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

Acute liver failure is a rare but potentially fatal disease. Adult definition of fulminant hepatic failure, which includes the development of hepatic necrosis and encephalopathy within 8 weeks of onset of liver disease does not apply to acute liver failure in children particularly if secondary to autoimmune or metabolic liver disease. The etiology of acute liver failure varies with the age of the child. In neonates, infection or an inborn error of metabolism are common, while viral hepatitis and drug induced liver failure are more likely in older children. The clinical presentation of acute liver failure includes jaundice, coagulopathy and encephalopathy. In neonates, encephalopathy may be subclinical. The management of acute liver failure includes assessment of prognosis for liver transplantation; prevention and treatment of complications while awaiting hepatic regeneration or a donor liver and hepatic support. The major complications of acute liver failure are sepsis, gastro-intestinal bleeding, cerebral edema, renal and cardiac failure. Selection for liver transplantation depends on the etiology of the disease, prognostic factors, the presence or absence of multisystem disease and/or reversible brain damage. Prognostic factors for survival are less well established in children than in adults but children with metabolic liver disease, prothrombin time > 50 seconds, rising bilirubin and falling transaminase, grade II or higher grade of hepatic coma indicate poor prognosis. Most children receive a reduced or split liver graft. Living related donations for acute liver failure are also carried out by some centres. Survival post liver transplantation for acute liver failure has improved and most recipients can expect a 70% five year survival.
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PMID:Acute liver failure. 1113 56

Myocardial infarction remains the leading cause of early and late death after abdominal aortic aneurysm (AAA) repair. Myocardial revascularization is staged either before or concomitant with AAA resection, but results are far from uniform. We retrospectively analyzed our experience with patients who underwent concomitant AAA resection and aortocoronary bypass (ACB) to examine the factors affecting early morbidity/mortality and early results. Forty-two patients (all men; mean age, 67.2 years) underwent simultaneous ACB grafting and AAA repair between 1975 and 1998. All were managed postoperatively in the cardiothoracic intensive care unit (mean stay, 6.1 days). The mean total hospital stay was 17.2 days. Two died in the early postoperative period (4.8%): 1 of sustained myocardial failure following a third ACB, and 1 of coagulopathy after concomitant ACB, aortic valve replacement, and AAA. One patient developed a nonfatal MI on postoperative day 3. The incidence of wound and bleeding complications was higher for patients undergoing both ACB and AAA repair than for patients undergoing AAA resection alone. On follow-up (mean, 10 years; range, 7 months to 15 years), only 2 of 10 late deaths were due to cardiovascular causes. We believe that concomitant myocardial revascularization is warranted in select patients requiring elective or urgent AAA resection in order to decrease perioperative risk and improve late survival. Cardiac failure or ischemia during aortic surgery can be prevented by proper perfusion with or without cardiopulmonary bypass. In patients undergoing simultaneous procedures, the increased risk is related to the severity of the vascular and coronary artery disease and not to the combined operations.
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PMID:Outcome after simultaneous abdominal aortic aneurysm repair and aortocoronary bypass. 1198 88

A term newborn infant developed hypovolaemic shock shortly after birth. She was pale with gross hepatomegaly. She required multiple boluses of intravenous fluids, blood products as well as inotropic support. Blood investigations showed persistent thrombocytopenia, anaemia and disseminated intravascular coagulopathy (DIC). She also developed heart failure. She finally succumbed on the eleventh day of life. Autopsy revealed haemangiomatosis involving the liver, lungs, gastrointestinal tract, kidneys and adrenals.
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PMID:Diffuse neonatal haemangiomatosis: a rare cause of haemorrhagic shock and refractory coagulopathy in the newborn. 1244 Feb 78

Hepatic hemangioendothelioma (HE) is a tumor that presents in infancy and toddler. It manifests hepatomegaly, abdominal mass, jaundice, abdominal distention, or high output cardiac failure. We reviewed patients with HE in our hospital in the past 15 years (from July 1986 to June 2001). The diagnosis was made by the histology specimen or various imaging studies. There were thirteen patients (9 males, 4 females) enrolled in our study. Their ages ranged from neonate to 2 years old. The common clinical manifestations included abdominal distention (53%), congestive heart failure (38.5%), abdominal mass (30.8%), jaundice (30.8%), and skin hemangioma (23.1%). Nine patients had serum alanine aminotransferase examination and were abnormal in 2. Anemia was noted in 7 of 13 (53.8%) patients, thrombocytopenia and hyperconsumptive coagulopathy were found in 4 and 5 patients, respectively. Serum alpha-fetoprotein was elevated in 4 of 7 patients. Abdominal ultrasonography (n = 13) showed heterogeneous and hypoechoic lesions in the liver. Computed tomography (n = 11) revealed central hypointensity with peripheral enhancement after contrast of the liver masses. Magnetic resonance imaging studies of the hepatic masses (n = 3) showed decreased signal intensity on T1 images and high signal intensity on T2. Most patients were treated with steroid. Other management included interferon, chemotherapy, embolization and/or surgery. Four patients were managed conservatively. Among the other nine patients, four patients died of sepsis, hepatic failure, disseminated intravascular coagulopathy or tumor rupture with hemorrhagic shock. HE appears to be a histologically benign tumor but may have a poor outcome because of complications. For its management, steroid is a first-line medication. Other methods of treatment were interferon, hepatic artery embolization, chemotherapy and surgery. Long term follow up is needed for the evaluation of treatment response.
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PMID:Hepatic hemangioendothelioma in children: analysis of thirteen cases. 1280 Mar 77

