eMedicine Specialties > Pediatrics: Cardiac Disease and Critical Care Medicine > Neonatology

Neonatal Hypertension

Joseph Flynn, MD, MS, Director of Pediatric Hypertension Program, Division of Nephrology, Children's Hospital and Regional Medical Center; Professor, Department of Pediatrics, University of Washington School of Medicine

Updated: Dec 4, 2008

Introduction

Background

Recent advances in the ability to identify, evaluate, and care for infants with hypertension, coupled with advances in the practice of neonatology in general, have led to an increased awareness of hypertension in modern neonatal ICUs (NICUs) since its first description in the 1970s. This article discusses an overview of the differential diagnosis of hypertension in the neonate, the optimal diagnostic evaluation, and both immediate and long-term antihypertensive therapy.

Pathophysiology

Hypertension in newborn infants primarily is of renal origin, although cardiac, endocrine, and pulmonary causes have been described as well. Therefore, the pathophysiology depends on the organ system involved. For example, hypertension related to renal emboli primarily is a high renin form of hypertension, whereas the hypertension associated with bronchopulmonary dysplasia (BPD) is likely related to hypoxia. Such differences in pathophysiology are very important because they can guide the clinician with respect to evaluation and treatment.

Frequency

United States

Although precise figures are difficult to obtain, available data suggest that the incidence of hypertension in newborns is low, with published figures ranging from 0.2-3%. Hypertension is so unusual in otherwise healthy term infants that routine blood pressure (BP) determination is not advocated for these patients.

A study of approximately 2600 infants treated at a single center in Australia over a 4-year period demonstrated a prevalence of hypertension of 1.3%.¹ Antenatal steroids, maternal hypertension, umbilical arterial catheter, postnatal acute renal failure, patent ductus arteriosus, treatment with indomethacin, and chronic lung disease were associated with the development of hypertension.

Hypertension may also be detected following discharge from the NICU. In 1987, Friedman and Hustead diagnosed hypertension (defined as a systolic BP >113 mm Hg on 3 consecutive visits over 6 wk) in 2.6% of infants discharged from a teaching hospital NICU.² The diagnosis of hypertension was made in these infants at a mean corrected age of approximately 2 months. Although the number of babies affected is likely to be relatively small, this study supports screening for hypertension in the follow-up of NICU graduates, especially those with more complicated NICU courses.

Clinical

History

• Identifying hypertension in the newborn
  • Blood pressure in newborn infants is influenced by various factors, including birthweight, gestational age, and postconceptual age.
  • Excellent normative data illustrating the importance of these factors was generated by Zubrow et al, who prospectively obtained serial blood pressure (BP) measurements from nearly 700 infants admitted to several neonatal ICUs (NICUs) in a large metropolitan area over 3 months.³ They used these data to define the mean plus upper and lower 95% confidence limits for BP; their data clearly demonstrated increases in BP with increasing gestational age, birthweight, and postconceptual age. The Zubrow data are probably most useful in identifying hypertension in premature and term newborns. Using their data, an infant's BP is considered elevated if it falls above the upper limit of the 95% confidence interval for infants of similar gestational or postconceptual age and size. The curves generated by the study have been widely published and should be consulted in assessing hypertension in a newborn.
  • For older infants found to be hypertensive following discharge from the nursery, the percentile curves generated by the 1987 Second Task Force on Blood Pressure Control in Childhood remain the most useful reference for infants aged 1 year or younger.⁴ These curves, which can be found in many reference texts and handbooks, allow BP to be characterized as normal or elevated not only by age and sex but also by size, albeit to a somewhat limited extent. Hypertension in this age group is defined as BP elevation ≥95th percentile for infants of similar age, size, and sex.
• Clinical presentation: In most newborns, hypertension is discovered on routine monitoring of vital signs. Other presentations of neonatal hypertension to be aware of in acutely ill infants include congestive heart failure (CHF) and cardiogenic shock, which are potentially life threatening. Fortunately, these consequences of hypertension gradually resolve with appropriate BP reduction. In the less acutely ill infant, feeding difficulties, unexplained tachypnea, apnea, lethargy, irritability, or seizures may constitute symptoms of unsuspected hypertension. In older infants who have been discharged from the nursery, unexplained irritability or failure to thrive may be the only manifestations of hypertension.
• Patient history: Focus the history on discovering any pertinent prenatal exposures, as well as to the particulars of the infant's nursery course and any concurrent conditions. Review the procedures that the infant has undergone, especially umbilical catheter placement, and analyze the baby's current medication list. If the infant has been discharged from the nursery, the history should also cover symptoms related to possible underlying causes of hypertension.

Physical

Issues pertinent to the physical examination in neonates with hypertension can be divided into two categories: proper BP measurement and other components of the physical examination.

• BP measurement
  • Proper identification of hypertension in the newborn requires accurate BP measurement. Fortunately, in most acutely ill infants, BP is usually monitored directly via an indwelling arterial catheter, either in the radial or umbilical artery. This method provides the most accurate BP readings and is clearly preferable to other methods. In infants who do not have indwelling umbilical lines, automated oscillometric devices are an acceptable alternative method of BP measurement.
  • Although BP readings obtained using such devices may differ slightly from intra-arterial readings, they are easy to use and facilitate monitoring BP trends over time. BP readings obtained using such devices are also useful for infants who require BP monitoring after discharge from the NICU. Pay attention to the size of the cuff and also to the extremity used. Most normative BP data, not only in infants but also in older children, have been collected using BP measurements obtained in the right arm. Because BP measurements obtained in the leg may be slightly higher than those obtained in the arm, the use of other extremities for routine BP determination may complicate the evaluation of hypertension. The nursing staff should document the extremity used for BP determinations and try to use the same extremity for all BP measurements, especially in infants who require antihypertensive treatment.
• Physical examination: The physical examination should begin with 4-extremity BP measurements in order to rule out aortic coarctation. Assess the general appearance of the infant and pay particular attention to the presence of dysmorphic features that may indicate an underlying genetic syndrome. Perform careful cardiac and abdominal examinations to rule out CHF or renal anomalies. Examine the genitalia to rule out congenital adrenal hyperplasia (CAH).

