Pulse Oximetry For Estimation Of Oxygenation In Dogs With Experimental Pneumothorax

The purpose of this study was the evaluation of pulse oximetry for estimating the oxygen saturation of hemoglobin (S_pO₂) in dogs with pneumothorax. Values for measured by pulse oximetry with transducers on the tongues and toes of six dogs were compared with saturation values (S_aO₂) computed from arterial oxygen tensions (P_aO₂) during experimentally induced pneumothorax (30,45, and 60 ml/kg of ambient air in the pleural space). Values for S_pO₂, S_aO₂, and P_aO₂ decreased with increasing volume of air. Compared to computed S_aO₂ values, S_pO₂ values obtained from the tongue tended to be less variable than those obtained from the toe, but both locations gave valuable information. Pulse oximetry appears to be a useful, relatively inexpensive method of estimating hemoglobin saturation in dogs with experimentally induced pneumothorax, and it appears to have clinical application in management of critical or traumartized dogs.     

Practicality, Usefulness, and Limits of Pulse Oximetry in Critical Small Animal Patients

Pulse oximetry holds the promise of wide application for monitoring and assessing pulmonary function in small animal patients. Although the saturation as read by pulse oximetry (SpO2) has previously been shown to be accurate in healthy dogs, its accuracy and usefulness have not been demonstrated in critical small animal patients. The present study assessed the accuracy and usefulness of a pulse oximeter (Ohmeda Biox 3740, Ohmeda, Louisville, CO) in a small animal intensive care unit. The instrument yielded readings in 48 of 51 attempts in 33 animals (25 dogs, 8 cats). Criteria were developed to reject spurious readings; when these criteria were applied, the actual calculated SaO2 differed from the SpO2 by O.26 +2.2%, with a correlation of 0.87 (p<0.0001). The 95% confidence interval was +4.4%, comparable to the accepted level in humans. No ill effects from SpO2 were apparent in the patients, and the instrument was useful in monitoring the progress of critical animals. However, uncritical use of the oximeter could have led to gross patient mismanagement, as SpO2 readings as much as 29% different from SaO2 were sometimes obtained.     

Evaluation of Transmittance and Reflectance Pulse Oximetry in a Canine Model of Hypotension and Desaturation

Ten, anesthetized dogs were instrumented with three pulse oximeter probes; two lingual transmittance probes and one rectal reflective probe. Arterial oxygen desaturation was produced by decreasing the inspired oxygen concentration. Hypotension was produced with an infusion of nitroprusside. Simultaneous pulse oximeter readings (SpO₂) were compared to co-oximeter measured arterial saturation (SaO₂) collected over a range of SaO₂ (50–100%) and mean arterial pressures (40–100mmHg). Each of the monitors and means of evaluating SpO₂ studied provided accurate SpO₂ measurements over a range of mean arterial pressure from 40–100mmHg. All of the monitors tested tended to overestimate the SaO₂ when the arterial saturation was less than 70%.     

Evaluation of the Nonin 8600V Veterinary Pulse Oximeter in Anesthetized Horses

S_pO₂ values from the Nonin 8600V veterinary pulse oximeter, using a lingual clip-type, transmittance sensor applied to the tongue, were compared to directly-measured S_aO₂ values from a co-oximeter, calibrated for equine blood, in 5 halothane-anesthetized horse. Normocapnia was maintained with controlled ventilartion. The inspired oxygen concentration was varied by mixing nitrogen in oxygen to obtain S_pO₂ readings of approximately 60, 65, 70, 75, 80, 85, 90, 92, and 100%. At the time of each S_pO₂ recording, an arterial blood sample was collected for immediate analysis of S_aO₂. A total of sixty paired measurements were made. The results showed excellent data correlation with a bias (precision) of 0.55 (2.57) and an R-value of 0.98 over the entire S_aO₂ range tested. Based on these findings, the Nonin 8600V veterinary pulse oximeter, with the lingual sensor, performed accurately and reliably, and appears to be suitable for clinical use in anesthetized horses. (Vet Emerg & Crit Care, 1999: 13–18)     