The differentiation of haemangiomas and vascular malformations is histological, clinical and prognostic. Although the majority of haemangiomas evolve towards spontaneous resolution, as many as 10% of cases can develop complications with ulceration, pain and haemorrhaging. Besides, the localisation of haemangiomas in the head and neck, next to vital structures, can compromise their functions. Hence, compression of the airway might be a vital emergency. Periorbital haemangiomas can give rise to amblyopia due to sensory deprivation or due to a restrictive strabismus. Lumbosacral haemangiomas must be studied with Nuclear Magnetic Resonance because of their frequent association with alterations in the midline at the level of the spine, anus, genitals or kidneys. Amongst visceral haemangiomas, hepatic haemangiomas are the most serious due to their association with congestive cardiac insufficiency. The association of extensive facial haemangiomas with anomalies of the central nervous system, vascular, cardiac, ocular and sternal anomalies, is denominated PHACE syndrome and is frequently complicated by mental deficiency, convulsions or ictus. Vascular malformations of trigeminal localisation are associated in up to 15% of cases with glaucoma or choroidal or leptomeningeal haemangiomas (Sturge-Weber syndrome). Combined vascular malformations localised in the extremities can become complicated with thrombophlebitis, regional osteolysis and even distant thromboembolisms (Klippel-Treneaunay Syndrome). On the other hand, there is a coagulopathy due to consumption (Kassabach-Merrit Syndrome) that can complicate some vascular tumours such as the Kaposiform haemangioendothelioma and the tufted angioma. Finally, the complications of the treatments employed are reviewed.
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PMID:[Complications in the evolution of haemangiomas and vascular malformations]. 1514 12

There is a very limited published material about experience with long-term pediatric mechanical circulatory support as a bridge to heart transplant. We report on a 2-year-old, 12 kg boy admitted with 2-week history of low-grade fever, ear pain, pulmonary edema, and congestive heart failure. Trans-thoracic echocardiography confirmed severe myocardial dysfunction with a left ventricular ejection fraction of 0.20 and percentage shortening of 13. After 2 days of ventilatory and inotropic support, the patient continued to deteriorate and subsequently required femoro-femoral extracorporeal life support (ECLS). This was later complicated by a progressive coagulopathy and massive bleeding. On day 17, a pulsatile pediatric paracorporeal biventricular assist device (VAD) (Berlin Heart) was implanted. The patient's condition improved significantly with all coagulopathies corrected, and the patient was extubated 21 days later. After 109 days of bi-VAD support, the patient was successfully transplanted and discharged home 45 days post transplant. Our early experience with initial ECLS bridge to VAD and subsequently to transplant was encouraging. It allowed for additional time to select the ideal organ donor and optimize the recipient's comorbid condition and multiorgan failure. VAD provides an additional armamentarium of circulatory support in pediatric patients with severe heart failure.
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PMID:The combined use of extracorporeal life support and the Berlin Heart pulsatile pediatric ventricular assist device as a bridge to transplant in a toddler. 1533 57

The HeartMate vented-electric left ventricular assist system (Thoratec Corp., Woburn, MA) has become widely accepted as a temporary bridge to transplantation. We describe a left thoracotomy technique in 3 patients for implanting this pump intrathoracically or intraperitoneally. In all 3 cases, long-term pump function was satisfactory. For HeartMate implantation, the left thoracotomy approach may be particularly useful when previous median sternotomies, coupled with the severe debilitation posed by chronic heart failure and hepatic dysfunction with resultant coagulopathy, would greatly increase the mortality and morbidity of a redo median sternotomy.
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PMID:HeartMate vented-electric left ventricular assist system: technique for intrathoracic or intraperitoneal implantation via a left thoracotomy. 1536 37

