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Children hypertension

Miller, J. Z-, Weinberger, M. H., and Christian, J. C. (1987). Blood pressure response to potassium supplementation in normotensive adults and children. Hypertension 10,437-442. [Pg.847]

Postoperative complications include ischemia of paraexstrophy flaps, thus leading to urethral strictures (Kelly 1998 Ben-Chaim et al. 1996 Ben-Chaim and Gearhart 1996). Suprapubic leakage is another problem, but usually there is spontaneous closure within several months. VUR is present in almost all cases postoperatively (Currarino et al. 1993). Two children were reported who developed significant hypertension postoperatively after primary bladder closure and pelvic osteotomies followed by immobilization using skin traction (Husmann et al. 1993). In both children hypertension subsided spontaneously after removal of the immobilization. [Pg.181]

If a pregnant woman is affected by mercury poisoning, the consequences may affect the child. As a result, the child may suffer from profound mental deficiency, atrophy of cerebral cortex, commisure and cerebellum neuron destruction. Acrodynia is a syndrome that affects children exposed to organic and inorganic mercury compounds. Symptoms include itchy, measles-like rash followed by desquamation of palm and foot skin, essential tachycardia, generalized swellings, hypertension and salivation (Harada, 1995). [Pg.341]

There are major consequences of alcoholism, from child abuse to domestic or public violence to traffic accidents and from cirrhosis to hypertension. Mean life expectancy of alcohol abusers is around 55 years. Alcohol seems involved in several hundred thousand deaths each year in Europe, with considerable added social and health care costs. This is in clear contrast with the little attention paid to the treatment of alcohol dependence and abuse. It is important to note that there is an increasing knowledge of similar effects on driving etc. from other psychoactive substances, particularly from the seda-tive/tranquillizer drugs and antihistamines. [Pg.268]

Can antidepressants such as tricyclics or buproprion augment the effect of stimulants on nondepressed children with ADHD Randomized controlled trials have yet to address this question. Nonetheless, such combinations are common in clinical practice. One case report showed leukopenia in a child treated with a combination of MPH and tricyclics for 4 months, although the doses were not specified (Burke et ah, 1995). Another case report indicated that obsessive-compulsive symptoms developed secondary to the combination of MPH and tricyclics (Pataki et ah, 1993). On a cautionary note, MPH has been found to interact with guanethidine to produce paradoxical hypotension. Patients on monoamine oxidose (MAO) inhibitors are likely to develop hypertensive crises if given a stimulant. [Pg.258]

Coadministration of beta-blockers can potentiate rebound hypertension upon discontinuation of medications, and it is therefore recommended that the beta-blocker be withdrawn before the tt2 agonist (Physicians Desk Reference, 2001). Tricyclic antidepressants may also produce changes in sinus node and AV conduction, and it is recommended that they be used cautiously in combination with tt2 agonists (Physicians Desk Reference, 2001). However, in child psychiatric practice, there has been debate about whether there are adverse interactions related to concomitant use of tricyclics and tt2 agonists. Finally, the tt2 agonists may potentiate the effects of CNS depressants (e.g., barbiturates) or other medications that produce sedation, so lower doses of each may be warranted. [Pg.270]

The adverse effects of TCAs are also similar to those reported in adults (see Chapter 7). The secondary amine TCAs (e.g., desipramine, nortriptyline) are generally as well tolerated as newer antidepressants. Increased blood pressure may be more likely to occur in children than in adults but hypertension per se is rare ( 135). The most common cardiovascular effect is mild tachycardia. Despite their generally favorable adverse effect profile, secondary amine TCAs can cause serious toxicity in children and adolescents just as in adults when a taken in an overdose or when a high TCA plasma level occurs as a result of slow metabolism ( 136). For that reason, most clinicians reserve TCAs for the child or adolescent who has at least a moderate depressive disorder unresponsive to a trial of one or more newer antidepressants. In such instances, TDM should be done at least once to ensure plasma concentrations greater than 450 ng/mL do not develop ( 137). Such levels are associated with an increased risk of the following ... [Pg.280]

