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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypocalcemia is a relatively uncommon reversible cause of congestive heart failure. There are a few reports of hypocalcemic children who developed congestive heart failure associated with hypoparathyroidism. In all these patients, however, cardiac failure did not occur before the age of nine years. In addition, other striking noncardial manifestations of hypoparathyroidism, e.g., convulsive seizures, had been present prior to cardiac symptoms. We report on a 3.7 year old girl with mitral insufficiency and severe cardiac failure due to hypocalcemia secondary to familial hypoparathyroidism. The infant's mother was suffering from idiopathic hypoparathyroidism, but her own history lacked any evidence for parathyroid hormone deficiency. On admission, she presented with fatigue, dyspnea, and pedal edema. Liver edge was palpable 4 cm below the right costal margin, and a 3/6 systolic murmur was heard. A chest x-ray showed cardiac enlargement; electrocardiogram demonstrated a prolonged QTc interval of 0.46 s. The echocardiography revealed a cleft in the mitral valve with mitral insufficiency and markedly reduced contractility of the left ventricle. Laboratory studies demonstrated a low total serum calcium level of 1.3 mmol/l; serum magnesium level was slightly decreased (0.5 mmol/l), and parathyroid hormone level was not detectable. Partial monosomy of chromosome 22 was excluded. Ophthalmological examination, audiometry, and renal ultrasonogram were normal. Oral calcium supplementation and anticongestive therapy with metildigoxin, furosemid, and captopril was initiated but no improvement of the heart failure occurred. However, normalization of serum calcium level by calcium infusions caused prompt clearing of the clinical symptoms, complete normalization of liver size, reduction of cardiac enlargement (thoracic ratio decreased from 0.68 to 0.57), and marked improvement in contractility (left ventricular shortening fraction increased from 21% to 34%). The QTc interval decreased to 0.39 s. The successful treatment following normalization of serum calcium level proved the superiority of hypocalcemia over mitral valve insufficiency in the etiology of the cardiac failure. To our knowledge, this is the first report of congestive heart failure due to hypocalcemia as the first manifestation of hypoparathyroidism in childhood. Hypocalcemia should be kept in mind in any congestive heart failure in children with or without underlying cardiac malformation.
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PMID:[Hypocalcemia-induced heart failure as the initial symptom of hypoparathyroidism]. 1102 Dec 71

On any given day a patient seen by the dental hygienist has the potential of experiencing a life-threatening medical emergency. All dental hygiene practitioners should be aware of potential risks that a patient may present, take steps to prevent life-threatening events from occurring, and plan for problems in advance of their happening. The primary goal of this course is to help dental hygienists carry out the ethical, moral, legal, and professional obligation owed any patient. The course will review the basics of medical emergencies, with particular emphasis on those that are most likely to occur in the dental office. Discussion will center on general aspects of prevention and preparation, and will focus on the recognition and emergency treatment of specific conditions. Vasodepressor syncope, orthostatic hypotension, acute adrenal insufficiency, hyperventilation, asthma, heart failure and acute pulmonary edema, cerebrovascular accident seizures, hyperglycemia, hypoglycemia, myocardial infarction, angina pectoris, and anaphylaxis will be emphasized.
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PMID:Medical emergencies in the oral health care setting. 1131 57

A drug overdose (OD) is the body's response to being overwhelmed by too much of a substance. Overdoses are not always life-threatening, but can lead to unconsciousness, failed breathing, heart failure, and seizures. Many overdoses are the result of taking drugs of inconsistent strength or drugs that are mixed with other substances. Guidelines are given to recognize and prevent drug overdoses.
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PMID:Overdose prevention & survival. Harm Reduction Coalition. 1136 71

This study reports observed toxicity in a child with acute lymphocytic leukemia who had received vincristine (VCR) with nifedipine and itraconazole. A 5-year-old-child with leukemia developed bilateral cranial nerve palsies, severe peripheral neuropathy involving upper and lower extremities, seizures, hypertension, heart failure, and syndrome of inappropriate antidiuretic hormone secretion after being treated with VCR, nifedipine, and itraconazole. Appropriate management of the above problems including discontinuation of VCR resulted in recovery from neurotoxic manifestations. Concurrent administration of VCR with nifedipine and itraconazole may enhance its neurotoxicity.
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PMID:Enhanced vincristine neurotoxicity from drug interactions: case report and review of literature. 1176 5

