The effect of feed restriction and the application of canola oil to broiler straw litter to contain respirable dust on growth performance, carcass traits, and the incidence of ascites was evaluated with 800 male broilers studied in two 6-wk periods. Two pens of birds were feed restricted. Two pens of birds received feed ad libitum for the 6-wk trial. One restricted and one ad libitum pen received biweekly addition of canola oil to the litter. At 6 wk of age, 30 birds from each pen were killed for determination of breast muscle, fat pad, and heart weights. All birds were scored for the incidence of ascites at processing. A cross sectional image of each heart was digitally recorded and, using image analysis, the right ventricular area (RVA), left ventricular area (LVA), and total heart area (HA) were determined. The right ventricular wall was removed and its weight was expressed as a percentage of total heart weight (PRVW). The 40-d BW was significantly greater in the ad libitum birds (2.07 kg) than in the feed-restricted birds (1.86 kg). The right ventricular weight (RVW) (1.69 and 1.92 g) and the RVA (0.35 and 0.40 cm2) were also significantly different between the two feeding treatments. The ascites score was significantly correlated to the RVW (r = 0.50) and RVA (r = 0.52). The RVA was also correlated to the RVW (r = 0.63). Oiling the litter did not result in differences in carcass characteristics. Litter oiling significantly reduced the RVA of the ad libitum birds (0.36 cm2) compared to the ad libitum birds that did not have oiled litter (0.44 cm2). Feed restriction reduced the incidence of ascites, but also reduced gain. Litter oiling in the feed-restricted groups reduced the RVA, but did not reduce mortality.
The effects of diurnal temperature fluctuations and removal of respirable dust, by application of canola oil to straw litter, on growth, carcass traits, and the degree of ascites was evaluated with 1,200 male broilers studied in two replicated 6-wk trials. Each trial used four pens of 150 birds. The temperature treatment consisted of a fluctuation of 3 C in temperature above the required temperature during the day (0600 to 1800 h) and 3 C below the required temperature at night (1800 to 0600 h) for a 6 C change in daily temperature. The control temperature was constant. All pens had the same mean daily temperature. In each trial, one control temperature pen and one fluctuation temperature pen received bi-weekly applications of canola oil to the litter (1.1 L/m2 of oil over 6 wk). At 6 wk of age, 30 birds from each pen were killed for determination of breast muscle, fatpad, and heart weights. All birds were scored for lesions of ascites at time of processing. A score of 0 or 1 represented slight pericardial effusion, slight pulmonary congestion, and edema. A score of 4 represented birds with marked accumulation of ascitic fluid in one or more ceolomic cavities (other than the pericardium) and advanced liver lesions. A cross-sectional image of each 4-mm heart slice (cross-section of the ventricles) was digitally recorded, and with image analysis we determined the right ventricular area (RVA), left ventricular area (LVA), and total heart area (HA). The final BW of the broilers were significantly different, the oiled-litter treatment (2,249 g) had lower weight gain compared with the nonoiled litter treatment (2,293 g). There were no differences in fatpad weight, shank length, lung weight, and percentage breast muscle between the main treatments. The Pectoralis minor and Pectoralis major weight were significantly heavier in the temperature fluctuation treatment than in the control temperature treatment by 3.0 and 12.0 g, respectively. The birds subjected to the control temperature treatment had a lower RVW than the birds subjected to the fluctuating temperature treatment. Temperature fluctuations also resulted in a 1.4% increase in the incidence of mortality. Temperature fluctuations negatively impact broiler growth due to heat loss when litter oiling was excessive.
Coagulopathy has proven to be a common complication of the novel coronavirus SARS-CoV-2, with evidence of elevated D-dimers and fibrin degradation products associated with an increased incidence of thromboembolism. Despite emerging evidence describing the coagulopathy and its clinical relevance in COVID-19, fewer studies have addressed the potential role of empiric therapeutic anticoagulation in this setting. We report the case of a patient admitted to our intensive care unit (ICU) with severe acute respiratory distress syndrome (ARDS) secondary to COVID-19 whose clinical trajectory improved dramatically after initiation of a therapeutic dose of LMWH. The patient showed progressive elevation of fibrinogen and D-dimers despite a prophylactic dose of LMWH during her ICU stay. This was met with a moderate increase of troponin T-hs, an escalating need for vasopressors, and a progressive decrease in her P/F ratio despite preserved lung static compliance. Her platelet count was normal and had an elevated fibrinogen during the first week of ICU stay. The ECG was normal, and a bedside transthoracic echocardiogram showed no evidence of pulmonary embolism and a preserved EF with no regional wall motion abnormalities (RMWA). The chest X-ray was not dissimilar to previous exams, and the ABG showed hypoxia with normal pCO2 values. The decision was made to commence empiric therapeutic enoxaparin. The patient did not experience bleeding complications, and her clinical trajectory appeared to change dramatically. She was successfully extubated three days later and proceeded to clinical recovery and eventual discharge from the ICU. The available evidence shows that there is undoubtedly coagulopathy associated with COVID-19 with various subsequent forms of clinical manifestation described in the literature. Evidence also shows the benefits of heparin as an anticoagulant. From the discussion of this case report, however, it can be concluded that despite the plausible theoretical rationale, studies pertaining to the role of empiric therapeutic anticoagulation in this setting fall short of providing compelling evidence. Subsequently the role of empiric therapeutic anticoagulation in COVID-19 remains unclear with a pressing call for further research.
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