Clinical evaluation of MAS is most common in infants with a history of postmaturine, fetal upset, and / or meconium staining. Infants with MAS are at risk of increasing respiratory distress with hypoxemia and hypercarbia, which can also be complicated by PPHN. The following therapies are used to treat newborns with MAS:
- Chest Physiotherapy and Suction
- transcutaneous monitoring oxygen saturation using supplemental oxygen to prevent hypoxia and hypoxic pulmonary vasoconstriction that could lead to PPHN
- ABG monitoring for the rapid recognition and treatment of acidosis, hypoxia , and hypercarbia
- CPAP or mechanical ventilation to maintain normal oxygenation and ventilation
- Sedation or neuromuscular paralysis for babies with high fan settings
- Regular antibiotic administration due to possible secondary bacterial pneumonia
- exogenous surface-active substance administration
Persistent pulmonary hypertension of the newborn
Persistent pulmonary hypertension of the newborn (PPHN), also historically known as continuous circulation of the fetus, is a combination of pulmonary hypertension and right to left shunting of unsaturated blood from the embryonic pathways (PFD) or PDA in a structurally normal heart. This pathological process is caused by a steady increase in the level of pulmonary vascular resistance (PVR) after birth. In contrast, systemic vascular resistance (CBP) rapidly increases with the fixation of the cord. These events lead to the functional closure of the VFD and the narrowing of the PDA with the separation of pulmonary and systemic blood circulation. An increase in PVR may be idiopathic or secondary to MAS, congenital diaphragmatic hernia, hyperviscosity, sepsis, or for other reasons. This anomaly leads to a decrease in the cross-sectional area of the pulmonary vascular bed and increased resistance to pulmonary blood flow. PPHN leadership has changed dramatically with recent medical advances.
Treatment regimens include the following:
- Rapid correction of hypoxia and acidosis (as strong pulmonary vasoconstrictor ) for reverse pulmonary vasospasm
- Supplemental Oxygen Injected Nasal cannula , hood or NCPAP
- intubation and mechanical ventilation if hypoxia preserved
- High frequency ventilation (often used in newborns with PPHN)
- Expansion and / or introduction inotropic agents like dopamine to provide adequate cardiac output and increase systemic pressure to counteract right-to-left shake
Clinical studies have shown that babies with PPHN benefit from surfactant replacement therapy, probably due to the fact that the initial lung damage was resolved by inactivating the surfactant. For infants who do not respond to these treatments, additional treatment may be required.
Bronchopulmonary dysplasia
Premature babies are diagnosed with bronchopulmonary dysplasia (BPD) (also called CLD) if they continue to need oxygen or positive pressure for 36 weeks of gestational age. The pathogenesis of BPD includes numerous etiological factors, such as immature alveoli, barotrauma resulting from prolonged mechanical ventilation, oxygen toxicity with the formation of oxygen radicals, infection, chronic aspiration caused by gastroesophageal reflux, pulmonary edema caused by volume overload, and PDA. Infants usually have a history that includes prematurity, prolonged mechanical ventilation, the need for a high concentration of oxygen in the breath, infection, and / or PDA. Pulmonary function tests usually indicate increased resistance to the airways and a decrease in lung dynamic compliance. Growth problems are common in babies with BPD, and intensive nutritional support is crucial.
APNEA and congenital neonatal infections
Apnea, defined as cessation of breathing for more than 10 seconds, is common in premature babies; incidence decreases with increasing gestational age. Apnea affects approximately 25% of infants who weighed less than 2500 g at birth and 84% of newborns who weighed less than 1000 g. Experts believe that the immaturity of central respiratory control is a key factor in the etiology of apnea in prematurity. The carbon reaction, reflecting the central activity of chemoreceptors, is not so developed in premature babies. Apnea is more common during rapid eye movement and transient sleep, when the respiratory pattern is irregular. The presence or absence of an upper airway obstruction determines three types of apnea. Central apnea (from 10% to 25% of cases) is characterized by a lack of inspiration; obstructive sleep apnea (10% to 20% of cases) by obstruction of the airways without nasal airflow; and mixed apnea (from 50% to 70% of cases) for elements of both types. In contrast, periodic breathing is defined as repeating sequences of cessation of breathing for 5 to 10 seconds, followed by 10 to 15 seconds of hyperventilation. This respiratory pattern is normal in premature babies. A history of feeding intolerance, vomiting, lethargy, temperature instability, seizures, and a maternal history of infection or drug use may indicate an alternative cause of apnea. Bradycardia and, sometimes, cyanosis often accompany apnea. Other features that may be present include tachypnea, respiratory distress, congenital anomalies, or neurological abnormalities, such as lethargy, hypotension, or nervousness. The identification of a potential cause of apnea, such as hypoxemia, infection or anemia, concerns the treatment of a causal condition. Exclusion of other etiologies leads to the diagnosis of idiopathic apnea of prematurity.
Congenital infections
Congenital infections can occur at any time during pregnancy, childbirth and childbirth. First trimester infections can affect almost any of the developing organ systems and often lead to significant IUGRs. Reduction TORCH (toxoplasmosis, rubella, cytomegalovirus [CMV], and herpes simplex) describes only some of the main causes of intrauterine infection; others include HIV, enterovirus, parvovirus, chicken pox and syphilis. Some of these infections, as well as viral hepatitis, can occur after contact after contact with the skin or through breast milk. Many serious congenital infections occur unexpectedly; they are often associated with a mild, non-specific disease in a pregnant woman. The risk of other congenital infections may have to be derived, and the effect of a congenital infection depends on the pathogen and the maternal and fetal hosts. Many affected fetuses are asymptomatic at birth. The most common effects include:
- Growth retardation
- Premature delivery
- Central nervous system ( CNS a) anomalies, including microcephaly, intracranial calcifications and chorioretinitis
- Hepatosplenomegaly often accompanied by jaundice
- Bruises or petechiae that may accompany thrombocytopenia
- Skin lesions
Infants with congenital viral infections may also have acute symptoms, such as interstitial pneumonitis, myocarditis, or encephalitis. Clinical data specific to certain conditions:
- Congenital rubella syndrome: cataract, hearing loss, heart damage, blueberry bun spots (palpable skin lesions associated with extramedullary hematopoiesis)
- Congenital herpes simplex: damage to the skin, eyes or mouth; more severe systemic symptoms, including convulsions or a system malfunction with several organs, usually occurring after the first week
- Parvovirus B19 : possible suppression of embryonic bone marrow associated with algae fetalis
Urine cultures best demonstrate active CMV infection. Blood, Berezpropinovaya fluid (CSF) and skin lesion cultures or viral polymerase chain reaction testing are usually diagnosed with herpes and enterovirus infections.
However, the following treatments may be useful in specific conditions:
- Neonatal herpes infection : antivirals acyclovir and vidarabine to reduce mortality and morbidity
- toxoplasmosis : regimen of pyrimethamine, sulfadiazine and folinic acid (newborns) or spiramycin (infected pregnant women)
- HIV infection : Zidovudine use in the prophylactic treatment of HIV-infected newborns.
Bacterial infections
Bacterial infections can be transmitted through the blood, cross the placenta, or rise through the birth canal, especially after prolonged rupture of the membranes. The specific pathogen depends on the colonization of the mother. It is important to get a complete obstetric history; maternal risk factors for neonatal bacterial sepsis include prolonged or premature rupture of membranes associated with childbirth, chorioamnionitis, and urinary tract infection. Learn more at healthinfants.com
