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Complications of Equine Anesthesia
Published in Michele Barletta, Jane Quandt, Rachel Reed, Equine Anesthesia and Pain Management, 2023
Treatment for pulmonary edema consists primarily of: Furosemide (1 mg/kg IV).Oxygen therapy. It can be useful to place a nasotracheal tube in the standing horse, so that high flows of oxygen can be administered without disturbing the horse. Nasopharyngeal tubes can be placed bilaterally and oxygen insufflated on both sides if necessary. 15 l/min O2 flow can be administered.
Congestive Heart Failure
Published in Jahangir Moini, Matthew Adams, Anthony LoGalbo, Complications of Diabetes Mellitus, 2022
Jahangir Moini, Matthew Adams, Anthony LoGalbo
Pulmonary edema causes signs and symptoms that can mimic an exacerbation of COPD. The edema may be the primary symptom when the patient has no history of cardiac disorders. An immediate chest X-ray is usually sufficient for diagnosis and reveals extreme interstitial edema. If the diagnosis is still not confirmed, the serum brain natriuretic peptide (BNP)/N-terminal (NT)-prohormone BNP levels can be measured. They are elevated if pulmonary edema is present, but are normal if COPD is exacerbated. Other evaluations include blood tests, ECG, and pulse oximetry. The blood tests include cardiac biomarkers, BUN, electrolytes, and creatinine. For extremely ill patients, arterial blood gas measurements are taken. To determine the cause of pulmonary edema and select the best treatment, echocardiography may be done. Other factors to evaluate include severe hypoxemia and carbon dioxide retention, which is a late and severely negative sign of secondary hypoventilation.
Battlefield Chemical Inhalation Injury
Published in Jacob Loke, Pathophysiology and Treatment of Inhalation Injuries, 2020
With mild exposure there is a reddened oropharynx with some endothelial inflammation extending peripherally to the level of the smaller airways. As exposure increases, the oropharynx becomes more intensely injected. There is edema of the epiglottis and larynx as well as the base of the tongue. A sharp line of demarcation may be seen separating the pharyngeal injection from the pale uninvolved esophagus. Pleural effusions may be seen in association with developing pulmonary edema. With even more severe exposures there are distended pulmonary lymphatics with a dense, heavy edematous consolidation of lung. Subcutaneous emphysema is common. A fibrinous exudate may be seen lining the bronchi at 1-2 days. There may be epithelial necrosis. With moderate exposures a purulent bronchitis may be seen with small areas of pneumonic consolidation that became larger with increasing severity of exposure. Infarction and gangrene have been reported by the French but is not a common finding in other pathologic reviews (Bunting, 1945c).
Pulmonary delivery of resveratrol-β-cyclodextrin inclusion complexes for the prevention of zinc chloride smoke-induced acute lung injury
Published in Drug Delivery, 2022
Wanmei Wang, Yan Liu, Pan Pan, Yueqi Huang, Ting Chen, Tianyu Yuan, Yulong Ma, Guang Han, Jiahuan Li, Yiguang Jin, Fei Xie
In this study, we detected pulmonary vascular permeability by the extravasation of this dye into the pulmonary extravascular space and the surrounding lung tissues. The lungs of model mice were obviously blue after 48 h post-smoke exposure; however, the mice administrated with BUD and RES-β-CD only showed little blue lungs compared to the healthy lung (Figure 3(A)). The content of Evans blue in the lung tissues of model mice was much more than those in the prevented mice and healthy mice while no significant difference was presented between the latter two groups (Figure 3(B)). Moreover, we used the lung W/D ratios to evaluate the extent of pulmonary edema. ZnCl2 smoke exposure markedly increased the lung W/D ratios while the prevention of RES-β-CD and BUD decreased the W/D ratios. However, the effect of RES-β-CD was much higher than that of BUD (p < .01) (Figure 3(C)). Therefore, RES-β-CD greatly ameliorated pulmonary vascular leakage and pulmonary edema induced by ZnCl2 smoke exposure.
Cardiomyopathy and heart failure secondary to anabolic-androgen steroid abuse
Published in Baylor University Medical Center Proceedings, 2022
Onyedika J. Ilonze, Chioma O. Enyi, Chibuzo C. Ilonze
An electrocardiogram (Figure 1a) showed atrial flutter with rapid ventricular response with 2:1 atrioventricular conduction. His heart rate was 130 to 150 beats/min, and his blood pressure was 109/64 mm Hg. He received intravenous adenosine 18 mg and a diltiazem bolus. He developed acute respiratory distress and was intubated and mechanically ventilated. Computed tomography of the chest showed bilateral interstitial pulmonary edema with pleural effusions. Transesophageal echocardiogram on day 2 showed severe left ventricular (LV) dysfunction with a left ventricular ejection fraction (LVEF) of 15%, mitral regurgitation, biatrial enlargement, and no left atrial appendage thrombus. He underwent direct current cardioversion with restoration of sinus rhythm; however, atrial flutter recurred within 24 hours. Pharmacologic therapy to maintain sinus rhythm included intravenous amiodarone followed by oral amiodarone.
Scorpion envenomation: a deadly illness requiring an effective therapy
Published in Toxin Reviews, 2021
Faez Amokrane Nait Mohamed, Fatima Laraba-Djebari
Experimental studies of scorpion envenomation have shown a first hyperdynamic phase characterized by tachycardia and hypertension followed by hypotension and bradycardia phases attributed to cholinergic effects. (Ismail 1995, Correa et al.1997, Hammoudi-Triki et al.2007, Adi-Bessalem et al.2008, Abroug et al.2015, Elatrous et al.2015). While the mechanisms of hemodynamic disorders are still not clearly defined, it seems that catecholamine release is the main cause (Abroug et al.2020). Several observed hemodynamic changes in severe scorpion envenomation could be due to the release of endogenous mediators, including such peptides as endothelin-1 and neuropeptides (D’suze et al.2003, Nouira et al.2005, Soualmia et al.2009). In severe cases of envenomation, death is caused by pulmonary edema followed by respiratory failure (Krifi et al.1998, Adi-Bessalem et al.2008). The mechanism of acute pulmonary edema has not yet been elucidated. Although some clinical reports have linked pulmonary edema to an increased capillary permeability, most experimental and clinical studies suggest a hemodynamic origin for this event (Abroug et al.1991, Bahloul et al.2013). Recently, the moment of envenomation has been shown to correlate with the severity and toxicological effects of Aah envenomation. It has been reported a pronounced inflammatory response on the hypothalamo-pituitary-adrenal axis when Aah venom is administered during the activity phase (daylight) (Daachi et al.2020).