Transient hyperammonaemia in an adult German shepherd dog : case report

Lobetti, Remo; Miller, David B.; Dippenaar, Johannes Marthinus

doi:10.4102/jsava.v68i2.873

Cited by 7 publications

(9 citation statements)

References 4 publications

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“…Similar cases of hyperammonemia of unknown origin have also been described in humans and dogs. [12][13][14][15][16] Several similarities between the horse reported in this study and other equine patients were found with regard to history, clinical findings, and laboratory abnormalities. A postmortem examination was performed on 4 of the previously reported horses and showed similar findings.…”

mentioning

confidence: 63%

Clostridium sordelli Infection as a Suspected Cause of Transient Hyperammonemia in an Adult Horse

Desrochers¹,

Dallap²,

Wilkins³

2003

J Vet Int Med

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A 5-year-old Dutch Warmblood gelding was referred to the University of Pennsylvania George D. Widener Hospital for the evaluation of abdominal discomfort and acute onset of neurologic deficits. The horse was imported from Holland 10 days before admission and was intended to be used for dressage. Vaccination for rhinopneumonitis, influenza, and tetanus was performed 11 months before importation, and the horse had no medical history that was relevant to this study. The day before presentation, the horse was depressed, febrile, and anorexic and showed mild abdominal discomfort. Treatment with 500 mg of flunixin meglumine IV and 2 g of phenylbutazone PO improved the horse's clinical signs. The following day, the horse became increasingly depressed and tachycardic and showed signs of abdominal discomfort. Progressive development of ataxia was also reported by the referring veterinarian. The horse received an additional 500 mg of flunixin meglumine IV and was referred for further medical evaluation and treatment.Upon arrival, the gelding was very depressed and showed signs of severe symmetric ataxia in all 4 limbs with hindlimb extensor rigidity. The horse was head pressing, leaning against walls, and propulsively circling. Rectal temperature, heart rate, and respiratory rate were 99.8ЊF, 60 beats/min, and 24 breaths/min, respectively. His mucus membranes were hyperemic and tacky with a capillary refill time of 1.5 seconds. The peripheral pulses were weak, the distal extremities were cold, and hypalgesia was present. No menace response was obtained in either eye, and pupillary light response was slow bilaterally. Cardiac and thoracic auscultation were normal. Borborygmi were decreased, and abdominal distention was present bilaterally. The horse showed intermittent signs of mild abdominal discomfort characterized by a regular pawing and looking at his flanks. Rectal palpation revealed a gas-distended large colon. Nasogastric intubation did not yield marked reflux. Abdominocentesis yielded grossly and cytologically normal peritoneal fluid. Urinalysis was unremarkable. Attempts to perform a sonographic evaluation of the abdomen were unsuccessful because of the horse's behavior. A CBC showed a PCV of 61% (reference range, 32-52%), a total protein concentration of 7.4 g/dL (reference range, 4.6-6.9 g/dL), and a white blood cell count of 1.39 ϫ 10 3 cells/L (ref-Medicine 0891-6640/03/1702-0019/$3.00/0 erence range, 5.5-12.5 ϫ 10 3 cells/L) with 26% segmented neutrophils (reference range, 30-65%) and 6% band cells (reference range, 0-2%) with toxic changes. Hypochloremia (91 mg/dL; reference range, 94-102 mg/dL), hypocalcemia (9.99 mg/dL; reference range, 10.7-13.4 mg/ dL), hypomagnesemia (0.91 mg/dL; reference range, 1.6-2.5 mg/dL), and hyperglycemia (191 mg/dL; reference range, 72-114 mg/dL) were shown on clinical chemistry evaluation. The plasma creatinine concentration was increased at 2.23 mg/dL (reference range, 0.6-1.8 mg/dL), and the lactate concentration was 13.6 mol/L (reference range, Ͻ2 mol/L). Because the horse's...

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mentioning

confidence: 63%

Clostridium sordelli Infection as a Suspected Cause of Transient Hyperammonemia in an Adult Horse

Desrochers¹,

Dallap²,

Wilkins³

2003

J Vet Int Med

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“…Transient HA has been reported in Irish wolfhound pups and a similar syndrome has been observed in a mature German Shepherd dog (Meyer et al . 1996; Lobetti et al . 1997; Zandvliet and Rothuizen 2007).…”

Section: Discussionmentioning

confidence: 99%

“…Portosystemic shunts were considered unlikely, as survivors recovered completely and permanently and post mortem findings in nonsurvivors were not supportive of the diagnosis (Buonanno et al 1988;Fortier et al 1996). Transient HA has been reported in Irish wolfhound pups and a similar syndrome has been observed in a mature German Shepherd dog (Meyer et al 1996;Lobetti et al 1997;Zandvliet and Rothuizen 2007). Affected pups show no clinical signs and NH 4 + concentrations normalise at age 3-4 months and the authors suspected that a transient defect in NH4 + metabolism as the underlying cause (Zandvliet and Rothuizen 2007).…”

Section: Discussionmentioning

confidence: 99%

Putative intestinal hyperammonaemia in horses: 36 cases

Dunkel¹,

Chaney

Dallap‐Schaer³

et al. 2011

Equine Veterinary Journal

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“…This disorder is thought to be due to a defective mitochondria1 ornithine transport protein, required in urea synthesis, resulting in hyperammonaemia and hyperornithinaemia. Transient hyperammonaemia has been described in a mature German Shepherd dog which presented with severe generalised seizures (Lobetti et al 1997). The dog was normoammonaemic during seizures, but developed severe hyperammonaemia when dosed with 100 mgkg bwt of ammonia.…”

Section: Discussionmentioning

confidence: 99%

Encephalopathy with idiopathic hyperammonaemia and Alzheimer type II astrocytes in Equidae

Hasel

Summers

Lahunta

1999

Equine Veterinary Journal

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Summary In 3 mature female horses of varying breeds, episodes of colic and depression for 1–4 days preceded an encephalopathic disorder with maniacal behaviour, anxiety, profuse sweating and, in one case, terminal opisthotonus. Blood ammonia levels were elevated approximately 10‐fold. At necropsy, there were gastrointestinal serosal and mesenteric haemorrhages. Histologically, all 3 cases revealed diffuse Alzheimer type II astrocytes in the cerebral grey matter. Alzheimer type II astrocytes were glial fibrillary acidic protein (GFAP) negative or only weakly positive, weakly S‐100 positive, and vimentin negative. In the absence of primary hepatic and/or renal lesions, an increase in intestinal ammonia absorption due to ileus or increased ammonia production by colonic bacteria is hypothesised.

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Transient hyperammonaemia in an adult German shepherd dog : case report

Cited by 7 publications

References 4 publications

Clostridium sordelli Infection as a Suspected Cause of Transient Hyperammonemia in an Adult Horse

Clostridium sordelli Infection as a Suspected Cause of Transient Hyperammonemia in an Adult Horse

Putative intestinal hyperammonaemia in horses: 36 cases

Encephalopathy with idiopathic hyperammonaemia and Alzheimer type II astrocytes in Equidae

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