Journal of the Practice of Cardiovascular Sciences

: 2016  |  Volume : 2  |  Issue : 3  |  Page : 183--186

A case of PDA with infective endocarditis

Danny Kumar, P Anand 
 Department of Cardiology, AIIMS, New Delhi, India

Correspondence Address:
Danny Kumar
Department of Cardiology, AIIMS, New Delhi


An 18-year-old girl presented with prolonged febrile illness with dyspnea. She was asymptomatic till an episode of infective endocarditis (IE). Patent ductus arteriosus (PDA) detection at this age is not unusual. IE is a common presentation of undiagnosed PDA in the second decade.

How to cite this article:
Kumar D, Anand P. A case of PDA with infective endocarditis.J Pract Cardiovasc Sci 2016;2:183-186

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Kumar D, Anand P. A case of PDA with infective endocarditis. J Pract Cardiovasc Sci [serial online] 2016 [cited 2023 May 28 ];2:183-186
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 Clinical Presentation

An 18-year-old girl, a class 12 student from Bihar, presented with:

Fever off and on for 7 months Exertional dyspnea for 6 months.

The patient was apparently well till 7 months back when she started to experience continuous fever documented to be 103–104°F associated with chills and rigor, requiring around-the-clock antipyretics. There were associated constitutional symptoms in the form of malaise and generalized body ache. It was not associated with localizing symptoms such as cough, running nose, expectoration, and abdominal pain, burning micturition, headache, or neck stiffness. She was shown in a local hospital, and with some treatment, the fever subsided in 7–8 days only to recur again in 3–4 days. With another course of treatment, the fever again stopped after a week. It recurred again within 5–6 days and was now associated with shortness of breath (Class II) on riding a bicycle. Along with dyspnea which slowly progressed to Class III, there were also exertional palpitations. There was no history of orthopnea, paroxysmal nocturnal dyspnea, or pedal edema. She did not receive intravenous medication during this period. There was no associated joint pain, skin rash, bleeding from any site, presyncope, or syncope.

This fever, shortness of breath, and palpitation continued for 7 months during which the girl lost about seven kilograms of weight.

There was no significant history of similar prolonged febrile illness. There was no history of episodes of arthralgia or arthritis in childhood, episodes of shortness of breath, recurrent pneumonia in childhood, hospitalization for any significant illness, and being diagnosed as having a heart disease or receiving penicillin prophylaxis. There were no details of any blood investigation having been done, but there was no history of having received any blood transfusion during the illness or having been told to be anemic. There was no history of bleeding from any site.

From the father, there was no evidence abnormal antenatal history. She was the 4th of 5 siblings, and the other siblings were normal. She was vegetarian, unmarried, and her menstrual history was normal.

There was no significant family history of any cardiovascular disorder.


This is an 18-year-old girl presenting with moderate- to high-grade fever for 7 months associated with slowly progressive shortness of breath and palpitations and weight loss but without any respiratory symptom.


The salient features to be discussed are:

Prolonged fever 7 months (not responded to usual oral therapy) Dyspnea (slowly progressive to Class III) Palpitations Negative history No respiratory symptoms No history of being diagnosed as having anemia or receiving blood transfusions.

The history of prolonged fever in a patient from Bihar leads immediate suspicion to noncardiac causes, and it is natural to think of causes such as kala-azar or tuberculosis or chronic malaria. However, for any of these causes to cause progressive shortness of breath, they would all need to cause severe anemia, and it would be reasonable to expect that, wherever this patient was treated, anemia would have been picked up. The fact that anemia was never diagnosed or treated (as per the history) nor is there a history of blood transfusion provides sufficient reason at this point to keep these causes low in the priority. Similarly, a total lack of respiratory symptoms in the form of cough and expectoration would again tend to exclude a primary respiratory focus of the entire illness.

 Cardiac Causes of a Febrile Illness

Fever with progressive dyspnea does point to a cardiac lesion when other causes have been excluded on history. Since she was asymptomatic at the onset of the illness (at age 18), we need to see what cardiac lesions can be prone to infective endocarditis (IE), be silent till the age of 18, and rapidly progress with IE.

