eMedicine Specialties > Pediatrics: Cardiac Disease and Critical Care Medicine > Cardiology

Holt-Oram Syndrome: Treatment & Medication

Author: Poothirikovil Venugopalan, MBBS, MD, FRCP (Glasg), FRCPCH, Consulting Staff, Department of Child Health, University Hospital of Hartlepool, UK
Contributor Information and Disclosures

Updated: Nov 7, 2008

Treatment

Medical Care

  • Acute-stage management in patients with Holt-Oram syndrome (HOS)
    • Treatment is directed at the cardiac manifestations.
    • Establish a complete diagnosis.
    • Counsel the patient and family.

Surgical Care

  • Treatment for the heart defect
    • Appropriate surgical or nonsurgical correction of the heart defect if indicated and possible
    • Palliative surgery, as indicated, if complete correction is not possible
  • Treatment for musculoskeletal defects
    • Take adequate measures to prevent acquired deformities and to treat existing deformities.
    • Surgical management of hand anomalies depends on the age, pattern, and degree of accompanying malformations of the upper limb.
    • Pollicization to improve function of index finger is recommended for patients with aplasia of the thumb. This is also recommended following amputation of a rudimental thumb.

Consultations

  • Pediatric cardiologist
  • Orthopedic specialist
  • Radiologist
  • Nuclear medicine specialist
  • Family physician
  • Occupational therapist
  • Physiotherapist
  • Psychologist
  • School teacher
  • Specialist nurse
  • Pharmacist
  • Dietitian

Diet

  • Diet may require modification because of the specific cardiac abnormality.

Activity

  • No restrictions are required unless specific cardiac abnormality indicates otherwise.

Medication

The specific cardiac defect and its effects dictate appropriate therapy. For example, treatment of congestive heart failure may include diuretics, an ACE inhibitor, and digoxin. Iron supplements are appropriate in patients with cyanotic heart disease.

Bacterial endocarditis prophylaxis is administered to patients with Holt-Oram syndrome (HOS) based on the specific cardiac condition. An isolated secundum atrial septal defect (ASD) does not require this treatment. For more information, see Antibiotic Prophylactic Regimens for Endocarditis.

Diuretics

These agents eliminate retained fluid and lower preload.


Furosemide (Lasix)

Increases excretion of water by interfering with chloride-binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption in ascending loop of Henle and distal renal tubule. DOC in acute heart failure and in exacerbations of CHF. Used for the long-term management of CHF.

Adult

20-80 mg/d PO/IV/IM; titrate up to 600 mg/d for severe edematous states

Pediatric

1-2 mg/kg/dose PO; not to exceed 6 mg/kg/dose; do not administer more frequently than q6h
0.5-2 mg/kg/d IV divided q8h; may titrate upward; not to exceed 6 mg/kg/d

Metformin decreases furosemide concentrations; furosemide interferes with hypoglycemic effect of antidiabetic agents and antagonizes muscle-relaxing effect of tubocurarine; auditory toxicity appears to be increased with coadministration of aminoglycosides and furosemide (varying degrees of hearing loss may occur); anticoagulant activity of warfarin may be enhanced when administered concurrently; increased plasma lithium levels and toxicity are possible when administered concurrently

Documented hypersensitivity; hepatic coma, anuria, and state of severe electrolyte depletion

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Monitor for hypokalemia, hyponatremia, and hypotension; use caution in pregnancy and breastfeeding


Spironolactone (Aldactone)

A potassium-sparing diuretic. For management of edema resulting from excessive aldosterone excretion. Competes with aldosterone for receptor sites in distal renal tubules, increasing water excretion while retaining potassium and hydrogen ions.

Adult

25-200 mg/d PO qd or divided bid

Pediatric

1.5-3.5 mg/kg/d PO divided q6-24h

May decrease effect of anticoagulants; potassium and potassium-sparing diuretics may increase toxicity of spironolactone

Documented hypersensitivity; anuria, renal failure, or hyperkalemia

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

GI upset, hyponatremia, hyperkalemia, lethargy, confusion, impotence and gynecomastia; caution in renal and hepatic impairment


Amiloride (Midamor)

Potassium-sparing diuretic that acts directly on the distal renal tubule. Usually used along with a potassium-losing diuretic.

Adult

5-10 mg PO bid

Pediatric

0.2 mg/kg PO bid

ACE inhibitors, cyclosporine, indomethacin, and potassium supplements increase risk of hyperkalemia; NSAIDs decrease the effect of amiloride; amiloride increases the risk of toxicity with lithium and amantadine

Documented hypersensitivity; hyperkalemia, potassium supplementation, or potassium-sparing diuretics; impaired renal function

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

GI upset, dry mouth, skin rash, confusion, postural hypotension, hyperkalemia, and hyponatremia

ACE inhibitors

These agents reduce afterload and decrease myocardial remodeling that worsen chronic heart failure.


Captopril (Capoten)

Widely accepted as an essential part of CHF treatment. Improves symptoms and prolongs survival. Prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion.

Adult

6.25-12.5 mg PO tid; not to exceed 150 mg tid

Pediatric

Infants: 0.1-0.5 mg/kg/dose PO q8-12h; not to exceed 4 mg/kg/d
Children: 0.1-2 mg/kg/dose PO q8-12h; not to exceed 6 mg/kg/d
Adolescents: 6.25-25 mg/dose PO q8-12h

NSAIDs may reduce hypotensive effects of captopril; ACE inhibitors may increase digoxin, lithium, and allopurinol levels; rifampin decreases captopril levels; probenecid may increase captopril levels; the hypotensive effects of ACE inhibitors may be enhanced when given concurrently with diuretics

Documented hypersensitivity; renal impairment

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Pregnancy category D in second and third trimester; caution in renal impairment, valvular stenosis, or severe congestive heart failure

Cardiac glycosides

These agents improve symptoms, exert a positive inotropic effect on both the normal and failing heart, and are mediated through inhibition of transmembranous active transport of sodium and potassium. Clinically important actions are on the sinoatrial (SA) and AV nodes. Cardiac glycosides increase efferent vagal impulses, reflexly reduce sympathetic tone, and decrease the sinus rate. They decrease conduction velocity through the AV node.


