Patent Ductus Arteriosus in infant - Nursing Case Study
Pathophysiology
• Primary Mechanism: In utero, the ductus arteriosus, a small vessel, connects the pulmonary artery to the aorta, bypassing the lungs as they are not yet needed for oxygenation. After birth, this duct normally closes within a few days, allowing the blood to flow correctly through the heart to the lungs for oxygenation. In Patent Ductus Arteriosus (PDA), this closure fails, causing an abnormal blood flow between the aorta and pulmonary artery.
• Secondary Mechanism: The continued patency of the ductus arteriosus results in a left-to-right shunt, leading to increased blood flow to the lungs. This can exacerbate pulmonary hypertension, cause left atrial and ventricular volume overload, and potentially lead to heart failure.
• Key Complication: Over time, if untreated, the excess blood flow to the lungs may cause pulmonary congestion, potentially resulting in respiratory distress. In severe cases, it can reverse the direction of the shunt (Eisenmenger syndrome), which can lead to life-thre
Patient Profile
Demographics:
6 months old, Female, Not applicable
History:
• Key past medical history: Premature birth at 28 weeks
• Current medications: Indomethacin for closure of PDA
• Allergies: No known allergies
Current Presentation:
• Chief complaint: Difficulty in feeding, rapid breathing
• Key symptoms: Shortness of breath, poor weight gain, excessive sweating, fatigue, and continuous, machine-like heart murmur
• Vital signs: Pulse rate - 160 bpm, Respiratory rate - 50 breaths per minute, Oxygen saturation - 90% on room air, Temperature - 98.6 F, Blood Pressure - 90/50 mmHg
Section 1
New Diagnostic Results:
Despite the administration of indomethacin, the infant's condition did not improve significantly. A follow-up echocardiogram revealed that the ductus arteriosus remained patent, with a large left-to-right shunt. This finding suggested that the indomethacin had not been effective in closing the PDA. Furthermore, the echocardiogram showed evidence of increased left ventricular volume, suggesting that the infant's heart was working harder to pump blood.
Laboratory results also indicated a worsening condition. The infant's blood gas analysis showed a pH of 7.28 (normal range: 7.35-7.45), PaCO2 of 50 mmHg (normal range: 35-45 mmHg), bicarbonate of 22 mEq/L (normal range: 22-28 mEq/L), and PaO2 of 80 mmHg (normal range: 80-100 mmHg). This suggested the presence of respiratory acidosis, likely due to her increased work of breathing.
These new diagnostic results indicate that the infant's condition is deteriorating, and the current treatment plan is not effectively managing her PDA. The medical team needs to consider alternative treatments, such as surgical closure of the ductus arteriosus, to prevent further complications. This situation requires careful clinical reasoning to determine the best course of action for this infant.
Section 2
Change in Patient Status:
Over the next several hours, the infant's condition continued to deteriorate. She exhibited noticeable difficulty with feeding, showing signs of fatigue and shortness of breath during and after feedings. Her heart rate increased to 180 beats per minute (normal range for a newborn: 100-160 beats per minute), indicating possible tachycardia. Additionally, the infant's respiratory rate was measured at 70 breaths per minute (normal range: 30-60 breaths per minute), suggesting tachypnea. Her oxygen saturation levels fluctuated, at times dropping to 86% (normal range: 95-100%), despite receiving supplemental oxygen.
Upon physical examination, the infant's skin appeared mottled and cool to touch, indicating poor peripheral perfusion. The nurse also noted a prominent precordial impulse and a continuous, machinery-like murmur on auscultation, classic signs of PDA. These changes in her condition indicate a worsening of her heart failure due to the PDA and the increased strain on her heart. It is critical to reassess the current treatment approach and consider more aggressive interventions to manage her condition. This situation requires a high level of clinical reasoning to balance the risks and benefits of potential treatment options.
Section 3
Change in Patient Status:
An urgent echocardiogram was ordered to confirm the suspected diagnosis of PDA. The results revealed a sizeable patent ductus arteriosus, causing a significant left-to-right shunt. The left atrium and left ventricle were enlarged, indicating volume overload due to the shunt.
Her blood gas measurements showed a pH of 7.28 (normal range: 7.35-7.45), indicating mild acidosis, and a PaCO2 of 52 mmHg (normal range: 35-45 mmHg), suggesting respiratory acidosis. Her bicarbonate levels were normal, and her base excess was -4 (normal range: -2 to +2), confirming a primary respiratory problem. These results suggested that the infant was unable to adequately oxygenate her blood due to the increased pulmonary blood flow caused by the PDA. This was contributing to her respiratory distress and the observed changes in her skin color and temperature.
New Complications:
The infant's worsening condition necessitated a change in management approach. However, the decision was complicated by the development of a new complication. The infant became increasingly irritable and exhibited symptoms of increased intracranial pressure, such as bulging fontanelles and high-pitched crying. This raised concerns about the possibility of an intraventricular hemorrhage (IVH), a common complication in infants with significant heart disease. An urgent head ultrasound was ordered to evaluate the possibility of IVH. The results of the ultrasound could have significant implications on the choice of intervention for her PDA, as surgical closure might be contraindicated if an IVH was present.
Section 4
Change in Patient Status:
The infant's condition continued to deteriorate. Her respiratory distress became more pronounced, with grunting, nasal flaring, and retractions observed. Her respiratory rate increased to 70 breaths per minute and oxygen saturation dropped to 86% on room air, indicating worsening hypoxemia. Additionally, the infant became tachycardic with a heart rate of 180 beats per minute. Her skin became increasingly mottled and cool to touch, suggesting poor perfusion. The infant also became lethargic, another sign of deteriorating brain perfusion.
Response to Interventions:
Despite these concerning signs, the nursing team continued to provide supportive care while awaiting the ultrasound results. The infant was placed on supplemental oxygen via nasal cannula at 2 L/min, which improved her oxygen saturation to 92%. Intravenous fluids were initiated to maintain hydration and support cardiac output. Simultaneously, the team was also preparing for the possibility of needing to start the infant on prostaglandin E1 to keep the ductus arteriosus open if IVH was confirmed, thus preventing further deterioration of the infant's condition. However, this decision would need to be balanced against the risks of worsening the infant's respiratory distress due to increased pulmonary blood flow. The team eagerly awaited the ultrasound results to guide the next steps in management.
Section 5
New Diagnostic Results:
The eagerly awaited echocardiogram results finally arrived, confirming the diagnosis of Patent Ductus Arteriosus (PDA). The ultrasound also showed a moderate-sized PDA with a significant left-to-right shunt, resulting in volume overload of the left heart. The infant's condition, paired with this confirmation, led the team to diagnose her with congestive heart failure secondary to the PDA. Additionally, the cranial ultrasound did not show any signs of intraventricular hemorrhage (IVH), eliminating that as a potential concern.
Change in Patient Status:
Despite the ongoing supportive care, the infant's condition further deteriorated. Her heart rate increased to 200 beats per minute, and despite the supplemental oxygen, her oxygen saturation fluctuated between 86% and 90%. She developed a new heart murmur, suggestive of the increased blood flow through the PDA. The infant also started showing signs of poor feeding and weight loss, indicating worsening heart failure. Furthermore, the infant's urine output decreased to less than 1 mL/kg/hr, suggesting reduced renal perfusion due to decreased cardiac output. This new information necessitated a change in management strategy.