PPHN condition results from failure to attain a smooth transition “from fetal to extrauterine pulmonary circulation after birth”. Diagnosis of this condition can be done through various ways including; physical examinations, looking at the history, undertaking laboratory tests, using chest x-ray, undertaking hyperoxia test, and echocardiogram.
We will write a custom Research Paper on Persistent Pulmonary Hypertension of the Newborn (PPHN) specifically for you
301 certified writers online
The signs and symptoms include; tachypnea or rapid breathing, increased heart beat rate, respiratory distress which may include signs like grunting and flaring nostrils, and cyanosis even at the time the infant is being given extra oxygen to help it in breathing and having heart murmur among others.
In this paper, there has also been describing of the causes, treatment, and outcomes of PPHN condition and the role of the respiratory therapist in dealing with this condition.
PPHN condition is an outcome of failure to attain a smooth transition “from fetal to extrauterine pulmonary circulation after birth” (Bartle, Patole & Rao, 2010, p.845). In most cases, pulmonary circulation experiences a noticeable drop from a high-resistance condition in the utero to a “low-resistance circuit”, within a very short period of time after birth (Mago, 2012, p.30).
Such reduction in the “pulmonary vascular resistance” or what is simply referred to as PVR, gives room for the lungs to turn out to be a gas exchange body organ (Kraemer, Krijger, Reiss, Rottier, Sluiter & Tibboel, 2011, p.245).
This paper is going to look at the “Persistent Pulmonary Hypertension of the Newborn” condition in much detail. The paper will discuss the diagnosis of this condition, its signs and symptoms, the population affected, causes, treatment, outcomes, and the role of the respiratory therapist. The last section of the paper will present a summary of the discussion.
The diagnosis of the “Persistent Pulmonary Hypertension of the Newborn” condition can be confirmed by echocardiography which gives demonstration of the “right-to-left shunt with normal anatomy” (Bartle, Patole & Rao, 2010, p.845).
There is suspicion of PPHN in the newborn children who shows liability in the progressive cyanosis oxygenation condition in the initial twelve to twenty four hours of the child’s life; and in other occasions, after the first good oxygenation period.
Establishing of diagnosis is carried out from the physical examinations, the history of the patient, “laboratory tests, chest x-ray, pre-ductal and post-ductal blood gases, hyperoxia test, and echocardiogram” (Natarajan, Ostrea, Uy, & Villanueva-Uy, 2006, p.181).
Revelation is made of either a term infant or post-term infant by the history with a perinatal asphyxia’s history or predisposing factors like persistent membrane rapturing, “oligohydramnios, maternal group B streptococcal colonization, maternal smoking, and antenatal use of NSAIDS” (Natarajan et al., 2006, p.181).
The purpose of the physical examination is to help reveal the intermittent or progressive cyanosis, the variable levels of the respiratory distress and an intimately “split second heart” (Natarajan et al., 2006, p.181). There may be an audible murmur within the tricuspid or pulmonary region or sometimes in mitral area.
Systematic BP maybe at the normal level or there may be exhibition of sigs of the congestive heart failure as well as low blood pressure or BP. Moreover, there may be saturations of differential oxygen with either the upper or the lower extremities resulting from deoxygenated blood shunting via ductus arteriosus (Natarajan et al., 2006, p.181).
On the other hand, considering the x-ray method, this is found to be non-specific. This may be either normal or there may be mild or moderate “parenchymal lung disease” (Natarajan et al., 2006, p.181).
This form of diagnosis is mostly important in diagnosing the cause of acute deterioration among the affected children suffering from the PPHN-related conditions like; pulmonary hemorrhage among others (Nakwan, Nakwan & Wannaro, 2011, p.311).
Get your first paper with 15% OFF
Diagnosing PPHN by applying echocardiographic diagnosis is carried out on the basis of demonstrating high pressures of the pulmonary artery that are usually higher than the systemic pressures, and a “right-to-left shunt” via the foramen oval and ductus arteriosus.
