EQUINE VETERINARY EDUCATION / AE / APRIL 2018
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Additional work-up and treatment Based on the major clinical signs, laboratory parameters and the rapid deterioration over the last 2 weeks significant inflammation or infection of the lungs and liver was presumed. Hepatic encephalopathy (HE) was considered most likely due to obtunded mentation and extreme elevations in hepatobiliary enzymes, in conjunction with chronic, severe weight loss. Initial budget was limited. Treatment was focused on improving demeanour, combating neurological signs, and reducing hepatic and airway inflammation possibly associated with bacterial infection. Initial treatment on Day 1 included enteral fluid therapy via
nasogastic tube (8 L water with electrolytes [one sachet Lectade] plus 500 mL lactulose), flunixin meglumine (1.1 mg/kg bwt i.v.), dexamethasone (0.1 mg/kg bwt i.v.) and trimethoprim–sulfonamide (TMPS; 20 mg/kg bwt i.m.). Nasogastric intubation was repeated on five more occasions within a 48-h period while other treatments were continued orally (dexamethasone 0.1 mg/kg per os s.i.d., flunixin meglumine 1.1 mg/kg per os s.i.d. and TMPS 20 mg/kg per os b.i.d.) for 3 more days. Appetite was stimulated by offering frequent small amounts of good quality hay and fibre nuts. Improvements in mentation and ataxia were noted on Day 3 and the pony showed a better appetite. Oral flunixin meglumine (1.1 mg/kg bwt per os s.i.d.), TMPS (20 mg/kg bwt per os b.i.d.) and dexamethasone (0.1 mg/kg bwt per os s.i.d.) were continued for another 2 days (Days 4 and 5). Oral prednisolone (1 mg/kg bwt per os s.i.d.) was substituted for dexamethasone from Day 5. During the following 10 days, the pony had occasional fever spikes (up to 42°C) that were treated with oral or intravenous flunixin meglumine (1.1 mg/kg bwt s.i.d.). A relapse in depression and ataxia presented on Day 10. Abdominocentesis was attempted (to rule out peritonitis) but was unsuccessful. The pony’s clinical parameters and demeanour improved following enteral fluids administered by nasogastric tube as previously described. With recurrent clinical signs and only marginal improvements in repeat haematology and biochemistry values at Day 10, hepatic ultrasound and biopsy was elected by the owner. Transabdominal ultrasound was performed on Day 15
(3.5-MHz curvilinear probe) revealing a subjectively small liver (10th–14th right intercostal space) with a subjectively hyperechoic parenchymous appearance. A single 3.8 cm anechoic structure compatible with an Echinococcus (hydatid) cyst could be imaged in the 14th intercostal space on the right side (Fig 1). Three ultrasound guided percutaneous Tru-cut biopsies were collected and submitted for histopathology. Following biopsy, the pony remained on TMPS (20 mg/kg bwt per os b.i.d.) pending results. On Day 18, while awaiting the liver biopsy results, the
pony deteriorated again, became recumbent and was subjected to euthanasia. A post-mortem examination was performed with samples collected for histopathology (fixed in 10% formal saline) and microbiology testing.
Post-mortem examination Upon opening the abdomen many coalescing, white, raised nodules were present throughout approximately 60% of the peritoneal and mesenteric surfaces (Fig 2). The liver appeared small and pale, containing four parenchymal cystic structures. Opening the cysts revealed they were Echinococcus cysts (Fig 3). Many white, granulomatous, caseous masses measuring approximately 1–4 cm in diameter were present
Fig 1: Ultrasound of the liver in the right hemithorax at the 14th intercostal space. A 3.8 cm diameter echinococcus cyst was evident within subjectively hyperechogenic hepatic parenchyma.
Fig 2: Post-mortem examination of the mesentery revealed multiple, coalescing white nodules forming plaques. This appearance was seen throughout the abdomen and on the gastric serosal surface.
throughout the splenic parenchyma (Fig 4). These masses extended into adjacent tissue as small nodules on juxtapositioned serosal surfaces. There was no evidence of adhesions or inflammation typical of peritonitis. Maximal small intestinal wall thickness was approximately 4 mm at one location. Two mesenteric lymph nodes appeared subjectively enlarged. Exploration of the thorax revealed identical cystic structures and white caseous masses spread throughout the lung and pleural surfaces. Bronchial walls were thickened on cut section. No other macroscopic abnormalities were detected.
Histopathology Antemortem tru-cut liver biopsy specimens revealed moderate portal fibrosis and moderate biliary hyperplasia with infiltrates of haemosiderophages. Two discrete pyogranulomatous inflammatory foci were seen. Ziehl– Neelsen staining of these was positive for acid-fast bacilli. The samples were given a liver biopsy score of 4/14 (Durham et al. 2003a,b). Bacterial culture was not performed due to
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