Hipertensión pulmonar secundaria a Sepsis en el neonato
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Fecha
2023
Autores
Yepes Padilla, María Patricia
Barrios Quintero, Jhony Alexander
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Ediciones Universidad Simón Bolívar
Facultad de Ciencias de la Salud
Facultad de Ciencias de la Salud
Resumen
La hipertensión pulmonar es un síndrome de falla respiratoria aguda caracterizado por elevación sostenida de las resistencias vasculares pulmonares (RVP), que produce hipertensión persistente de la arteria pulmonar después del nacimiento, que ocasiona cortocircuito extrapulmonar de derecha a izquierda de sangre no oxigenada a través del conducto arterioso (CA) y foramen oval (FO) con hipoxemia severa y acidosis secundaria. La hipertensión pulmonar secundaria a sepsis (HTP-S) es una de las complicaciones de mayor preocupación en los neonatos por las implicaciones que puede conllevar a corto, media y largo plazo, algunas incluso pudiendo a comprometer la vida del niño, por los compromisos a nivel renal, cardiaco y evidentemente respiratorio. La HTP-S puede explicarse por varios mecanismos; ejemplo: gérmenes comunes en la etapa neonatal como (Streptococcus del grupo B y bacterias gramnegativas), liberan endotoxinas bacterianas desencadenando una respuesta inflamatoria secundaria, con liberación de tromboxano endotelial y de varias citoquinas (como el factor de necrosis tumoral-alfa) que lleva a un aumento en las resistencias vasculares pulmonares. Aunque la HTP es una causa frecuente de ingreso a la Unidad de Cuidados intensivos neonatales, la causa que termina en hipertensión pulmonar puede pasar desapercibida ya sea por poca asociación a la patología o por su baja frecuencia, como es el caso de la HTP secundaria a sepsis, considerada como un desafío debido a la dificultad de identificar a los recién nacidos en riesgo de sepsis, especialmente a los que tienen un buen aspecto general.
Pulmonary hypertension is a syndrome of acute respiratory failure characterized by sustained elevation of pulmonary vascular resistance (PVR), leading to persistent pulmonary artery hypertension after birth, leading to right-to-left extrapulmonary shunting of deoxygenated blood through the pulmonary artery. ductus arteriosus (CA) and foramen ovale (FO) with severe hypoxemia and secondary acidosis. Pulmonary hypertension secondary to sepsis (HTP-S) is one of the complications of greatest concern in neonates due to the implications that it may entail in the short, medium and long term, some of which may even compromise the life of the child, due to the commitments to renal, cardiac and obviously respiratory level. HTP-S can be explained by several mechanisms; example: common germs in the neonatal stage such as (group B Streptococcus and gram-negative bacteria), release bacterial endotoxins triggering a secondary inflammatory response, with release of endothelial thromboxane and several cytokines (such as tumor necrosis factor-alpha) that leads to an increase in pulmonary vascular resistance. Although PHT is a frequent cause of admission to the Neonatal Intensive Care Unit, the cause that ends in pulmonary hypertension may go unnoticed, either due to little association with the pathology or its low frequency, as is the case of PHT secondary to sepsis, considered a challenge due to the difficulty of identifying newborns at risk of sepsis, especially those with a good general appearance.
Pulmonary hypertension is a syndrome of acute respiratory failure characterized by sustained elevation of pulmonary vascular resistance (PVR), leading to persistent pulmonary artery hypertension after birth, leading to right-to-left extrapulmonary shunting of deoxygenated blood through the pulmonary artery. ductus arteriosus (CA) and foramen ovale (FO) with severe hypoxemia and secondary acidosis. Pulmonary hypertension secondary to sepsis (HTP-S) is one of the complications of greatest concern in neonates due to the implications that it may entail in the short, medium and long term, some of which may even compromise the life of the child, due to the commitments to renal, cardiac and obviously respiratory level. HTP-S can be explained by several mechanisms; example: common germs in the neonatal stage such as (group B Streptococcus and gram-negative bacteria), release bacterial endotoxins triggering a secondary inflammatory response, with release of endothelial thromboxane and several cytokines (such as tumor necrosis factor-alpha) that leads to an increase in pulmonary vascular resistance. Although PHT is a frequent cause of admission to the Neonatal Intensive Care Unit, the cause that ends in pulmonary hypertension may go unnoticed, either due to little association with the pathology or its low frequency, as is the case of PHT secondary to sepsis, considered a challenge due to the difficulty of identifying newborns at risk of sepsis, especially those with a good general appearance.
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Palabras clave
Hipertensión segundaria a sepsis, Sepsis neonatal, Unidad de cuidados intensivos neonatal, Síndrome de Dificultad Respiratoria, Taquipnea, Mortalidad, Antibiótico, Resistencia antibiótica, Hypertension secondary to sepsis, Neonatal sepsis, Neonatal intensive care unit, Respiratory Distress Syndrome, Tachypnea, Mortality, Antibiotic, Antibiotic resistance