Indicators that suggest higher levels of the pressure in the pulmonary artery are; prolonged time interval of the ventricular systole and a short “pulmonary flow velocity ratio” (Natarajan et al., 2006, p.181). A prolonged “left ventricular systolic” interval of time indicates ventricular dysfunction.
Failing of the acceleration of “systolic blood flow” between the major pulmonary artery and the minor peripheral artery on the Doppler also indicates ductal shunt. Conversely, echocardiogram might be normal and “the right-to-left shunt across the ductus arteriosus or foramen may not be seen depending on the level of the pulmonary artery pressure at the time of examination” (Natarajan et al., 2006, pp.181-182).
Signs and Symptoms
The signs and symptoms for the PPHN condition include; tachypnea or rapid breathing, increased heart beat rate, respiratory distress which may include signs like grunting and flaring nostrils, and cyanosis even at the time the infant is being given extra oxygen to help it in breathing (Natarajan et al., 2006, p.181).
On some occasions when the infant is being examined for PPHN, the physician may be able to hear an abnormal heart sound or what is called a “heart murmur” (Natarajan et al., 2006, p.181).
Some sections of the population are affected by PPHN, and this basically depends on the risk factors to which they may be exposed.
For instance, Cornfield & Delaney (2012, p.18) present a report that in a well-considered, case-control trial carried out in the U.S Army population, it was found out that babies that were delivered through cesarean section were at about five times increased risk of developing the condition of PPHN in comparison with a control population that is well-matched demographically.
As on one hand this study encompassed nearly twelve thousand infants, it is only 20 of them that were found to have developed the PPHN condition (Cornfield & Delaney, 2012, p.18). In the study, choramnionitis as well deliberated a considerably higher risk of the PPHN (Cornfield & Delaney, 2012, p.18).
The idea that imply that Cesarean section delivery leads to having increased risk of developing PPHN is offered support to by data that was obtained from a study conducted previously in which the delivery mode, maternal race, and “high maternal body mass index each increased the likelihood of PPHN” (Cornfield & Delaney, 2012, p.18).
It is also found that the risk of any woman delivering a baby that is affected by PPHN within the overall population is found to be approximately two babies among every one thousand live births (Cornfield & Delaney, 2012, p.18).
It has been found that in otherwise fit newborn, “the cause of PPHN is usually unknown” (Cornfield & Delaney, 2012, p.16). Among the researchers, there are those who hold a belief that stress among mothers while they are carrying babies in their wombs, linked to particular pregnancy complications may raise the level of the risk of having the PPHN condition.
The occurrence of PPHN may take place with particular congenital conditions or diseases of babies that have some effects on the lungs (Weijerman, Van Furth, Van der Mooren, Van Weissenbruch, Rammeloo, Broers, & Gemke, 2010, p.1195).
The PPHN condition has as well been associated with such health conditions as hypoglycemia, anemia, birth asphyxia and severe pneumonia. Such conditions may lead to high BP within the blood vessels that subsequently, leads to the lungs to rise to the level where the blood of the infant goes on passing by lungs after delivery.
In most cases, these conditions are found to be reversible and are also normally temporary. Some particular congenital conditions which contribute towards having incomplete development of the lungs may as well be linked to PPHN (Cornfield & Delaney, 2012, p.17).
Maintaining sufficient oxygenation is the fundamental objective in PPHN management and mechanical ventilation is among treatment modalities that can be applied to realize this objective (Goissen, Ghyselen, Tourneux, Krim, Storme, Bou, & Maingourd, 2008, p.437-438).
Among the very early strategies within the conventional ventilator therapy was the hyperventilation to raise the level of the blood PH, facilitate the reversing of ductal shunting and inducting pulmonary vasodilatation. In comparing hyperventilation with alkali infusion, it was found out that hyperventilation brought down the level the “extracorporeal membrane oxygenation” risk (Oden & Cheifetz, 2005, p.105).
