• Hypertension (HTN) is rare in neonates, unlike hypotension 
• Low-birth-weight and prematurity (<32 weeks’ gestation) have been linked to HTN in the paediatric demographic and other cardiovascular disease later in life
• Normal blood pressure (BP) values increase with increasing weight and postnatal age
  
  • rises by 1–2 mmHg/day in the first week and then 1–2 mmHg/week over the next 6 weeks
  • these changes are significant, particularly in preterm babies

Systolic blood pressure (SBP) and/or diastolic blood pressure (DBP) >95th percentile for gestation and postnatal age

Table 1: BP values beyond 2 weeks of age in babies 26–44 weeks’ post-conceptional age

• Asymptomatic
• Respiratory distress
• Increased tone
• Lethargy
• Cyanosis
• Apnoea
• Feeding difficulties
• Congestive heart failure
• Mottling
• Irritability/seizures
• Abdominal distension
• Cardiogenic shock
• Cerebral haemorrhage

Method

• Invasive: intra-arterial BP monitoring (umbilical artery, radial artery, posterior tibial artery) 
• Non-invasive: oscillometric device, doppler flow ultrasonography (most reliable non-invasive method of BP measurement) 

Technique

• Cuff length must cover ≥80% length of right upper arm and bladder width should be 60% of circumference (narrow cuffs give falsely raised readings)
• For oscillometric readings, measure BP 1.5 hr after feeds/medical intervention with baby supine or prone
• Place cuff, wait 15 min and note state of baby (awake/asleep). Take 3 readings at 2 min intervals
• Check BP in legs (normally higher) as well as arms. If leg BP < arm BP consider diagnosis of coarctation of the aorta (COA)
• For umbilical arterial catheter (UAC) in situ, ensure catheter free of clots/air bubbles and that transducer is calibrated 

Physiological variance

• Transient rise: feeding, sucking, in pain (post-surgical babies), agitated, being suctioned, crying (increases SBP 17–25 mmHg) or an upright position 
• Physiological rise in BP (increasing weight and postnatal age) in the first few weeks of life 
• SBP can be 5 mmHg lower in sleeping babies 

• Antenatal history (fetal scans, maternal HTN, TORCH screen, maternal drug abuse, e.g. cocaine, heroin)
• Perinatal history (mode of delivery, type of anaesthesia given during delivery)
• Postnatal history (neonatal drugs e.g. caffeine, steroids, inotropes; umbilical lines, neurological status, BP measurement technique) 

• Full general examination (check for syndromic facies)
• Systemic examination including checking for murmurs, bruits; femoral pulses in both lower limbs (absent or decreased in COA) and abdomen for palpable renal masses (tumours, polycystic kidneys)

• Renal function tests
  
  • elevated serum creatinine/urea signifies renal insufficiency which may be associated with HTN
• Urinalysis
  
  • haematuria: obstruction, infection, renal vein thrombosis 
  • proteinuria: renal parenchymal disease
• Urine culture
  
  • exclude pyelonephritis
• Thyroid function tests, cortisol, plasma renin and aldosterone
  
  • plasma renin elevated in renovascular disease and low in primary hyperaldosteronism
  • renin levels higher in neonates than children and adults. Elevated plasma renin activity may not always indicate underlying renal disease 
  • medication such as caffeine can raise renin levels 
• Abdominal ultrasound 
  
  • abdominal masses and renal obstruction
  • Doppler flow ultrasonography can rule out arterial/venous causes (detects renal artery stenosis but can miss branch artery stenosis)
  • if UAC in situ, check aorta and renal arteries for thrombi
• Cranial ultrasound
  
  • intra-ventricular haemorrhage (IVH)
  • cerebral oedema
• Echocardiogram
  
  • COA
  • signs of end organ damage (left ventricular hypertrophy or decreased contractility)
• Other investigations to consider following discussion with the relevant specialist
  
  • arteriography – renovascular disease
  • venocavography – renal vein thrombosis 
  • CT/MR angiogram – renovascular disease and middle aortic pathology
  • MCUG
  • DMSA
  • serum and urine metanephrines – exclude pheochromocytoma
  • urine 17-hydroxysteroid and 17-ketosteroid levels – Cushing’s and CAH
  • gene expression array
  • fundoscopy
  • ECG
  • CXR

• Renal parenchymal disease
• Reno-vascular causes 
• Pain
• Acquired renal conditions
• Neurological 
• Pulmonary 
• Cardiovascular causes 
• Medication related (maternal and neonatal)
• Endocrine causes 
• Idiopathic

• Determined by severity of HTN, whether baby is symptomatic and presence of end organ damage (e.g. LVH, encephalopathy, haematuria, proteinuria) 
• Treat cause (e.g. correcting fluid overload, treating pain, removing iatrogenic agents that may have contributed to HTN)
• Start each medication at lowest recommended dose 
• Monitor BP at least every 15 min in the first 2 hr of treatment and then hourly to avoid hypotension and hypoperfusion
• Surgery may be indicated for the treatment of secondary HTN, e.g. COA, renal artery stenosis HTN, renal vein thrombosis, polycystic kidney disease, tumours or ureteral obstruction to avoid long-term anti-hypertensive medical treatment although, in some cases, this is not guaranteed
• Treat the following 3 categories of neonates:
  
  • SBP 95–99th centile and symptomatic or evidence of end organ damage
  • asymptomatic with SBP >99th centile
  • symptomatic with SBP >99th centile (hypertensive crisis)

• Discuss with renal and cardiac teams
• IV treatment to reduce BP slowly to <90th centile 
  
  • one third total reduction in first 12 hr
  • next one third total reduction in second 12 hr
  • final one third total reduction over next 24 hr
• If BP drops suddenly – fluid bolus and reduce drug dose
• IV drug options include: 
  
  • labetalol 
  • hydralazine 
  • nicardipine (caution with perinatal asphyxia)
  • esmolol (on the advice of paediatric cardiologist) 

• Use oral agents, options include:
  
  • amlodipine oral  
  • hydralazine 
  • propranolol 
• diuretics e.g. furosemide and spironolactone ACE inhibitors (enalapril or captopril) not usually used due to significant side effect profile (profound hypotension, acute renal failure, delayed renal maturity in preterms, neurological complications)

• Depends on aetiology, timing of diagnosis and management 
• Usually resolves in majority of babies, especially those with UAC complications
• HTN secondary to renal parenchymal disease requires long-term specialist follow-up