Seven related Quarter Horse foals that died by 7 weeks of age were examined for glycogen branching enzyme (GBE) deficiency. Clinical signs varied from stillbirth, transient flexural limb deformities, seizures, and respiratory or cardiac failure to persistent recumbency. Leukopenia (5 of 5 foals) as well as high serum creatine kinase (CK; 5 of 5), aspartate transaminase (AST; 4 of 4), and gamma glutamyl transferase (GGT; 5 of 5) activities were present in most foals, and intermittent hypoglycemia was present in 2 foals. Gross postmortem lesions were minor, except for pulmonary edema in 2 foals. Muscle, heart, or liver samples from the foals contained abnormal periodic acid Schiff's (PAS)-positive globular or crystalline intracellular inclusions in amounts proportional to the foal's age at death. Accumulation of an unbranched polysaccharide in tissues was suggested by a shift in the iodine absorption spectra of polysaccharide isolated from the liver and muscle of affected foals. Skeletal muscle total polysaccharide concentrations were reduced by 30%, but liver and cardiac muscle glycogen concentrations were normal. Several glycolytic enzyme activities were normal, whereas GBE activity was virtually absent in cardiac and skeletal muscle, as well as in liver and peripheral blood cells of affected foals. GBE activities in peripheral blood cells of dams of affected foals and several of their half-siblings or full siblings were approximately 50% of controls. GBE protein in liver determined by Western blot was markedly reduced to absent in affected foals, and in a half-sibling of an affected foal, it was approximately one-half the amount of normal controls. Pedigree analysis also supported an autosomal recessive mode of inheritance. The affected foals have at least 2,600 half-siblings. Consequently, GBE deficiency may be a common cause of neonatal mortality in Quarter Horses that is obscured by the variety of clinical signs that resemble other equine neonatal diseases.
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PMID:Glycogen branching enzyme deficiency in quarter horse foals. 1181 63

There are almost one hundred inborn errors of metabolism which can start in the neonatal period, but less than 20 are amenable to treatment. In general, an extremely evocative clinical setting is the course of a full-term baby born after normal pregnancy and delivery who, after an initial symptom-free period deteriorates relentlessly for no apparent reason and does not respond to symptomatic therapy. Investigations routinely performed in all sick neonates yield normal results. Emergency treatment must be undertaken in parallel with investigations. Five main presentations can be observed: a neurologic deterioration 'intoxication' type mostly suggests maple syrup urine disease, methylmalonic, propionic, isovaleric acidaemias and urea cycle disorders. Isolated seizures is the revealing symptom of pyridoxine-responsive and folinic acid responsive seizures. A jaundice or a liver failure suggest galactosaemia, fructosaemia, tyrosinaemia type I (after 3 weeks), phosphomannoisomerase deficiency or bile acid synthesis defects. Cardiac failure and heartbeat disorders should first suggest mitochondrial fatty acid oxidation (FAO) disorders. Persistent hypoglycaemia is the presenting sign of glyco/gluconeogeneis defects, hyperinsulinism and FAO disorders. The first line investigation relies upon the collection at the same time of a few samples including blood gases electrolytes, prothrombin time, transaminases, ammonia and lactic acid, and the search for ketonuria. The storage of plasma, urine and blood (on filter paper) is an important element in the diagnosis. The utilization of these samples should be carefully planned after taking advice from specialists in inborn errors.
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PMID:Clinical approach to inherited metabolic disorders in neonates: an overview. 1206 34

Infants with Down syndrome are known to have a high frequency of birth defects, particularly cardiac and gastrointestinal defects. Mental retardation of different degrees is common, but accompanying central nervous system malformations are rare. We report a boy born spontaneously in the 37th postconceptional week with multiple malformations: microcephaly, hypertelorism, blepharophimosis, medial cleft palate, micrognathia, omphalocele, and pathologic palmar and plantar creases. Cardial sonography revealed a ventricular septal defect and mild pulmonary stenosis. Cranial magnetic resonance imaging demonstrated a general but infratentorial stressed brain atrophy with widening of the inner and outer cerebrospinal fluid spaces and dysplasia of the corpus callosum. Chromosomal analysis showed a free trisomy 21. The boy had muscular hypotonia and developed severe motor and mental retardation, accompanied by microsomia and generalized epileptic seizures. At age 8 months, he died of sudden nocturnal respiratory and cardiac failure. The peculiarity of this case is the combination of Down syndrome with midline developmental defects (callosal dysplasia, medial cleft palate, omphalocele) accompanied by severe malformative encephalopathy. There are no previous reports of this combination, but there are genetic links between Down syndrome and midline defects concerning the Drosophila single-minded (sim) gene. The expression pattern of the human sim corresponding gene suggests that it might be involved in the pathogenesis of midline defects in Down syndrome.
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PMID:Midline developmental anomalies in Down syndrome. 1217 71

