**6. Hemodynamic significance of the PDA**

There is no consensus regarding the definition of a hemodynamically significant PDA (hsPDA), yet it is a key indicator for clinicians when determining whether intervention is needed to close the ductus. Historically, clinical signs have been used as indicators of hsPDA, such as the presence of a systolic murmur, wide pulse pressures,

#### **Figure 1.**

*Transthoracic echocardiogram (TTE) demonstrating a large, hsPDA in a 3 weeks old ex-24 week ELBW infant. (A) 2D-TTE demonstrating a large PDA between the aorta and the pulmonary artery (PA). (B) Color Doppler demonstrating left to right shunt in the PDA from the aorta to the PA. (C) Severe left atrial (LA) and left ventricular (LV) enlargement relative to the right atrium (RA) and the right ventricle (RV).*

bounding pulses, pulmonary edema, and increased oxygen requirements. With the advent of echocardiography in the 1970s, more sophisticated measures can be used to determine hemodynamic significance. Approaches to determine hsPDA now include (1) establishing thresholds based on clinical signs and echocardiographic parameters, (2) the need for treatment as determined by the size of the PDA and its likelihood of closing based on age/size of the infant, (3) probable outcomes based on identifying populations most likely to experience complications related to PDA.

Echocardiographic indices to determine hsPDA can be established by PDA shunt size, the extent of volume overload [19–21], the degree of pulmonary overload, and the magnitude of systemic hypoperfusion (**Figure 1**). Moderate to large PDAs may be hemodynamically significant if flow patterns through the duct indicate significant left-to-right shunting. Volume overload is determined by calculating the left atrium diameter (LA) relative to a constant, the aortic root diameter (Ao). An LA:Ao ratio greater than 1.4 is one of the most commonly used indicators of hsPDA, since increased volume through the PDA will return to the left atrium and cause dilation [19–21]. Left ventricular output (LVO), a key indicator of pulmonary overload, may be large due to additional volume from the PDA, or may be small to normal (an ominous sign) if the left ventricle fails to compensate for the additional volume through

#### **Figure 2.**

*Pulse wave Doppler assessment in the descending aorta by TTE in the same patient in Figure 1. (A) There is diastolic flow reversal in the descending aorta (arrows) suggesting a large left to right shunt from the aorta to the PA leading to systemic hypoperfusion. (B) Following transcatheter closure, there is normalization in the Doppler pattern.*


**45**

**Table 2.**

*PDA Closure in ELBW Infants: If, When, and How to Do It*

feeding intolerance, and rising creatinine levels.

**7. Established techniques for closure**

certain contraindications are noted below:

• Severe pulmonary vascular disease.

• Duct dependent congenital heart disease

• Pulmonary artery hypoplasia.

**7.1 Medical therapy**

**Advantages:** • Non-Invasive • Efficacy 50–70% • May take a few days to be

effective

**Disadvantages:**

hyperkalemia • Cerebral white-matter

damage

perfusion

• Impairment in renal function, oliguria, proteinuria,

• Impairment in cerebral

• NEC, Gastrointestinal perforation • Platelet dysfunction

*Advantages and disadvantages of therapies.*

flow may be assessed to further quantify these effects [19–21].

increased cardiac output. Another indicator of pulmonary overload is the enddiastolic velocity in the PA, where high velocities may indicate pulmonary overload. Retrograde diastolic blood flow through the descending aorta (**Figure 2**) may be the most telling sign of systemic hypoperfusion due to a PDA, although end-organ blood

Echocardiographic evidence alone cannot determine hsPDA, but should be used in conjunction with clinical factors (**Table 1**), vulnerability of the infant due to gestational and chronological age, and risk of organ overflow (lungs) or hypoperfusion (brain, kidneys, intestines). Clinical findings that may help identify hsPDA include the need for vasopressors/inotropes, ventilator support and pulmonary edema,

Treatment options are continuously evolving [25], and have included routine pharmacological treatment, conservative management, surgical ligation and transcatheter closure (**Table 2**). While indications for closure are not fully agreed upon,

Pharmacological treatment with COX inhibitors is usually the initial treatment for PDA. Currently, pharmacological therapy consists of intravenous or oral

