LAUSR

Hypertension was initially recognized clinically in neonates in the 1970s, but recent technological advances in the NICU have led to heightened awareness and increased diagnostic frequency. Neonatal hypertension is defined as systolic blood pressure (BP) of at least the 95th percentile for gestational age, birthweight, and sex on 3 separate occasions. The incidence of neonatal hypertension in the NICU ranges from 0.2% to 3% and most commonly affects term and preterm infants in the intensive care setting. Abnormally elevated BP, especially severe (defined by systolic BP >99th percentile) in critically ill or premature infants can result in vascular injury, left ventricular hypertrophy, encephalopathy, and hypertensive retinopathy. In addition to complications from end organ damage, certain forms of neonatal hypertension are linked to hypertension beyond infancy, making it imperative to swiftly diagnose and aggressively manage severe or persistent hypertension. As with older children and adults, there are multiple causes of neonatal hypertension (Table 1), with the most common being renal parenchymal and renovascular abnormalities. A well-established renovascular etiology is umbilical arterial catheter-associated hypertension, both with and without demonstrable thromboembolic events. Umbilical catheter placement is thought to disrupt vascular endothelium, resulting in decreased perfusion and increased renin and aldosterone production. Chronic lung disease or bronchopulmonary dysplasia (BPD) is the most common nonrenal cause of hypertension in premature infants, with an incidence ranging from 13% to 43% in neonates with BPD, especially in those severely affected. In fact, among very low birthweight infants, those with BPD are twice as likely to develop hypertension as those without BPD. In other clinical scenarios, other diagnoses associated with hypertension should be considered: patent ductus arteriosus, intraventricular hemorrhage, endocrine abnormalities, neoplasia, and medication adverse effects. The clinical presentation of hypertension in neonates is quite variable, with nonspecific signs and symptoms such as irritability, poor feeding, lethargy, tachypnea, cyanosis, seizures, apnea, and poor perfusion, ormore life-threatening events such as congestive heart failure and cardiogenic shock. For term neonates, routine evaluation of BP is not recommended by the American Academy of Pediatrics (AAP), and because most of this group will be asymptomatic, hypertension may be diagnosed incidentally during vital sign monitoring. Given the variation in clinical presentation, it is important to determine BP accurately in tertiary settings. The gold standard for reliable measurement of BP, especially in critically ill neonates, remains invasive arterial BP monitoring through an indwelling radial or umbilical catheter. However, in the absence of other indications for catheter insertion, noninvasive BP monitoring has become the clinical mainstay for diagnosis. Ultrasonic Doppler was routinely used in previous studies of hypertension but can underestimate systolic BP. Sphygmomanometry is not recommended because Korotkoff sounds are often barely AUTHORDISCLOSUREDrs Giri and Roth have disclosed no financial relationships relevant to this article. This commentary does not contain a discussion of an unapproved/investigative use of a commercial product/device.