Rheumatic heart disease (RHD) is the most common cardiac disorder to consider at the age of 18, and among the silent lesions, mild to moderate mitral regurgitation and mild to moderate aortic regurgitation are possible lesions which can suddenly worsen with IE A bicuspid aortic valve with mild aortic regurgitation can also present like this with IE. Same is true for mitral valve prolapse with mitral regurgitation Left to right shunts: small left to right shunts such as a small ventricular septal defect (VSD) or a VSD with aortic regurgitation can progress with IE. Similarly, a patent ductus arteriosus (PDA) can be asymptomatic and then present with IE.

 What Is the Risk of Infective Endocarditis of Condition Listed Above?

RHD is most common underlying condition in IE patients in the Indian scenario. In a recent study of 2-year follow-up of 3000 patients, 0.7% develop IE, with an incidence of 3.65/1000 patient-years, which would be more if only regurgitant lesions were included.[1] Small shunts such as small VSD had a 20 times higher risk than the general population. In a recent study, the incidence of IE was 1.7–2.7/1000 patient-years.[2] The risk of developing IE on a bicuspid aortic valve is 10%–30% over a lifetime.[3]

Is it possible for IE to have fever for 6 month? Can IE present without fever?

Antibiotic modified IE can present for long periods as partially treated, and some less virulent organisms can present with prolonged fever. Many low-virulence organisms present with low-grade fever or no fever, for example, Brucella, Bartonella, Coxiella, Treponema whippelii. Fever (>38°C) is the most common presenting symptom in up to 95% of patients but may be absent in up to 20% of cases. The absence of fever can be due to low-virulence organisms, in immunocompromised patients, in heart failure, in elderly patients, with previous empirical antibiotic therapy, or patients with infections of implantable cardiac devices.[4],[5]

 On Examination

The patient was conscious and oriented to time, place, and person. Her height was 157 cm, weight was 30, and body mass index = 12 kg/m 2.

Her pulse rate was 110/min, regular, bounding, and collapsing (water hammer). There was no radioradial or radiofemoral delay. She was febrile to touch. The blood pressure in the right upper limb was 126/50 mm of mercury (Hg) and in the right lower limb was 138/70 mm Hg. The respiratory rate was 20/min and regular.

She had mild anemia with Grade II clubbing. The jugular venous pressure was not raised, and there was no icterus, cyanosis, and pedal edema.

The oral hygiene was good, and there was no dental caries. There were no peripheral signs of IE other than anemia and clubbing. There were no peripheral signs of a high volume pulse.

On cardiovascular examination, the precordium was normal in shape and contoured, with the apex impulse in the fifth intercostal space in the midclavicular line, with prominent suprasternal pulsations. There were no scars, sinuses, or any other pulsations. The apex was localized but hyperdynamic. There was a Grade II parasternal heave. Second sound was not palpable. There was no thrill. There was no epigastric pulsation. The second intercostal space was resonant, and the liver dullness was in the 5th intercostal space.

The first sound was normal, but the second sound could not be appreciated well due to a continuous murmur. There was no third or fourth sound.

There was a Grade 3/6 continuous murmur in the first intercostal space along the left sternal border with crescendo-decrescendo pattern reaching its peak around the second sound and terminating just before the end of diastole with no eddy sounds.

Chest features were suggestive of right lower lobe consolidation in the form of decreased breath sound and increased tactile vocal fremitus and vocal resonance.

Abdomen examination revealed an enlarged spleen (2 cm, firm, and nontender) but no enlargement of the liver.

Diagnosis Acyanotic congenital heart disease Increased pulmonary blood flow PDA with moderate pulmonary arterial hypertension (PAH), mild pulmonary venous hypertension IE, Class III Anemia (mild) Embolization of vegetation to the right lung.

Question - This is a patient with fever and a continuous murmur. What are differential diagnoses? What are other causes of continuous murmur?

