Skip to Main Content

++

GENERAL

++

The patent ductus arteriosus (PDA) is usually functionally closed within 12 hours of life. Anatomic closure normally occurs within 10 days. In the premature infant, closure often will not occur until term.

++

Left-to-right shunting through the ductus may contribute to increasing pulmonary edema, persistent need for ventilator support, and the development of bronchopulmonary dysplasia (BPD). Decreased systemic perfusion to end organs such as the brain, kidney, and intestines may also occur. These potential complications have traditionally been the motivation to achieve ductal closure.

++

It remains unclear if treatment of a PDA results in improved long-term outcomes. Recent analyses have shown that treatment of a PDA does not reduce the common complications of prematurity, including death, BPD, intraventricular hemorrhage (IVH), or necrotizing enterocolitis (NEC).1 Risks of medical or surgical closure also exist. Therefore, determination of the hemodynamic significance of the PDA in a particular patient is essential to approaching management strategies until further evidence from clinical studies can be acquired to guide optimal treatment.

++

DIAGNOSIS

++

Clinical Signs and Symptoms

++

Suspect a hemodynamically significant PDA in premature infants when the following exist:

++

  1. A systolic or continuous “grating” murmur heard in the left upper sternal border (LUSB).

  2. Bounding pulses (often palmar pulses are palpated).

  3. Wide pulse pressure greater than 20 mm Hg with decreased diastolic pressure may be present but has poor diagnostic power in very low birth weight infants.

  4. Difficulty weaning from the ventilator (above what is expected for the typical respiratory distress syndrome [RDS] picture); increased arterial partial pressure of carbon dioxide (PaCO2) may be the only finding.

  5. Congestive heart failure (CHF), cardiomegaly, and pulmonary edema visible on chest x-ray.

  6. Metabolic acidosis from retrograde aortic flow (“ductal steal”).

  7. Feeding intolerance.

  8. Oliguria, rising creatinine levels, from decreased renal perfusion (ductal steal).

  9. Note: Not uncommonly, a PDA is asymptomatic (“silent ductus”) in small, sick premature infants.

++

Echocardiographic Findings

++

Confirmation of clinical suspicion is by echocardiogram (echo):

++

  1. Echo characteristics to consider include

    1. Size of the duct,

    2. Direction of blood flow (left to right, bidirectional), and

    3. Evidence of fluid overload (eg, elevated ratio of left atrial to aortic root [La:Ao ratio] or atrial enlargement), and

    4. Evidence of holoretrograde diastolic flow, or

    5. Mitral regurgitation.

  2. The echo will only capture a moment in time. As the PDA is dynamic, multiple echo studies may be necessary for clinical correlation.

  3. If ductal closure is considered, it is important to rule out a ductal-dependent lesion.

++

TREATMENT

++

Conservative Management

++

In the asymptomatic patient, consider waiting for spontaneous closure with conservative management.

++

  1. Limit the fluid volume to the essential amount necessary to meet estimated needs.

  2. Diuretic therapy may be necessary to minimize pulmonary edema.

  3. Treat hypotension with pressors until ductal closure is confirmed.

  4. Maintain higher positive ...

Pop-up div Successfully Displayed

This div only appears when the trigger link is hovered over. Otherwise it is hidden from view.