Long-term prognosis in dialysis is poor compared to that in healthy control persons. A worsening of the prognosis is noted especially for patients who at initiation of dialysis have congestive heart failure, ischemic heart disease, or left ventricular dysfunction or hypertrophy. This is the main reason that cardiovascular causes are the most common for morbidity in these patients. The weight obtained when normal urine output is present is the dry weight. With reduced ability to excrete the volume by the kidneys in end-stage renal disease (ESRD), the body will retain water and the patient will gain weight. This extra weight is due to volume overload. While volume overload may induce a rise in blood pressure, if the heart is in acceptable condition, a fast removal of fluid by ultrafiltration (UF) during dialysis may instead cause hypotension. Ultrafiltration failure in peritoneal dialysis (PD) patients may lead to successive water retention and overhydration with subsequent cardiac failure, while volume overload may occur over a few days in hemodialysis (HD) patients. Anemia or even too-high hematocrit may impair cardiac function further and worsen conditions caused by wrong dry weight. Thus, during long-term and sustained volume overload, left ventricular (LV) hypertrophy will occur in an eccentric manner. A sustained overload then may lead to cell death and LV dilatation and, eventually, systolic dysfunction. Once a severe left ventricular dilatation has developed, the blood pressure may decrease during volume overload. A worsened prognosis is seen if malnutrition and low albumin levels are present. Volume overload necessitates ultrafiltration to achieve dry weight. Thereby, volume contraction contributes to exaggerated stimulation of or response to activation of the RAS and alpha-adrenergic sympathetic systems. If ultrafiltration goes beyond these compensatory mechanisms, hypotension will occur and increase the risk for hypoperfusion of vital organs. Such episodes may cause cardiac morbidity, aspiration pneumonia, vascular access closure, or neurological complications (seizures, cerebral infarction), besides a more rapid lowering of residual renal function. Preventive measures are, first, finding the right dry weight; second, minimizing interdialytic weight gain; third, optimizing the target for hemoglobin (110-120 g/l); fourth, lowering dialysate calcium (1.25 mmol/l); and fifth, eventually using higher dialysate potassium if long dialyses are performed.
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PMID:Ultrafiltration and dry weight-what are the cardiovascular effects? 1266 7

Autosomal dominant hypocalcemia (ADH) caused by activating mutations of calcium-sensing receptor (CaSR) is characterized by hypocalcemia with inappropriately low concentration of PTH and relative hypercalciuria. Active vitamin D treatment often leads to nephrolithiasis and renal impairment in patients with ADH. However, differential diagnosis between ADH and idiopathic hypoparathyroidism is sometimes very difficult. Here, we report a mutation of CaSR and its functional property found in three generations of a Japanese family. The proband developed seizures at 7 days of age. His mother and elder sister were discovered to have hypoparathyroidism by family survey, but his father was normocalcemic. His grandfather developed heart failure and was found to have hypoparathyroidism. All affected members had been treated with active vitamin D3 and bilateral nephrolithiasis were detected in three of them. DNA sequencing revealed that all affected patients had a heterozygous mutation in CaSR gene that causes proline to leucine substitution at codon 221 (P221L). In vitro functional analysis of the mutant CaSR by measuring inositol 1,4,5-trisphosphate production in response to changes of extracellular Ca indicated that this mutation is an activating one and responsible for ADH in this family. Therefore, careful monitoring of urinary Ca excretion before and during treatment of PTH-deficient hypoparathyroidism is very important, and screening of CaSR mutation should be considered in patients with relative hypercalciuria or with a family history of hypocalcemia.
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PMID:A family of autosomal dominant hypocalcemia with an activating mutation of calcium-sensing receptor gene. 1273 14

A case is presented of a fatal drug interaction caused by ingestion of oxycodone (Oxycontin) and clonazepam (Klonapin). Oxycodone is an opium alkaloid used in long-term pain management therapy. Clonazepam is a benzodiazepine used for the treatment of seizures and panic disorders. The Drug Abuse Warning Network (DAWN) has reported an increase of 108% in the last two years of emergency department episodes related to Oxycontin. Six billion prescriptions were written for Oxycontin in the year 2000, an 18-fold increase from four years previous (1). Oxycontin has recently gained enormous notoriety at the local and national levels; however, there are very few previously documented cases of lethal drug interactions between oxycodone and clonazepam. Synergistic effects between these two drugs are postulated to arise from different agonistic mechanisms producing similar physiological changes. It is also theorized that clonazepam may inhibit the metabolism of oxycodone. A 38-year-old white female was found dead in Jefferson County, Tennessee in March of 2001. The deceased had physical evidence of previous drug abuse and positive serological findings of hepatitis B and C. Prescription pill bottles filled under the name of the deceased, as well as another name, were found with the body. Serum, urine and gastric contents from the deceased were screened for numerous drugs and metabolites using a combination of thin layer chromatography and immunoassay techniques (EMIT and FPIA). Analysis of biological specimens from the deceased revealed the presence of: benzodiazepines, opiates (oxycodone), and trazodone metabolites in the serum; cannabinoids, benzodiazepines, opiates (oxycodone), trazodone, trazodone metabolites, nicotine, and nicotine metabolite in the urine; and benzodiazepines, opiates (oxycodone), nicotine, and nicotine metabolite in the gastric contents. Quantitative analyses for clonazepam was performed by high performance liquid chromatography (HPLC) and revealed a plasma concentration of 1.41 microg/mL. Plasma oxycodone and urine 11-nor-carboxy-delta-9-tetrahydrocannabinol concentrations were determined by gas chromatography/mass spectrometry and revealed concentrations of 0.60 microg/mL and 27.9 ng/mL, respectively. The deceased had pathologies consistent with severe central nervous system (CNS) and respiratory depression produced by high concentrations of clonazepam and oxycodone including collapsed lungs, aspirated mucus, and heart failure. The pathologies were sufficient to cause death, which was officially attributed to a drug overdose; however, the manner of death was unknown.
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PMID:A fatal drug interaction between oxycodone and clonazepam. 1517 Nov 97


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