Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019209 (hepatomegaly)
 5,798 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Emergencies in pediatric cardiology are heart failure, cyanosis and rhythm disturbances. The signs of heart failure are tachycardia, tachypnea and hepatomegaly. The therapy consists of oxygen, diuretics and digoxin. Occasionally, intubation with mechanical ventilation and intravenous catecholamines are needed. Cyanosis is often the only sign of a severe heart malformation, and prompt hospitalization is mandatory. Oxygen and warm environment is important during transport, correction of a possible metabolic acidosis and prostaglandin infusion are done in the hospital. Beyond the newborn period, so-called cyanotic spells are seen, particularly in tetralogy of Fallot. In supraventricular tachycardia, vagal manoeuvres can be tried first, if not successful, intravenous adenosine or electroconversion will restore sinus rhythm. In the older child, intravenous isoptin can be given. Slow heart rates from total AV block or sinus node affection are treated with atrophic, isuprel or electrical pacing.
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PMID:[Pediatric cardiological emergencies]. 797 84

Two patients with serologically-proven dengue virus infection and Morbitz type I second degree atrioventricular (AV) block are described. A 7 years old boy (patient 1) with grade 2 and a 7 years old girl (patient 2) with grade 3 illness were admitted to the hospital on the 3rd and the 5th day of the illness, respectively. Both had typical resentation for dengue hemorrhagic fever including fever, hepatomegaly, thrombocytopenia and signs of extravascular leakage. The 7 year old girl also had epistaxis and anemia (Hct 24%). Morbitz type I second degree and 2:1 AV block developed on day 7 (patient 1) and day 8 (patient 2) of the illness, both during recovery periods. Patient 1 also had occasional monomorphic premature ventricular contraction (PVC). There was no other abnormality in the 12-lead EKGS and echocardiograms showed normal ventricular systolic function in both. Other than mild hypokalemia (3.3 and 3.4 mgq/l), serum electrolytes were normal. Neither patients had elevation of serum creatine phosphokinase (CPK). In patient 1, exercise (on day 10) normalized AV conduction and abolished the PVC. Follow up EKG and physical examination at 10 months after the illness was normal. The rhythm in patient 2 resolved to 1st degree AV block (with occasional morbitz type I second degree at night) on day 12. In this patient, exercise resulted in shortening of the PR interval and Valsalva maneuver resulted in further PR prolongation. The patient was well at 1-month follow up with a mormal EKG. Morbitz type I second degree AV block during recovery from dengue hemorrhagic fever may be a transient functional impairment of the AV node, in which altered autonomic tone may play a role.
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PMID:Morbitz type I second degree AV block during recovery from dengue hemorrhagic fever. 1141 4

Technical advances in health care have improved patient survival and quality of life, but are not devoid of complications. We present the case of a 74-year-old woman with a history of hypertensive heart disease with preserved systolic function, atrial fibrillation and dyslipidemia. She had a DDDR pacemaker implanted in 2005 due to symptomatic complete atrioventricular block. The patient reported progressive fatigue, weakness, ascites with abdominal discomfort, and lower limb edema, accompanied by non-specific hepatic cholestasis on biochemical testing. Abdominal ultrasound revealed homogeneous hepatomegaly and dilatation of the inferior vena cava and upper hepatic veins, suggestive of congestive hepatopathy. Echocardiography revealed tricuspid regurgitation progressively worsening over the previous four years and dilatation and progressive dysfunction of the right ventricle, with preserved left ventricular function. The transesophageal echocardiogram revealed severe tricuspid regurgitation with flail septal leaflet and marked dilatation of the tricuspid annulus due to mechanical interference of the pacemaker lead, which was adhering to the septal leaflet. Minimally invasive surgical treatment was performed with partial resection of the leaflet, placement of a tricuspid annuloplasty ring and replacement of the pacemaker lead. Regression of the congestive symptoms was observed, and the postoperative echocardiogram showed the tricuspid annuloplasty ring with no evidence of stenosis and only slightly dilated right chambers with moderate pulmonary hypertension. Six months after the procedure, the patient suffered an acute neurological event and died.
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PMID:Pacemaker lead as an iatrogenic cause of right heart failure: Case report. 3180 83