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M Rudman

Publications and source records attributed to M Rudman.

3 recordsLinked to original sources

Analytical modeling and numerical simulation of forces in an endoluminal graft.

PURPOSE: To utilize mathematical analysis and computational fluid dynamics (CFD) to investigate the forces acting within the pressurized aorta and upon a stent-graft and how these forces may affect the ongoing performance of the stent-graft. METHODS: Analytical force balance analysis and CFD simulations using the Fluent code were used to mimic blood flow through a bifurcated stent-graft in a person at rest. Steady-state blood flow was assumed in which the inlet pressure approximated the mean blood pressure (100 mm Hg) and the blood flow velocity was an approximation of the peak systolic flow rate (0.6 m/s). Two sizes of endoluminal grafts were analyzed: the larger graft had an inlet diameter of 3 cm and outlet diameters of 1 cm; the smaller graft diameters measured 2.4 cm proximally and 1.2 cm distally. The endografts were studied in 2 configurations: with the limbs straight and with one bent. RESULTS: For the larger graft model, the normal peak blood flow induced a downward force of 7 to 9 N on the bifurcated grafts. Bending one of the limbs of the graft produced a sideways force of 1.3 N. For the smaller endograft, the downward force was in the range of 3.1 to 5.1 N and the sideways force on a curved limb was approximately 1.5 N. The magnitude of the forces given by the analytical formulae and the CFD results agreed to within 2 significant figures. CONCLUSIONS: These results suggest that the downward force on a bifurcated stent-graft, which may exceed the force required to dislodge it when relying on radial attachment alone, is determined mostly by the proximal graft diameter. Curvature of the graft limbs creates an additional sideways force that works to displace the distal limbs of the graft from the iliac arteries.

Angioplasty↗

[Acute renal failure as a complication of cholera].

We present a 72-year-old man who had episodes of severe, acute renal failure during severe attacks of diarrhea caused by Vibrio cholerae. Patterns of acute tubular necrosis and tubulointerstitial nephritis developed following hypotension and decrease in renal blood flow, causing secondary renal ischemia. There was severe dehydration with profound hypovolemia and infection. The clinical picture included fever, weakness, arthralgia, pedal edema, mild bilateral pleural effusions, anemia, leukocytosis, azotemia with a maximum of 330 mg/dl of urea, creatine to a maximum of 9.8 mg/dl, hypoproteinemia, severe metabolic acidosis, marked increase in lactate dehydrogenase (LDH) and creatine phosphokinase (CPK), microscopic hematuria, sterile leukocyturia, normoglycemic glucosuria and phosphaturia with diminished tubular reabsorption of phosphorus. A short oliguric phase was followed by a polyuric phase lasting about 10 days, and glomerular and tubular function became normal after about 3 weeks. Treatment was by intensive infusions of fluids, electrolytes, sodium bicarbonate, salt-free albumin and antibiotics. To the best of our knowledge, this renal complication of cholera has not yet been described in Israel.

Acute Kidney Injury↗

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