BackgroundPericardial effusion cytology is believed by many to be of limited value, yet few studies have evaluated its diagnostic utility.ObjectivesTo determine the diagnostic utility of cytologic analysis of pericardial effusion in dogs and to determine if consideration of additional data could improve the diagnostic yield.AnimalsTwo hundred and fifty‐nine dogs with cytologic analysis of pericardial effusion performed between April 1990 and June 2012.MethodsElectronic medical records from a university teaching hospital were retrospectively reviewed; signalment, complete blood count, serum biochemistry, cytologic analysis of pericardial effusion, and echocardiographic data were recorded. Cytology was classified as diagnostic (infectious or neoplastic) or nondiagnostic (hemorrhagic or other) and groups were compared with multiple Student's t‐tests.ResultsCytology was grouped as nondiagnostic (92.3%) or diagnostic (7.7%) and characterized as hemorrhagic (90%), neoplastic (4.6%), infectious (3.1%), or other (2.3%). Overall cytologic analysis of pericardial effusion diagnostic utility was 7.7% and increased to 20.3% if the effusion hematocrit (HCT) <10%; echocardiographic evidence of a mass did not result in a significant increase in the diagnostic utility.Conclusions and Clinical ImportanceThe diagnostic utility of cytologic analysis of canine pericardial effusion is variable depending on the underlying etiology. In this group of dogs, the diagnostic yield of cytologic analysis was greater for pericardial effusion samples in which the HCT was less than 10%.
Objective:To evaluate the ability of arterial hemoglobin oxygen saturation measurement via pulse oximetry (SpO 2 ) to serve as a surrogate for PaO 2 in dogs.Design: Two-part study: prospective observational and retrospective components. Setting: University teaching hospital.Animals: Ninety-two dogs breathing room air prospectively enrolled on a convenience basis. Retrospective evaluation of 1,033 paired SpO 2 and PaO 2 measurements from 62 dogs on mechanical ventilation.Interventions: Dogs with concurrent SpO 2 and PaO 2 measured on room air had a data sheet completed with blood gas analysis. SpO 2 , PaO 2 , and FiO 2 values were collected from medical records of dogs on mechanical ventilation. Measurements and Main Results:Predicted PaO 2 was calculated from SpO 2 using the dog oxyhemoglobin dissociation curve. The correlation coefficient between measured and predicted PaO 2 was 0.49 (P < 0.0001) in room air dogs and 0.74 (P < 0.0001) in ventilated dogs. In room air dogs, Bland-Altman analysis between measured minus predicted PaO 2 versus the average showed a mean bias of −6.0 mm Hg (95% limit of agreement, −35 to 23 mm Hg). The correlation coefficient between PaO 2 /FiO 2 and SpO 2 /FiO 2 ratios was 0.76 (P < 0.0001). After combining data sets, receiver operating characteristic curve analysis showed the optimal cutoff value for detecting hypoxemia (PaO 2 < 80 mm Hg) was an SpO 2 of 95%, with sensitivity and specificity of 77.8% and 89.5%, respectively. Using this cutoff, 6.9% of SpO 2 readings failed to detect hypoxemia, whereas 7.2% predicted hypoxemia that was not present. Conclusions:The SpO 2 was not clinically suitable as a surrogate for PaO 2 , though it performed better in mechanically ventilated dogs. As sensitivity for the detection of hypoxemia was poor, pulse oximetry does not appear to be an acceptable screening test. The SpO 2 /FiO 2 ratio may have value for evaluation of anesthetized dogs on supplemental oxygen. Arterial blood gas analysis remains ideal for assessment of oxygenation.
Anesthetic protocols for murine models are varied within the literature and medetomidine has been implicated in the development of urethral plugs in male mice. Our objective was to evaluate the combination of butorphanol, dexmedetomidine, and tiletamine-zolazepam. A secondary objective was to identify which class of agent was associated with urethral obstructions in male mice. BALB/c male (n = 13) and female (n = 23) mice were assigned to dexmedetomidine and tiletamine-zolazepam with or without butorphanol or to single agent dexmedetomidine or tiletamine-zolazepam. Anesthesia was achieved in 58% (14/24) of mice without butorphanol and in 100% (24/24) of mice with butorphanol. The combination of dexmedetomidine (0.2 mg/kg), tiletamine-zolazepam (40 mg/kg), and butorphanol (3 mg/kg) resulted in an induction and anesthetic duration of 12 and 143 minutes, respectively. Urethral obstructions occurred in 66% (25/38) of trials in male mice that received dexmedetomidine with a mortality rate of 38% (5/13). Tiletamine-zolazepam, when used alone, resulted in a 0% (0/21) incidence of urethral obstructions. Combination use of dexmedetomidine, tiletamine-zolazepam, and butorphanol results in a longer and more reliable duration of anesthesia than the use of dexmedetomidine and tiletamine-zolazepam alone. Dexmedetomidine is not recommended for use in nonterminal procedures in male mice due to the high incidence of urethral obstructions and resultant high mortality rate.
