Technician Update

Neonatal foal with uroperitoneum and severe electrolyte and metabolic imbalances

By Cheyenne Wilkins, RVT, VTS-EVN

A 4-day-old Quarter Horse colt was evaluated for progressive lethargy, dysuria, sheath edema and poor nursing behavior. The owner had observed abnormal urination approximately 48 hours prior to presentation, followed by rapid clinical deterioration. The foal was born after an unremarkable delivery and initially nursed well.

On presentation, the foal was weak, ataxic and obtunded. Physical examination revealed mild tachycardia, slightly tacky mucous membranes, umbilical thickening, marked sheath edema and reduced borborygmi. Initial ultrasonography identified a markedly distended urinary bladder with no evidence of free abdominal fluid. Following urinary catheterization and decompression, repeat ultrasonography demonstrated progressive accumulation of abdominal fluid, raising suspicion for uroperitoneum secondary to urinary tract rupture.

Shortly after admission, the foal developed intermittent seizure activity characterized by rigidity, nystagmus, muscle fasciculations and collapse. Laboratory evaluation revealed hemoconcentration and significant electrolyte abnormalities, including severe hyponatremia and hypochloremia, with potassium at the upper end of the reference range. These findings were consistent with uroperitoneum, in which diffusion of urine into the peritoneal cavity results in dilutional electrolyte disturbances and progressive metabolic imbalance.

Hyponatremia is a particularly critical abnormality in neonatal foals, as sodium plays a key role in maintaining neuronal membrane potential and cerebral osmotic balance. Severe decreases in serum sodium can lead to cerebral edema, increased intracranial pressure and neurologic dysfunction, including seizures. In this case, the degree of hyponatremia was considered a primary contributor to the foal’s neurologic signs. While uroperitoneum is associated with azotemia and hyperkalemia, pronounced neurologic manifestations are less common, highlighting the clinical significance of the electrolyte disturbance in this patient.

Based on clinical findings and diagnostic results, the foal was diagnosed with uroperitoneum with secondary hyponatremic encephalopathy, along with suspected neonatal maladjustment syndrome (NMS). Uroperitoneum in neonatal foals most commonly results from rupture of the urinary bladder during parturition, particularly in male foals, due to increased intravesical pressure as the fetus passes through the birth canal. Affected foals are often normal at birth but typically develop clinical signs within 24 to 48 hours after birth. Signs include lethargy, abdominal distension, dysuria and progressive electrolyte abnormalities.

NMS, commonly referred to as “dummy foal syndrome,” is a neurologic condition associated with
periparturient hypoxia or ischemia. Affected foals may exhibit abnormal mentation, failure to nurse, disorientation, and intermittent seizure activity. Prognosis generally is favorable with prompt recognition and supportive care.

Given the foal’s initial instability and severe electrolyte derangements, he was considered a high risk for surgical intervention, so the staff focused on stabilization and gradual correction of metabolic abnormalities. Diluted isotonic saline was administered to safely increase sodium levels and avoid complications associated with rapid correction. Glucose supplementation was provided to address inadequate nursing, and calcium was administered to support cardiac function. Seizure activity was managed with benzodiazepines, and anti-inflammatory and gastroprotective therapies were initiated.

A Madigan squeeze procedure was performed to address suspected NMS, resulting in improved mentation and nursing behavior. As abdominal fluid increased during fluid therapy, an abdominal drain was placed to reduce ongoing electrolyte shifts and allow time for the urinary tract to heal.

Over the course of hospitalization, the foal demonstrated steady neurologic and metabolic improvement. Electrolyte abnormalities resolved with controlled correction, and serial ultrasonography confirmed resolution of abdominal fluid without further evidence of urine leakage. The urinary catheter and abdominal drain were removed following confirmation of normal bladder function.

After 8 days of hospitalization, the foal was discharged; he was nursing independently, urinating normally and exhibiting no residual neurologic deficits. Follow-up confirmed continued normal growth and appropriate development.

This case highlights the significant role of electrolyte imbalances in the clinical progression of uroperitoneum in neonatal foals. Severe hyponatremia can result in life-threatening neurologic complications, and careful, controlled correction is essential to avoid secondary injury. Early recognition, close monitoring, and targeted stabilization allowed for a successful outcome without surgical intervention. MeV

Related: Stabilizing a Foal Born Via Emergency Cesarean-Section follows a technician through the first hours of another critical neonatal case.