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)

9 figures form the core of this article describing and discussing a case of sudden death, 2 hours after a 30-year old woman presented at a hospital emergency with chest pains. She had taken no medications other than oral contraceptives (OCs) for 10 years. The patient was admitted to the coronary care unit where findings included a palpable blood pressure of 94 mm of Hg, a heart rate of 128/min, and a respiratory rate of 28/minute. Cyanosis was noted, jugular veins were distended, and there were rales over the lung bases bilaterally; cardiac sounds were soft and a third heart sound was audible. Arterial oxygen tension was 15 mm of Hg, and carbon dioxide tension was 42 mm of Hg; pH was 7.2. Ventricular tachycardia developed and ventricular fibrillation ensued. The patient was intubated and well oxygenated, external cardiac compression was performed, sodium bicarbonate, epinephrine, and calcium were administered, and electrical defibrillation was performed. After several attempts, the latter resulted in a slow idioventricular rhythm on the electrocardiogram, but neither the blood pressure nor pulse was detectable. Asystole subsequently developed, and cardiac activity could not be restored. After discussion by a panel of physicians, the final anatomic diagnoses are chronic active nonspecific myocarditis; organizing and acute myocardial microvascular and endocardial mural thrombi; platelet-rich microthrombi in the heart, lungs, and liver; chronic passive pulmonary congestion and edema; and congestive hepatomegaly (2900 g). Any of these may be assciated with longterm OC usage.
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PMID:Chest pain, shock, arrhythmias and death in a young woman. 44 59

Twelve patients with tricuspid atresia underwent physiological operative repair. The criteria for their selection for operation included normal pulmonary vascular resistance and normal left atrial and left ventricular end-diastolic pressures. Four patients died (30% mortality). The 8 surviving patients developed pleural effusion, ascites, and hepatomegaly, which markedly improved in the subsequent weeks. Five of the 8 survivors underwent cardiac catheterization. The arterial oxygen saturation in these patients averaged 82% preoperatively, 89% immediately postoperatively, and 94% or better six months later. All had improved subjectively and developed increased exercise tolerance.
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PMID:Operative repair for tricuspid atresia. 127 2

Hypoxemia in liver cirrhosis has been attributed to increased pulmonary perfusion; lung function abnormalities have rarely been found in adults. In infants, however, smaller airways and the disproportion in size between the enlarged liver and abdominal cavity leading to lung compression by elevated diaphragms may well suggest that ventilation disturbances play an important role in the development of hypoxemia. We examined lung functions, ventilation-perfusion scans, chest radiographs, and blood gases in air and 80% oxygen in 19 infants with biliary atresia (mean age 14 months) and found maximum flows at functional residual capacity (VmaxFRC) markedly decreased [48% +/- 29% (mean +/- SD)] and thoracic gas volume (TGV) elevated (156% +/- 30.2%). PO2 was less than 9.3 kPa in seven of 19 patients, in whom TGV was higher compared with the other patients (182% vs. 141%, p less than 0.005). However, the decrease in PO2, was much more closely correlated to the amount of shunting (r = 0.62, p less than 0.05) than to the reduced airway patency (VmaxFRC/TGV, r = 0.41, p = 0.08). We conclude that airway narrowing probably by lung compression is present more frequently in infants than in adults with liver disease. We found some evidence that hyperinflation contributes to the observed low PO2 values, possibly aggravated by inadequate vasoconstriction to hypoxic stimuli. However, pulmonary shunting independent of ventilatory disturbances more readily explained hypoxemia already present in these infants.
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PMID:Hypoxemia in infants with biliary atresia: the role of airway obstruction. 140 65

A 14-month-old baby weighing 4300 g was a giant infant with macroglossia. Exomphalos was not present, but diastasis recti abdominis was observed. The patient was therefore diagnosed as having Beckwith-Wiedemann syndrome (EMG syndrome). Other characteristic signs such as neonatal hypoglycemia, hemihypertrophy, and a small ventricular septal defect were also recognized, but nephromegaly or hepatomegaly was not present. Tongue reduction by wedge resection was performed under general anesthesia. Some of the problems associated with anesthetic management in this syndrome are hypoglycemia, airway obstruction and cardiovascular status. After induction with increasing concentration of halothane (0.5-4.0%) and 66% nitrous oxide in oxygen, a nasotracheal tube was inserted. Endotracheal intubation was easy without using a neuromuscular blocking agent. Anesthetic maintenance was accomplished with nitrous oxide 66% in oxygen and halothane 0.5-1.0% and no neuromuscular blocking agent was used. The plasma glucose level was kept within normal ranges during and after the operation by infusion of acetate Ringer's solution with 5% glucose. The postoperative progress was uneventful.
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PMID:[Anesthetic management for partial tongue resection in a patient with Beckwith-Wiedemann syndrome]. 160 68