Objectives:To determine the complications associated with positive-pressure ventilation (PPV) in dogs and cats.
Objectives: To determine the indications and outcomes of positive-pressure ventilation (PPV) and identify factors associated with successful weaning.
Positive-pressure ventilation results in ventilator-induced lung injury, and few therapeutic modalities have been successful at limiting the degree of injury to the lungs. Understanding the primary drivers of ventilator-induced lung injury will aid in the development of specific treatments to ameliorate the progression of this syndrome. There are conflicting data for the role of neutrophils in acute respiratory distress syndrome pathogenesis. Here, we specifically examined the importance of neutrophils as a primary driver of ventilator-induced lung injury in a mouse model known to have impaired ability to recruit neutrophils in previous models of inflammation. We exposed Duoxa 1/1 and Duoxa 2/2 mice to lowor high-tidal volume ventilation with or without positive endexpiratory pressure (PEEP) and recruitment maneuvers for 4 hours. Absolute neutrophils in BAL fluid were significantly reduced in Duoxa 2/2 mice compared with Duoxa 1/1 mice (6.7 cells/ml; 16.4 cells/ml; P = 0.003), consistent with our hypothesis that neutrophil translocation across the capillary endothelium is reduced in the absence of DUOX1 or DUOX2 in response to ventilator-induced lung injury. Reduced lung neutrophilia was not associated with a reduction in overall lung injury in this study, suggesting that neutrophils do not play an important role in early features of acute lung injury. Surprisingly, Duoxa 2/2 mice exhibited significant hypoxemia, as measured by the arterial oxygen tension/fraction of inspired oxygen ratio and arterial oxygen content, which was out of proportion with that seen in the Duoxa 1/1 mice (141, 257, P = 0.012). These findings suggest a role for dual oxidases to limit physiologic impairment during early ventilator-induced lung injury.
BackgroundPositive-pressure mechanical ventilation is an essential therapeutic intervention, yet it causes the clinical syndrome known as ventilator-induced lung injury. Various lung protective mechanical ventilation strategies have attempted to reduce or prevent ventilator-induced lung injury but few modalities have proven effective. A model that isolates the contribution of mechanical ventilation on the development of acute lung injury is needed to better understand biologic mechanisms that lead to ventilator-induced lung injury.ObjectivesTo evaluate the effects of positive end-expiratory pressure and recruitment maneuvers in reducing lung injury in a ventilator-induced lung injury murine model in short- and longer-term ventilation.Methods5–12 week-old female BALB/c mice (n = 85) were anesthetized, placed on mechanical ventilation for either 2 hrs or 4 hrs with either low tidal volume (8 ml/kg) or high tidal volume (15 ml/kg) with or without positive end-expiratory pressure and recruitment maneuvers.ResultsAlteration of the alveolar-capillary barrier was noted at 2 hrs of high tidal volume ventilation. Standardized histology scores, influx of bronchoalveolar lavage albumin, proinflammatory cytokines, and absolute neutrophils were significantly higher in the high-tidal volume ventilation group at 4 hours of ventilation. Application of positive end-expiratory pressure resulted in significantly decreased standardized histology scores and bronchoalveolar absolute neutrophil counts at low- and high-tidal volume ventilation, respectively. Recruitment maneuvers were essential to maintain pulmonary compliance at both 2 and 4 hrs of ventilation.ConclusionsSigns of ventilator-induced lung injury are evident soon after high tidal volume ventilation (as early as 2 hours) and lung injury worsens with longer-term ventilation (4 hrs). Application of positive end-expiratory pressure and recruitment maneuvers are protective against worsening VILI across all time points. Dynamic compliance can be used guide the frequency of recruitment maneuvers to help ameloriate ventilator-induced lung injury.
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