Ruptured sinus of Valsalva

This is always a differential for a continuous murmur. Usually, a ruptured sinus of Valsalva (RSOV) has a more abrupt onset, and fever is less common. Chest pain is often present at presentation. Progressive dyspnea is rapid in these patients. Patients with RSOV deteriorate fast with early presentation with congestive heart failure.

The continuous murmur in this patient is usually lower down, prominent in the 2–4 spaces with right ventricular rupture and 4–5th space and right of sternum also in right atrial rupture. Its murmur often is to-and-fro continuous murmur which tends to be louder in diastole.

Coronary arteriovenous fistula can also present with continuous murmurs but since the shunt size is very small, they usually do not present with hemodynamic consequences. The location, duration, and character of the continuous murmur depend on the anatomical type of fistula. Involvement of the right coronary artery produces a murmur located along the parasternal area. Left circumflex and coronary sinus communication is located in the left axilla. The configuration of the murmur and its systolic and diastolic intensities are variable.

VSD with aortic regurgitation is often a differential for a continuous murmur; however then, careful auscultation can separate the systolic and diastolic components of the two murmurs.

Peripheral pulmonary artery stenosis: a continuous murmur is audible all over the thorax.

Aortopulmonary window: an extremely rare cause. Due to the large size of the communication, PAH develops rapidly and so the diastolic component disappears.

Coarctation of aorta, bronchial arterial collaterals, innocent murmur-venous hum, and mammary soufflé are other causes of continuous murmur.

Peaking of continuous murmur at S2 is a feature of PDA as the pulmonary artery flow in the start of systole is by RV outflow and then duct start contributing before S2 combined flow makes it peak, and in diastole, flow is from duct only. Early part of systole and last part of diastole may be free of murmur. Uninterrupted progression of the murmur through S2 is a must for a continuous murmur. Eddies sound around S2 can be heard.

 How Did You Judge the Severity of Pulmonary Arterial Hypertension in Patent Ductus Arteriosus?

In this patient, the second sound was drowned by the murmur and was not helpful. A Grade II parasternal heave suggests at least moderate pulmonary artery hypertension. Since the PDA murmur is continuous, it suggests that the shunt is still left to right and the PAH is not severe and irreversible. As the PAH becomes severe, the diastolic component disappears.

 What Is Natural History of Patent Ductus Arteriosus?

In the 1st year of life, a large shunt can present as heart failure. After the 1st year, most patients with PDA are asymptomatic. In the second decade, infective endarteritis at the narrow pulmonary end as presentation is more common, and in the third decade, a moderate PDA presenting with heart failure is again common.[6],[7],[8] Nearly 50% of large PDA eisenmengerized at a mean age of 20 years.[9]

 What Is This X-Ray Showing, Is it Compatible With Your Diagnosis?

[Figure 1] showing the X-ray shows cardiomegaly present, with 60% cardiothoracic ratio, signs of increased vascularity with end on vessels and a left ventricular type of apex. There is moderate pulmonary artery hypertension as there is some enlargement of the pulmonary artery segment making the left border straight. However, there is no PDA shadow or any calcification at the site of the PDA. Ascending aorta is not dilated, chambers, for example, RA and LA are not dilated, which rules out a large shunt. X-ray shows features suggestive of increased pulmonary flow but not much confirmative of PDA as X-ray had low sensitivity for diagnosing a PDA. Lung fields show mild haziness in the right lower zone, but it is not typical of pulmonary infarct and more likely a breast shadow [Figure 2].{Figure 1}{Figure 2}

[Figure 3] shows the echocardiogram, with a continuous flow across the PDA and vegetation in the pulmonary artery.{Figure 3}

This confirms the diagnosis of a PDA with IE.


The patient will be treated for IE, and after completion of the full course, PDA ligation will be done. In the case of infective endarteritis, device closure is not feasible due to the risk of distal embolization of vegetation.

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Conflicts of interest

There are no conflicts of interest.


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