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| CONSIDER THIS CASE acoustic enhancement. The pancreas was prominent and moderately hypoechoic with hyperechoic striations and stippling throughout the parenchyma). No abnor- malities were noted with regard to the size, shape, or consistency of the adrenal glands. Preferential consideration was given to possible hepa- tocutaneous syndrome; neoplasia was less likely. Differential Diagnoses Liver Disease Abscess/inflammation Atypical nodular regeneration Chronic liver diseases affecting liver function, including: r *OGFDUJPVT r *OGMBNNBUPSZ r .FEJDBUJPO JOEVDFE r /POJOGMBNNBUPSZ FH DISPOJD IFQBUJUJT BOUJ- convulsant & glucocorticoid hepatopathy, portosystemic shunt, amyloidosis) Neoplasia Skin Biopsy Based upon radiographic and ultrasonographic find- ings, as well as previous historical findings, an ACTH- stimulation test was not performed. The patient was prepared for biopsy of the feet and footpads. After administering a lidocaine block (0.1 mg/kg SC), samples were obtained from the left front and right hind feet using a 6-mm circular punch biopsy instrument. The samples were submitted to a patholo- gist for histopathologic evaluation. The dog was dis- charged with tramadol (5 mg/kg PO Q 12 H), an opioid class of analgesic. Pathology Results Pathology results were consistent with superficial necro- lytic dermatitis (hepatocutaneous syndrome [HCS], met- abolic epidermal necrosis). The owner was advised to consider ultrasound- guided hepatic biopsy to achieve diagnosis. Further Diagnostics The owner declined biopsy due to concerns regard- ing anesthesia but did elect to pursue glucagon and ammonia measurements. Both ammonia and glucagon levels were within normal limits. Based upon these levels, the liver was eliminating ammonia normally. The possibility of a glu- cagonoma as the cause of skin disease was less likely. Without a hepatic biopsy, neoplasia could not be ruled out definitively; however, the ultrasound report listed neoplasia as very unlikely. Therefore, the patient was treated for HCS. TREATMENT Currently published supportive therapy for HCS is multifaceted and consists of: UÊ ««Ào«Ài>ÌiÊ>nÌimiVÀoLi>lÊÌhiÀ>«ÞÊ UÊ-Õ««oÀÌiÛiÊ ÌhiÀ>«ÞÊ ovÊ VÕÀÀinÌÊ hi«>ÌiVÊ `iÃi>ÃiÊ ÜiÌhÊ -->`inoÃÞlmiÌhioniniÊ - i®]Ê ÕÀÃo`iol]Ê >n`ÊÛiÌ>minÊ Ê UÊParenteral amino acid supplementation (Note: oniÌoÀin}Ê ÌhiÊ«>ÌiinÌÊ voÀÊniÕÀolo}iVÊ Ãi}nÃÊ`ÕÀin}Ê amino acid administration is important due to the potential risk for hepatoencephalopathy.) WHAT YOU NEED TO KNOW ABOUT… HEPATOCUTANEOUS SYNDROME HCS is generally considered a rare disease in the veterinary literature with 1 institution report- ing only 0.3% of all nonneoplastic skin biopsy samples having changes consistent with the disease.1 Although most commonly reported in canines; it has been diagnosed in felines and captive black rhinoceros populations in the United States. Known by other names, such as superficial a definitive necrolytic dermatitis (SND), metabolic epider- mal necrolysis (MEN), diabetic dermatopathy, and necrolytic migratory erythema (NME), HCS is a progressive dermatologic disorder that typ- ically develops secondary to hepatic dysfunc- tion. The term HCS is given when evidence of hepatic abnormalities are present. MEN, SND, and NME are used to describe the dermatologic component.2 Although this syndrome is primarily diag- nosed in dogs, its human counterpart is referred to as NME. It is associated primarily with a pancreatic endocrine tumor, whereas in dogs, HCS is associated with glucagonomas in only in a minority of cases.3 40 Today’s Veterinary Practice July/August 2011