We present a case of an obese young man who developed ischemic hepatitis, severe coagulopathy, acute renal failure, and encephalopathy. Heart failure and hypovolemia were absent. Oxygen arterial saturation was very low, between 77% and 99% during the day, with no history of respiratory failure. A diagnosis of obstructive sleep apnea was made clinically and confirmed by performing formal polysomnography. The polysomnographic study showed multiple episodes of apneas and hypopneas with severe oxygen desaturation. The patient was treated with continuous positive airway pressure through a nose mask and clinical manifestations related to profound nocturnal desaturation were ameliorated. He was discharged 32 days after admission with normal results of laboratory tests. This case report is presented to support the hypothesis that hypoxic hepatitis was directly related to severe arterial hypoxemia.
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PMID:A case of ischemic hepatitis. 1538 90

The pathogenesis of preeclampsia stems from aberrant changes at the placental interface. The trophoblastic endovascular invasion of tonic spiral arteries that converts them to passive conduits falters. Uteroplacental insufficiency and fetoplacental hypoxemia result. Secondary maternal oxidative stress and an excessive inflammatory response to pregnancy generate the clinical syndrome of preeclampsia. Current treatment focuses on preventing seizures, controlling hypertension, preserving renal function and delivering the baby. We propose that the pathophysiological changes induced by preeclampsia in the placenta parallel those caused by persistent hypoxemia in the lungs at high altitude or with chronic obstructive pulmonary disease. Unrelenting pulmonary hypoxic vasoconstriction induces pulmonary hypertension and cor pulmonale. Inhalation of nitric oxide and phosphodiesterase-5 inhibitors opposes pulmonary hypoxic vasoconstriction, alleviates pulmonary hypertension and improves systemic oxygenation. Notably nitric oxide donor therapy also counters hypoxemic fetoplacental vasoconstriction, a biological response analogous to pulmonary hypoxic vasoconstriction. Fetal oxygenation and nutrition improve. Placental upstream resistance to umbilical arterial blood flow decreases. Fetal right ventricular impedance falls. Heart failure (cor placentale) is avoided. Emergency preterm delivery can be postponed. Other than low dose aspirin and antioxidants vitamins C and E no available therapy specifically targets the underlying disease profile. We hypothesize that, like nitric oxide donation, pharmacological inhibition of placental phosphodiesterase-5 will also protect the fetus but for a longer time. Biological availability of guanosine 3'5'-cyclic monophosphate is boosted due to slowed hydrolysis. Adenosine 3'5'-cyclic monphosphate levels increase in parallel. Cyclic nucleotide accumulation dilates intact tonic spiral arteries and counters hypoxemic fetoplacental vasoconstriction. Intervillous and intravillous perfusion pick up. Maternal to fetal placental circulatory matching improves. Enhanced placental oxygen uptake alleviates hypoxemic fetal stress. Appropriate fetal nutrition resumes. Cor placentale and severe intrauterine growth restriction are averted. Increased maternal cyclic nucleotide concentrations promote systemic vasodilatation so that blood pressures fall. Preemption of oxidative stress initiated by "consumptive" oxidation of nitric oxide stabilizes the vascular endothelium and corrects coagulopathy. Anti-inflammatory and immunosuppressant adenosine 3'5'-cyclic monphosphate offsets the extreme gestational inflammatory response. Cellular injury and multi-organ damage are prevented. One tablet a day of the new long acting phosphodiesterase-5 inhibitor, tadalafil (half life of 17.5 h) theoretically should allow a preterm pregnancy affected by preeclampsia to continue safely. Selective monitoring of vital organ functions guards against life-threatening maternal complications. Regular biophysical profiling warns the obstetrician of impending fetal compromise. Fetal growth and vital organ maturation can continue. As a result workloads imposed upon neonatal intensivists will lighten. Parental anxiety and concern will be allayed. The cost of treating preeclamptic mothers and their extremely low birth weight infants will decrease. Money saved by midwifery services in poorer states can be used to pay for better prenatal care. Severe preeclampsia/eclampsia will be less common. Maternal and perinatal morbidity and mortality will be reduced. Because the human immunodeficiency virus often infects individuals at a workforce eligible age, the global acquired immunodeficiency syndrome pandemic has already brought many nations to the brink of economic ruin. Potentially productive lives saved for the future will help restore them fiscally.
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PMID:Hypothesis: selective phosphodiesterase-5 inhibition improves outcome in preeclampsia. 1550 76

Systemic thromboembolism is well recognized in patients with left ventricular (LV) impairment. We report a case of cardiac failure presenting with systemic coagulopathy and an unusual pattern of thrombotic manifestations as a consequence of LV impairment.
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PMID:Multisite thrombosis: a late presentation of myocardial infarction. 1577 5


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