The case is reported of a 49-year-old chronic alcoholic woman, who presented with severe pulmonary arterial hypertension (PAH) mimicking as an acute abdomen. She was admitted with right-sided hypochondrial abdominal pain and hepatomegaly, with a moderate jaundice. On admission to intensive care unit, she had an arterial blood pressure of 110/70 mmHg, a heart rate of 100 b.min-1, and a respiratory rate of 36 c.min-1. An electrocardiogram showed sinus rhythm and right-sided heart failure. Whilst breathing 6 l.min-1 oxygen, her arterial blood gases were: PaO2 47 mmHg PaCO2 29 mmHg. Severe PAH was confirmed by measuring her mean pulmonary arterial pressure, which was 46 mmHg, whilst her pulmonary wedge pressure was 7 mmHg. Hepatic function was also altered: total bilirubin 41 mumol.l-1, alkaline phosphatase 145 UI.l-1 and gamma glutamyl transferase 1 340 UI.l-1. She developed arterial hypotension, which did not respond to increasing doses of isoproterenol. She died on the third day. Necropsy confirmed the diagnosis of primary PAH, with acute "cardiac liver".
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PMID:[Pseudosurgical acute abdomen syndrome in primary pulmonary hypertension]. 175 58

A 14-year-old girl was admitted with chief complaints of edema and chest pain. She had hepatomegaly, but did not have heart murmur and accentuation of the pulmonary component of the second heart sound. The electrocardiogram showed right axis deviation, negative T wave in V3,4 and ST depression in III, aVF. But right ventricular hypertrophy was not dominant. Chest radiography showed a cardiothoracic ratio of 54% and a slight prominence of proximal pulmonary arteries. The edema was soon diminished only by the diuretics, but it appeared again without the diuretics. At the cardiac catheterization 3 months after the onset of symptoms, the pulmonary arterial pressure was 150/85 mmHg and the pulmonary resistance was 3,232 dyn/sec/cm5. The right atrial pressure was 9.5 mmHg and oxygen saturation at the pulmonary artery was 31.0%. Prostaglandin E1 reduced the pulmonary artery pressure only a little, but raised the systemic pressure. The patient was treated with several vasodilators, but her condition deteriorated rapidly and she developed severe right ventricular failure. She died only 8 months after the onset of symptoms and 5 months after the catheterization. At autopsy, histological examination demonstrated intimal fibrotic thickening of the small-sized pulmonary arteries and organizing thrombus. But there was not plexiform lesion. Heart failure was easily improved when she was first admitted. But after 3 months the cardiac catheterization revealed that her condition was already severe. Several vasodilators was not effective to such a rapidly progressive primary pulmonary hypertension.
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PMID:[A case of rapidly progressive pulmonary pulmonary hypertension in a 14-year-old girl]. 259 31

A three-day-old female infant was transferred to the Pediatric Intensive Care Unit with chief presenting problems of progressive change of cyanosis and respiratory distress. Physical examination revealed tachypnea, acrocyanosis, hepatomegaly, undetectable pulse of extremities and oozing over the place of venous puncture. Chest roentgenograms revealed slight cardiomegaly; other X-rays were within normal limits. Complete electrocardiograms showed right axis deviation and right ventricular hypertrophy. Because of an impression of neonatal sepsis, the patient was put in an incubator with oxygen and antibiotics were given. Persistent anuria appeared associated with sighs of cardiac and renal failure; the ventilator was applied; dopamine and lasix were also given. Unfortunately, the cyanosis worsened progressive. Despite several attempts at resuscitations, the infant expired eight hours later. Pathology disclosed the heart size as normal; hypoplasia of ascending aorta as 0.4 cm in diameter; a PDA with 1 cm in diameter; a diminutive bean-sized left ventricle; hypertrophy of right ventricle and atresias of aortic and mitral valves. There was no evidence of septicemia.
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PMID:[Hypoplastic left heart syndrome due to aortic and mitral atresias: report of one case]. 263 9

