Summary The clinical findings and outcome of 161 horses diagnosed with 174 episodes of nephrosplenic entrapment (NSE) were reviewed retrospectively. The median age at presentation was 5 years (9 months to 24 years), and duration of colic was 2–92 h. Nasogastric reflux was present in 49 of 113 horses (43.4%) and was significant (≥ 21) in 32 (28.3%) horses. The recurrence rate was 13/161 (8.1%). Thirteen horses (13/174, 7.5%) had other lesions including small intestinal obstruction (4), 360° large colon torsion (5), gastric rupture (2), thromboembolic colic (1) and small colon infarction (1). Of 115 cases, in 107 horses treated by surgery alone, 2 horses required a large colon resection, and 8 (8/107, 7.5%) horses died or were subjected to euthanasia. Twenty‐six of 35 horses (74%) were successfully corrected by rolling under general anesthesia and, of the 9 horses taken to surgery after rolling, 4 had other lesions and 2 were corrected at surgery. Phenylephrine was used in 20 of 35 horses that were rolled and 2 horses required surgery after rolling with phenylephrine. Five horses were jogged after phenylephrine administration and all were successfully corrected. Eleven horses presented with the left colon located between the spleen and the body wall were treated successfully by fasting and/or i.v. fluids. One horse had a gastric rupture after rolling. The overall success rate was 92.5%. In conclusion, NSE is a condition associated with a good prognosis for medical or surgical correction. A small number of horses may have additional gastrointestinal lesions, which may affect outcome.

Based on MIC for common equine pathogens, administration of gentamicin intra-articularly or by regional intravenous perfusion should be useful for treatment of osteomyelitis.

Oscillations of arterial pressure during sleep are the hemodynamic hallmark of the sleep apnea syndrome. The mechanism of these transient pressure elevations is incompletely understood. To investigate the role of the arterial chemoreflex in the neurocirculatory responses to apnea, we measured mean arterial pressure (MAP; Finapres) and muscle sympathetic nerve activity (MSNA; peroneal microneurography) during voluntary end-expiratory apnea during exposure to room air, 10.5% O2 in N2 (hypoxemia), and 100% O2 (hyperoxia) in 11 healthy men. While the men breathed spontaneously, MSNA (in bursts/min) rose during hypoxemia and decreased during hyperoxia and MAP remained unchanged. During room air exposure, apnea led to a rise of 94 +/- 54% in MSNA total amplitude and a rise of 6.5 +/- 2.1 mmHg in MAP. MSNA and MAP increased by 616 +/- 158% and 10.8 +/- 2.4 mmHg, respectively, during hypoxemic apnea of equal duration (time-matched responses) and by 98 +/- 41% and 4.9 +/- 2.0 mmHg, respectively, during hyperoxic apnea (P < 0.05 for hypoxemic vs. hyperoxic apnea for both). Thus, in awake healthy humans, activation of the arterial chemoreflex by hypoxemia appears to contribute importantly to the sympathetic and blood pressure responses to apnea.

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