The human reproductive process does not fit perfectly into the animal model of reproductive and developmental toxicity. Conditions of the fetal-maternal unit that affect both mother and child have not been adequately addressed in this monograph, although there is some evidence that some of these adverse outcomes, such as pregnancy-induced hypertension, may be related to environmental exposure (Tabacova et al., 1998 Dawson et al., 1999). This is a promising frontier for new research. We have also not dealt with genetic susceptibility to developmental toxicants. Advances in this field may illuminate many of the mysteries of how toxicants act, and on whom. Limited data are available on mechanisms of action (see section 5.2.4). The work on oxidative stress in pregnancy (Tabacova et al., 1998 Hubei,... [Pg.108]

Shackleton CH, Honour JW, Dillon MJ, Chantler C, Jones RW (1980c) Hypertension in a four-year-old child gas chromatographic and mass spectrometric evidence for deficient hepatic metabolism of steroids. J Clin Endocrinol Metab 50 786-802... [Pg.604]

Benign intracranial hypertension occurred in a 7-month-old child after withdrawal of topical betamethasone ointment and in a 7-year-old boy treated with a 1% cortisol ointment in large amounts. [Pg.10]

Children have more frequent, more severe, and more rapid ocular hypertensive responses to topical dexamethasone than adults. In one case a systemic glucocorticoid caused significant but asymptomatic ocular hypertension in a child (67). [Pg.11]

Chua JK, Fan DS, Leung AT, Lam DS. Accelerated ocular hypertensive response after application of corticosteroid ointment to a child s eyelid. Mayo Clin Proc 2000 75(5) 539. [Pg.67]

Bindl L, Fahnenstich H, Peukert U. Aerosolised prostacyclin for pulmonary hypertension in neonates. Arch Dis Child Fetal Neonatal Ed 1994 71(3) F214-6. [Pg.110]

Clonidine is one of the most widely used sedating medications in pediatric and child psychiatry practice, particularly in children with sleep onset delay and ADHD. It is a central alpha2 agonist. Pharmacokinetics show rapid absorption, with an onset action within 1 h, peak effects at 2-4 h and a half-life 6-24 h. Effects on sleep architecture are fairly minimal but may include decreased REM, so that discontinuation can lead to REM rebound. Clonidine has a narrow therapeutic index, and there has been a recent dramatic increase in reports of overdose with this medication. Potentially significant side effects including hypotension, bradycardia, anticholinergic effects, irritability, and dysphoria rebound hypertension may occur on abrupt discontinuation. Tolerance often develops, necessitating increases in dose. [Pg.142]

The chance that an obese child will become an obese adult is estimated to increase from approximately 20% if overweight at age 4 years to approximately 80% if overweight during adolescence (Guo and Chumlea, 1999). Patients who are overweight are at a higher risk for type 2 diabetes, hypertension, and dyslipidemia. [Pg.247]

A 6-year-old boy developed general malaise and mild agitation, tachycardia, hypertension, and dilated pupils. His mother was a cocaine addict. Cocaine and benzodiazepines were found in significant amounts in the child s urine and hair the urine contained 109 ng/ ml of cocaine and 145 ng/ml of benzodiazepines. Hair samples contained 16 ng/ml of cocaine and 0.6 ng/ml of benzodiazepines. [Pg.523]

A 14-month-old boy began convulsing 40 minutes after taking an unknown medication. The convulsions lasted for 20 minutes. He became cyanotic with a heart rate of 130/minute and a temperature of 38°C. He was treated with oxygen, intravenous benzodiazepines, and dipyrone, but continued to have isolated ventricular extra beats, hypertension, and tachycardia. The serum and urine concentrations of MDMA 8 hours after ingestion were 0.591 and 1477 mg/1 respectively. After 12 hours, the tachycardia and hypertension resolved and the child was discharged 9 days later with no residual symptoms. [Pg.610]

Hypertension can develop rapidly during the third trimester of pregnancy. Untreated, it can pose a danger to both mother and child. So-called gestational hypertension commonly disappears after pregnancy but not always. And if your blood pressure was elevated prior to pregnancy it s particularly important to monitor it on a regular basis. [Pg.41]

Liver transplantation not only removes the continued risk of variceal bleeding, but also eliminates the underlying liver disease causing portal hypertension. However, due to the scarcity of liver donors, limited financial resources and the life-long immunosuppression required, this major surgical intervention can only rarely be considered - perhaps in cases where a previous shunt operation or the creation of a TIPS was not possible. The survival rate for transplantation is higher than when recurrent bleeding is treated by repeated sclerotherapy (73% versus 17% after 4 years). The indication for transplantation (e. g. cirrhosis Child B or C) should be set as early as possible, (s. p. 872)... [Pg.260]

