Biomedical subjects
Publications and source records attributed to O Adler.
Two cases of endocrine inactive malignant islet cell tumors diagnosed by angiography are presented. The angiographic features are described and the differential diagnosis of the tumor and its metastases are discussed. Radiological literature of the past decade on this subject is reviewed.
A young girl in whom severe hypertension was cured by the surgical removal of a unilateral hypoplastic kidney (Ask-Upmark kidney) is described. The clinicopathological features of the Ask-Upmark kidney are described with particular reference to the aetiology of the hypertension as well as the selection of patients for surgery. No abnormality of the renin-angiotensin system was detected.
The early and late radiological features of damage to the stomach and duodenum caused by acid ingestion are described based on our experience with ten patients. The radiological features of early corrosive damage to the stomach caused by acid are: gastric atony, thickened mucosal folds and mural filling defects representing mucosal edema, mural hematoma and necrosis. Similar changes, although to a lesser degree, can be seen in the duodenum. Within a few weeks after ingestion there is rapid progression to antropyloric stenosis, leading to gastric outlet obstruction. The clinical and radiological picture of corrosive gastritis may closely resemble that of malignancy of the stomach. Acid ingestion, particularly with suicidal intent, is not a rare occurrence, and the radiologist has an important part in its diagnosis, evaluation and management.
Renal venography was performed in a patient suffereing from hypertension due to fibromuscular dysplasia of the renal artery. The venogram revealed morphological changes in the renal veins similar to those seen in fibromuscular dysplasia of the arteries. Histological examination of the veins showed fibrosis of the medial wall layer.
Severe, unremitting bleeding of the upper gastrointestinal tract could be controlled by Gelfoam embolization of the posterior pancreaticoduodenal artery. The technique and indications of the method are presented.
Two patients with kidney transplants had hypertensive encephalopathy and rapidly progressive kidney failure 10 weeks and 18 months postoperatively. In one patient renal failure was associated with erythrocytosis. Absence of proteinuria, despite progressive renal insufficiency in both patients, suggested that these abnormalities were not due to rejection episodes. Subsequently, angiography proved that each of these patients had renal-artery stenosis. Surgical repair of this lesion increased creatinine clearance at least threefold, and the hypertension and erythrocytosis disappeared. Apparent "rejection" episodes in which there is no proteinuria should alert clinicians to the possiblity of renal-artery stenosis of the graft. Restoration of kidney function and amelioration of hypertension may follow revascularisation, even after many months of renal ischaemia producing severe uraemia.
1) In major vein trauma, an attempt should be made to repair the vein. 2) Whenever possible, lateral suture seems to be the ideal type of repair. However, excellent results can be obtained with end-to-end anastomosis. 3) When the damaged segment of the vein is too long to permit end-to-end approximation, a vein interposition graft (and if necessary, a composite tube) appropriate to the width of the injured vein and length of the gap should be employed. Use of synthetic grafts should be avoided. 4) Although the importance of a distal temporary A-V fistula is still disputed, the present authors have adopted this method in the graft repair of the femoral vein in the groin. Better results were obtained in the cases in which the fistula functioned than in those in which it became occluded.
A case is presented in which extreme hydronephrosis simulated absence of the right kidney. The hydronephrosis occurred as a result of surgical ligation of the right ureter 10 years previously. There was no visualization of the excretory system by intravenous urography or retrograde pyelography. Abdominal aortography did not show the renal artery. Selective renal venography revealed a patent venous bed with splaying and thinning of the intrarenal veins. The contribution of renal venography is discussed in clarifying cases in which the kidney and the renal artery were not visualized.
A young girl suffering from anuria due to periarteritis nodosa developed severe bleeding after left kidney needle biopsy. Angiography revealed, in addition to changes in the renal vascular tree, two saccular pseudoaneurysms in the course of a lobar artery in the left kidney. These caused life-threatening bleeding from the urinary tract. An autologous blood clot was injected into the bleeding artery by selective catherization, which resulted in cessation of bleeding for a period of 15 h, and thus permitted the performance of surgical intervention - nephrectomy - under more suitable conditions.
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This report concerns an apparently healthy elderly woman who presented with gradually worsening mitral regurgitation secondary to chordae tendineae rupture leading to pulmonary edema in the presence of discrete subvalvular aortic stenosis with a severe gradient reflecting the left ventricular outflow tract obstruction. The gradual worsening of heart failure took place parallel to the increase in severity of mitral regurgitation in a short period. The patient underwent successful mitral valve replacement with myectomy. Surgical inspection revealed rupture of the chordae tendineae to the posterior leaflets without any significant primary intrinsic disease of the mitral valve. The predominant mechanism of chordae tendineae rupture in this patient with discrete subvalvular aortic stenosis is a severe pressure gradient. It is suggested that increased awareness of chordae tendineae rupture as a cause of mitral regurgitation and the prompt use of appropriate diagnostic tools may facilitate the timely recognition of this potentially fatal, but treatable, cause of mitral regurgitation in patients with left ventricular outflow tract obstruction.
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