[A case report of type B WPW syndrome with Ebstein's anomaly; division of Kent bundle by epicardial approach].
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Biomedical subjects
Publications and source records attributed to M Otaki.
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The patient was a 48-year-old housewife, who had a sudden onset of severe headache followed by loss of consciousness for a few hours on the day of admission. Initially she showed slight restlessness due to headache, neck stiffness and subhyaloid hemorrhage. Four-vessel study revealed a basilar aneurysm on right retrograde brachial angiography and anterior communicating aneurysm on left carotid angiography. Two weeks after the onset, when she had no neurological deficit except for intermittent appearance of disorientation, both aneurysms were successfully clipped through right pterional approach of Yasargil. The subarachnoid hemorrhage was apparently due to basilar bifurcation aneurysm. Postoperatively, she showed right hemiparesis including her face, aniscocoria (left, 4 mm, oval: right, 1.5 mm, round) and conjugate deviation toward the left. The disturbance of conjugate eye movement and the hemiparesis completely disappeared in 2 and 7 days respectively. The patient was discharged 4 weeks postoperatively with mild left 3rd nerve palsy. At present, one year postoperatively, she is fully engaged in her housewife life without any neurological deficits. A case of superior Foville syndrome combined with Weber syndrome after clipping of basilar bifurcation aneurysm was reported and its anatomicoclinical mechanism was reviewed. The pathogenesis was supposed to be left midbrain ischemic lesion due to circulatory disturbance of P-1 perforators (P-1: proximal posterior cerebral artery); e.g., occlusion on clipping of vasospasm. This P-1 perforator syndrome after aneurysmal clipping has been reported only little. The importance of preservation of these perforators with careful dissection and manipulation under microscopy was emphasized.
UNLABELLED: CASEs of primary brain stem lesion following closed head injury, verified on CT scan, have been increasingly reported recently. However, most of them have supratentorial lesions in addition to brain stem, resulting in a poor outcome. In this paper, a case of localized brain stem hematoma following closed head injury, is reported based on CT findings. CASE: A 26-year-old man slipped down on his back and hit the right occipital area with following loss of consciousness for several minutes. Since then, he continued to have gait disturbance and visited our hospital on the next day. On admission, he presented truncal ataxia, left trochlear nerve palsy, right Horner's syndrome and left hemihypesthesia. CT scan revealed a small hematoma localized to the right midbrain tegmentum at the level of inferior colliculus, well correlating with his clinical presentation. He gradually improved on conservative treatment and returned to his former work one month after the accident. This case suggests that there may be cases of primary brain stem injury with no other intracranial lesion based on CT findings and with a good prognosis. Shear strain is said to be a probable mechanism for explaining brain stem injury, which is usually combined with other parenchymal lesions. In our case, however, more focal factor--nervous and/or vascular compression against the tentorial edge--is suspected for producing this localized midbrain lesion.
The application of computed tomography to cardiovascular diagnosis was attempted. One hundred and four consecutive patients with various cardiovascular diseases were studied with a third-generation computed tomographic three-second whole body scanner. Identification and evaluation of abnormalities of the great vessels, atria, ventricles and interventricular septum were possible by cardiac computed tomography. Sizes and locations of intracardiac thrombi were accurately assessed by computed tomography. Computed tomography was valuable for the evaluation of pericardial effusion because distribution of the effusion as well as the gross nature of the fluid could be estimated by the CT number.
Electrophysiological studies were performed in five patients, two with the three without Wolff-Parkinson-White (WPW) syndrome. In the former patients group, the paroxysmal supraventricular tachycardia (PSVT) was concluded to reflect the circus movement utilizing the normal atrioventricular (A-V) conduction system for antegrade conduction and the Kent bundle for the retrograde conduction. Ventriculoatrial conduction time (VACT) was measured during ventricular pacing before and after the administration of atropine sulfate. In patients without WPW syndrome, the VACT prolonged and subsequently second degree ventriculoatrial block developed when the pacing rate was increased progressively and atropine facilitated the retrograde conduction, suggesting the ventriculoatrial conduction took place via the normal A-V pathway. In contrast, the VACT in patients with WPW syndrome remained unchanged during ventricular pacing at rates of 145/min and more before and after atropine, indicating the retrograde conduction was taking place through the Kent bundle. It is discussed that the analysis of the VACT before and after atropine serves as an aid to differentiate the underlying mechanisms of PSVT in patients with WPW syndrome.
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Fifteen cases of multiple myeloma and 6 cases of macroglobulin emia Waldenstrom were followed up from 1957 to 1974. As for administration of drugs a low continuous dose regimen was mainly employed instead of a high intermittent dose regimen. 50% survival time from the onset of the disease was 18 months for multiple myeloma and 25 months for macroglobulinemia Waldenstrom. 3 cases of multiple myeloma are still living 44 months after the onset of symptoms. Cyclophosphamide and melphalan seem to have contributed much to the prolonged survival of these patients as well as improved supportive care.
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Reports of patients with idiopathic thrombocytopenic purpura (ITP) undergoing cardiac surgery are rare, and almost all of the reported cases required platelet transfusion. ITP patients, especially those having a history of splenectomy or a history of heavy bleeding, may have to undergo multiple platelet transfusions. Such transfusions may induce alloimmunization against the human leukocyte antigen (HLA) and result in refractoriness to subsequent platelet transfusions. We report a case of a 63-year-old female with ITP, with a history of splenectomy and multiple platelet transfusions, who underwent aortic and mitral valve replacement. Although corticosteroid administration, high-dose immunoglobulin therapy, and repeated platelet transfusion led to a temporary increase in platelet count and successful hemostasis, refractoriness to platelet transfusion occurred postoperatively because of the presence of the anti-HLA antibody. In addition, the patient showed complications of pyothorax. Corticosteroids might have exerted an inhibitory influence on the occurrence of pyothorax.