Medical treatment of cholangiohepatitis and cholelithiasis in mature horses: 9 cases (1991–1998)

Abstract

The medical approach to treatment of cholangiohepatitis and cholelithiasis in 9 horses is described. Seven horses were treated successfully and returned to normal use, with a minimum follow-up period of 12 months. Long-term antimicrobial therapy was believed to be critical in those cases that survived, with a median treatment duration of 51 days (range 17-124 days). Treatment failure was associated with severe periportal and bridging hepatic fibrosis from biopsy material obtained at admission in 2 horses, one of whom also presented with hyperammonaemic hepatic encephalopathy. Transabdominal ultrasound was used diagnostically in each case to obtain hepatic biopsy material for histopathology and bacterial culture, to evaluate hepatic size and echogenicity and to identify and monitor the dissolution of hepatoliths. Histologically, all horses had evidence of suppurative cholangiohepatitis with varying degrees of periportal and bridging fibrosis. Discrete hyperechoic calculi were identified in 4 cases, but all horses had ultrasonographic evidence of biliary obstruction with numerous dilated bile ducts. Aerobic and anaerobic cultures of liver biopsy material were negative from 7 horses, but 2 different species of Escherichia coli were obtained from one horse, and Bacteroides vulgatus and Escherichia coli were isolated from another. In all 7 horses that survived, clinical recovery was seen before normalisation of biochemical indices of hepatobiliary function including gammaglutamyl transaminopeptidase (GGT), alkaline phosphatase (AP), bile acids and serum bilirubin. Serum GGT levels were monitored extensively as a marker of hepatobiliary disease and actually increased during the initial period of clinical improvement in horses that recovered. Supportive medical therapy with i.v. fluids was also a critical part of the therapy of several cases in this report, both acutely and in the management of chronic cases that deteriorated clinically during treatment. Previous therapeutic failures may well be related to treatment periods of inadequate duration, and the authors recommend that antimicrobial therapy should be continued until GGT values are normal.

Cholelithiasis - a cause of hepatocirrhosis and hepatic encephalopathy in a 10-year-old warmblood mare

“…Die genaue Entstehungsweise von Gallensteinen beim Pferd ist noch nicht vollständig geklärt, jedoch werden aus dem Dünn-darm aufsteigende bakterielle Infektionen als Hauptursache angesehen (Barton 2004, Donovan 1999 (Donovan 1999, Barton 2004. Der Nachweis von überwiegend gramnegativen Enterobakterien aus Lebergewebe von Pferden mit Cholelithiasis unterstützt diese These (Reed et al 1990, Johnston et al 1989, Peek and Divers 2000.…”

“…Diese Entstehungsweise von Gallensteinen, insbesondere von Cholesterolsteinen, ist beim Pferd ebenso denkbar. Des Weiteren ist auch vorstellbar, dass Gallensteine durch parasitäre Infektionen der Leber hervorgerufen werden (Gerros 1996 (Grabner 1997, Peek und Divers 2000, Johnston et al 1989, Tulleners et al 1985. Die frühe Erkennung einer Cholelithiasis ist also für eine erfolgreiche Therapie von großer Bedeutung.…”

“…Es gibt verschiedene Berichte über die erfolgreiche medikamentöse (Grabner 1997, Peek and Divers 2000, Graves 2006) und chirurgische Therapie (Traub et al 1983, Tulleners et al 1985, Johnston et al 1989 der Cholelithiasis des Pferdes. Sobald jedoch eine Leberfibrose mit Insuffizienz des Leberparenchyms eingetreten ist, steigt die Mortalitätsrate erheblich an, was zahlreiche Berichte belegen (Traub et al 1982, van der Luer and Kroneman 1982, Johnston et al 1989, Freestone 1989, Reed et al 1990, Holland et al 1991, Ryu et al 2004 …”

Equine Hepatic Encephalopathy

“…In one paper, the recommendation to continue therapy until serum GGT concentrations normalize was suggested. 5 The median treatment time was 51 days (range 17 to 124 days) with antibiotics. Table 20.5 gives suggested doses for drugs used in the symptomatic treatment of HE in the horse.…”

“…Pathological features that have been identified include processes affecting glial cell and neuronal function, hyperammonemia, changes in the concentration of excitatory and inhibitory neurotransmitter systems, as well as osmotic changes with consequential cell swelling. 3 The frequently documented liver diseases in the horse are acute hepatic necrosis, 4 chronic active hepatitis 4 caused by pyrrolizidine alkaloids, cholelithiasis, 5 and hemachromatosis. 4 In foals, a toxic hepatopathy causing HE has been described following the oral administration of a viable Aspergillus sp.…”