2. ESTRUCTURA METÁLICA
2.6. CIMENTACIÓN
Direct vasodilators (hydralazine, minoxidil), -blockers (prazosin, doxazosin), and centrally acting agents (clonidine) can also be considered but are not usually first-line agents for hypertension in children.
Treatment aims
To reduce blood pressure to levels that diminish the risk of associated organ involvement.
To maximize compliance by using long-acting agents and monotherapy, if possi-ble.
To monitor for and address adverse effects, should they arise.
Other treatments
• Some forms of secondary hyperten-sion require surgical correction, such as coarctation of the aorta and some forms of renovascular hypertension.
• Percutaneous transluminal angioplasty can be considered in some cases of ren-ovascular hypertension.
Prognosis
• The patient’s prognosis depends on the underlying cause of the hypertension.
Follow-up and management
• Patients should be followed up for life.
• In cases of mild hypertension, medica-tion tapering can be considered.
General references
Dillon MJ, Ingelfinger JR: Pharmacologic treat-ment of hypertension. In Pediatric Nephrology, ed 3. Edited by Holliday MA, Barratt TM, Avner ED. Baltimore:Williams & Wilkins;
1994:1165–1174.
Ingelfinger JR, Dillon MJ: Evaluation of sec-ondary hypertension. In Pediatric Nephrology, ed 3. Edited by Holliday MA, Barratt TM, Avner ED: Baltimore:Williams and Wilkins;
1994:1146–1164.
Rocchini AP: Childhood hypertension. Pediatr Clin North Am 1993, 40:1–212.
Task Force on Blood Pressure Control in Children: Report of the Second Task Force on Blood Pressure Control in Children. Pediatrics 1987, 79:1–25.
Yetman RJ, Bonilla-Felix MA, Portman RJ:
Primary hypertension in children and adoles-cents. In Pediatric Nephrology, ed 3. Edited by Holliday MA, Barratt TM, Avner ED. Baltimore:
Williams & Wilkins; 1994:1117–1145.
Hyperthyroidism
Diagnosis
Symptoms
Hyperactivity; often mistaken for attention deficit disorder.
Weight loss, polyphagia.
Anxious, palpitations, shortness of breath, weakness.
Heat intolerance, sweating.
Staring.
Signs
Increased systolic blood pressure, tachycardia.
Goiter with or without nodules, often with bruit.
Exopthalmos, tremors, and proximal muscle weakness.
Investigations
Thyroid function tests: T4 is generally elevated; total T3 is almost always elevated; thyroid-stimulating hormone (TSH) is suppressed and is the best indicator of thyroid hormone excess; a normal TSH suggests the possibility of familial dysalbuninemic hyperthyroxinemia, familial thyroxine-binding globulin excess, or familial thyroxine resistance.
123Thyroid uptake and scan: will demonstrate a rapid elevated uptake and enlarged thyroid gland; a single hyperfunctioning nodule will depress radioactive iodine uptake in the rest of the gland; in subacute and chronic thyroiditis (Hashimoto thyroiditis hyperthyroidism or “Hashi-toxicosis”), the uptake is low.
Anti-TSH receptor antibodies or thyroid-stimulating immunoglobulins: will be elevated in Graves’ disease.
Antithyroglobulin, antimicrosomal, and antiperoxidase antibodies: can be elevated in Graves’ disease as well as chronic lymphocytic thyroiditis.
Complications
Excessive growth with advancement of bone age.
Cardiac high-output failure is unlikely in children.
Differential diagnosis Factitious thyroxine ingestion.
Attention deficit disorder.
Familial thyroxine resistance.
Familial dysalbuminemic hyperthyroxine-mia.
Etiology
Autoimmune: Graves’ disease.
Autoimmune: toxic phase of Hashimoto’s thyroiditis.
Postviral: subacute thyroiditis.
Hyperfunctioning nodule.
Neonatal Graves’ secondary to maternal transfer of thyroid-stimulating antibodies.
Epidemiology
Most common in second to fourth decade of life.
Four to five times more frequent in females.
Hyperthyroidism
Treatment
Lifestyle
• Avoid frequent use of sympathomimetic drugs and significant iodide ingestion.
Pharmacological treatment
Thionamide drugs (propylthiouracil and methimazole) comprise first line of treatment.
Standard dosage Propylthiouracil, 300 mg, or methimazole, 30 mg is the usual starting dose (the dose of propylthiouracil is 10 times greater than methimazole) but may need to be higher in older and larger children then titrate down after controlling hyperthyroidism.
Propranolol, 20–60 mg/d during the first 6–12 wk of treatment, is often useful to ameliorate the symptoms.
Special points Some groups add L-thyroxine when the patient is biochemically hypothyroid on the initial higher dose of thionamide. Other groups titrate the dose down to 100–150 mg of propythiouracil (10–15 mg
methimazole) and then add L-thyroxine if the patient remains hypothyroid.
Other treatments
• In those children who are nonresponsive or noncompliant with medical therapy, radioablation is the second line of therapy.
• As a third option, especially in very large thyroid glands, subtotal thyroidectomy is extremely effective. In nodular hyperthyroidism, subtotal thyroidectomy is the first line of treatment.
Treatment aims
To restore the patient to a normal metabolic state.
• The relief of clinical symptoms and signs, coupled with normal biochemical studies of thyroid function, are the goals of therapy.
Prognosis
• Restoration of the child to normal thy-roid metabolic function can be achieved with treatment (medical, surgical, or with radioablation and use of L-thyroxine to treat iatrogenic hypothyroidism) in greater than 90% of patients.
• In children, remission occurs in 25%–40$ of patients in 2 y and approxi-mately another 25% each following 2 y.
Approximately 80% of patients will be in remission in 8 y. Relapses occur in 3%–30% of patients, however.
Follow-up and management
• Patients should be followed at 6–8-wk intervals both clinically and biochemical-ly until a euthyroid state is achieved.
Once a maintenance program is achieved, the patients can be followed at 3-mo intervals.
• Discontinuation of pharmacologic therapy can be attempted after 2 y of stability and if levels of thyroid-stimulat-ing antibodies are found to be low.
General references
Alter CA, Moshang T: Diagnostic dilemma: the goiter. Pediatr Clin North Am 1991, 38:567–578.
Foley TP:Thyrotoxicosis in childhood. Pediatr Ann 1992, 21:43–49.
Lippe B, Landau EM, Kaplan SA:
Hyperthyroidism in children treated with long term medical therapy: twenty-five percent remission every 2 years. J Clin Endocrinol Metab 1987, 65:1241–1245.
Hypoglycemia
Diagnosis
Symptoms
Sweating, shakiness, anxiety, blurry vision: due to sympathetic adrenergic responses to low blood glucose concentrations.
Dizziness, lethargy, confusion: due to impaired cerebral function resulting from low blood glucose concentrations.
Signs
Pallor, diaphoresis, tachycardia, occasional hypothermia (adrenergic).
Altered behavior, lethargy, irritability, coma, seizure (neuroglycopenic).