Tierarztl Prax Ausg K Kleintiere Heimtiere 2010; 38(03): 157-162
DOI: 10.1055/s-0038-1622842
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Schattauer GmbH

Kastrationsnebenwirkungen Harninkontinenz und Welpenfell bei der Hündin

Eine Übersicht zu Pathophysiologie, Diagnose und TherapieUrinary incontinence and puppy coat due to spaying in the bitchAn overview of pathophysiology, diagnosis and therapy
I. M. Reichler
1   Klinik für Fortpflanzungsmedizin (Prof. Dr. Dr. h. c. U. Braun), Vetsuisse-Fakultät Universität Zürich
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Publikationsverlauf

Eingegangen: 19. Februar 2010

Akzeptiert nach Revision: 04. Mai 2010

Publikationsdatum:
05. Januar 2018 (online)

Zusammenfassung

Harninkontinenz (HI) als Folge eines nicht ausreichenden Verschlussmechanismus der Harnröhre (urethrale Sphinkterinkompetenz [USMI]) oder einer gestörten Speicherfunktion der Blase ist eine gefürchtete Nebenwirkung der Kastration bei Hündinnen. Das Risiko für HI wird von Faktoren wie Rassezugehörigkeit, Körpergewicht und Zeitpunkt der Kastration beeinflusst. Typisch ist der Harnverlust im Liegen, der im Mittel 2,8 Jahre nach Kastration erstmals auftritt. Die Diagnose wird mittels Ausschlussverfahren gestellt, wobei insbesondere eine gezielte Anamnese sehr hilfreich ist. Die Therapie hat zum Ziel, den Verschlussdruck der Harnröhre und/oder die Blasencompliance zu erhöhen. In der Regel führt eine medikamentöse Therapie zum Erfolg, sodass eine chirurgische Intervention nicht notwendig ist. Neben der HI werden als unerwünschte Kastrationsfolge bei bestimmten Hunderassen auch Fell-veränderungen beobachtet. Die durch die Kastration ausgelösten pathophysiologischen Mechanismen, die zur Abnahme des Harnröhrenverschlussdrucks, zu einer veränderten Speicherfunktion der Harnblase sowie zu Fellveränderungen führen, sind bis heute nicht vollständig geklärt. Außer die in einer altbekannten Hypothese genannte Östrogendefizienz könnte die nach Kastration veränderte Sekretion der übergeordneten Sexualhormone, FSH, LH und GnRH eine Rolle spielen. Neben α-Adrenergika, Flavoxat und Estriol wird auch der erfolgreiche Einsatz von GnRH-Agonist-Depotformulierungen zur Therapie der kastrationsbedingten HI beschrieben. Diese Depotformulierungen erwiesen sich auch zur Therapie bei Fellveränderungen nach Kastration als geeignet.

Summary

Urinary incontinence as a consequence of an insufficient urethral closure mechanism (urethral sphincter mechanism incompetence, USMI) or an impaired storing capacity of the urinary bladder is a considerable side effect of castration in the female dog. Different factors such as breed, body weight and time of spaying have an impact on the risk of urinary incontinence. Loss of urine while the patient is recumbent is the most typical symptom which is first observed at a mean time of 2.8 years after castration. Diagnosis is obtained by excluding other causes, whereas a precise patient history is particularly helpful. Therapy is aimed at increasing the closing pressure of the urethra and/or the compliance of the urinary bladder. Usually success can be achieved by medical therapy, thus surgical intervention is normally not required. In addition to urinary incontinence, coat changes can be observed as an undesirable effect of castration in certain dog breeds. To date, the patho-physiology of decreased urethral closing pressure, altered storing function of the urinary bladder and coat changes induced by castration are still not fully understood. Apart from the well-known hypothesis of estrogen deficiency, altered secretion of the hypothalamic and pituitary hormones GnRH, FSH and LH due to castration may have an influence. In addition to α-adrenergic medication, Flavoxate and Estriol, depot formulations of GnRH analogues have been successfully used to treat urinary incontinence. These depot formulations have also been described for the treatment of coat changes due to spaying.

 
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