Causes

As in older infants and children, most cases of neonatal hypertension are of renal origin, with the 2 largest categories being renovascular and other renal parenchymal diseases (see Differentials). Other predisposing factors include a history of umbilical catheterization and chronic lung disease.

• A 1992 study by Singh and colleagues clearly demonstrated that hypertension was considerably more common in infants with bronchopulmonary dysplasia (BPD), patent ductus arteriosus, or intraventricular hemorrhage or in those who had indwelling umbilical arterial catheters. Approximately 9% of the infants in their series who had indwelling umbilical arterial catheters developed hypertension.⁵
• Complexity of the infant’s nursery course also appears to be important in the development of hypertension. Freidman et al studied hypertension in NICU graduates and reported that infants who developed hypertension tended to have lower initial Apgar scores and slightly longer NICU stays than infants who remained normotensive, indicating that sicker babies have a somewhat greater likelihood of developing hypertension.²
• With respect to renovascular disease, umbilical artery catheter–associated thromboembolism affecting the aorta, the renal arteries, or both probably is the most common cause observed in the typical NICU. In 1972, Neal et al were the first investigators to demonstrate an association between the use of umbilical arterial catheters and development of arterial thrombi. Using aortography at the time of umbilical artery removal as well as autopsy data, they demonstrated thrombus formation in 25 of 31 infants studied (81%).⁶
• Following Neal's report, the association between umbilical arterial catheter–associated thrombi and the development of hypertension was confirmed by several other groups of investigators. Although potential predisposing factors such as duration of line placement and line position (low versus high) have been studied, these studies have not been conclusive, leading to the assumption that the cause of hypertension in such cases is related to thrombus formation at the time of line placement, which is probably related to disruption of the vascular endothelium of the umbilical artery. Such thrombi may then embolize into the kidneys, causing areas of infarction and increased renin release.
• Other renovascular problems that may lead to neonatal hypertension include renal venous thrombosis (RVT) and renal artery stenosis secondary to fibromuscular dysplasia (FMD). Many infants with FMD may have main renal arteries that appear fairly normal on angiography but demonstrate significant branch vessel disease that can cause severe hypertension.
• Other vascular abnormalities may also lead to hypertension in the newborn, including idiopathic arterial calcification and renal artery stenosis secondary to congenital rubella infection.
• Finally, mechanical compression of one or both renal arteries by tumors, hydronephrotic kidneys, or other abdominal masses may also lead to hypertension.
• Numerous congenital renal parenchymal abnormalities can lead to hypertension in the newborn period. For example, patients with autosomal dominant or autosomal recessive polycystic kidney disease (PKD) may present in the newborn period with severe nephromegaly and hypertension. The most severely affected infants with PKD are at risk for development of CHF due to severe malignant hypertension. Although much less common than in PKD, hypertension has also been reported in infants with unilateral multicystic dysplastic kidneys. Renal obstruction may be accompanied by hypertension, even in the absence of renal arterial compression. This has been observed, for example, in infants with congenital ureteropelvic junction obstruction and in infants with ureteral obstruction by other intra-abdominal masses. The mechanism of hypertension in such instances is unclear, although the renin-angiotensin system (RAS) may be involved.
• Additional renal parenchymal causes of hypertension in the newborn period include severe acute tubular necrosis, interstitial nephritis, and cortical necrosis. Hemolytic uremic syndrome, although rare in the newborn period, is usually accompanied by hypertension that can be quite difficult to control, frequently requiring multiple agents.
• The most important nonrenal cause of neonatal hypertension is BPD. This association was first described in 1984 by Abman et al, who studied 65 infants discharged from a NICU.⁷ Abman et al reported that the incidence of hypertension in infants with BPD was 43% versus an incidence of 4.5% in infants without BPD. More than half of the infants with BPD who developed hypertension did not manifest it until following discharge from the NICU, highlighting the need for measurement of BP in NICU graduates. Investigators were unable to identify a clear cause of hypertension but postulated that hypoxemia may be involved.
• These findings have subsequently been reproduced by several other investigators, most recently in 1998 by Alagappan, who found that hypertension was twice as common in very low birthweight infants with BPD compared to the incidence in all very low birthweight infants.⁸ As in Abman's report, the development of hypertension appeared to be correlated with the severity of pulmonary disease because all of the hypertensive infants were receiving supplemental oxygen and aminophylline. These observations reinforce the impression that infants with severe lung disease are clearly at increased risk of developing hypertension and need close monitoring for this problem.
• Numerous other causes of hypertension in newborns are recognized, a comprehensive listing of which can be found in Differentials. Of these, hypertension associated with coarctation of the thoracic aorta deserves further comment. This is perhaps one of the most easily detected forms of hypertension in the newborn period and has been included in the differential diagnosis of this problem since the earliest reported case series of neonatal hypertension. Repair early in infancy seems to lead to an improved long-term outcome compared to delayed repair, which may be followed by persistent hypertension.
• Endocrinologic disorders that may produce hypertension in the newborn period include CAH, hyperaldosteronism, and hyperthyroidism.
• Iatrogenic hypertension can be the result of medications administered to infants for treatment of pulmonary disease, such as dexamethasone and aminophylline, high doses of adrenergic agents, prolonged use of pancuronium, or administration of phenylephrine ophthalmic drops. Hypertension in such cases typically resolves when the offending agent is discontinued or its dose is reduced.
• For infants receiving prolonged total parenteral nutrition (TPN), hypertension may result from salt and water overload or from hypercalcemia. Patients with certain tumors, including neuroblastoma, Wilms tumor, and mesoblastic nephroma, may present in the neonatal period, and the tumors may produce hypertension either because of compression of the renal vessels or ureters or because of production of vasoactive substances such as catecholamines. Neurologic problems, such as seizures, intracranial hypertension, and pain, constitute fairly common causes of episodic hypertension. Finally, illicit substances ingested by the mother during pregnancy, most notably cocaine and heroin, may also lead to significant problems with hypertension in the newborn either because of direct effects on the developing kidney or because of drug withdrawal.

