Page 911 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition
P. 911

886                                        CHAPTER 5



  VetBooks.ir  of histopathology; therefore, approximately 2–4 cm   where possible, that biopsies are collected from at
                                                          least two different sites or, at least, from slightly dif-
           of biopsy material is collected in total where possible
           (Fig. 5.15). Biopsy specimens should be placed in
                                                            Examination of liver biopsy specimens is the most
           10% buffered formalin for histopathology, although   ferent angles at the same site.
           where suspicions of bacterial cholangiohepatitis exist   likely means by which the aetiology of liver disease is
           then culture of fresh biopsy material might also be   identified, although this will still prove to be evasive
           useful given the caveat that even successful culture   in the majority of cases. Certain types of liver dis-
           might not necessarily comprise all bacterial species   ease such as septic cholangiohepatitis, pyrrolizidine
           present.                                       alkaloid toxicosis (Fig. 5.16), neoplasia and severe
             It is a commonly stated dogma that liver disease   haemosiderosis may well provide characteristic histo-
           in horses is diffuse and it is generally assumed that   pathological findings, although the majority of clini-
           collection of a biopsy from any site is likely to be rep-  cal cases of liver disease examined in equine practice
           resentative of the underlying hepatopathy. Although   will reveal patterns of pathology that are not specific
           this generally appears to be the case, variation can be   for any precise causation. One should also be mind-
           seen in biopsies taken from different sites of the same   ful that minor pathological insults are commonly
           liver in up to 30% of cases, albeit in most cases the   encountered in horses showing no clinical or clinico-
           variation is mild. Furthermore, even at a microscopic   pathological evidence of liver disease, including mild
           level hepatic pathology is very rarely genuinely dif-  periportal lymphoplasmacytic infiltrates and mild to
           fuse. For example, fibroplasia tends to preferentially   moderate haemosiderin accumulation in hepatocytes
           have a porto-portal pattern in most equine liver dis-  and Kupffer cells. Despite these diagnostic limita-
           ease cases. However, adjacent portal tracts may be   tions, there are further clinical benefits from exam-
           variably affected (intrabiopsy variability) and,  fur-  ining the biopsy specimens in addition to confirming
           thermore, a very different impression of the degree   that liver disease is definitely present, even if the pre-
           of fibrosis can be made from two adjacent biopsies   cise aetiological factors are often elusive.
           (interbiopsy variability), depending on the relative   Alongside neoplasia, megaolcytosis and extensive
           proportion of acinar margins that are included in   necrosis, marked periportal and bridging porto-
           the specimen. Thus, it is generally recommended,   portal fibrosis is the most prognostically concerning



           5.15                                           5.16
                                                                      F






                                                                              BH


                                                                   H

                                                                                M



           Fig. 5.15  Liver biopsy specimens of mixed individual   Fig. 5.16  Biopsy specimen demonstrating typical
           lengths collected from the same horse (approximately   signs of pyrrolizidine alkaloid toxicosis including
           33 mm of biopsy specimens in total).           fibrosis (F), megalocytosis (M) and biliary hyperplasia
                                                          (BH), with an additional finding of orange granular
                                                          haemosiderosis (H).
   906   907   908   909   910   911   912   913   914   915   916