Digoxin (Lanoxin)

Improves myocardial contractility, reduces heart rate, and lowers sympathetic stimulation in chronic heart failure.

Adult

0.125-0.375 mg PO qd

Pediatric

5-10 mcg/kg/d PO divided q12h

Medications that may increase digoxin levels include alprazolam, benzodiazepines, bepridil, captopril, cyclosporine, propafenone, propantheline, quinidine, diltiazem, aminoglycosides, PO amiodarone, anticholinergics, diphenoxylate, erythromycin, felodipine, flecainide, hydroxychloroquine, itraconazole, nifedipine, omeprazole, quinine, ibuprofen, indomethacin, esmolol, tetracycline, tolbutamide, and verapamil; medications that may decrease serum digoxin levels include aminoglutethimide, antihistamines, cholestyramine, neomycin, penicillamine, aminoglycosides, oral colestipol, hydantoins, hypoglycemic agents, antineoplastic treatment combinations (including carmustine, bleomycin, methotrexate, cytarabine, doxorubicin, cyclophosphamide, vincristine, and procarbazine), aluminum or magnesium antacids, rifampin, sucralfate, sulfasalazine, barbiturates, kaolin/pectin, and aminosalicylic acid

Documented hypersensitivity; beriberi heart disease, idiopathic hypertrophic subaortic stenosis, constrictive pericarditis, and carotid sinus syndrome

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Hypokalemia may reduce positive inotropic effect of digitalis; IV calcium may produce arrhythmias in digitalized patients; hypercalcemia predisposes patient to digitalis toxicity, and hypocalcemia can make digoxin ineffective until serum calcium levels are normal; magnesium replacement therapy must be instituted in patients with hypomagnesemia to prevent digitalis toxicity; patients diagnosed with incomplete AV block may progress to complete block when treated with digoxin; exercise caution in hypothyroidism, hypoxia, and acute myocarditis

Beta-adrenoceptor blockers

These agents relieve infundibular spasm in hypercyanotic spells.


Propranolol (Inderal)

Inhibits both beta1- and beta2-adrenergic receptors. The exact mechanism of benefit is uncertain, although it is believed to relieve infundibular spasm that precipitates hypercyanotic spells.

Adult

Not used for this indication

Pediatric

1-2 mg/kg/d PO divided bid/tid
0.01-0.1 mg/kg/dose IV administered slowly (over at least 10 min) in ICU; not to exceed 1 mg/dose in infants or 3 mg/dose in children

Coadministration with aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease propranolol effects; calcium channel blockers, cimetidine, loop diuretics, and MAOIs may increase toxicity of propranolol; toxicity of hydralazine, haloperidol, benzodiazepines, and phenothiazines may increase with propranolol

Documented hypersensitivity; uncompensated CHF; bradycardia; cardiogenic shock; AV conduction abnormalities

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Beta-adrenergic blockade may decrease signs of acute hypoglycemia and hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism, including thyroid storm (withdraw drug slowly and monitor closely)

More on Holt-Oram Syndrome

Overview: Holt-Oram Syndrome
Differential Diagnoses & Workup: Holt-Oram Syndrome
Treatment & Medication: Holt-Oram Syndrome
Follow-up: Holt-Oram Syndrome
Multimedia: Holt-Oram Syndrome
References
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Further Reading

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Keywords

Holt-Oram syndrome, HOS, embryonic radial ray, triphalangeal thumbs, absent thumbs, foreshortened arms, phocomelia, TBX5, atriodigital hypoplasia, cardiac-limb syndrome, cardiomelic syndrome, heart-hand syndrome, upper limb–cardiovascular syndrome, ventricular septal defect, VSD, atrial septal defect, ASD

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Contributor Information and Disclosures

Author

Poothirikovil Venugopalan, MBBS, MD, FRCP (Glasg), FRCPCH, Consulting Staff, Department of Child Health, University Hospital of Hartlepool, UK
Poothirikovil Venugopalan, MBBS, MD, FRCP (Glasg), FRCPCH is a member of the following medical societies: British Cardiac Society and Royal College of Physicians and Surgeons of Glasgow
Disclosure: Nothing to disclose.

Medical Editor

Ira H Gessner, MD, Professor Emeritus, Pediatric Cardiology
Ira H Gessner, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, American Pediatric Society, and Society for Pediatric Research
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

John W Moore, MD, MPH, Professor of Clinical Pediatrics, Section of Pediatric Cardiology, Department of Pediatrics, University of California San Diego School of Medicine; Director of Cardiology, Rady Children's Hospital
John W Moore, MD, MPH is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, and Society for Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

CME Editor

Gilbert Z Herzberg, MD, Assistant Professor, Department of Pediatrics, Section of Pediatric Cardiology, New York Medical College; Consulting Staff, Department of Pediatrics, Sound Shore Medical Center
Gilbert Z Herzberg, MD is a member of the following medical societies: American Academy of Pediatrics
Disclosure: Nothing to disclose.

Chief Editor

Steven R Neish, MD, SM, Director of Pediatric Cardiology Fellowship Program, Associate Professor, Department of Pediatrics, Baylor College of Medicine
Steven R Neish, MD, SM is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, and American Heart Association
Disclosure: Nothing to disclose.

 
 
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