Case Report: Cardiac Tamponade in Dengue Hemorrhagic Fever: An Unusual Manifestation of a Common Disease

Abstract.

Dengue hemorrhagic fever is one of the most commonly encountered mosquito-borne viral infections of humans worldwide with multiple reported outbreaks. Cardiac involvement is a known manifestation of the disease usually presenting as rhythm abnormalities, myocarditis, or pericardial effusion, which may be clinically asymptomatic. We describe a case of a 30-year-old woman who presented to us with high-grade fever, headache, retro-orbital pain, generalized maculopapular rash with bilateral pleural effusion, and hypotension. Dengue non-structural protein 1 (NS1) antigen and IgM antibodies were positive on admission, supporting a diagnosis of dengue hemorrhagic fever. Cardiac troponin-I was elevated on admission (65 ng/L) with diffuse convex ST segment elevations on electrocardiogram, suggestive of possible myopericarditis. Echocardiogram on admission revealed minimal pericardial effusion with preserved ejection fraction. Despite administration of fluids and inotrope use, the patient’s hypotension progressively deteriorated over the next 6 hours, associated with decreased urine output and worsening sensorium. Clinical examination revealed muffled heart sounds and raised jugular venous pressure. A repeat echocardiogram confirmed an increase in the pericardial effusion manifesting as cardiac tamponade. Ultrasound-guided pigtail catheter insertion led to a prompt removal of the excessive pericardial fluid and correction of hypotension. Early identification of this uncommon but important complication of dengue hemorrhagic fever led to a good outcome in our case.

INTRODUCTION

Dengue is the most widely distributed mosquito-borne viral infection of humans worldwide, affecting an estimated 100 million people annually.¹ It usually presents as an acute febrile illness with body ache, retro-orbital pain, and generalized rashes. Treatment is largely supportive, comprising fluid replacement during the phase of increased vascular permeability and management of secondary complications. However, as the incidence of dengue increases, atypical manifestations of the disease are reported with increasing frequency. Cardiac involvement in dengue encompasses a wide spectrum of presentations ranging from silent disease to fatal myocarditis. Rhythm abnormalities are seen in almost 62.5% cases, most commonly manifesting as an asymptomatic bradycardia.¹ It may also present with mild pericardial effusion due to serositis, pericarditis, or even myocarditis, but these are less commonly reported. Rapidly accumulating pericardial effusion is known to cause an embarrassment of cardiac function, but its occurrence in cases of dengue hemorrhagic fever is uncommon with only a few cases reported worldwide. It is important to recognize this as patients with cardiac tamponade have a rapid decline in cardiac function and present with sudden onset of hypotension and features of shock, which must be differentiated with dengue shock syndrome occurring because of increased vascular permeability. We present a case of myopericarditis in dengue hemorrhagic fever eventually progressing to cardiac tamponade.

CASE REPORT

A 30-year-old woman presented to us with complaints of high-grade fever and headache for 6 days, associated with retro-orbital pain. She reported that the fever was higher initially (highest documented temperature 104°F) associated with chills but had decreased significantly 2 days before her presentation. However, she had been experiencing shortness of breath over the last 2 days, which she felt was increasing, along with a sensation of generalized fatigue for which she had presented to us for evaluation. She had previously approached a local clinician for her fever who had advised her to do an NS1 antigen test, which was positive. He had reassured her regarding the illness and asked her to follow up with him, which she had neglected. On evaluation, she was febrile (100°F) with tachycardia (120 minutes⁻¹), tachypnea (26 minutes⁻¹), and hypotension (80/50 mm of Hg). General physical examination revealed a generalized, blanchable erythematous maculopapular rash sparing the palms and soles. Her body mass index was 27.2 kg/m². Auscultation of the chest revealed decreased air entry bilaterally up to the mid-zone, suggestive of bilateral pleural effusion. Rest of the systemic examination was within normal limits.