But on the other hand, from some study findings, it has been established that hyperventilation as well as “metabolic and respiratory alkanosis” induction in PPHN treatment, have not improved the clinical outcome to a significant level and have been linked to “adverse neurologic sequelae” (Natarajan et al., 2006, p.183).
On the other hand, pulmonary vasodilation using a number of drugs has undergone evaluation for PPHN treatment, but there has been no recommendation of any, apart from NO (Nassi, Daniotti, Agostiniani, Lombardi, Favilli, & Donzelli., 2010, p.104).
Some special cases of adenosine infusion have indicated improved oxygenation but have some adverse effects of “bradycardia, hypotension, and prolonged breeding time, which have precluded its clinical use” (Natarajan et al., 2006, p.183).
Initially, there was utilizing of tolazoline as a “vasolidilating, α-adrenergic blocking agent” (Natarajan et al., 2006, p.183). However, it facilitates inducing of histamine release and brings in adverse effects like having higher levels of gastric secretions as well as bleeding. It also leads to frequent occurrence of oliguria and systematic hypotension.
On the other hand, “Extracorporeal membrane oxygenation” (ECMO) is found to be a final therapy mode among infants that has reversible cardiac or respiratory failure at a time the rest of non-invasive measures have not succeeded. This method is an improved cardiopulmonary bypass which makes sure that there is sufficient delivery of oxygen and gas exchange among the PPHN patients having or not having cardiac support.
In this manner, the innate organs of the patient are rested to ensure facilitation of repair as well as to evade barotrauma and also volutrauma of the management of mechanical ventilation. Apart from PPHN, ECMO has as well been employed in “meconium aspiration syndrome, CDH, and cardiac anomalies” (Natarajan et al., 2006, p.184).
Basing on the fact that ECMO is an invasive method, this method or procedure is reserved for the young children that are receiving maximum “ventilatory support” and the ones that meet Barlett standards, which is suggestive of at least eighty percent risk of incurring death.
In the course of the last ten years or so, there has been a decline in the frequency of the utilization of ECMO technique because of the coming up of alternative techniques like inhaled NO or iNO (Natarajan et al., 2006, p.184).
Inhaled nitric oxide or (iNO) is a technique that has been identified to be safe and very effective treatment method for PPHN in the near-term as well as term newborns (Fashaw, Hale, Lee, Rosenberg, Vaver, Waas, & Werner, 2010, p.27; Hosono, Ohno, Kimoto, Shimizu, Takahashi, & Harada, 2009, p.79).
It has also been found out that using iNO has contributed to 3.4 percent more lives saved and a six percent rise in “average utility gained per infant (Lorch, Cnaan & Barnhart, 2004, p.417). Moreover, utilization of this technique has helped to bring improvement in oxygenation and also in decreasing the need for having ECMO among term newborns having PPHN (Kinsella & Abman, 1998,p.28).
In the current day, there has been extending of iNO utilization to the pre-term infants as being a rescue therapy among the infants having respiratory failure in spite of “surfactant replacement therapy”, and also more prevalent utilization among the infants who are less sick in an effort to bring down the level of frequency of the “chronic lung disease of the premature” (Fashaw et al., 2010, p.127).
While the use of this technique becomes more and more prevalent, it remains vital to go on evaluating short-term as well as long-term outcomes for the infants (Walsh-Sukys & Tyson, 2000, p.20).
The follow-up studies that were conducted previously about the infants who underwent treatment using iNO as “neonates have not found a short-term increase in medical, neurodevelopmental or behavioral problems when compared historically or concurrently with infants treated conventionally or with ECMO” (Fashaw et al., 2010, p.127).
A number of studies of young children of up to the age of 2 years, who received treatment using iNO as neonates have been somehow encouraging concerning short-term “developmental outcomes” (Fashaw et al., 2010, p.127).