Differential Diagnoses

Other Problems to Be Considered

Renovascular conditions

Thromboembolism
Renal artery stenosis
Midabdominal aortic coarctation
Renal venous thrombosis
Compression of renal artery
Idiopathic arterial calcification
Congenital rubella syndrome

Renal parenchymal disease

Polycystic kidney disease
Multicystic-dysplastic kidney disease
Tuberous sclerosis
Ureteropelvic junction obstruction
Acute tubular necrosis
Cortical necrosis
Interstitial nephritis
Hemolytic-uremic syndrome

Pulmonary conditions

Bronchopulmonary dysplasia (BPD)
Pneumothorax

Cardiac conditions

Thoracic aortic coarctation

Endocrine conditions

Congenital adrenal hyperplasia
Hyperaldosteronism
Hyperthyroidism
Pseudohypoaldosteronism type II

Medications/Intoxications

Dexamethasone
Adrenergic agents
Vitamin D intoxication
Theophylline
Caffeine
Pancuronium
Phenylephrine
Maternal cocaine or heroin use

Tumors

Neoplasia
Wilms tumor
Mesoblastic nephroma
Neuroblastoma
Pheochromocytoma

Neurologic conditions

Pain
Intracranial hypertension
Seizures
Familial dysautonomia
Subdural hematoma

Miscellaneous conditions

Closure of abdominal wall defect
Adrenal hemorrhage
Hypercalcemia
Traction
Extracorporeal membrane oxygenation (ECMO)
Birth asphyxia
Urological neoplasms

Workup

Laboratory Studies

• Usually only a limited set of laboratory data are needed in the evaluation of neonatal hypertension. Obtain serum electrolyte, creatinine, and BUN levels as well as urinalysis in order to look for renal parenchymal disease. Obtain endocrinologic studies, such as cortisol, aldosterone, or thyroxine, when pertinent history is noted.
• Measurement of plasma renin activity (PRA) is usually recommended as part of the laboratory assessment in newborns with hypertension, although elevated peripheral renin levels may not signify the presence of underlying pathology because renin values are typically high in infancy. In addition, plasma renin levels may be falsely elevated by medications that are commonly used in the neonatal ICU (NICU), such as aminophylline. Furthermore, many laboratories have switched from measurement of PRA to the direct renin assay, which is easier to perform. However, normative values for the direct renin assay in neonates are not widely available. Keep these factors in mind when interpreting renin values.
• Alternatively, suppressed PRA in an infant with hypertension is a significant finding, possibly indicating the presence of a genetic form of hypertension associated with volume overload, such as glucocorticoid-remediable aldosteronism or Liddle Syndrome.

Imaging Studies

• Chest radiography may be helpful in infants with congestive heart failure (CHF) or in those with a murmur upon physical examination.
• Perform renal ultrasonography with Doppler of the renal vessels in all hypertensive infants. Accurate renal ultrasonography may help uncover potentially correctable causes of hypertension (eg, renal venous thrombosis [RVT]); it may detect aortic thrombi, renal arterial thrombi, or both; and it can reveal anatomic renal abnormalities or other congenital renal parenchymal disease. Ultrasonography is fast, noninvasive, and relatively inexpensive. Ultrasonography has largely replaced intravenous pyelography, which has little, if any, use in the routine assessment of neonatal hypertension.
• For infants with extremely severe blood pressure (BP) elevation, angiography may be necessary. Although some investigators have used aortography via the umbilical artery catheter, formal renal arteriography using the traditional femoral vascular approach is much more accurate for diagnosing renal arterial stenosis, primarily because of the high incidence of intrarenal branch vessel abnormalities observed in children with fibromuscular dysplasia (FMD). Depending on the expertise available, this may need to be deferred until the infant is larger. MR and CT angiography are of little value in infants as they do not provide sufficient resolution to identify branch vessel stenoses.
• Nuclear scanning may demonstrate abnormalities of renal perfusion caused by thromboembolic phenomenon, although obtaining good studies in infants is difficult because of their immature renal function.
• Obtain other studies, including echocardiography and voiding cystourethrography, as indicated.

Treatment

Medical Care

Numerous medications are available that may be used in the treatment of neonatal hypertension. Assess the clinical status of the infant and correct any easily correctable iatrogenic causes of hypertension (eg, infusions of inotropic agents, volume overload, pain) prior to instituting drug therapy. Next, choose an antihypertensive agent that is most appropriate for the specific clinical situation.

