Background It is highly desirable to assess the probability of survival in sick neonatal foals upon admission. The foal survival score (FSS) is a published scoring system used to estimate the probability of survival in hospitalized neonatal foals <4 days old. Hypothesis/Objectives To evaluate the ability of the FSS to predict survival in older foals from a geographically different area compared to the original study. Animals Five‐hundred ninety hospitalized neonatal foals ≤14 days of age. Methods Retrospective Danish‐Swedish multicenter study that included details of signalment, history, clinical examination, laboratory results, necropsy findings, and outcome. Scores and score variables were compared between survivors and nonsurvivors using logistic regression. The optimal cutoff and its test parameters were calculated using a receiver operator characteristic curve. Results Prematurity, cold extremities, ≥2 infectious or inflammatory sites, blood glucose concentration, and total white blood cell counts were significantly associated with nonsurvival ( P ≤ .02). The optimal cutoff to predict survival was ≥6, resulting in sensitivity 78%, specificity 58%, 92% positive predictive value, and 31% negative predictive value. The test performed equally well in foals <4 days old compared to those 4‐14 days old. Conclusions and Clinical Importance Using the suggested optimal cutoff of ≥6, the FSS performed moderately well and may aid in early determination of prognosis for survival. However, the FSS did perform differently in another population and therefore should be assessed under local conditions so that its diagnostic potential is not overestimated.

Background Serum amyloid A (SAA) has been reported to hold promise as diagnostic and prognostic marker in foals. This has not been investigated thoroughly. Objectives Evaluate admission SAA concentrations as predictor of sepsis and outcome. Animals Five hundred and ninety hospitalized foals <14 days old. Methods Retrospective multicenter study. Foals were scored with sepsis and survival scores, grouped according to health category (septic, sick but nonseptic, uncertain sepsis status) and outcome; septic foals were further categorized according to severity (normal sepsis, severe sepsis, and septic shock). SAA was compared between groups using Mann‐Whitney test and Kruskal‐Wallis test. Receiver operating characteristic curves identified optimal SAA cut off values for detecting sepsis and predicting outcome. Results Admission SAA concentrations differed significantly between sick nonseptic foals (312.1 ± 685.4 mg/L) and septic foals (1079.7 ± 1254.5 mg/L) and increased with increasing sepsis score. SAA did not differ between sepsis severity groups. The optimal cut off for sepsis detection was 1050 mg/L (sensitivity 30.2%, specificity 90.7%). Admission SAA concentrations were lower in surviving (435.0 ± 723.6 mg/L) compared to nonsurviving foals (1062.7 ± 1440.1 mg/L) and decreased with increasing survival score. The optimal cut off for nonsurvival prediction was 1250 mg/L (sensitivity 22.1%, specificity 90.8%). Conclusions and Clinical Importance SAA concentration was higher in septic foals and nonsurviving foals. Even though optimal cut offs for SAA to detect sepsis and predict outcome had low sensitivity, they had good specificity. SAA can therefore be used as a marker to rule out sepsis and nonsurvival.

An 8-year-old, 167 kg mule was scheduled for surgical treatment of a hip luxation in lateral recumbency. During general anaesthesia, after a short phase of spontaneous breathing followed by mechanical ventilation at standard settings, the mule developed hypoxaemia (arterial oxygen partial pressure (PaO 2 ) 8.3 kPa). First, respiratory rate, tidal volume and fraction of inspired oxygen (FiO 2 ) were increased; 5 cmH 2 0 of positive end-expiratory pressure (PEEP) and nebulized salbutamol were administered. Second, three vital capacity manoeuvres were executed (tidal volume of 20 ml kg −1 ). No immediate improvement in PaO 2 (8.0 kPa) was observed. A further recruitment manoeuvre with increased peak inspiratory pressure (up to 44 cmH 2 O) and PEEP (25 cmH 2 O) was performed. Over the following 120 min, PaO 2 increased progressively. The mule recovered without complications. This case reports that mules can develop hypoxaemia during general anaesthesia that can be treated with recruitment manoeuvres. However, the effect may not be immediate.This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

ObjectivesTo investigate whether morphine causes a change in mean arterial blood pressure (MAP) heart rate (HR) and oxygen extraction (OE) rate in healthy horses anesthetized with isoflurane and a dexmedetomidine infusion.Material and methodsThe study design was prospective clinical, randomized, blinded two groups including 33 horses. All horses were sedated with romifidine IV, and anesthesia was induced with midazolam IV and ketamine IV and maintained with isoflurane in oxygen and medical air and a dexmedetomidine infusion. As a baseline venous and arterial blood, HR and MAP were sampled. Thereafter either morphine 0.1 mg kg−1 IV or an equivalent volume of NaCl 0.9% IV was administered. HR and MAP were then further sampled for 5 min before venous and arterial blood was again sampled. OE was calculated based upon arterial and venous blood gas analysis. To evaluate the change in minimum MAP, mean HR, and OE, the differences between baseline and observation period values were further termed delta MAP, delta HR, and delta OE. Individual delta MAPs were normalized to the minimum baseline value and are reported as a percentage. Alpha was set to 0.05. Confidence intervals 95% (CI) were calculated for delta MAP, delta HR, and delta OE within groups, and for the difference between groups.ResultsThe 95% CIs for delta MAP (%), delta HR (min−1), and delta OE (mL/dL) in the morphine group were −20.5 to −9.0, 0.6 to 3.1, and −0.1 to 0.6 and in the placebo group were −17.4 to −10.1, 0.2 to 2.0, and −0.2 to 0.3, respectively. The 95% CI for the differences in delta MAP (%), delta HR (min−1), and delta OE (mL/dL) were −5.5 to 7.6, −2.3 to 0.7, and −0.7 to 0.2, respectively. The minimum MAP of one horse in the morphine group decreased around 50% between baseline and observation period with almost unchanged OE and HR.Conclusion and clinical relevanceThe effects of morphine 0.1 mg kg−1 IV on HR, MAP, and OE in healthy horses anesthetized with isoflurane and a CRI of dexmedetomidine are minimal.