Minimal-invasive Adrenalektomie beim Phäochromozytom

ZusammenfassungHintergrund Bedingt durch die intraoperative Katecholaminsekretion mit hämodynamischen Veränderungen, einem größeren Tumordurchmesser und einer deutlichen Neovaskularisation ist die Adrenalektomie beim Phäochromozytom im Vergleich zu anderen Nebennierenerkrankungen schwieriger und potenziell komplikationsträchtiger. Ziel unserer Studie war die Frage, ob das Risiko intraoperativer kardiovaskulärer Komplikationen durch das minimal-invasive Vorgehen potenziert wird.Patienten und Methodik Im Zeitraum zwischen Februar 1992 und Mai 2005 wurden in unserer Klinik 82 Eingriffe wegen eines Phäochromozytoms bei 71 Patienten durchgeführt. Davon wurden 8 (1) Patient(en) bi-(tri-)lateral adrenalektomiert und bei 2 Patienten erfolgte eine ipsilaterale Rezidivoperation. Eingeschlossen sind 5 weitere Patienten mit Rezidiv nach Erstoperation vor 1992. Sechsunddreißig Eingriffe erfolgten konventionell (transperitoneal n=35, retroperitoneal n=1) und 46 Operationen endoskopisch (transperitoneal n=28, retroperitoneal n=18), davon keine Konversion zum offenen Vorgehen.Ergebnisse Das mediane Alter zum Zeitpunkt der Operation betrug 45 (24–75) Jahre bei einer Anamnesedauer von 12 (0–180) Monaten. Die offen operierten Phäochromozytome waren mit 5,5 (1–19) cm vs. 3,5 (0,5–8) cm (endoskopisch) signifikant größer (p=0,0011). Patienten mit endoskopischer, insbesondere mit retroperitoneoskopischer Adrenalektomie hatten im Vergleich zum konventionellen Vorgehen intraoperativ höhere systolische und diastolische maximale Blutdruckwerte sowie Spitzen über 200 mmHg (statistisch nicht signifikant). Faktoren mit möglichem Einfluss auf intraoperative hämodynamische Veränderungen waren in der multivariaten Analyse das Geschlecht (p=0,0107), der operative Zugangsweg (p=0,0153), das Patientenalter (p=0,0364) und die Tumorgröße (p=0,0484). Die postoperative stationäre Verweildauer war nach endoskopischer Operation signifikant kürzer (p<0,0001).Schlussfolgerung Die endoskopische Adrenalektomie beim Phäochromozytom ist in der Routine ohne vermehrtes Risiko kardiovaskulärer Komplikationen die Methode der Wahl. Das offene Vorgehen sollte extraadrenalen Befunden oder sehr großen Tumoren mit Malignitätsverdacht vorbehalten bleiben.      

Stones, bones, and heredity

Genetic disorders of mineral metabolism cause urolithiasis, renal disease, and osteodystrophy. Most are rare, such that the full spectrum of clinical expression is difficult to appreciate. Diagnosis is further complicated by overlap of clinical features. Dent's disease and primary hyperoxaluria, inherited causes of calcium urolithiasis, are both associated with nephrocalcinosis and urolithiasis in early childhood and renal failure that can occur at any age but is seen more often in adulthood. Bone disease is an inconsistent feature of each. Dent's disease is caused by mutations of the CLCN-5 gene with impaired kidney-specific CLC-5 chloride channel expression in the proximal tubule, thick ascending limb of Henle, and the collecting ducts. Resulting hypercalciuria and proximal tubule dysfunction, including phosphate wasting, are primarily responsible for the clinical manifestations. Low-molecular-weight proteinuria is characteristic. Definitive diagnosis is made by DNA mutation analysis. Primary hyperoxaluria, type I, is due to mutations of the AGXT gene leading to deficient hepatic alanine–glyoxylate aminotransferase activity. Marked overproduction of oxalate by hepatic cells results in the hyperoxaluria responsible for clinical features. Definitive diagnosis is by liver biopsy with measurement of enzyme activity, with DNA mutation analysis used increasingly as mutations and their frequency are defined.

Conclusion

These disorders of calcium urolithiasis illustrate the value of molecular medicine for diagnosis and the promise it provides for innovative and more effective future treatments.     

Image formation in vibro-acoustography with depth-of-field effects.

We study the image formation of vibro-acoustography systems based on a concave sector array transducer taking into account depth-of-field effects. The system point-spread function (PSF) is defined in terms of the acoustic emission of a point-target in response to the dynamic radiation stress of ultrasound. The PSF on the focal plane and the axis of the transducer are presented. To extend the obtained PSF to the 3D-space, we assume it is a separable function in the axial direction and the focal plane of the transducer. In this model, an image is formed through the 3D convolution of the PSF with an object function. Experimental vibro-acoustography images of a breast phantom with lesion-like inclusions were compared with simulated images. Results show that the experimental images are in good agreement with the proposed model.     

Effect of sequential administration of an opioid and cholecystokinin on gallbladder ejection fraction: brief communication.

This study was undertaken to test the effect of sequential administration of an opioid and intravenous cholecystokinin (CCK) on gallbladder ejection fraction. METHODS: Forty-nine patients who had received an opioid underwent quantitative cholescintigraphy with octapeptide of CCK (CCK-8). Gallbladder ejection fraction and CCK-8-induced paradoxical filling were calculated. RESULTS: In the basal state, more of the hepatic bile entered the gallbladder (67%) than the small intestine (33%). After CCK-8 infusion, gallbladder ejection fraction was low in 37 (76%) of 49 patients and normal in 12 (24%). All 5 types of opioids lowered ejection fraction. CCK-induced paradoxical filling of the gallbladder was noted in 7 patients, but only one showed paradoxical filling of greater than 20% and none had a normal gallbladder ejection fraction. The lowering effect of opioids on gallbladder ejection fraction may last as long as 18 h after intake. CONCLUSION: CCK-8 produced a normal gallbladder ejection fraction in 24% of patients who had received an opioid and thus could exclude both acute and chronic cholecystitis during a single hepatobiliary study.