Point-of-care ultrasound (POCUS) revealed bilateral moderate pleural effusion with minimal ascites. Minimal pericardial effusion was present with ejection fraction greater than 65% and no generalized or regional wall motion abnormalities. She was commenced on intravenous fluids (1 L bolus followed by maintenance fluids at 75 mL/hour of 0.9% saline) and subsequently inotropes (intravenous noradrenaline at 5.3 μg/hour) to maintain a mean arterial pressure above 65 mm of Hg. Hematocrit on admission was 42.2% with thrombocytopenia (113,000 mm⁻³). Renal and liver function test results are provided in Table 1. An electrocardiogram revealed diffuse convex ST segment elevation in leads I, II, III, aVF, and V_5–6 with PR depression and reciprocal changes in lead aVR (Figure 1). Serum troponin-I levels were elevated (65 ng/L). A chest X-ray confirmed bilateral pleural effusion with mild cardiomegaly.

Table 1.

Laboratory parameters of the patient

Days of hospitalization	Day 1	Day 3	Day 5	Day 7
Hemogram
HGB (g/dL)	10.5	10.1	10.0	10.2
HCT (%)	42.2	42.0	39.7	38.0
PLT (μL−1)	113,000	105,000	122,000	150,000
TLC (mm−3)	4,200	4,400	6,400	7,300
Renal function tests
Urea (mg/dL)	42	40	28	30
Creatinine (mg/dL)	1.5	1.1	0.9	0.3
Calcium (mg/dL)	7.5	7.1	7.2	7.5
Phosphate (mg/dL)	3.5	2.9	3.3	3.3
Uric acid (mg/dL)	4.5	8.0	8.2	4.3
Na+ (mEq/L)	138	147	143	143
K+ (mEq/L)	3.6	3.5	3.9	4.2
Liver function tests
Bilirubin (total) (mg/dL)	1.0	0.9	0.7	0.8
Direct (mg/dL)	0.6	0.6	0.4	0.6
Indirect (mg/dL)	0.4	0.3	0.3	0.2
Protein (total) (g/dL)	6.0	6.0	6.3	6.5
Albumin (g/dL)	3.5	3.5	3.8	3.8
Globulin (g/dL)	2.5	2.5	2.5	2.7
SGOT (IU/L)	94	76	56	50
SGPT (IU/L)	73	88	47	40
ALP (IU/L)	251	296	200	175
PT (seconds)	15.1	–	–	–
INR	1.37	–	–	–

HGB = hemoglobin; HCT = hematocrit; PLT = platelet; TLC = total leucocyte count; BIL = bilirubin; SGOT = serum glutamic oxaloacetic transaminase; SGPT = serum glutamic pyruvic transaminase; ALP = alkaline phosphatase; PT = prothrombin time; INR = internationalized normalized ratio.

Figure 1.

Electrocardiogram revealing diffuse convex ST segment elevation in leads I, II, III, aVF, and V5-6 with PR depression and reciprocal changes in lead aVR.

Despite the institution of appropriate supportive care, she continued to deteriorate clinically over the next 6 hours, with worsening hypotension and persistently increasing inotrope requirement. During this period, her sensorium also worsened and she was electively intubated. Her urine output had also declined and she had passed only 150 mL of urine over the 6 hours of admission.

The patient was reassessed and found to have raised jugular venous pressure with muffled heart sounds. Repeat echocardiogram revealed diastolic collapse of the right ventricle with increased pericardial collection suggestive of cardiac tamponade. A pigtail catheter was inserted under ultrasound guidance and 200 mL of serous fluid was drained (Figure 2). Her vitals stabilized progressively over the next 4 hours, and she was extubated the next day following a successful spontaneous breathing trial. The pigtail catheter was removed on day 4 of insertion after minimal output was documented on three successive days, and a repeat echocardiogram showed resolution of the pericardial effusion.

Figure 2.

Bedside skiagram of the patient revealing cardiomegaly with pigtail in situ. This figure appears in color at www.ajtmh.org.

Evaluations for malaria, leptospirosis, scrub typhus, and enteric fever were negative. IgM dengue serology was positive by ELISA, but IgG was negative. Repeat NS1 antigen value was negative. Pericardial fluid analysis showed 10 lymphocytes, and tests for tuberculosis (adenosine deaminase and GeneXpert) were negative. Thyroid function tests, antinuclear antibodies, anti–double-stranded DNA, and angiotensin-converting enzyme levels were normal.