• Intravenous antihypertensive infusions
  • Usually, continuous intravenous infusions are the most appropriate initial therapy, especially in acutely ill infants with severe hypertension. The advantages of intravenous infusions are numerous, most importantly including the ability to quickly increase or decrease the rate of infusion to achieve the desired blood pressure (BP). As in patients of any age with malignant hypertension, take care to avoid too rapid a reduction in BP in order to avoid cerebral ischemia and hemorrhage; premature infants in particular are already at an increased risk because of the immaturity of their periventricular circulation. Because of the paucity of available data regarding the use of these agents in newborns, the choice of agent depends on the individual clinician's experience.
  • Currently available drugs for continuous infusion include sodium nitroprusside, labetalol, esmolol, fenoldopam and nicardipine (see Table 1). Nicardipine, which is a dihydropyridine calcium channel blocker, has been reported to be effective most often in neonates and appears to have some advantages compared with older drugs that may make it the drug of choice in this population. Regardless of the drug chosen, continuously monitor BP via an indwelling arterial catheter or by frequently repeated (every 10-15 min) cuff readings so that the rate of infusion can be titrated to achieve the desired degree of BP control.   Table 1. Intravenous Drugs for Severe Hypertension in Neonates⁹
    

    Drug	Class	Intravenous (IV) Dosage	Comments
    Diazoxide	Vasodilator (arteriolar)	2-5 mg/kg/dose rapid IV bolus	Slow IV injection ineffective; duration unpredictable; use with caution, may cause rapid hypotension; increases blood glucose levels
    Esmolol	Beta-blocker	100-300 mcg/kg/min IV infusion	Very short-acting; constant IV infusion necessary
    Hydralazine	Vasodilator (arteriolar)	0.15-0.6 mg/kg/dose IV bolus or 0.75-5 mcg/kg/min IV constant infusion	Tachycardia is frequent adverse effect; must administer q4h when administered as IV bolus
    Labetalol	Alpha-blocker and beta-blocker	0.2-1 mg/kg/dose IV bolus or 0.25-3 mg/kg/h IV constant infusion	Heart failure, bronchopulmonary dysplasia (BPD), relative contraindications
    Nicardipine	Calcium channel blocker	1-5 mcg/kg/min IV constant infusion	May cause reflex tachycardia
    Sodium nitroprusside	Vasodilator (arteriolar and venous)	0.5-10 mcg/kg/min IV constant infusion	Thiocyanate toxicity can occur with prolonged use (>72 h) or in renal failure; usual maintenance dose <2 mcg/kg/min, may use 10 mcg/kg/min for short duration (ie, <10-15 min)

• Intermittently administered intravenous antihypertensive agents: For some infants, intermittently administered intravenous agents have a role in therapy (see Table 1). Hydralazine and labetalol, in particular, may be useful in infants with mild-to-moderate hypertension who are not yet candidates for oral therapy because of GI dysfunction. Enalaprilat, the intravenous ACE inhibitor, has also been reported to be useful in the treatment of neonatal renovascular hypertension; however, it should be used with great caution. Even doses at the lower end of published ranges may lead to significant prolonged hypotension and oliguric acute renal failure.
• Oral antihypertensive agents
  • Oral antihypertensive agents (see Table 2) are best reserved for infants with less severe hypertension or infants whose acute hypertension has been controlled with intravenous drugs and who are ready to be converted to long-term therapy. Although captopril had once been considered by many authorities to be the oral drug of choice for neonatal hypertension, this has recently come under question because of the possibility of adverse effects on renal development, particularly in premature infants. It is probably acceptable for use in infants aged 38-40 weeks.
  • Beta-blockers may need to be avoided in long-term antihypertensive therapy in infants with BPD. In such infants, diuretics may have a beneficial effect, not only in controlling BP, but also in improving pulmonary function. Other drugs that may be useful in some infants include vasodilators, such as hydralazine and minoxidil (because it can be compounded into a stable suspension) and the calcium channel blocker isradipine, which may be superior to the older agents. Nifedipine is a poor choice for long-term therapy because of the difficulty in administering small doses and because of the rapid, profound, and short-lived drops in BP that are typically produced by this agent.  Table 2. Oral Antihypertensive Agents Useful for Treatment of Neonatal Hypertension⁹

    Drug	Class	Oral Dosage	Comments
    Captopril	ACE inhibitor	<3 months: 0.01-0.5 mg/kg/dose three times daily; not to exceed 2 mg/kg/d >3 months: 0.15-0.3 mg/kg/dose three times daily; not to exceed 6 mg/kg/d	Monitor serum creatinine and potassium levels
    Clonidine	Central agonist	0.05-0.1 mg/dose 2-3 times daily	Adverse effects include dry mouth and sedation; rebound hypertension with abrupt discontinuation
    Hydralazine	Vasodilator (arteriolar)	0.25-1 mg/kg/dose tid-qid; not to exceed 7.5 mg/kg/d	Suspension stable up to 1 wk; tachycardia and fluid retention are common adverse effects; lupuslike syndrome may develop in slow acetylators
    Isradipine	Calcium channel blocker	0.05-0.15 mg/kg/dose 4 times daily; not to exceed 0.8 mg/kg/d or 20 mg/d	Suspension may be compounded; useful for both acute and chronic hypertension
    Amlodipine	Calcium channel blocker	0.1-0.3 mg/kg/dose bid; not to exceed 0.6 mg/kg/d or 20 mg/d	Less likely to cause sudden hypotension than isradipine
    Minoxidil	Vasodilator (arteriolar)	0.1-0.2 mg/kg/dose 2-3 times daily	Most potent oral vasodilator; excellent for refractory hypertension
    Propranolol	Beta-blocker	0.5-1 mg/kg/dose three times daily	Maximal dose depends on heart rate; may administer as much as 8-10 mg/kg/d if no bradycardia; avoid in infants with BPD
    Labetalol	Alpha- and beta-blocker	1 mg/kg/dose 2-3 times daily, up to 12 mg/kg/d	Monitor heart rate; avoid in infants with BPD
    Spironolactone	Aldosterone antagonist	0.5-1.5 mg/kg/dose twice daily	Potassium-sparing diuretic; monitor electrolytes; several days necessary to observe maximum effectiveness
    Hydrochlorothiazide	Thiazide diuretic	2-3 mg/kg/d orally every day or divided twice daily	Monitor electrolytes
    Chlorothiazide	Thiazide diuretic	5-15 mg/kg/dose twice daily	Monitor electrolytes

