A 44-year-old male with the past medical history of essential hypertension and tuberculosis presented to the emergency room (ER) with the complaints of high grade fever, fatigue, and shortness of breath. According to patient, he developed high grade fever 1 week ago that was accompanied by myalgias, frontal headache, and generalized weakness. Fever was followed by shortness of breath and exercise intolerance which started 3 days ago and worsened with time. History was positive for mild paroxysmal nocturnal dyspnea and orthopnea though he denied any chest pain, palpitations, cough, or syncope. He also had frequent light headedness and got 1 episode of coffee ground emesis after which he was brought to ER. There was no history of blood in stools or urine. The patient denied any history of diabetes, ischemic heart disease, or hyperlipidemia. The patient was only taking HCTZ for hypertension and did not have any allergies. He was an active smoker with a history of one pack of cigarettes daily but denied use of alcohol or illicit drugs. The family history was positive for myocardial infarction in father at the age of 77. The patient did have a history of recent sick contact with one of his brothers who had dengue fever 3 weeks ago.
Review of patient's past medical records indicated that patient had dengue fever 1 year ago for which he was admitted on the floor but fever got resolved on its own with no complications. At that time patient developed vague chest discomfort for which EKG was done which showed widespread T wave inversions. Cardiac enzymes were mildly elevated and echocardiography showed normal wall thickness and ejection fraction of 58%. Taking into account above findings, a tentative diagnosis of mild dengue myocarditis was made. CXR was normal and patient was discharged. Endomyocardial biopsy and cardiac MRI were not done as the patient had mild myocarditis with normal myocardial functions. Follow-up CXR, Echo, and EKGs were normal and patient remained healthy other than having slight fatigue.
In ER patient was lethargic and seemed anxious due to generalised body aches and headache. On physical examination, vital signs were as follows: blood pressure of 89/52 mmHg, temperature of 103 F, heart rate of 116/min, and respiratory rate of 19. Chest examination revealed reduced breath sounds at lung bases bilaterally with scattered fine crackles in both lungs; no rhonchi or wheeze was heard. Examination of heart was remarkable for normal S1 and S2 with no murmur or clicks; an S3 gallop sound was audible. There was no pallor, scleral icterus, cyanosis, clubbing, or peripheral edema. The rest of the physical examination was unremarkable.
Patient was suspected to have dengue shock syndrome and was immediately admitted on floor and resuscitated with IV fluids. Antiemetics and Tylenol was also given. Routine EKG was done which showed sinus rhythm and frequent premature ventricular contractions (PVC) with no ST or T wave ischemic changes (Figure 1). CXR showed bilateral interstitial edema, cardiomegaly, and pleural effusion in both lungs (Figure 2). The X-ray findings were suggestive of acute congestive heart failure. Elevated BNP (1040) supported the X-ray findings His haematological investigations revealed slight thrombocytopenia (127000), leucopenia (3100), and haemoglobin of 12. Cardiac enzymes were initially slightly elevated but remained stable over the course of hospital stay (Table 1). Urgent transthoracic echocardiography was done which showed ejection fraction of 10% and left ventricle dilation without focal wall motion defect and or focal thinning (Figure 3). Cardiac catheterization revealed EF of 13% and normal coronary arteries (Figure 4). Patient was started on dobutamine infusion along with ACEIs, spironolactone, and Lasix. Blood cultures, ESR, hepatitis panel, thyroid profile, and urine drug screen were all within normal limits. Malarial antigen test and typhoid serology were also negative. Anti-dengue IGM by ELISA was negative at the time of admission but was positive for IGG antibodies at that time. Repeat testing on day 3 showed positive IGM antibodies for dengue. The diagnosis was confirmed with reverse transcriptase polymerised chain reaction (RT-PCR) which was positive for dengue virus serotype 3 (DEN-3). In view of above clinical scenario with positive dengue serology, history of myocarditis during primary dengue infection 1 year ago, and echocardiographic findings, diagnosis of dengue virus induced dilated cardiomyopathy (DCM) was made. Fulminant myocarditis with acute myocardial failure was ruled out as cardiac enzymes were almost normal in the setting of dilated cardiac chambers on Echo.
Patient condition worsened gradually and he developed acute hypoxic respiratory failure for which he was intubated on day 4. Patent developed severe thrombocytopenia and despite platelet transfusions he developed massive lower GI bleed leading to refractory shock. Patient was transfused 2 units of PRBC and platelets, but despite aggressive resuscitation and intensive care, patient died on day 5.