In addition, the interviews conducted among parents that had children aged slightly above four years, that underwent treatment using iNO for PPHN, did not give out any findings of having increased neurologic, pulmonary, cognitive, “behavioral or neurosensory outcomes in infants treated with iNO when compared to those managed without iNO” (Fashaw et al., 2010, p.129).
Even if neurodevelopmental disabilities are given different definitions depending on the study being carried out, there has been reporting of these disabilities in between ten to thirty percent of the infants having no differences pointed out where comparison was made between the infants that received treatment with iNO and a control population that received treatment for PPHN.
Such numbers were as well comparable to those infants that received treatment with ECMO “followed out to 7 years of age” (Fashaw et al., 2010, p.129).
Therefore, outcomes for the infants treated as being neonates for “Persistent Pulmonary Hypertension of the Newborn” tends not to be related to the “specifics of individual intensive care treatment regimens, rather to events clinically associated with PPHN such as prenatal asphyxia” (Fashaw et al., 2010, p.129).
In general terms, the children that receive treatment with iNO have the same outcomes as those that receive treatment with ECMO and those that are treated with the conventional ways for the Persistent Pulmonary Hypertension of the Newborn.
The Role of the Respiratory Therapist
The respiratory therapist may be requested to offer supplemental oxygen and may also offer supplemental pressure to any patient who may be grunting in order to relieve the patient from some of the breathing hardships. The respiratory therapist can give this through either the nasal CPAP or through any other more appropriate means.
The therapist is then supposed to watch the infant (patient) closely for any symptoms of tiring. By making any observation of any sign of tiring, it may now become essential to apply more interventions. It is quite imperative for the therapist to watch closely this kind of patient.
The respiratory rate as well as the oxygen saturation of the patient has to be constantly monitored. In case there is any deterioration in the patient, quick intervention must take place (Tibballs & Chow, 2002, p.399).
PPHN condition results from failure to attain a smooth transition “from fetal to extrauterine pulmonary circulation after birth”. The diagnosis of this condition can be carried by undertaking physical examinations, looking at the history, undertaking laboratory tests, using chest x-ray, undertaking hyperoxia test, and echocardiogram.
The signs and symptoms for the PPHN condition include; tachypnea or rapid breathing, increased heart beat rate, respiratory distress which may include signs like grunting and flaring nostrils, and cyanosis even at the time the infant is being given extra oxygen to help it in breathing and having heart murmur among others.
It is believed that PPHN is brought about by stress among mothers while they are carrying babies in their wombs, linked to particular pregnancy complications which may raise the level of the risk of having the PPHN condition. Moreover, the occurrence of PPHN may take place with particular congenital conditions or diseases of babies that have some effects on the lungs.
Considering treatment, maintaining sufficient oxygenation is the main goal in PPHN management and mechanical ventilation is among treatment modalities that can be applied to achieve the goal. ECMO has been found to be a final therapy mode among infants that has reversible cardiac or respiratory failure at a time the rest of non-invasive measures have not been successful.
The technique is an improvement of the cardiopulmonary bypass which makes sure that there is sufficient delivery of oxygen and gas exchange among the PPHN patients having or not having cardiac support. But on the other, in the last few year, there has been a decline in the frequency of the utilization of ECMO technique because of the coming up of alternative techniques like inhaled NO or iNO.
This new technique has been found to be very safe and very effective for treating PPHN in the near-term as well as term newborns. It has also been found out that using iNO has contributed to 3.4 percent more lives saved.
Moreover, utilization of this technique has helped to bring improvement in oxygenation and also in decreasing the need for having ECMO among term newborns having PPHN.
The respiratory therapist can play an important role of offering supplemental oxygen as well as providing supplemental pressure to any patient who may be grunting in order to relieve the patient from some of the breathing problems. The therapists also closely watches the patient in order to help carry out any interventions when need arises.
Bartle, D., Patole, S., & Rao, S. (2010). Current and future therapeutic options for persistent pulmonary hypertension in the newborn. Expert Review of Cardiovascular Therapy, 8(6), 845-873.