A boy weighing 4 kg was born by spontaneous normal delivery at 39 weeks to a 38-year-old Afro-Caribbean woman, whose pregnancy was complicated by essential hypertension treated with amlodipine. On day 1 the child developed firm, red, pea-sized nodular lesions on the face, buttocks, back, shoulders, and arms. [Pg.176]

An 18-month-old boy who had regularly consumed a herbal tea mixture since the 3rd month of hfe developed veno-occlusive disease with portal hypertension and severe ascites (46). Histology of the liver showed centrilobular sinusoidal congestion with perivenular bleeding and parenchymal necrosis without cirrhosis. The child was given conservative treatment only and recovered completely within 2 months. [Pg.364]

The ocular hypertensive response in this case could have been due to systemic absorption of glucocorticoid through the skin of the eyelid, especially when there was a surgical wound. Alternatively, a sufficient amount of ointment could have seeped over the eyelid margins, causing the rise in intraocular pressure, similar to the application of eye-drops, as has been reported in another child, who also had Cushing s syndrome, a rare result of ophthalmic glucocorticoids (370). [Pg.941]

A 14-year-old child developed hypertensive encephalopathy, a known rare adverse effect of erythropoietin, after 2 months (69). [Pg.1244]

Taylor J, Pahl M, Rajpoot D. Erythropoietin-induced hypertensive encephalopathy in a child possible mechanisms. Dial Transplant 2002 31 170-88. [Pg.1250]

Johnson TR, Tobias JD. Hypotension following the initiation of tizanidine in a patient treated with an angiotensin converting enzyme inhibitor for chronic hypertension. J Child Neurol 2000 15(12) 818-19. [Pg.2073]

Wilkinson AR, Aynsley-Green A, Mitchell MD. Persistent pulmonary hypertension and abnormal prostaglandin E levels in preterm infants after maternal treatment with naproxen. Arch Dis Child 1979 54(12) 942-5. [Pg.2429]

The use of nifedipine during pregnancy and labor has been widely debated, although its effects on child development have not been well evaluated. In one study nifedipine did not affect the development and health of 190 children, aged 18 months, born to women with mild to moderate hypertension who had been randomized to nifedipine, given for 12-34 gestational weeks before delivery, or expectant management (45). [Pg.2520]

A child developed cardiac dysrhythmias, severe hypertension, and pulmonary edema after the intraoperative administration of ocular phenylephrine (1). [Pg.2809]

A 2-month-old child given perioperative phenylephrine drops during cataract extraction developed ventricular extra beats, very severe hypertension, and pulmonary edema requiring intensive therapy (5). Extubation was possible within 3 hours, and she recovered with no untoward consequences. [Pg.2809]

Greher M, Hartmann T, Winkler M, Zimpfer M, Crabnor CM. Hypertension and pulmonary edema associated with subconjunctival phenylephrine in a 2-month-old child during cataract extraction. Anesthesiology 1998 88(5) 1394-6. [Pg.2810]

Complete atrioventricular block occurred in a 10-year-old child with a history of hypertension, severe renal dysfunction, incomplete right bundle branch block, and a ventricular septal defect that had been repaired at birth (10). After slow induction with sevoflurane and nitrous oxide 66%, complete atrioventricular block occurred when the inspired sevoflurane concentration was 3% and reverted to sinus rhythm after withdrawal of the sevoflurane. The dysrhjrthmia recurred at the end of the procedure, possibly caused by lidocaine, which had infiltrated into the abdominal wound, and again at 24 hours in association with congestive cardiac failure following absorption of peritoneal dialysis fluid. [Pg.3123]


See other pages where Children hypertension is mentioned: [Pg.10]    [Pg.239]    [Pg.357]    [Pg.12]    [Pg.543]    [Pg.848]    [Pg.264]    [Pg.299]    [Pg.435]    [Pg.693]    [Pg.1230]    [Pg.449]    [Pg.245]    [Pg.26]    [Pg.37]    [Pg.109]    [Pg.153]    [Pg.357]    [Pg.727]   
See also in sourсe #XX -- [ Pg.202 ]




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Hypertension in children

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