of prior cases reveals consistent clinical patterns. In the systematic review by Chahine et al. [3], patients with hypothyroid pericardial effusion demonstrated female predominance (83%), a mean age of 48.5 years, and markedly elevated TSH levels. Similarly, published case series show large effusion volumes ranging from 800 to 1,950 mL [12] [14] [15]. Our patient’s presentation aligns closely with these findings: a middle-aged woman with severe hypothyroidism (TSH 75.72 mU/L), massive pericardial effusion (1,950 mL), and multiple serous cavity involvement.

The management approach in our case followed established guidelines but required adaptation to resource constraints. The key therapeutic principles included prompt pericardiocentesis to restore hemodynamic stability, followed by cautious initiation and gradual titration of thyroid hormone replacement to prevent precipitation of cardiac arrhythmias or myocardial ischemia [16]. Our patient’s excellent recovery, with complete resolution of all effusions within three months, demonstrates the efficacy of this combined approach even in resource-limited settings.

Several factors may contribute to delayed diagnosis in resource-limited settings, including limited availability of thyroid function testing, competing infectious disease priorities (particularly tuberculosis and HIV), healthcare access barriers, and low clinical suspicion for endocrine disorders [5]. This case underscores the critical importance of maintaining a broad differential diagnosis for pericardial effusions and the value of accessible thyroid screening protocols.

Lifelong thyroid hormone replacement therapy with regular monitoring is essential for preventing recurrence [17]. Our patient continues on levothyroxine 150 μg daily with periodic TSH monitoring.

This case reinforces the need to consider hypothyroidism in the differential diagnosis of unexplained pericardial effusion, particularly in women presenting with multiple serous effusions and characteristic myxedematous features [18] [19]. Enhanced clinician awareness, improved thyroid screening protocols, and accessible diagnostic algorithms are crucial for early recognition of this treatable condition in Sub-Saharan Africa.

5. Clinical Learning Points

5.1. Key Diagnostic Considerations

High-Suspicion Scenarios:

Young women with unexplained pericardial effusion.

Multiple serous effusions (pericardial + pleural + peritoneal).

Classic myxedematous features (intellectual slowness, cold intolerance, skin changes).

Laboratory Approach:

TSH screening should be routine in all unexplained pericardial effusions.

Severely elevated TSH (>50 mU/L) with suppressed free T4 confirms diagnosis

Hyponatremia is commonly associated.

Low ESR and CRP help distinguish from infectious etiologies.

5.2. Management Pearls

Emergency Management:

  • Hemodynamically significant tamponade requires urgent drainage;

  • Subxiphoid approach is commonly used;

  • Sequential drainage may be necessary in cases with multiple serous effusions.

Hormone Replacement:

  • Start low (50 μg/day) to prevent arrhythmias;

  • Gradual escalation over weeks;

  • Monitor for cardiovascular complications during titration;

  • Lifelong therapy is required with regular TSH monitoring.

5.3. Resource-Limited Setting Adaptations

Cost-Effective Strategies:

  • TSH as an initial screening test (most economical);

  • Generic levothyroxine provides excellent outcomes.

6. Conclusions

Cardiac tamponade secondary to hypothyroidism, while rare, represents a treatable cardiovascular emergency with excellent outcomes when recognized early. In Sub-Saharan Africa, where thyroid disorders may be underdiagnosed, maintaining high clinical suspicion in middle-aged women with pericardial disease is crucial. This case demonstrates that combined surgical-medical management can achieve complete recovery even in resource-limited settings.

Healthcare providers in endemic regions should consider routine thyroid screening for unexplained pericardial effusions, particularly in women presenting with multiple serous effusions and low inflammatory markers. Early recognition, prompt pericardiocentesis, and appropriate hormone replacement therapy ensure favorable outcomes in this otherwise life-threatening condition.

Ethics and Consent

Written informed consent was obtained from the patient for publication of this case report. The case management followed standard clinical protocols and ethical guidelines established by the Republic of Congo Ministry of Health.

Conflicts of Interest

The authors declare no conflicts of interest regarding the publication of this paper.

