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Case 36 Slide 08-193 The little calf that couldn’t. Julia Lankton, Natalie Durrett Crawford, Ondrej Becvar, Tanya LeRoith Virginia-Maryland Regional College of Veterinary Medicine. Signalment and History. Three week old Holstein heifer calf from large dairy Abdominal distension.
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Case 36Slide 08-193The little calf that couldn’t Julia Lankton, Natalie Durrett Crawford, Ondrej Becvar, Tanya LeRoith Virginia-Maryland Regional College of Veterinary Medicine Presented at SEVPAC 2008 – Permission granted for use on SEVPAC website only
Signalmentand History • Three week old Holstein heifer calf from large dairy • Abdominal distension Presented at SEVPAC 2008 – Permission granted for use on SEVPAC website only
Physical Exam and Initial Treatment • Ataxia • Thiamine • Diarrhea • Sulfamethazine • Florfenicol • Electrolytes • Poor muscle tone Presented at SEVPAC 2008 – Permission granted for use on SEVPAC website only
3-Week Progression • Good appetite with little weight gain • Chemistry panel: Low BUN • EMG: WNL • Continued/Worsening ataxia • Rx corticosteroids – no improvement • Euthanized at 6 weeks Presented at SEVPAC 2008 – Permission granted for use on SEVPAC website only
Differentials • Bacterial • TEME • Vertebral osteomyelitis • Viral • Rabies • Pseudorabies • Parasitic • Nervous coccidiosis • Parelaphostrongylus tenuis • Nutritional • Polioencephalomalacia • Vitamin A deficiency • Toxic • Lead toxicosis • Urea toxicosis • Congenital • Hydranencephaly • Hydrocephalus • Porto-systemic shunt? • Nah, that’s in small animals Presented at SEVPAC 2008 – Permission granted for use on SEVPAC website only
Gross Lesions • Body weight: 68 kg (150 lbs) • Normal: 82 kg (180 lbs) • Minimal fat stores • Small liver • Cerebral cyst Presented at SEVPAC 2008 – Permission granted for use on SEVPAC website only
Abdomen Presented at SEVPAC 2008 – Permission granted for use on SEVPAC website only
Liver Presented at SEVPAC 2008 – Permission granted for use on SEVPAC website only
Liver and Kidney Presented at SEVPAC 2008 – Permission granted for use on SEVPAC website only
Histopathology: Liver • Lobules small and irregular • Lymphatics and sinusoids dilated • Portal regions: • Small portal veins • Numerous portal arterioles Presented at SEVPAC 2008 – Permission granted for use on SEVPAC website only
Liver H&E Presented at SEVPAC 2008 – Permission granted for use on SEVPAC website only
Liver H&E Presented at SEVPAC 2008 – Permission granted for use on SEVPAC website only
Liver H&E Presented at SEVPAC 2008 – Permission granted for use on SEVPAC website only
Histopathology: Brain • White matter vacuolization • Pronounced in white matter tracts bordering grey matter • Severity increases caudally • Scattered neuronal necrosis • 1.4 mm diameter ependymal lined space • Rostral cerebral white matter Presented at SEVPAC 2008 – Permission granted for use on SEVPAC website only
Cerebrum H&E Presented at SEVPAC 2008 – Permission granted for use on SEVPAC website only
Cerebrum LFB-PAS Presented at SEVPAC 2008 – Permission granted for use on SEVPAC website only
Brainstem H&E Presented at SEVPAC 2008 – Permission granted for use on SEVPAC website only
Brainstem LFB-PAS Presented at SEVPAC 2008 – Permission granted for use on SEVPAC website only
Spinal Cord H&E Presented at SEVPAC 2008 – Permission granted for use on SEVPAC website only
Cerebrum H&E Presented at SEVPAC 2008 – Permission granted for use on SEVPAC website only
Diagnosis • Morphologic : • Liver: arteriolar reduplication, lobular atrophy and lymphatic dilation • Brain: white matter, polymicrocavitation; focal syringoencephalocele • Disease : Portosystemic shunt with hepatic encephalopathy Presented at SEVPAC 2008 – Permission granted for use on SEVPAC website only
PSS Pathogenesis • Rare in large animals (4 cases in calves) • Normal fetal communications patent • Portal blood bypasses liver and enters circulation • Decreased portal vein perfusion • Liver lobules atrophy • Portal veins are hypoplastic • Hepatic arterioles are hyperplastic Presented at SEVPAC 2008 – Permission granted for use on SEVPAC website only
HE Pathogenesis • Toxins from portal blood access CNS • Ammonia astrocytes decreased BBB • Ammonia, fatty acids, amino acids and other neurotoxins enter CNS • Astrocyte hypertrophy and degeneration • Alzheimer type II cells • More prominent in other spp. • Intramyelinic Edema • Diffuse bilaterally symmetrical polymicrocavitaton, predominantly of white matter and at grey-white border Presented at SEVPAC 2008 – Permission granted for use on SEVPAC website only
In Conclusion Presented at SEVPAC 2008 – Permission granted for use on SEVPAC website only
Thank You • Dr. Natalie Durrett Crawford • Dr. Tanya LeRoith • Dr. Ondrej Becvar • Dr. Bernard Jortner • VMRCVM histopathology lab Presented at SEVPAC 2008 – Permission granted for use on SEVPAC website only
References • 1.Buczinski, Sebastien, et. al. Portacaval shunt in a calf: Clinical, pathologic, and ultrasonographic findings. Can Vet J 2007; 48: 407-410. • 2. Van Den Ingh, et. al. Congenital portosystemic shunts in three pigs and one calf. Vet Pathol 1990; 27: 56-58 • 3. Reimer JM, et. al. Diagnosis and surgical correction of a patent ductus venosus in a calf. JAVMA 1988; 193: 1539-1541. Presented at SEVPAC 2008 – Permission granted for use on SEVPAC website only