Cornfield, D., & Delaney, C. (2012). Risk factors for persistent pulmonary hypertension of the newborn. Pulmonary Circulation, 2(1), 15-23.
Fashaw, L., Hale, K., Lee, N. R., Rosenberg, A. A., Vaver, K. N., Waas, N., & Werner, D. (2010). School-age outcomes of newborns treated for persistent pulmonary hypertension. Journal of Perinatology, 30(2), 127-139.
Goissen, C. C., Ghyselen, L. L., Tourneux, P. P., Krim, G. G., Storme, L. L., Bou, P. P., & Maingourd, Y. Y. (2008). Persistent pulmonary hypertension of the newborn with transposition of the great arteries: successful treatment with bosentan. European Journal Of Pediatrics, 167(4), 437-440
Hosono, S., Ohno, T., Kimoto, H., Shimizu, M., Takahashi, S., & Harada, K. (2009). Developmental outcomes in persistent pulmonary hypertension treated with nitric oxide therapy. Pediatrics International, 51(1), 79-83.
Kinsella, J. P., & Abman, S. H. (1998). Inhaled nitric oxide and high frequency oscillatory ventilation in persistent pulmonary hypertension of the newborn. European Journal Of Pediatrics. Supplement, 157S28-S30.
Kraemer, U., Krijger, R. D., Reiss, I., Rottier, R. J., Sluiter, I., & Tibboel, D. (2011). Vascular abnormalities in human newborns with pulmonary hypertension. Expert Review of Respiratory Medicine, 5(2), 245-264.
Lorch, S. A., Cnaan, A., & Barnhart, K. (2004). Cost-Effectiveness of Inhaled Nitric Oxide for the Management of Persistent Pulmonary Hypertension of the Newborn. Pediatrics, 114(2), 417-426.
Mago, R. (2012, August). Antidepressants and persistent pulmonary hypertension of the newborn. Psychiatric Times, 29(8), 30.
Nakwan, N., Nakwan, N., & Wannaro, J. (2011). Predicting mortality in infants with persistent pulmonary hypertension of the newborn with the score for neonatal acute physiology-version II (SNAP-II) in Thai neonates. Journal of Perinatal Medicine, 39(3), 311-321.
Nassi, N. N., Daniotti, M. M., Agostiniani, S. S., Lombardi, E. E., Favilli, S. S., & Donzelli, G. P. (2010). Sildenafil as ‘first line therapy’ in pulmonary persistent hypertension of the newborn?. Journal Of Maternal-Fetal & Neonatal Medicine, 23(1),104-105.
Natarajan, G., Ostrea, E. M., Jr., Uy, H. G., & Villanueva-Uy, E. T. (2006). Persistent pulmonary hypertension of the newborn: pathogenesis, etiology, and management. Pediatric Drugs, 8(3), 179-188.
Oden, J., & Cheifetz, I. M. (2005). Neonatal Thyrotoxicosis and Persistent Pulmonary Hypertension Necessitating Extracorporeal Life Support. Pediatrics, 115(1), 105-108.
Tibballs, J., & Chow, C. (2002). Incidence of alveolar capillary dysplasia in severe idiopathic persistent pulmonary hypertension of the newborn. Journal Of Paediatrics & Child Health, 38(4), 397-400
Walsh-Sukys, M. C., & Tyson, J. E. (2000). Persistent Pulmonary Hypertension of the Newborn in the Era Before Nitric Oxide: Practice Pediatrics, 105(1), 14.
Weijerman, M., Van Furth, A., Van der Mooren, M., Van Weissenbruch, M. M., Rammeloo, L., Broers, C. M., & Gemke, R. J. (2010). Prevalence of congenital heart defects and persistent pulmonary hypertension of the neonate with Down syndrome. European Journal Of Pediatrics, 169(10), 1195-1199.