Evaluation of Pulse Oximetry as a Continuous Monitoring Technique in Critically Ill Dogs in the Small Animal Intensive Care Unit

To assess the clinical applicability of pulse oximetry in the intensive care setting, a comparison was made of arterial hemoglobin saturation values determined by in vitro oximetry (SaO₂) and pulse oximetry (SpO₂) in 21 critically ill dogs. Single SaO₂ measurements were compared to simultaneously obtained SpO₂ readings. The correlation between these two methods was statistically significant (r = 0.8944, p = 0.0001). In addition, heart rates read by the pulse oximeter were compared to simultaneously obtained electrocardiograms (ECG). The correlation between these two methods was statistically significant (r = 0.9966, p = 0.0001). The pulse oximeter was easy to use, and recorded trends in oxygenation virtually instantaneously. Pulse oximetry appears to be an accurate and practical technique for the continuous non-invasive monitoring of oxygenation in critically ill dogs in the intensive care unit.     

Cantharidin Toxicosis in Horses

Cantharidin toxicosis in horses has become an increasing problem in certain regions of the United States. Toxicosis occurs when horses ingest alfalfa hay or products that are contaminated with "blister" beetles. Clinical signs may vary from depression to severe shock and death, depending upon the amount of toxin ingested. The most frequently observed signs include varying degrees of abdominal pain, anorexia, depression, and signs suggestive of oral irritation. Many horses make frequent attempts to void urine. Less commonly observed signs include synchronous diaphragmatic flutter and erosions of the oral mucosal surfaces. Clinical laboratory abnormalities suggestive of cantharidin toxicosis include persistent hypocalcemia and hypomagnesemia, development of hypoproteinemia, microscopic hematuria, and mild azotemia with inappropriate urine specific gravity. Chemical analysis for cantharidin is accomplished by evaluation of urine or stomach contents. Treatment of cantharidin toxicosis is symptomatic, but must include removal of toxin source. Gastrointestinal protectants, laxative, intravenous fluids, analgesics, diuretics, calcium gluconate, and magnesium are all included in the treatment regimen. Early and vigorous therapy is imperative if it is to be successful. In horses that remain alive for several days, persistence of elevated heart and respiratory rates and increasing serum creatine kinase concentration are associated with a deteriorating condition. Prevention is aimed at timely harvesting of alfalfa hay. Hay fields should be inspected for the presence of beetle clusters before harvesting. Involved areas of the field should not be harvested.     

Gastric Neoplasia in Horses

Background: Gastric neoplasia of horses is incompletely described.
Objective: Provide history, clinical signs, and clinicopathological and pathological findings associated with gastric neoplasia in horses.
Animals: Twenty-four horses with gastric neoplasia.
Methods: Retrospective study. History, clinical signs, and clinicopathological and pathologic findings in horses diagnosed histologically with gastric neoplasia were reviewed.
Results: Horses ranged in age from 9 to 25 years (median 18 years at presentation). There was no apparent breed or sex predisposition. The most common presenting complaints were inappetance (17/24), weight loss (14/24), lethargy (7/24), hypersalivation (7/24), colic (5/24), and fever (5/24). The most consistent clinical signs were tachypnea (10/19), decreased borborygmi (8/19), and low body weight (7/17). Useful diagnostic tests included rectal examination, routine blood analysis, gastroscopy, abdominocentesis, and transabdominal ultrasound examination. Anemia was the most common hematologic abnormality encountered (7/19), and hypercalcemia of malignancy was seen in 4/16 horses. Squamous cell carcinoma was the most common tumor identified (19/24), and was most often (14/19) found as a single ulcerated, necrotic mass in the nonglandular portion of the stomach. Other gastric neoplasms encountered were leiomyoma (n=2), mesothelioma (n=1), adenocarcinoma (n=1), and lymphoma (n=1). Metastatic neoplasia was found in 18/23 horses. The median time from onset of clinical signs to death was 4 weeks, and all horses died or were euthanized because of gastric neoplasia.
Conclusions: Squamous cell carcinoma is the most common primary gastric neoplasia in horses. The survival time after diagnosis of gastric neoplasia in horses is short.