Right Ventricular and Saphenous Vein Thrombi Associated with Sepsis in a Quarter Horse Foal

Abstract

A 41-kg, 12-hour-old Quarter Horse filly presented to the Boren Veterinary Medical Teaching Hospital for a 12-hour history of weakness and recumbency. The mare had a history of premature lactation and presumptive placentitis, which was treated with trimethoprim-sulfamethoxazole by the referring veterinarian. The filly was born at 315 days gestation; parturition was unattended. The filly was found recumbent and unable to stand. Before referral, the attending veterinarian administered 1 L of colostrum via nasogastric tube. Upon presentation to the veterinary teaching hospital, the filly was recumbent and lethargic with intermittent bouts of hyperresponsiveness. Rectal temperature was 94°F, heart rate was 132 beats per minute, and respiratory rate was 24 breaths per minute. A grade 3/5 systolic murmur was auscultated over the left heart base. Mucous membranes were hyperemic with a capillary refill time of approximately 2 seconds. Abrasions were present along the gingiva and around the eyes and muzzle. Petechiae were observed in both pinnae. The foal's distal limbs were cool and edematous, peripheral pulses were weak, and the coronets of all 4 feet were circumferentially dark red.Presumptive diagnoses of neonatal encephalopathy and sepsis were made. An IV jugular catheter was placed. Blood was collected for bacterial culture and sensitivity, CBC, fibrinogen concentration, serum biochemistry, and quantification of serum immunoglobulin G (IgG) concentration. The CBC disclosed immature (band) neutrophilia (558 bands/lL; reference range, <200 bands/lL) and toxic polymorphonuclear leukocytes. A biochemistry profile identified hypoproteinemia (3.8 g/dL; reference range, 5.6-8.0 g/dL) characterized by hypoglobulinemia (1.1 g/dL; reference range, 2.6-5.6 g/dL), azotemia (creatinine, 4 mg/dL; reference range, 1.2-2.0 mg/dL), hypoglycemia (37 mg/ dL; reference range, 70-120 mg/dL), hypernatremia (156 mEq/L; reference range, 130-146 mEq/L), hyperchloremia (112 mEq/L; reference range, 95-110 mEq/ L), and increased creatine kinase activity (40016 IU/L; reference range, 20-500 IU/L). Quantification of IgG a concentration was consistent with failure of passive transfer (IgG < 400 mg/dL). Neonatal sepsis score was calculated to be 18.1 Arterial blood gas sampling was not attempted because of limb edema and weak peripheral pulses. Blood pressure measured using an oscillometric blood pressure monitor b applied to the middle coccygeal artery yielded a mean arterial pressure of 70 mmHg.Initial medical treatment consisted of a plasma c transfusion (25 mL/kg), IV fluids (1 L bolus of 0.45% sodium chloride followed by 0.45% sodium chloride with 10% dextrose at 6 mg/kg/min), broad spectrum antimicrobials (ceftiofur, d 10 mg/kg IV q6h), dimethyl sulfoxide e (1 g/kg/d diluted to a 10% solution IV), thiamine (10 mg/kg IV q24h), and magnesium sulfate (25 mg/kg/h). After plasma c transfusion, quantification of serum IgG a concentration indicated persistent hypogammaglobulinemia (IgG, 400-800 mg/dL); an additional plasma c transfusion (25 mL/kg)...

Pulmonary embolism as a complication after abdominal surgery and colitis in a foal

“…Echocardiography could have been considered in this case for detection of systemic thrombus formation but is more indicated if there is a clinical suspicion of endocarditis (Banse et al . ).…”

“…Ultrasonographic monitoring of every catheter could be seen as excessive; however, application in high risk patients such as this foal could be appropriate, as early removal and application of therapy are the most important factors for successful treatment and outcome. Echocardiography could have been considered in this case for detection of systemic thrombus formation but is more indicated if there is a clinical suspicion of endocarditis (Banse et al 2012).…”

Hyperammonemic Encephalopathy Associated with Portal Vein Thrombosis in a Thoroughbred Foal

“…12,13 Experimental bacteremia and endotoxemia induce intravascular fibrin deposition in kidneys, lungs, liver, and brain, manifesting clinically as disseminated intravascular coagulation (DIC), a syndrome frequently observed in septicemic and endotoxemic patients. 13 Consumptive coagulopathies have been observed in septicemic foals, [14][15][16][17] and in 1 study, evidence of DIC and microvascular thrombosis were identified in the tissues of 28/32 septic nonsurviving foals. 15 When compared with healthy foals, septic foals have lower aPC and ATIII activities and higher PAI-1, TNF-a, and interleukin-6 (IL-6) activities, suggesting that sepsis induces prothrombotic, antifibrinolytic shifts in hemostasis that may contribute to systemic hypercoagulation and DIC.…”