Most children with HTN have no symptoms. Signs and symptoms associated with severe HTN include encephalopathy (headache, vomiting, seizures), heart failure, stroke, and retinopathy (blurred vision, flame hemorrhage, and cotton wool spots on retinal exam). Neonatal history (low birth weight or use of umbilical artery catheter); family history of HTN, stroke, or heart disease; and dietary history (excessive salt or caffeine, drugs) are important. Additional findings that may suggest specific causes include abdominal bruit; diminished leg pressure and weak femoral pulse (coarctation of aorta); cafe-au-lait spots (neurofibromatosis associated renal artery stenosis); flank mass (hydronephrosis, Wilms tumor); tachycardia with flushing and diaphoresis (pheochromocytoma); and truncal obesity, acne, striae, and buffalo hump (Cushing syndrome). Signs of underlying kidney disease may be present.
In addition to history and physical examination, the evaluation of children with confirmed HTN includes the following: 1.
Baseline etiologic assessment (urinalysis, electrolytes, blood urea nitrogen, creatinine, and renal ultrasound) 2.
Focused studies based on clinical suspicion (e.g., plasma metanephrines, thyroid studies, vascular imaging) 3.
4.
Assessment of other cardiovascular risk factors (lipids, fasting glucose, uric acid)
Therapeutic lifestyle changes (diet, exercise) should be initiated for asymptomatic stage 1 HTN without target organ damage or systemic disease. Medication should be started for stage 2 or symptomatic HTN and stage 1 HTN, which fails to respond to lifestyle changes. Calcium channel blockers or angiotensin-converting enzyme inhibitors are the most frequently chosen first-line options in children. Angiotensin receptor blockers, β-blockers, or diuretics are also recommended as first-line antihypertensive agents. More than one agent may be needed. Hypertensive emergency requires prompt hospitalization and may require parenteral antihypertensive treatment with nicardipine, labetalol, esmolol, or sodium nitroprusside.
Prognosis depends on the underlying etiology and BP control. Essential HTN, when present in adolescents, is usually not associated with morbidity at presentation. Left untreated, however, even asymptomatic stage 1 HTN may increase risk for cardiovascular, central nervous system, and renal morbidity in adults.
Vesicoureteral reflux (VUR) is the retrograde flow of urine from the bladder up to the ureter or even up to the kidney. Most VUR results from congenital incompetence of the ureterovesical (UV) junction, a structure that matures through early childhood. In a significant minority of children, structural UV abnormalities exist that never resolve. VUR may be familial; 30% to 40% of siblings of a child with VUR also have VUR. VUR may also be secondary to distal bladder obstruction or other urinary tract anomalies.