  • Few medications are approved for use in treating hypertension in neonates; therefore, all such use must be considered off-label.

Surgical Care

Surgery is rarely indicated for treatment of neonatal hypertension, except for specific diagnoses, such as ureteral obstruction, aortic coarctation, or certain tumors. Unilateral renal venous thrombosis (RVT) is commonly treated with nephrectomy to avoid the need for long-term drug therapy. For infants with renal arterial stenosis, managing the infant medically may be necessary until growth is sufficient to undergo definitive repair of the vascular abnormalities. Infants with malignant hypertension secondary to polycystic kidney disease (PKD) may require bilateral nephrectomy. Fortunately, such severely affected infants are quite rare.

Consultations

Consultation with a cardiologist may be indicated for performance of echocardiography or evaluation of congestive heart failure (CHF) or both. Consultation with an interventional radiologist may also be needed in some cases for performance of renal angiography.

Diet

A low-sodium diet may assist in treatment of infants with persistent hypertension; however, because most infant formula is relatively low in sodium content, no special dietary modifications are usually necessary in the neonatal period.

Medication

Most medications discussed in this article have not been specifically studied in newborns; however, through empiric use of these medications, a reasonable clinical experience has been accumulated. The information below has been summarized in Table 1 and Table 2; the tables also contain information on several other drugs, which are not included in this section because of space limitations.

Vasodilators

These agents relax blood vessels; thus, they decrease peripheral vascular resistance.

Hydralazine (Apresoline)

Decreases systemic resistance through direct vasodilation of arterioles.

Dosing

Adult

Pediatric

0.15-0.6 mg/kg/dose IV bolus or 0.75-5 mcg/kg/min IV constant infusion
0.25-1 mg/kg/dose PO q6-8h; not to exceed 7.5 mg/kg/d

Interactions

MAOIs and beta-blockers may increase hydralazine toxicity; pharmacologic effects of hydralazine may be decreased by indomethacin

Contraindications

Documented hypersensitivity; mitral valve rheumatic heart disease

Precautions

Pregnancy

Precautions

Tachycardia may develop; lupuslike syndrome may occur in nonacetylators

Sodium nitroprusside (Nipride, Nitropress)

Produces vasodilation and increases inotropic activity of the heart.

Dosing

Adult

Pediatric

0.5-10 mcg/kg/min continuous IV infusion; initiate at lower dose, may titrate by increments of 0.5 mcg/kg/min to desired effect

Interactions

Effects are additive when administered with other hypotensive agents

Contraindications

Documented hypersensitivity; subaortic stenosis; idiopathic hypertrophic and atrial fibrillation or flutter

Precautions

Pregnancy

Precautions

Caution in increased intracranial pressure, hepatic failure, severe renal impairment, and hypothyroidism; in renal or hepatic insufficiency, nitroprusside levels may increase and can cause cyanide toxicity

Diazoxide (Hyperstat)

Produces direct smooth muscle relaxation of peripheral arterioles, which decreases BP. May no longer be available in the United States.

Dosing

Adult

Pediatric

2-5 mg/kg/dose IV push as a single injection

Interactions

May decrease serum hydantoins, possibly resulting in decreased anticonvulsant effects; thiazide diuretics may potentiate hyperuricemic and antihypertensive effects of diazoxide

Contraindications

Documented hypersensitivity; aortic coarctation; pheochromocytoma; arteriovenous shunts; aortic aneurysm

Precautions

Pregnancy

Precautions

Inject rapidly; magnitude and duration of effect may vary; patients with diabetes mellitus may require treatment for hyperglycemia; when administered before delivery, may produce fetal or neonatal hyperbilirubinemia, thrombocytopenia, altered carbohydrate metabolism, and other adverse reactions

Calcium channel blockers

These agents block calcium channels in vascular smooth muscle, which leads to vasodilatation.

Amlodipine (Norvasc)

Relaxes coronary smooth muscle and produces coronary vasodilation, which, in turn, improves myocardial oxygen delivery. Good choice for long-term outpatient treatment; may be compounded into a stable suspension (1 mg/mL).

Dosing

Adult

Pediatric

0.1-0.3 mg/kg/dose PO bid; not to exceed 0.6 mg/kg/d or 20 mg/d

Interactions

Coadministration with amiodarone can cause bradycardia and a decrease in cardiac output; triazole antifungals may increase levels

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

Precautions

Slow onset of action; caution in hepatic insufficiency

Isradipine (DynaCirc)

Dihydropyridine calcium channel blocker. It binds to calcium channels with high affinity and specificity and inhibits calcium flux into cardiac and smooth muscle. The resultant effect is arteriole dilation, which reduces systemic resistance and BP, with a small increase in resting heart rate. Rapid onset of action. May be compounded into a stable suspension.