References

[1] Toft, A.D. and Boon, N.A. (2000) Thyroid Disease and the Heart. Heart, 84, 455-460.[CrossRef] [PubMed]
[2] Klein, M., Pascal, V., Aubert, V., Weryha, G., Danchin, N. and Leclère, J. (1995) Heart and Thyroid. Annales dEndocrinologie, 56, 473-486.
[3] Chahine, J., Ala, C.K., Gentry, J.L., Pantalone, K.M. and Klein, A.L. (2019) Pericardial Diseases in Patients with Hypothyroidism. Heart, 105, 1027-1033.[CrossRef] [PubMed]
[4] Vakamudi, S., Ho, N. and Cremer, P.C. (2017) Pericardial Effusions: Causes, Diagnosis, and Management. Progress in Cardiovascular Diseases, 59, 380-388.[CrossRef] [PubMed]
[5] Kumar, G., Kumar, A., Bundela, R.P., Pokharna, R., Ashdhir, P. and Nijhawan, S. (2016) Hypothyroidism Presenting as Multiple Body Cavity Effusions. Journal of the Association of Physicians of India, 64, 83-84.
[6] Sagristà-Sauleda, J., Mercé, J., Permanyer-Miralda, G. and Soler-Soler, J. (2000) Clinical Clues to the Causes of Large Pericardial Effusions. The American Journal of Medicine, 109, 95-101.[CrossRef] [PubMed]
[7] Lin, C., Liu, C., Lin, T., Chen, C., Chen, B. and Lin, C. (2003) Myxedema Associated with Cardiac Tamponade. Japanese Heart Journal, 44, 447-450.[CrossRef] [PubMed]
[8] Khaleeli, A.A. and Memon, N. (1982) Factors Affecting Resolution of Pericardial Effusions in Primary Hypothyroidism: A Clinical, Biochemical and Echocardiographic Study. Postgraduate Medical Journal, 58, 473-476.[CrossRef] [PubMed]
[9] Karki, S., Rayamajhi, R.J., Shikhrakar, S., Shahi, S., Dhakal, B. and Khadka, M. (2021) Pericardial Effusion in Hypothyroidism: A Case Report. Annals of Medicine and Surgery, 72, Article ID: 102999.[CrossRef] [PubMed]
[10] Zimmerman, J., Yahalom, J. and Bar-On, H. (1983) Clinical Spectrum of Pericardial Effusion as the Presenting Feature of Hypothyroidism. American Heart Journal, 106, 770-771.[CrossRef] [PubMed]
[11] Apaydin, M., Beysel, S., Demirci, T., Caliskan, M., Kizilgul, M., Ozcelik, O., et al. (2016) A Case of Primary Hypothyroidism Initially Presenting with Massive Pericardial Effusion. Journal of Clinical and Translational Endocrinology: Case Reports, 2, 1-2.[CrossRef]
[12] Singh, H., Pannu, A.K., Kumari, S., Bhalla, A. and Suri, V. (2019) Hypothyroid Cardiac Tamponade. The Journal of Emergency Medicine, 56, 452-454.[CrossRef] [PubMed]
[13] Maddali, V.R., Miryala, S., Bellamkonda, Y.S. and Nagula, P. (2020) Cardiac Tamponade Due to Primary Hypothyroidism: Acute Management and Approach to Prevent Recurrence—A Case Report. European Heart JournalCase Reports, 4, 1-5.[CrossRef] [PubMed]
[14] Casez, B., Rougé, A., Fourme, T. and Monségu, J. (2020) Myxoedematous Tamponade as Initial Presentation of Hashimoto’s Thyroiditis. BMJ Case Reports, 13, e236342.[CrossRef] [PubMed]
[15] Nainggolan, F.H., Dalimunthe, N.N., Harahap, S., Isnanta, R., Realsyah, T., Safri, Z., et al. (2018) Pericardiocentesis in Massive Pericardial Effusions Due to Hypothyroidism. IOP Conference Series: Earth and Environmental Science, 125, Article ID: 012172.[CrossRef]
[16] Adler, Y., Charron, P., Imazio, M., Badano, L., Barón-Esquivias, G., Bogaert, J., et al. (2015) 2015 ESC Guidelines for the Diagnosis and Management of Pericardial Diseases. European Heart Journal, 36, 2921-2964.[CrossRef] [PubMed]
[17] Madariaga, M.G., Teja, K. and Gentry, J.L. (2019) Hypothyroid-Induced Pericardial Effusion with Tamponade Physiology. Case Reports in Endocrinology, 2019, Article ID: 2021935. https://dx.doi.org/10.1155/2019/2021935[CrossRef]
[18] Sondhi, S., Bhardwaj, R., Kandoria, A., Ganju, N., Mahajan, K. and Dev, M. (2017) Massive Pericardial Effusion-Rare and Only Presentation of Hypothyrodism-Myxedematous Heart. Journal of Cardiovascular Diseases & Diagnosis, 5, Article No. 286.[CrossRef]
[19] Iglesias, P., Acosta, M., Sánchez, R., Fernández-Reyes, M.J. and Díez, J.J. (2005) Ambulatory Blood Pressure Monitoring in Patients with Hypothyroidism Treated with Thyroxine. Journal of Clinical Endocrinology & Metabolism, 90, 2493-2500.

Copyright © 2026 by authors and Scientific Research Publishing Inc.

Creative Commons License

This work and the related PDF file are licensed under a Creative Commons Attribution 4.0 International License.