Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018991 (hemiplegia)
 3,997 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Between 1971 and 1981, 108 patients with pericardial effusion were treated by subxyphoid pericardial decompression. 68 patients (63%) had local anesthesia, while general anesthesia was used in 40 (37%). The total group included nonspecific (viral) pericarditis in 35 patients (32.4%), uremic pericarditis in 30 (27.8%); and 20 patients (18.5%) with a malignant etiology, traumatic in ten patients (9.3%), six patients (5.6%) following radiation for malignant disease, and seven patients (6.5%) due to other causes. Echocardiography was diagnostic in all cases. Acute cardiac tamponade necessitated pericardiocentesis as an initial procedure in seven patients (6.5%). Subxyphoid pericardial decompression included drainage of the pericardial fluid and performance of a 5 X 5 cm pericardial window and biopsy of all patients. There were two (1.8%) operative deaths in the general anesthesia group but none in the local anesthesia group. There were no major complication in the local anesthesia group, but one patient in the general anesthesia group, who was severely hypertensive preoperatively, developed hemiplegia on the left side. There were five recurrences (4.6%) requiring total pericardiectomy at a later date. Subxyphoid pericardial decompression under local anesthesia was seen to be a safe and effective procedure for primary decompression and diagnosis of acute or chronic pericardial effusion.
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PMID:Clinical experience with subxyphoid pericardial decompression. 401 84

Twelve cases of Stanford Type-A aortic dissection were operated in an acute phase. The male vs female ratio was 3:9, and their ages ranged from 47 to 79 (mean 61.3) years old. Most of them complained of chest and/or back pain, and four of them complained of syncope. Eight patients had the history of hypertension. As to the complications of aortic dissection, cardiac tamponade was seen in two cases, myocardial infarction in one, and transient hemiplegia and paraplegia in one case each. In five cases, moderate to severe aortic regurgitation was also noted. All but one case were operated within twenty-four hours after admission. The replacement of the ascending aorta with a tube graft was performed in all cases including the two cases whose entries were located in the aortic arch. CABG was done concomitantly in three cases, and aortic valve replacement and CABG in one case. The open distal anastomosis was carried out under the systemic circulatory arrest combined with the retrograde cerebral perfusion. The systemic perfusion was reinstituted after the distal anastomosis was completed. In cases whose dissecting pseudo-lumen of the distal aorta was not thrombosed, the arterial cannulation site was shifted from the femoral artery to the tube graft. All but two cases were discharged from the hospital in good condition. One case, who had been transferred to the operating room under cardiac massage due to myocardial infarction, was lost by severe LOS three weeks postoperatively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Surgical treatment of acute Stanford Type-A aortic dissection]. 783 14

The ruptured thoracic aortic aneurysm has had severely high mortality. A 71-year-old male who suddenly fainted away was admitted to our hospital. He was in shock on arrival. Computed tomography and echo cardiogram demonstrated ruptured aortic arch aneurysm with hemorrhagic cardiac tamponade. Aortic arch replacement was performed using the selective cerebral perfusion under deep hypothermia. The recovery of his consciousness was delayed, and he had right hemiplegia postoperatively, but his state was improved gradually. Finally he complained only slight degree of aphasia, paralysis. An immediate and aggressive emergency operation is a only method to salvage the patient who has ruptured aneurysm of the thoracic aorta.
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PMID:[Ruptured aortic arch aneurysm with hemorrhagic cardiac tamponade: report a case]. 983 83

Carbohydrate-deficient glycoprotein syndrome type 1 (CDGS-1) is an autosomal recessive hereditary metabolic disorder, the gene locus of which is chromosome 16p13. The disorder is characterised by genetic heterogeneity, and by decrease in the gene product, phosphomannomutase 2, though the heterogeneity is far less manifest in affected Swedish families. Its incidence is 1/80,000 live births, and the under-5 mortality rate over 30 per cent. The causes of death are liver failure, cardiac tamponade, haemorrhaging, and severe infection. The characteristic biochemical aberration is the occurrence of deficient carbohydrate chains in many but not all circulating glycoproteins, and the serum and blood concentrations of some glycoproteins may be above or below normal. These changes may improve over time, but never normalise. The clinical picture is generally more problematic during the first years of life when psychomotor retardation is complicated by failure to thrive, liver dysfunction, pericardial effusions, and stroke-like episodes. In addition, strabismus, lipocutaneous anomalies, and gluteal fat pads are always present, and muscular hypotonia and restricted joint mobility are common. Failure to thrive is common, with vomiting and diarrhoea and subsequent slow growth. Inflammation is a constant finding in the liver, and very common in the small bowel. Pancreatic function is also affected. Pericardial effusion has been reported in 50 per cent of the youngest children, requiring pericardectomy in 30 per cent of cases. Haemorrhaging and thromboembolic complications may occur, and the serum concentrations of several factors and inhibitors are low, particularly those of factors V and XI, protein C and antithrombin. Stroke-like episodes occur in about 30 per cent of cases, often following an infection, with coma lasting for hours to several days. Such sequelae as hemiplegia, blindness, and other focal neurological pathology have been observed transiently. Diagnosis is based on the serum carbohydrate-deficient transferrin level, verified by isoelectric focusing. Molecular genetic procedures enable point mutations to be identified and prenatal diagnosis to be performed in many families.
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PMID:[CDGS-1--a recently discovered hereditary metabolic disease. Multiple organ manifestations, incidence 1/80,000, difficult to treat]. 988 93

One-hundred-one surgeries for aortic arch aneurysm were divided into 2 groups: 52 aortic dissection cases (AD) and 49 non-dissecting aneurysm (TA). In group AD, 30 cases were operated in acute phase (acute AD) and 22 were in chronic phase (chronic AD). Preoperative shock were observed in 21 cases (15 in acute AD mostly due to cardiac tamponade, 1 in chronic AD and 5 in TA due to rupture). Through median sternotomy, 59 total arch replacement and 25 hemi-arch replacement were carried out under deep hypothermia (16 degrees C:DH) and retrograde (RCP) or selective (SCP) cerebral perfusion or arch-first technique. Through thoracotomy, distal arch replacement were carried out with DH + RCP in 8 cases and with partial bypass in 9. Early mortality were observed in 7 patients (6.9%) and 24 months survival rates (Kaplan-Meier) were 86.1% overall, 76.1% in acute AD, 95.5% in chronic AD, 87.8% in TA. The survival rates in patients with preoperative shock was 61.2%, however, without shock, 92.9% in acute AD, 95.2% in chronic AD, and 91.4% in TA. Other than mortality, 4 re-operations for aortic arch, 4 operations for descending to abdominal aorta and 1 late hemiplegia were observed. Aortic event free ratio at 24 months was 55.4% in acute AD, 94.4% in chronic AD, and 75.7% in TA. For the further improvement of aortic arch surgery, early mortality and residual false lumen in acute aortic dissection and atherosclerotic aneurysm in descending to abdominal aorta are focused.
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PMID:[Mid-term results of the surgery for aortic arch aneurysm]. 1196 15