Dosing

Adult

Pediatric

0.05-0.15 mg/kg/dose PO q6-8h; not to exceed 0.8 mg/kg/d or 20 mg/d

Interactions

Coadministration with amiodarone can cause bradycardia and a decrease in cardiac output; triazole antifungals or cimetidine may increase levels

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

Precautions

May cause tachycardia and flushing; caution in aortic stenosis or hepatic insufficiency; may cause dizziness or syncope upon treatment initiation

Nicardipine (Cardene)

Relaxes coronary smooth muscle and produces coronary vasodilation, which, in turn, improves myocardial oxygen delivery and reduces myocardial oxygen consumption. Intravenous nicardipine is the DOC for initial management of severe neonatal hypertension.

Dosing

Adult

Pediatric

1-5 mcg/kg/min IV continuous infusion

Interactions

When administered concurrently with beta-blockers, may increase cardiac depression; triazole antifungals may increase levels; PO formulation increases cyclosporine levels.

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

Precautions

Have arterial line in place for continuous BP monitoring; tachycardia may develop

Beta-adrenergic blockers

These agents decrease heart rate and cardiac output.

Labetalol (Normodyne, Trandate)

Blocks beta1-adrenergic, alpha-adrenergic, and beta2-adrenergic receptor sites, decreasing BP.

Dosing

Adult

Pediatric

0.2-1 mg/kg/dose IV bolus or 0.25-3 mg/kg/h continuous IV infusion
1 mg/kg/dose PO bid/tid; not to exceed 12 mg/kg/d

Interactions

Labetalol decreases effect of diuretics and increases toxicity of methotrexate, lithium, and salicylates; may diminish reflex tachycardia resulting from nitroglycerin use without interfering with hypotensive effects; cimetidine may increase labetalol blood levels; glutethimide may decrease labetalol effects by inducing microsomal enzymes

Contraindications

Documented hypersensitivity; cardiogenic shock; pulmonary edema; bradycardia; atrioventricular block; uncompensated congestive heart failure; reactive airway disease

Precautions

Pregnancy

Precautions

Caution in impaired hepatic function; discontinue therapy if signs of liver dysfunction are present; use with caution in infants with BPD because may cause bronchospasm

Propranolol (Inderal)

Has membrane-stabilizing activity and decreases automaticity of contractions.
Not suitable for emergency treatment of hypertension. Do not administer IV in hypertensive emergencies.

Dosing

Adult

Pediatric

0.5-1 mg/kg/dose PO q8h; not to exceed 10 mg/kg/d

Interactions

Coadministration with aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease propranolol effects; calcium channel blockers, cimetidine, loop diuretics, and MAOIs may increase toxicity of propranolol; toxicity of hydralazine, haloperidol, benzodiazepines, and phenothiazines may increase with propranolol

Contraindications

Documented hypersensitivity; uncompensated congestive heart failure; bradycardia; cardiogenic shock; AV conduction abnormalities

Precautions

Pregnancy

Precautions

Beta-adrenergic blockade may decrease signs of acute hypoglycemia and hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism, including thyroid storm; slowly withdraw drug and closely monitor; use with caution in infant with BPD because may cause bronchospasm

Esmolol (Brevibloc)

Excellent drug for use in patients at risk for experiencing complications from beta-blockade, particularly those with reactive airway disease, mild-to-moderate LV dysfunction, and/or peripheral vascular disease. Short half-life of 8 min allows for titration to desired effect and quick discontinuation if needed.

Dosing

Adult

Pediatric

100-300 mcg/kg/min continuous IV infusion

Interactions

Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease bioavailability and plasma levels of esmolol, possibly resulting in decreased pharmacologic effect; cardiotoxicity of esmolol may increase when administered concurrently with sparfloxacin, astemizole, calcium channel blockers, quinidine, flecainide, and contraceptives; toxicity of esmolol increases when administered concurrently with digoxin, flecainide, acetaminophen, clonidine, epinephrine, nifedipine, prazosin, haloperidol, phenothiazines, and catecholamine-depleting agents

Contraindications

Documented hypersensitivity; uncompensated congestive heart failure; bradycardia; cardiogenic shock; AV conduction abnormalities

Precautions

Pregnancy

Precautions

Beta-adrenergic blockers may mask signs and symptoms of acute hypoglycemia and clinical signs of hyperthyroidism; symptoms of hyperthyroidism, including thyroid storm, may worsen when medication is abruptly withdrawn; slowly withdraw drug and closely monitor patient

Angiotensin-converting enzyme (ACE) inhibitors

These agents inhibit conversion of angiotensin I to angiotensin II.

Captopril (Capoten)

Prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, and reduces aldosterone secretion.

Dosing

Adult

Pediatric

<3 months: 0.01-0.5 mg/kg/dose PO tid; not to exceed 2 mg/kg/d
>3 months: 0.15-0.3 mg/kg/dose PO tid; not to exceed 6 mg/kg/d

Interactions

NSAIDs may reduce hypotensive effects of captopril; ACE inhibitors may increase digoxin, lithium, and allopurinol levels; rifampin decreases captopril levels; probenecid may increase captopril levels; the hypotensive effects of ACE inhibitors may be enhanced when administered concurrently with diuretics

Contraindications

Documented hypersensitivity; renal impairment

Precautions

Pregnancy

Precautions

Caution in renal impairment, valvular stenosis, or severe congestive heart failure; may produce profound drops in BP in neonates; consider restricting use to infants whose postconceptual age has reached full term

Enalapril (Vasotec)

Competitive inhibitor of ACE. Reduces angiotensin II levels, decreasing aldosterone secretion.

