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Congestive heart failur infants

Infantile, generalized cardiomegalic AMD, or Pompe s disease, usually becomes manifest in the first weeks or months of life, with failure to thrive, poor suck, generalized hypotonia and weakness, also termed floppy infant syndrome. Macroglossia is common, as is hepatomegaly, which, however, is rarely severe. There is massive cardio-megaly, with congestive heart failure. Weak respiratory muscles make these infants susceptible to pulmonary infection death usually occurs before the age of 1 year and invariably before the age of 2 years [6]. [Pg.699]

The safety and efficacy of amiodarone for supraventricular tachycardia have been studied in 50 infants (mean age 1.0 month, 35 boys) (222). They had congenital heart disease (24%), congestive heart failure (36%), or ventricular dysfunction (44%). Six, who were critically ill, received a loading dose of intravenous amiodarone 5 mg/kg over 1 hour, and all took 20 mg/kg/day orally for 7-10 days, followed by 100 mg/day if this failed to control the dysrhythmia, oral propranolol (2 mg/kg/day) was added. Follow-up was for an average of 16 months. Rhythm control was achieved in aU patients. Growth and... [Pg.162]

A population pharmacokinetic study in 172 neonates and infants showed that the clearance of digoxin is affected significantly by total body weight, age, renal function, and congestive heart failure (143). [Pg.655]

Several cases of furosemide-associated fever have been reported (SEDA-20, 204) (SEDA-21, 229) (SEDA-22, 238). These had certain features in common (1) the affected infants were in their first year of life (2) there was congestive heart failure as a result of congenital abnormahties or cardiomyopathy (3) the temperature was raised to 38.5-40 C and there was a resemblance to septic fever (4) concomitant treatment with digoxin (5) negative physical examination and investigations for a source of infection (6) withdrawal of furosemide was followed by disappearance of fever within 1-2 days. In some cases, the use of furosemide in lower dosages or on alternate days avoided fever. The mechanism of this adverse effect is unclear, but it appears to be dose-related. Consideration of furosemide as a cause of fever in such patients may save unnecessary laboratory studies and lead to early resolution. [Pg.1457]

The Austrian Adverse Drug Reactions Advisory Committee received three reports of severe electroljde disturbances associated with an oral bowel-cleansing solution containing sodium phosphate solution (Fleet Phospho-Soda Buffered Saline Laxative Mixture), used as a bowel preparation for colonoscopy (5). Prescribers are advised to be aware of complications of the use of phosphate enemas, particularly in infants, elderly or debilitated patients, patients with congestive heart failure, and patients with impaired renal function. [Pg.2821]

Loop diuretic therapy has been implicated in the development of renal calcifications in both preterm and full-term infants [99-105]. In a study by Jacinto et al., nephrocalcinosis occurred in 20 of 31 (64%) of premature infants with birth weights less than 1500 g, with 65% of affected infants having received furo-semide [103]. Nephrocalcinosis was found in 14% of full-term infants with congestive heart failure receiving long-term furosemide therapy [104]- Furosemide may induce high urinary calcium excretion rates and low urinary citrate to creatinine ratio, risk factors for renal calcification [106]. [Pg.500]

Alon US, Scagliotti D, Garola RE. Nephrocalcinosis and nephrolithiasis in infants with congestive heart failure treated with furo-semide. J Pediatr 1994 125 149-151. [Pg.507]

SaarelaT, fanning P, Koivisto M, PaavilainenT. Nephrocalcinosis in full-term Infants receiving furosemide treatment for congestive heart failure a study of the Incidence and 2-year follow up. Eur J Pediatr 1999 158 668-672. [Pg.507]

Nadolol is contraindicated in severe bradyarrhythmias or bronchospasm. It should be used cautiously in overt congestive heart failure (CHF), severe peripheral vascular disorder with claudication, and severe diabetes mellitus. As nadolol is largely excreted by the kidneys, decreased renal function affects the clearance of the drug. Nadolol concentrates fivefold in human breast milk and that should be taken into consideration in prescribing the drug for a mother nursing an infant. [Pg.478]

Myocardial infarction, profound congestive heart failure, multiorgan failure, and perinatal stroke have been reported in infants born of mothers using blue cohosh, sometimes in combination with black cohosh or other herbs, before birth (Finkel and Zarlengo 2004 Gunn and Wright 1996 Jones and Lawson 1998). [Pg.180]

Acute myocardial infarction, congestive heart failure, and cardiogenic shock were reported in a newborn infant whose mother had taken blue cohosh. The mother had taken 3 tablets of blue cohosh daily for 3 weeks at the end of her pregnancy, although the recommended dose was 1 tablet daily (Jones and Lawson 1998). A review of the traditional herbal literature indicated that the dose taken in the case constituted an overdose (Bergner 2001). [Pg.180]

But back to that phone call. The incident it announced was the accidental death of a six-week-old infant. The child had been admitted to our hospital for an initial loading dose of digoxin, a powerful medication that was expected to control his symptoms of early congestive heart failure, but a conversion error from micrograms to milligrams, and a misplaced decimal point written by a distracted medical resident, produced an order for ten times the prescribed amount. That order set in motion a chain of events that transformed a healing medication into a lethal overdose. [Pg.7]

Relative active or latent peptic ulcer disease, recent intestinal anastomoses, nonspecific ulcerative colitis (increased risk of perforation), diabetes, adrenocortical insufficiency (may persist for months after discontinuing therapy), active or latent tuberculosis, cerebral malaria, chicken pox, meades, latent amebiasis or strongyloides infection, inactivated viral or bacterial vaccines where antibody response may not be induced, cirrhosis, congestive heart failure, renal failure or hypertension (increased risk of sodium retention, edema and potassium loss), hypokalemia or hypocalcemia, emotional instability or psychotic tendencies, hypothyroidism, growth retardation in infants and children. [Pg.389]

Alon US (1997) Nephrocalcinosis. Pediatrics 9 160-165 Alon US, Scagliotti D, Garola RE (1994) Nephrocalcinosis and nephrolithiasis in infants with congestive heart failure treated with furosemide. J Pediatr 125 149-151 Arikyants N, Sarkissian A, Hesse A et al (2007) Xanthinuria type I-a rare cause of urolithiasis. Pediatr Nephrol 22 310-314... [Pg.397]


See other pages where Congestive heart failur infants is mentioned: [Pg.2167]    [Pg.257]    [Pg.950]    [Pg.1436]    [Pg.1950]    [Pg.1165]    [Pg.920]    [Pg.399]    [Pg.333]    [Pg.127]   


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