She became afebrile on day 2 of hospitalization and was discharged on day 7 in a hemodynamically stable condition.

DISCUSSION

Myopericarditis is defined as pericarditis with mild myocardial involvement without any wall motion abnormalities or reduced ejection fraction.² Myocarditis in dengue hemorrhagic fever is usually subtle but may rarely be life-threatening. It is believed to result from cytokine-mediated injury to the myocardium. Direct invasion of myocardial tissue by the dengue virus may have a role but is controversial.³

Pericardial effusion in dengue hemorrhagic fever is generally mild and not clinically significant, occurring as a part of serositis. Setiawan et al.⁴ demonstrated the presence of mild pericardial effusion in only 8% cases of severe dengue. Rapidly accumulating pericardial effusion causing life-threatening cardiac tamponade is rarely encountered. The underlying mechanism is likely cytokine-mediated endothelial dysfunction causing increased vascular permeability and subsequent third-space fluid loss.⁵ To the best of our knowledge, only three such cases have been reported so far.^5–7 Two cases had prior comorbidities such as systemic lupus erythematosus and the other was postpartum. Of the reported cases, two had secondary dengue infection and one had primary infection (Table 2).

Table 2.

Comparison of the present case with previously reported cases of dengue fever with cardiac tamponade

Article	Age (years), gender	Prior comorbidities	Symptoms	Nature of dengue infection	Platelet count at admission (1,000 mm−3)	Cardiac enzyme	Amount of pericardial fluid drained (mL)
Kumar et al.5	59, F	Lupus nephritis	Fever, headache, and vomiting	Secondary	120	Normal	500
Bendwal et al.6	34, F	None	Fever and dyspnea	Secondary	42	Normal	1,500
Fernandes et al.7	26, F	Postpartum	Fever, headache, and dyspnea	Primary	165	NA	NA
Present case	30, F	None	Fever, chest pain, and dyspnea	Primary	113	Raised	280

Although uncommonly encountered, knowledge of the occurrence of cardiac tamponade in dengue hemorrhagic fever is of paramount importance. The features of hypotension and shock in association with respiratory distress may occur in patients of dengue hemorrhagic fever in the phase of increased vascular permeability with “plasma leak.”⁸ The treatment in such cases is usually supportive and involves close monitoring of the patient. In our case, the rapid clinical decline and the presence of mild effusion did not account for the rapid development of shock. Features of cardiac dysfunction such as raised jugular venous pressure, muffled heart sounds, and hypotension indicated a likely cardiac tamponade, which was confirmed on echocardiography. Elevated troponin-I and changes in electrocardiogram were suggestive of myopericarditis. There was no evidence of regional or global wall motion anomalies on echocardiogram and normal ejection fraction, which made myocardial ischemia unlikely. Thus, the threshold for repeat clinical examination and POCUS in a patient of dengue should be low, and alternative explanations for the presentation should be eliminated before diagnosing as dengue shock syndrome. The importance of this lies in the fact that cardiac tamponade is easily correctable by means of pericardiocentesis but requires immediate intervention, unlike dengue shock syndrome where treatment is supportive.⁹

Cardiac manifestations are common in dengue hemorrhagic fever, and the spectrum of involvement ranges from asymptomatic bradycardia to severe myocarditis and indeed cardiac tamponade, as in our case. This index case of severe dengue hemorrhagic fever with myopericarditis and cardiac tamponade, thus, further widens the domain of expanded dengue syndrome. Four serotypes of the dengue virus are known, namely, DEN 1, 2, 3, and 4, but cardiac complications occur with DEN2 and DEN3 serotypes.¹⁰ A recent study in India by Arora and Patil showed that 15.8% patients had abnormal rhythm and 37.50% patients had myocarditis, and these patients also exhibited a positive correlation with the severity of dengue fever as defined by the WHO criteria. They concluded that dengue patients require close cardiac monitoring, primarily to monitor for cardiac complications.¹¹