Perinatal foreign body aspiration in a Thoroughbred foal

Abstract

A 65-kg newborn Thoroughbred colt was referred approximately 30 min after birth. The foal was born from dystocia characterised by premature placental separation (i.e. 'red bag'). Following birth, the foal appeared poorly responsive to unresponsive, and signs of paddling consistent with seizure activity were observed. A single dose of i.v. diazepam (0.8 mg/kg bwt, Diazepam, Hospira Inc.) was administered, and intranasal oxygen (IN O2) therapy was initiated on the farm and maintained during transportation to the referral hospital. Tracheal intubation and cerebro-cardiopulmonary resuscitation were not performed since the foal was breathing spontaneously. CLINIC AL FINDING S AND TRE ATMENTOn arrival at the clinic, the foal was profoundly lethargic and recumbent and only occasionally showed brief states of arousal. Pupillary light and palpebral reflexes were present bilaterally. Suckle reflex was absent. Rectal temperature was 35.8°C. Pale and dry oral mucous membranes, prolonged capillary refill time (CRT 3 s), weak brachial arterial pulse, prolonged jugular refill time, passive enophthalmos and cold limb extremities were supportive of abnormal peripheral tissue perfusion. Heart rate was within normal limits, with regular rhythm upon auscultation. A grade 4/6 systolic murmur was auscultated with point of maximum intensity on the left side. Respiratory system examination revealed moist rattles upon tracheal and thoracic auscultation. Respiratory rate and effort were within normal limits. Rib cage and appendicular systems examination did not show any evidence of trauma or congenital abnormalities. The foal's coat appeared normal and without evidence of meconium staining. Blood samples were drawn via direct jugular puncture for the measurement of packed cell volume (PCV), total solids (TS), glucose, electrolyte and creatinine concentrations. Results indicated moderate hyperglycaemia (13.6 mmol/L; ref. range 4.4-10.0 mmol/L), significant hypercreatinaemia (>1525 µmol/L; ref. range 61-152 µmol/L), moderate leukopenia (5.3 × 10 9 /L; ref. range 7-12 × 10 9 /L) and mildly increased PCV and TS, 45.4% (ref. range 30-44%) and 58 g/L (ref. range 54-76 g/L), respectively. Thoracic and abdominal ultrasonography was performed, which showed diffuse bilateral, coalescent, comet tail artefacts, suggestive of pulmonary consolidation, extending from caudoventral to caudodorsal lung fields. The remainder of the examination was within normal limits for the patient's age. Based on historical, clinical and laboratory findings, a primary diagnosis of neonatal encephalopathy was made. An intravenous over-the-wire catheter (Arrow International Inc.) was aseptically placed in the patient's right jugular vein and a blood sample collected for haemoculture. According to physical examination findings, resuscitation fluid therapy was started with crystalloid isotonic solution (lactated Ringer's solution -LRS, Dechra Veterinary Products) at 30 ml/kg for a total of 2 litres administered as a bolus. Maintenance fluid therapy was started with LRS at 2....

Practical management and treatment of foals with neonatal encephalopathy/neonatal maladjustment syndrome in an ICU setting

“…In this issue, Migliorisi et al. describe a case where a colt displayed signs compatible with NE secondary to perinatal asphyxia (Migliorisi et al., 2023).…”

“…Other terminologies have been used to describe the disease, including hypoxic ischaemic encephalopathy and perinatal asphyxia; however, these imply a specific pathogenesis relating to hypoxia, ischaemia and asphyxia, which may not be recognised in all cases (Ferriero, 2004;Toribio, 2019;Wong et al, 2011). In this issue, Migliorisi et al describe a case where a colt displayed signs compatible with NE secondary to perinatal asphyxia (Migliorisi et al, 2023).Reviews, case reports and ongoing investigations demonstrate how our understanding of the disease in foals has evolved and continues to do so (Diesch & Mellor, 2013;Madigan et al, 2012;Mahaffey & Rossdale, 1957;Wong et al, 2011). In newborn babies, the causes of NE include hypoxic ischaemic encephalopathy, perinatal infections, placental abnormalities, metabolic disorders, coagulopathies and neonatal vascular stroke (Aslam et al, 2019).…”

“…Other terminologies have been used to describe the disease, including hypoxic ischaemic encephalopathy and perinatal asphyxia; however, these imply a specific pathogenesis relating to hypoxia, ischaemia and asphyxia, which may not be recognised in all cases (Ferriero, 2004;Toribio, 2019;Wong et al, 2011). In this issue, Migliorisi et al describe a case where a colt displayed signs compatible with NE secondary to perinatal asphyxia (Migliorisi et al, 2023).…”