Complications
There also appears to be an association with severe RDS, with a much higher incidence of PDA seen in premature infants ill with RDS.[22]
This complication is usually limited to premature infants with increased haemodynamic instability. Left-to-right shunting at the level of the ductus can lead to systemic steal. This can result in hypoperfusion of end organs including the gut. The presence of a ductus has been found to be independently associated with an increased incidence of necrotising enterocolitis.[24] Treatment varies from medical therapy with gut rest to surgical intervention. Prevention is attempted by not feeding premature infants who have suspected patent ductus arteriosus, and by attempting medical or surgical closure of significant ducts.
Isolated to premature infants, pulmonary haemorrhage can result from increased pulmonary blood flow. This was directly related to the size of the duct in one study.[19]
A large non-restrictive patent ductus arteriosus (PDA) can lead to the eventual development of pulmonary hypertensive disease in patients if left untreated. This occurs because of chronic volume and pressure overload on the pulmonary circulation that can lead to irreversible vascular changes. Symptoms of pulmonary HTN in children are frequently subtle, which can result in delayed diagnosis. In infants, poor feeding, tachypnoea, tachycardia, and poor growth are common. Physical signs may include a loud split second heart sound, right ventricular heave, gallop, and holosystolic murmur of tricuspid regurgitation.[113] Elevated pulmonary pressures may eventually lead to right-to-left shunting through the duct, resulting in cyanosis, shortness of breath, and clubbing (Eisenmenger syndrome). Oedema of the face, hands, and ankles, and hepatomegaly, are later signs of right-sided heart failure.[113] Chest radiography may provide clues as to the degree of shunting; congested vasculature is often seen in large left-to-right intracardiac shunts. Oligemia may be present in patients with restricted blood flow, such as those with Eisenmenger syndrome. However, radiographic findings do not always correlate with disease severity.[113] Transthoracic echocardiography is the first-line cardiovascular laboratory modality for the diagnosis and monitoring of pulmonary HTN. Cross-sectional laboratory (computed tomography and magnetic resonance imaging) are also used in diagnosis and management. Cardiac catheterisation is considered the gold standard for measuring haemodynamics in patients with congenital heart disease and pulmonary HTN, especially to assess operability; duct occlusion to determine the feasibility of closure of patent ductus arteriosus can be performed during the procedure.[113] For patients with pulmonary HTN and PDA, early repair and elimination of the shunt is paramount to reduce the overall burden of cardiovascular disease; the pulmonary HTN may be reversible with timely treatment of the PDA.[113][114] In those patients with irreversible pulmonary HTN, treatment options are limited to medical therapy, including oxygen and pulmonary vasodilators.
An untreated patent ductus with a significant shunt can result in symptoms of CHF. When and if CHF occurs depends on the size of the shunt and the degree of volume overload on the heart. While larger shunts may present in infancy, more moderate shunts may not present until later in childhood or into adulthood.[31] Once symptoms of heart failure are noted, patients can initially be managed medically with digoxin and diuretic therapy until the ductus can be dealt with definitively, either by catheter closure or surgical ligation.
The challenges associated with living with congenital heart disease can lead to depression and anxiety in as many as half of patients. Early-life stressors such as time in intensive care units and other traumatic healthcare experiences can also have a significant impact.[119]
Psychological care should be a routine part of congenital heart disease treatment, with access given to psychotherapy and pharmacotherapy where needed.[119]
Prior to surgical and catheter closure, the incidence of infective arteritis associated with the lesion was as high as 1% per year.[31] However, in the current era this has decreased dramatically to almost negligible numbers of case reports.[108] When they occur, vegetations usually form on the pulmonary end of the duct as a result of turbulent flow, and can result in pulmonary emboli. If suspected endarteritis can be diagnosed by transthoracic or trans-oesophageal echo. Treatment usually consists of long-term antibiotics followed by definitive closure of the duct.
A ductal aneurysm is an enlargement of the ductal tissue near the point of attachment to the aorta. It is thought to be related to abnormal elastin/ductal tissue. The reported incidence varies significantly from 1.5% to 8%.[115][116] It usually presents in infancy but has been reported in adults.[117] While some of the aneurysms resolve on their own, complications such as thromboses or rupture can occur.[116][118] The presence of a ductal aneurysm often points to an underlying connective tissue disorder. Spontaneous resolution of ductal aneurysms in infancy has been reported. If persistent or discovered at a later age, surgery is recommended.
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