> **Advantages:** • Minimally-Invasive • Efficacy 100%

**Disadvantages:**

• LPA stenosis (1%) • Aortic arch stenosis (1%) • Device embolization (1%) • Tricuspid valve regurgitation

(1%)

(2%)

medium • Hypothermia

• Immediate and definitive closure

• Vascular access complications

• Exposure to X-Rays and contrast

**Pharmacologic therapy Surgical ligation Transcatheter closure**

• Immediate and definitive

• Risk of worsening of BPD

• Diaphragmatic paralysis

• Cardiorespiratory failure

• Post-Ligation Syndrome (30%) • Vocal cord dysfunction (30%) • Impaired neurodevelopmental

**Advantages:** • Invasive • Efficacy 100%

closure

**Disadvantages:**

outcomes

• Chylothorax

• Bleeding • Pneumothorax

*DOI: http://dx.doi.org/10.5772/intechopen.88857*

### **Table 1.**

*Clinical and echocardiographic criteria for hemodynamic significance.*

*PDA Closure in ELBW Infants: If, When, and How to Do It DOI: http://dx.doi.org/10.5772/intechopen.88857*

*Update on Critical Issues on Infant and Neonatal Care*

bounding pulses, pulmonary edema, and increased oxygen requirements. With the advent of echocardiography in the 1970s, more sophisticated measures can be used to determine hemodynamic significance. Approaches to determine hsPDA now include (1) establishing thresholds based on clinical signs and echocardiographic parameters, (2) the need for treatment as determined by the size of the PDA and its likelihood of closing based on age/size of the infant, (3) probable outcomes based on identifying

Echocardiographic indices to determine hsPDA can be established by PDA shunt size, the extent of volume overload [19–21], the degree of pulmonary overload, and the magnitude of systemic hypoperfusion (**Figure 1**). Moderate to large PDAs may be hemodynamically significant if flow patterns through the duct indicate significant left-to-right shunting. Volume overload is determined by calculating the left atrium diameter (LA) relative to a constant, the aortic root diameter (Ao). An LA:Ao ratio greater than 1.4 is one of the most commonly used indicators of hsPDA, since increased volume through the PDA will return to the left atrium and cause dilation [19–21]. Left ventricular output (LVO), a key indicator of pulmonary overload, may be large due to additional volume from the PDA, or may be small to normal (an ominous sign) if the left ventricle fails to compensate for the additional volume through

populations most likely to experience complications related to PDA.

**Clinical criteria Echocardiographic criteria** • Oxygenation difficulty (oxygenation index ≥ 10) • PDA diameter ≥ 2 mm

• Inability to feed/abdominal distention • Left heart enlargement (LA:Ao ratio ≥1.4)

*Pulse wave Doppler assessment in the descending aorta by TTE in the same patient in Figure 1. (A) There is diastolic flow reversal in the descending aorta (arrows) suggesting a large left to right shunt from the aorta to the PA leading to systemic hypoperfusion. (B) Following transcatheter closure, there is normalization in the* 

> • Absent diastolic flow or reversal of enddiastolic flow in descending aorta, superior mesenteric, middle cerebral or renal artery

• Unrestrictive pulsatile transductal flow

• High ventilator settings (Mean airway

• Frequent episodes of oxygen desaturations, apnea or

• Systemic hypotension (low mean or diastolic BP) • Cardiomegaly ± Pulmonary edema on chest X-ray

*Clinical and echocardiographic criteria for hemodynamic significance.*

pressure ≥ 10)

bradycardia

• Metabolic acidosis

**44**

**Table 1.**

**Figure 2.**

*Doppler pattern.*

increased cardiac output. Another indicator of pulmonary overload is the enddiastolic velocity in the PA, where high velocities may indicate pulmonary overload. Retrograde diastolic blood flow through the descending aorta (**Figure 2**) may be the most telling sign of systemic hypoperfusion due to a PDA, although end-organ blood flow may be assessed to further quantify these effects [19–21].

Echocardiographic evidence alone cannot determine hsPDA, but should be used in conjunction with clinical factors (**Table 1**), vulnerability of the infant due to gestational and chronological age, and risk of organ overflow (lungs) or hypoperfusion (brain, kidneys, intestines). Clinical findings that may help identify hsPDA include the need for vasopressors/inotropes, ventilator support and pulmonary edema, feeding intolerance, and rising creatinine levels.
