Hypertrophic pyloric stenosis following persistent pulmonary hypertension of the newborn: a case report and literature review

Iijima, Shigeo; Ueno, Daizo; Baba, Toru; Ohishi, Akira

doi:10.1186/s12887-018-1270-0

Cited by 4 publications

(6 citation statements)

References 19 publications

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“…This study also suggested the importance of exclusive breastfeeding in decreasing the risk of HPS (5). Due breast milk may have lower osmolality, which could provide better gastric emptying (6). The breast milk field contains macronutrients that affected the growth of a child (7).…”

Section: Introductionmentioning

confidence: 74%

Congenital hypertrophic pyloric stenosis of 21 days infant

Kurniawan

Atmaja

2022

ijhs

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Hypertrophic Pyloric Stenosis (HPS) is a condition that occurs in infants with an abnormally thickened pyloric stomach, presented with a symptom of projectile vomiting. The cause of HPS is still unclear. However, it may occur due to multiple factors, including racial, environmental, and genetic factors, with the incidence of one to two out of 1000 live births. We reported a Hypertrophic Pyloric Stenosis (HPS) case in a 21-day-old baby girl (baby I) with projectile vomiting and yellowish diarrhea about six days before admission, which was recorded to be more than five times a day. The patient was hospitalized at Anwar Medika Hospital for five days before being referred to dr. Soetomo Hospital, Surabaya, and a pyloromyotomy were performed. Physical examination and radiological investigations (plain radiographs, Upper Gastrointestinal (UGI), and ultrasonography (USG)) supported the diagnosis of HPS. Ramstedt pyloromyotomy procedure had been conducted with a diagnosis of post-pyloromyotomy hypertrophic pyloric stenosis.

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Section: Introductionmentioning

confidence: 74%

Congenital hypertrophic pyloric stenosis of 21 days infant

Kurniawan

Atmaja

2022

ijhs

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“…This work is carried out by the placenta, which is responsible for guaranteeing the essential oxygenation of the blood, which will be directed to the fetal heart and brain to meet the high metabolic demands of the developing fetus. In fetal circulation, all blood that returns to the fetal cardiac system flows preferentially from the right atrium, through the foramen ovale to the left atrium, and is expelled through the left ventricle to be made available for the coronary and cerebral circulation (Verklan, 2006;Storme, et al, 2013;Iijima et al, 2018).…”

Section: Physiology Of Fetal Pulmonary Vascular Regulationmentioning

confidence: 99%

“…Pulmonary hypertension in the newborn may be primary (idiopathic) or secondary to lung tissue disease (such as surfactant deficiency, meconium aspiration syndrome or alveolar-capillary dysplasia), polycythemia, hypoglycemia, sepsis or maternal ingestion of prostaglandin inhibitors (Storme et al, 2013;Iijima et al, 2018).…”

Section: Pathogenesis Of Neonatal Persistent Pulmonary Hypertensionmentioning

confidence: 99%

“…Exaggerated vasoconstriction is the result of an imbalance between vasodilatory and vasoconstrictor factors, produced mainly by PAECs (pulmonary artery endothelial cells), which, in turn, stimulates increased contraction of PASMCs (pulmonary artery smooth muscle cells) and, therefore, increased vascular tone. Asphyxia and sepsis are some examples of etiologies that led to an exacerbated increase in pulmonary vessel constriction, either directly, through hypoxia and acidosis, or indirectly, through the release of pulmonary vessel constricting substances, such as TXA2 and leukotrienes (Storme L et al, 2013;Iijima et al, 2018).…”

Section: Pathogenesis Of Neonatal Persistent Pulmonary Hypertensionmentioning

confidence: 99%

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Use of sildenafil for the treatment of neonatal persistent pulmonary hypertension

Jucá Neto,

Mapurunga,

Belchior

et al. 2024

RSD

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Introduction: Persistent pulmonary hypertension of the newborn is a neonatal respiratory and vascular pathology with a high mortality rate. Furthermore, its prevalence is 1 to 2 per 1000 live births, accounting for 8%-10% of neonatal deaths. The therapeutic approach involves supporting pulmonary recruitment and pharmacological vasodilation, most notably sildenafil. Methodology: The study is a narrative review of the literature that was carried out from the PUBMED database using the keywords “Persistent Pulmonary Hypertension of the Newborn” and “Sildenafil”, with the time filter in the last 30 years (1994- 2023). Discussion: Physiologically, during fetal life, the lungs remain filled with fluids, but immediately after birth, pulmonary vascular resistance decreases drastically, allowing alveolar oxygen tension and ventilation to be possible. However, in the pathogenesis of neonatal persistent pulmonary hypertension, there is an increase in pulmonary vascular resistance and remodeling of the vascular structure after birth, which potentiate this exaggerated vasoconstriction. Therefore, the standard exam for investigating the pathology is echocardiography. Sildenafil is a drug used to treat neonatal persistent pulmonary hypertension, as it enhances better blood flow and better delivery of oxygen to tissues, through its physiopharmacology aimed at vasodilation secondary to inhibition of phosphodiesterase-5. Conclusion: Neonatal persistent pulmonary hypertension is still one of the main neonatal pathologies with high morbidity and mortality in the neonatal population, due to the complexity of presentations and the variation in therapeutic responses to pharmacotherapy.

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“…[ 4 , 5 , 9 , 11 , 13 – 15 , 19 , 22 , 24 , 39 , 44 , 45 , 47 , 48 , 52 ]…”

Section: The Clinical Algorythmunclassified

Life-threatening PPHN refractory to nitric oxide: proposal for a rational therapeutic algorithm

et al. 2021

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Persistent pulmonary hypertension of the neonate (PPHN) refractory to inhaled nitric oxide still represents a frequent clinical challenge with negative outcomes in neonatal critical care. Several pulmonary vasodilators have become available thanks to improved understanding of pulmonary hypertension pathobiology. These drugs are commonly used in adults and there are numerous case series and small studies describing their potential usefulness in neonates, as well. New vasodilators act on different pathways, some of them can have additive effects and all have different pharmacology features. This information has never been summarized so far and no comprehensive pathobiology-driven algorithm is available to guide the treatment of refractory PPHN. Conclusion : We offer a rational clinical algorithm to guide the treatment of refractory PPHN based on expert advice and the more recent pathobiology and pharmacology knowledge. What is Known: • Refractory PPHN occurs in 30–40% of iNO-treated neonates and represents a significant clinical problem. Several pulmonary vasodilators have become available thanks to a better understanding of pulmonary hypertension pathobiology. What is New: • Available vasodilators have different pharmacology, mechanisms of action and may provide additive effect. We provide a rational clinical algorithm to guide the treatment of refractory PPHN based on expert advice and the more recent pathobiology and pharmacology knowledge .

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Hypertrophic pyloric stenosis following persistent pulmonary hypertension of the newborn: a case report and literature review

Cited by 4 publications

References 19 publications

Congenital hypertrophic pyloric stenosis of 21 days infant

Congenital hypertrophic pyloric stenosis of 21 days infant

Use of sildenafil for the treatment of neonatal persistent pulmonary hypertension

Life-threatening PPHN refractory to nitric oxide: proposal for a rational therapeutic algorithm

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