Dosing

Adult

Pediatric

IV: Not recommended (see precautions)
PO: Not FDA approved for neonates; limited data exist, 0.08 mg/kg/d PO qd initially; may increase gradually, not to exceed 0.6 mg/kg/d

Interactions

NSAIDs may reduce hypotensive effects of enalapril; ACE inhibitors may increase digoxin, lithium, and allopurinol levels; rifampin decreases enalapril levels; probenecid may increase enalapril levels; the hypotensive effects of ACE inhibitors may be enhanced when administered concurrently with diuretics

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

Precautions

IV formulation is not recommended in managing neonatal hypertension due to risk of acute renal failure and oliguria; PO administration may be useful in the neonatal hypertension long-term management

Diuretic agents

These agents decrease plasma volume and promote excretion of water and electrolytes by the kidneys. They may be used as monotherapy or combination therapy to treat hypertension.

Chlorothiazide (Diuril)

Inhibits reabsorption of sodium in distal tubules, causing increased excretion of sodium and water as well as potassium and hydrogen ions.

Dosing

Adult

Pediatric

5-20 mg/kg/dose PO bid

Interactions

Thiazides may decrease effects of anticoagulants, antigout agents, and sulfonylureas; thiazides may increase toxicity of allopurinol, anesthetics, antineoplastics, calcium salts, loop diuretics, lithium, diazoxide, digitalis, amphotericin B, and nondepolarizing muscle relaxants

Contraindications

Documented hypersensitivity; anuria

Precautions

Pregnancy

Precautions

Caution in renal disease, hepatic disease, gout, diabetes mellitus, and erythematosus

Hydrochlorothiazide (Esidrix, HydroDIURIL)

Inhibits reabsorption of sodium in distal tubules, causing increased excretion of sodium and water as well as potassium and hydrogen ions. Good second agent to add to ACE inhibitor or vasodilator therapy.

Dosing

Adult

Pediatric

2-3 mg/kg/d PO qd or divided bid

Interactions

Thiazides may decrease effects of anticoagulants, antigout agents, and sulfonylureas; thiazides may increase toxicity of allopurinol, anesthetics, antineoplastics, calcium salts, loop diuretics, lithium, diazoxide, digitalis, amphotericin B, and nondepolarizing muscle relaxants

Contraindications

Documented hypersensitivity; anuria; renal decompensation

Precautions

Pregnancy

Precautions

Caution in renal disease, hepatic disease, gout, diabetes mellitus, and erythematosus. Liquid formulation no longer commercially available.

Spironolactone (Aldactone)

Potassium-sparing diuretic. Used for management of hypertension. May block effects of aldosterone on arteriolar smooth muscles.

Dosing

Adult

Pediatric

0.5-2.0 mg/kg/dose PO bid

Interactions

May decrease effect of anticoagulants; potassium and potassium-sparing diuretics may increase toxicity of spironolactone

Contraindications

Documented hypersensitivity; anuria; renal failure; hyperkalemia

Precautions

Pregnancy

Precautions

Caution in renal and hepatic impairment

Central agonists

These agents decrease central adrenergic output.

Clonidine (Catapres)

Stimulates alpha2-adrenoreceptors in brain stem, activating an inhibitory neuron, which, in turn, results in reduced sympathetic outflow. These effects result in a decrease in vasomotor tone and heart rate.

Dosing

Adult

Pediatric

Not established for neonates, limited data suggest 0.05-0.1 mg/dose PO bid/tid

Interactions

Tricyclic antidepressants inhibit hypotensive effects of clonidine; coadministration of clonidine with beta-blockers may potentiate bradycardia; tricyclic antidepressants may enhance hypertensive response associated with abrupt clonidine withdrawal; hypotensive effects of clonidine are enhanced by narcotic analgesics

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

Precautions

Adverse effects include dry mouth and sedation; rebound hypertension with abrupt discontinuation; caution in cerebrovascular disease, coronary insufficiency, sinus node dysfunction, and renal impairment

Follow-up

Further Inpatient Care

• Monitor blood pressure (BP) regularly in neonates with hypertension until the infant is ready for discharge from the neonatal ICU (NICU). Infants treated with ACE inhibitors or diuretics should have electrolyte levels and renal function monitored periodically until discharge.
• Arrangements for home BP monitoring should be part of the discharge plan for any infant sent home on antihypertensive therapy. The optimal device for home BP measurements in an infant is a Dinamap or similar oscillometric device. A second choice is a Doppler device: however, this only measures systolic BP and is difficult to teach parents to use. Therefore, oscillometric devices should be prescribed.

Further Outpatient Care

• Include BP measurement at all follow-up visits for infants with neonatal hypertension. In addition, monitor infants with bronchopulmonary dysplasia (BPD) at discharge and those who had complicated NICU courses for the development of hypertension following discharge.
• Ultrasonography should be obtained 6-12 months after discharge in infants with hypertension to ensure that the kidneys are growing normally.

Inpatient & Outpatient Medications

• Refer to preceding sections.

Transfer

• Occasionally, infants may need to be transferred to specialized centers for advanced diagnostic or therapeutic procedures, such as angiography or vascular surgery.

Deterrence/Prevention

• Although several studies have examined the role of placement of umbilical artery catheters (ie, low versus high lines), no definitive proof has emerged that changes in catheter placement can prevent thromboembolism and the subsequent development of hypertension.

Complications

• As mentioned above, the long-term sequelae of neonatal hypertension on renal growth, renal function, and future BP are unknown at this time. Long-term effects related to certain antihypertensive medications (eg, ACE inhibitors, calcium channel blockers) are also unknown. These infants may need to be monitored closely even after their hypertension has resolved, particularly with respect to renal growth and the redevelopment of hypertension in later childhood.