Centrilobular hypoxia mediated by enhanced hepatic consumption of oxygen has been hypothesized to be a factor of pathogenetic importance in ethanol-induced liver injury. In the present study, this hypothesis was tested in a rat model which developed alcoholic centrilobular liver necrosis. Male Wistar rats were infused with high fat diet plus ethanol or isocaloric glucose for 7 weeks, a duration which resulted in induction of balloon cell degeneration, focal necrosis, and inflammation in the centrilobular region of the liver of the ethanol-fed animals. Hepatic blood flow, oxygen consumption and oxygen delivery were determined by the radiolabeled microsphere method and measurement of oxygen content in arterial, portal venous, and hepatic venous blood. Hepatic oxygen consumption was markedly increased by 159% in the ethanol-fed animals compared to that in the controls when results were expressed as relative to body weight. Even after these results were standardized per gram of liver weight, hepatic oxygen consumption was still significantly elevated in the ethanol-fed group, but the magnitude of the elevation was reduced to 70%, due to marked hepatomegaly observed in these animals. There was a concomitant 59% increase in hepatic oxygen delivery in the ethanol-fed rats when expressed per kilogram of body weight, and this effect was attributable entirely to increased portal blood flow. However, the increment of this increase in oxygen delivery was much too small to compensate for the 159% increase in oxygen consumption. In addition, this increase in hepatic oxygen delivery was no longer observable when the results were reexpressed based on the liver weight.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Incomplete compensation of enhanced hepatic oxygen consumption in rats with alcoholic centrilobular liver necrosis. 291 30

Heart-lung transplantation for treatment of end-stage cardiopulmonary disease continues to be plagued by many problems. Three primary ones are the technical difficulties that can be encountered, particularly in those patients who have undergone previous cardiac operations, the additional restriction on donor availability imposed by the lack of satisfactory preservation techniques, and the need for lung size compatibility. Two of these difficulties and others surfaced postoperatively in a heart-lung transplant recipient who presented a series of unique operative and therapeutic challenges. A 42-year-old woman with chronic pulmonary hypertension and previous atrial septal defect repair underwent a heart-lung transplantation in August 1985. The operative procedure was expectedly complicated by bleeding from extensive mediastinal adhesions from the previous sternotomy and bronchial collateralization. Excessive chest tube drainage postoperatively necessitated reoperation to control bleeding from a right bronchial artery tributary. Phrenic nerve paresis, hepatomegaly, and marked abdominal distention caused persistent atelectasis and eventual right lower lobe collapse. Arteriovenous shunting and low oxygen saturation necessitated right lower lobectomy 15 days after transplantation, believed to be the first use of this procedure in a heart-lung graft recipient. Although oxygenation improved dramatically, continued ventilatory support led to tracheostomy. An intensive, psychologically oriented physical therapy program was initiated to access and retrain intercostal and accessory muscles. The tracheostomy cannula was removed after 43 days and gradual weaning from supplemental oxygen was accomplished. During this protracted recovery period, an episode of rejection was also encountered and successfully managed with steroid therapy. The patient continued to progress satisfactorily and was discharged 83 days after transplantation. She is well and active 20 months after discharge.
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PMID:Postoperative complications necessitating right lower lobectomy in a heart-lung transplant recipient with previous sternotomy. 311 65

Isoflurane inhibits oxidative metabolism of halothane. Because hepatotoxicity of chemicals may be associated with their metabolism, whether isoflurane can protect the liver against chemical injury was investigated. Hepatic injury was produced in female F344 rats by a 30-minute exposure to 250 ppm of carbon tetrachloride. In this and all other parts of the study, the inspired oxygen concentration was maintained at 21%. The injury was accompanied by elevated activity of liver enzymes in serum (SGOT, SGPT, and SDH), enlarged liver, fatty infiltration of the liver, and vacuolar degeneration of hepatocytes. These signs of toxicity were partly or completely suppressed by concurrent exposure to subanesthetic concentrations of isoflurane (0.2 or 0.038%, respectively). The protective effect was concentration-dependent. Enflurane was protective, but less so than isoflurane. Nitrous oxide and fentanyl had no protective effect.
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PMID:Hepatic protection from chemical injury by isoflurane. 341 97


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