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Blood: idiopathic hyperammonemia

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Introduction

  • Cause: idiopathic hyperammonemia has been documented as a rare complication of severe GI disease in adult horses, typically those with enterocolitis and/or colic.  
  • Significantly elevated blood ammonia (>150 mmol/L) in affected horses is not associated with elevations in other standard biochemical markers of liver disease. 
  • It is theorized that the high blood ammonia occurs due to massive enteric ammonia release associated with the primary GI disease that overwhelms the livers ability to metabolize the ammonia. 
  • Overgrowth of urease producing bacteria within the colon and cecum have been implicated.
  • Signs: acute encephalopathy associated with GI disease.
  • Diagnosis: biochemical evaluation, liver function tests, cerebrospinal fluid analysis, fecal microbiological investigation.
  • Treatment: analgesia, sedation/tranquilization, fluid therapy, 
  • Prognosis: very good if horse successfully treated through acute encephalopathic stage; mortality rates highest in first 72 h of treatment.

Presenting signs

  • Acute encephalopathy associated with concurrent or pre-existing GI disease.

Acute presentation

  • Encephalopathy wide ranging neurologic signs can be seen, including head-pressing, aimless walking, somnia, mania and seizures.
  • Blindness   Eye: blindness - overview  is commonly documented during encephalopathy with this condition.
  • Acute gastrointestinal signs colic   Abdomen: pain - adult  and/or diarrhea   Diarrhea: chronic  .

Geographic incidence

  • Documented in the US and UK, anecdotal reports from other parts of the world.

Age predisposition

  • Mature horses.

Public health considerations

  • Encephalopathic mature horses are potentially highly dangerous to themselves and people around them.

Cost considerations

  • Affected horses need aggressive supportive treatment, hospitalization for control of encephalopathy and intravenous treatment of metabolic abnormalities.

Special risks

  • High risk of acute musculoskeletal catastrophe during encephalopathic episodes.
  • Rarely need anesthesia but some individuals are extremely colicky and refractory to analgesics.
  • Clinicians should be mindful of severe metabolic and acid-base disturbances associated with this condition (metabolic acidosis   Acid-base imbalance  , hypokalemia, hyperglycemia, hyperammonemia) that make them poor anesthetic candidates.

Pathogenesis

Etiology

  • Unknown, but theorized to occur due to massive ammonia production in large intestine that overwhelms the livers ability to detoxify. 
  • Potential role for urease producing bacteria in enterocolitis cases, egClostridium sordelli
  • Temporally the hyperammonemia and encephalopathy seem to be preceded by GI disease.

Specific

Pathophysiology

  • High blood ammonia of enteric origin causes the neurologic signs. 
  • Ammonia disrupts normal neuronal and neurotransmitter physiology within the central nervous system, with subsequent behavioral and encephalopathic changes. 
  • The metabolic status of affected horses (severe metabolic acidemia   Acid-base imbalance  , dehydration, hypoproteinemia   Hypoproteinemia  and endotoxemia   Endotoxemia: overview  ) exacerbates the animal's general condition and complicates therapy.

Timecourse

  • Peracute-acute: 6-48 h from onset of GI disease.

Epidemiology

  • Sporadic disease, only affecting one horse at a time.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Unt V E et al (2012) Gastrointestinal hyperammonaemia in a 35-day-old Warmblood cross filly. Equine Vet Educ 24 (8), 387-391 VetMedResource.
  • Dunkel B et al (2010) Putative intestinal hyperammonaemia in horses: 36 cases. Equine Vet J 43 (2), 133-140 PubMed.
  • Dunkel B (2010) Intestinal hyperammonaemia in horses. Equine Vet Educ 22 (7), 340-345 VetMedResource.
  • Desrochers A M, Dallap B L & Wilkins P A (2003) Clostridium sordelli infection as a suspected cause of transient hyperammonemia in an adult horse. J Vet Intern Med 17 (2), 238-241 PubMed.
  • Hasel K M, Summers B A & De Lahunta A (1999) Encephalopathy with idiopathic hyperammonaemia and Alzheimer type II astrocytes in equidae. Equine Vet J 31 (6), 478-482 PubMed.
  • Peek S F, Divers T J & Jackson C J (1997) Hyperammonaemia associated with encephalopathy and abdominal pain without evidence of liver disease in four mature horses. Equine Vet J 29 (1), 70-74 PubMed.
  • Mair T S & Jones R D (1995) Acute encephalopathy and hyperammonaemia in a horse without evidence of liver disease. Vet Rec 137 (25), 642-643 PubMed.