Prognosis

• The long-term prognosis for most infants with hypertension is quite good. For infants with hypertension related to an umbilical arterial catheter, the hypertension usually resolves over time. These infants may require increases in their antihypertensive medications in the first several months following discharge from the nursery as they undergo rapid growth. Following this, weaning the patient off antihypertensive therapy is usually possible by making no further dose increases as the infant continues to grow. Home BP monitoring by the parents is a crucially important component of this process. Provide proper equipment, either a Doppler or oscillometric device, for all infants discharged from the NICU on long-term antihypertensive medications. Such infants may benefit from referral to a comprehensive pediatric hypertension clinic if their primary care provider is inexperienced in managing hypertension.
• Other forms of neonatal hypertension may persist beyond infancy. In particular, polycystic kidney disease (PKD) and other forms of renal parenchymal disease may continue to cause hypertension throughout childhood. Infants with renal venous thrombosis (RVT) may also remain hypertensive, and some of these children ultimately benefit from nephrectomy. Persistent or recurrent hypertension may also be observed in children who have undergone repair of renal arterial stenosis or coarctation of the aorta. Reappearance of hypertension in these situations should prompt a search for restenosis using the appropriate imaging studies.
• BP in newborns depends on various factors, including gestational age, postnatal age, and birth weight. Hypertension can be observed in various situations in the modern NICU and is especially common in infants who have undergone umbilical arterial catheterization. A careful diagnostic evaluation should lead to determination of the underlying cause of hypertension in most infants. Tailor treatment decisions, which may include intravenous therapy, oral therapy, or both, to the severity of the hypertension. Hypertension resolves in most infants over time, although a small number of infants may have persistent BP elevation throughout childhood.

Patient Education

• Educate the parents of infants who develop hypertension requiring drug therapy about the expected effects and side effects of their infant's antihypertensive medications. In addition, arrange home BP monitoring equipment and educate the parents in its use prior to the infant's discharge from the NICU. Parents must monitor the BP of all infants discharged on antihypertensive medications on a regular basis (ie, usually daily); parents should call the prescribing clinician if the infant's BP exceeds or falls below the target range.
• Patient education information on childhood hypertension can be found at the International Pediatric Hypertension Association web site. Also, visit eMedicine's patient education article, High Blood Pressure.

Miscellaneous

Medicolegal Pitfalls

• Failure to diagnose or treat neonatal hypertension (A major concern is missing an underlying cause of hypertension such as renal disease that might require specific therapy.)

References

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Keywords

neonatal hypertension, high blood pressure, high BP, premature infants, bronchopulmonary dysplasia, BPD, steroids, maternal hypertension, umbilical arterial catheter, postnatal acute renal failure, patent ductus arteriosus, chronic lung disease, congestive heart failure, cardiogenic shock, congenital adrenal hyperplasia, CAH, umbilical artery catheter–associated thromboembolism, renal venous thrombosis, RVT, renal artery stenosis, fibromuscular dysplasia, FMD, rubella, polycystic kidney disease, PKD, hydronephrotic kidney, nephromegaly, multicystic dysplastic kidney, congenital ureteropelvic junction obstruction, ureteral obstruction, hyperaldosteronism, hyperthyroidism, hypercalcemia, neuroblastoma, Wilms tumor, mesoblastic nephroma

Contributor Information and Disclosures

Author

Joseph Flynn, MD, MS, Director of Pediatric Hypertension Program, Division of Nephrology, Children's Hospital and Regional Medical Center; Professor, Department of Pediatrics, University of Washington School of Medicine
Joseph Flynn, MD, MS is a member of the following medical societies: American Academy of Pediatrics, American Heart Association, American Society of Hypertension, American Society of Nephrology, American Society of Pediatric Nephrology, National Kidney Foundation, and Phi Beta Kappa
Disclosure: Novartis Pharmaceuticals Consulting fee Consulting; Pfizer, Inc Consulting fee Review panel membership

Medical Editor

Steven M Donn, MD, Professor of Pediatrics, Director, Neonatal-Perinatal Medicine, Department of Pediatrics, University of Michigan Health System
Steven M Donn, MD is a member of the following medical societies: American Pediatric Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from broker recommendation; Avanir Pharma Stock Investment from broker recommendation

Managing Editor

Arun K Pramanik, MD, MBBS, Professor of Pediatrics, Director of Neonatal Fellowship, Louisiana State University Health Sciences Center
Arun K Pramanik, MD, MBBS is a member of the following medical societies: American Academy of Pediatrics, American Thoracic Society, National Perinatal Association, and Southern Society for Pediatric Research
Disclosure: Nothing to disclose.

CME Editor

Carol L Wagner, MD, Professor of Pediatrics, Medical University of South Carolina
Carol L Wagner, MD is a member of the following medical societies: American Academy of Pediatrics, American Chemical Society, American Medical Women's Association, American Public Health Association, American Society for Bone and Mineral Research, American Society for Clinical Nutrition, Massachusetts Medical Society, National Perinatal Association, and Society for Pediatric Research
Disclosure: Nothing to disclose.

Chief Editor

Ted Rosenkrantz, MD, Professor, Departments of Pediatrics and Obstetrics/Gynecology, Division of Neonatal-Perinatal Medicine, University of Connecticut School of Medicine
Ted Rosenkrantz, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Pediatric Society, Connecticut State Medical Society, Eastern Society for Pediatric Research, and Society for Pediatric Research
Disclosure: Nothing to disclose.

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