Study Case - Hyponatremia in a Foal

Matthew R. Barber, DVM, PhD, Heather L. Tarpley, DVM, Bruce E. LeRoy, DVM, PhD

Class of 2005 (Barber) and Department of Pathology (Tarpley, LeRoy), College of Veterinary Medicine, University of Georgia, Athens, GA 30602-7388

Signalment – Warm Blood filly, born 3 weeks prematurely.

Presenting Problems - sepsis, possible meconium impaction, hypoxic ischemic encephalopathy (HIE).

Physical examinantion – The foal was recumbent and mildly responsive. She showed evidence of premature development and incomplete ossification of distal limbs. The foal had a sepsis score of 17, characterized by a thickened umbilicus, petechia of the ears, injected mucus membranes, 3+ scleral injection and reddened coronary bands. A complete blood count and biochemical profile revealed a leukocytosis with a left shift, monocytosis, hyperfibrinogenemia, hypoglycemia, hypernatremia, hyperchloremia, and alkalosis.

Laboratory data -

Problems:

1. Leukocytosis consisting of a mature neutrophilia with a left shift, monocytosis and increased fibrinogen. The severe leukocytosis with increased fibrinogen was consistent with acute inflammation. The source of the inflammation was thought to be an in utero infection such as placentitis, which may also have been an inciting factor for the foals premature birth. The monocytosis is also most likely due to inflammation/infection.

2. Hypoproteinemia. The foal had failure of passive transfer which resulted in a decreased globulin concentration and contributed to the hypoproteinemia.

3. Hypoglycemia. Likely causes in this foal include her being a neonatal foal born 3 weeks prematurely, as well as sepsis.

4. Elevated bicarbonate (HCO₃) concentration. The very mildly increased bicarbonate concentration suggests alkalosis. In this foal, considerations include respiratory (hyperventilation due to sepsis) and metabolic (decreased renal excretion of bicarbonate due to dehydration) mechanisms.

5. Hypocalcemia. Some potential causes in this foal include sepsis and gastrointestinal disease.

6. Elevated creatine kinase (CK) activity. Increased CK activity is most likely a reflection of muscle damage, possibly due to prolonged recumbency.

7. Elevated gamma-glutamyl transferase activity (GGT). GGT activity may be increased in cholestatic/biliary tract disease, but in this case the very mild increase may be due to ingestion of a small amount of colostrum, even though the foal was not nursing well.

8. Electrolyte abnormalities: Day 1 – Hypernatremia and hyperchloremia. Most likely due to dehydration, as the foal was suckling poorly at presentation. Intravenous fluid supplementation included 5% dextrose, 0.45% sodium chloride, and lactated Ringers solution. This fluid was chosen to assist correction of the hypernatremia, hyerpchloremia and hypoglycemia. The biochemical abnormalities had normalized by Day 5.

9. Electrolyte abnormalities: Day 20 – Hyponatremia and hypochloremia. A subsequent serum biochemical profile indicated a significant hyponatremia and hypochloremia of 114 mmol/L and 74 mmol/L respectively. Rule-outs for hyponatremia and hypochloremia include 1) renal disease, 2) uroabdomen, 3) syndrome of inappropriate antidiuretic hormone secretion (SIADH), and 4) excess water consumption.

Additional Diagnostics:

A complete urinalysis, serum and urine creatinine concentrations, urine GGT activity, and urine fractional excretion of electrolytes were performed to rule out renal disease. These diagnostics were performed due to concerns about renal damage subsequent to aminoglycoside antibiotic treatment, or possibly a congenital renal abnormality. The fractional excretion of sodium, chloride, and potassium were within reference limits, as were the serum and urine creatinine concentrations. Urinary GGT activity was measured as an early biomarker of renal tubular epithelial cell damage and was within the reference interval. The kidneys were scanned via ultrasound and showed no abnormal findings. Based on these results, renal disease was considered to be very unlikely. Additionally, an abdominal ultrasound was performed. There was no evidence of fluid in the peritoneal space and the bladder was within normal limits, suggesting that a rupture of the urinary tract was very unlikely.

In animals with inappropriate antidiuretic hormone secretion (SIADH), the release of ADH occurs in the absence of normal stimuli, thus causing an extremely high urine osmolality. In this foal, the urine osmolality of 68 mOsm made SIADH very unlikely, as the osmolality in these cases is usually greater than 300 mOsm. This information allowed differentiation of SIADH from psychogenic polydypsia in this foal. The foal’s urine specific gravity of 1.002, combined with the urine osmolality of 68, are most compatible with a diagnosis of inappropriate water consumption or psychogenic polydypsia. Psychogenic polydypsia was the provisional diagnosis in this foal, as it had been hospitalized for some time and commonly drank large amounts of water from the mare’s water bucket.

Therapy:

The foal was treated with intravenous antibiotics (penicillin and amikacin) and hyperimmune plasma for sepsis. Glucose-containing fluids were administered to correct hypoglycemia.

Conclusions:

The foal responded well to medical management of her sepsis, prematurity, hypoxic ischemic encephalopathy and meconium impaction. The foal was placed in a stall with its mother when she was able to stand and nurse. Treatment for hyponatremia due to psychogenic polydypsia is to eliminate the source of water for the foal as well as supplement sodium and chloride. The foal should be receiving an adequate amount of fluid from nursing alone, around 20% of her body weight, so she should not need to consume any water. Once the foal was prevented from drinking water from the mare’s water bucket and given oral supplementation of sodium and chloride, her hyponatremia and hypochloremia normalized.

References:

1. Spurlock SL, Furr M: Fluid Therapy. In Koterba AM, Drummond WH, Kosch PC (eds): Equine Clinical Neonatology. Philadelphia, Lea & Febiger, 1990, pp. 671-699.

2. Madigan JE (ed): Manual of Equine Neonatal Medicine, 3rd ed. Woodland, California, Live Oak Publishing, 1997.

3. Rose BD: Clinical Physiology of Acid-Base and Electrolyte Disorders. New York, McGraw-Hill, 1984, pp. 482-508.

Acknowledgement:

The image "Wading Horse" is from the Île de Sable website of the Nova Scotia Museum of Natural History and the Sable Island Preservation Trust.

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