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Injuries Due to Burns and Cold
Published in Ian Greaves, Keith Porter, Jeff Garner, Trauma Care Manual, 2021
Ian Greaves, Keith Porter, Jeff Garner
The inflammatory process associated with burn injury evolves during the 8–24 hours after the burn and can cause further local and systemic injury. There is increased capillary permeability with fluid loss from the intravascular space. The magnitude of the inflammatory response is related to the extent of the tissue injury and is most easily expressed as the percentage of the total body surface area (% TBSA) that is burnt. Superficial burns cause only erythema with no significant capillary leakage. In burns greater than approximately 20% TBSA, the inflammatory mediators affect the whole body and patients may develop a systemic inflammatory response syndrome (SIRS)3 over several hours, with significant intravascular fluid loss and the potential for the development of hypovolaemic shock.4 Other causes of hypovolaemia, for example, from associated traumatic injuries from jumping to escape a fire, should be excluded before attributing hypovolaemia solely to the burn injury.
The immune and lymphatic systems, infection and sepsis
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
Michelle Treacy, Caroline Smales, Helen Dutton
Remembering the processes for the inflammatory response, there will be increased capillary permeability leading to the sequestering of fluids in the tissues and giving rise to swelling and oedema. If left untreated, the patient may go on to develop cardiac arrest.
Inhalational Durg Abuse
Published in Jacob Loke, Pathophysiology and Treatment of Inhalation Injuries, 2020
Jacob Loke, Richard Rowley, Herbert D. Kleber, Peter Jatlow
The pathophysiological mechanism of opiate pulmonary edema remains unclear. In patients with heroin pulmonary edema, the concentration of protein in the pulmonary edema fluid (obtained immediately after endotracheal intubation) has been shown to be higher than in serum when compared with those patients who have congestive heart failure (98.3 versus 40.0%). This finding supports the concept of increased pulmonary capillary permeability (Katz et al, 1972). Proposed mechanisms leading to increased capillary permeability include hypoxia; hypersensitivity reaction; histamine mediated effect; neurogenic effect; or a direct toxic effect of heroin, diluents, or adulterants (Frand, 1972).
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).
Pro-inflammatory cytokines as potential predictors for intradialytic hypotension
Published in Renal Failure, 2021
Jinbo Yu, Xiaohong Chen, Yang Li, Yaqiong Wang, Xuesen Cao, Zhonghua Liu, Bo Shen, Jianzhou Zou, Xiaoqiang Ding
Association between fluid overload (FO) and inflammation was revealed in MHD patients [25–27]. Inflammation might theoretically contribute to FO because of hypoalbuminemia. Hypoalbuminemia can lead to vascular volume migration to the interstitial chamber, which hinders fluid removal during dialysis [28]. However, FO itself can also reduce serum albumin levels by dilution, as serum albumin levels increased after excessive ultrafiltration [29]. Inflammation may also result in interstitial fluid accumulation by increasing capillary permeability. FO may also bring about inflammation by endotoxin fragment passing through a congested intestinal wall or visceral ischemia [30,31]. As volume overload, hypoalbuminemia and malnutrition are common predictors of IDH. We presumed that inflammatory markers might play a part in the onset of IDH. Serum TNF-α and IL-1β were observed elevated in the IDH group (p < 0.001).
Comparative pharmacokinetics of quercitrin, astragalin, afzelin and taxifolin in plasma after oral administration of Polygonum orientale inflorescence in sham-operated and myocardial ischemia–reperfusion injury rats
Published in Xenobiotica, 2020
Lin Zheng, Yueting Li, Zuying Zhou, Wenying Xiang, Zipeng Gong, Siying Chen, Yonglin Wang, Aimin Wang, Yanyu Lan, Yongjun Li, Yong Huang
The main reason is that the ischemic body causes the elimination of metabolites to slow down (Dong et al., 2016). Moreover, the vascular response is a central part of the inflammatory response, and inflammation can lead to an increase in tissue vasodilation and capillary permeability (Gao et al., 2013). As such, another possibility is microvascular dysfunction caused by myocardial ischemia–reperfusion injury (MIRI), including increased vascular permeability, endothelial cell inflammation, vasodilation, vasoconstriction factors and an imbalance between coagulation activation and the complement system (Li, 2014; Chai & Yu, 2014; Elizabeth & Charles, 2008; Gao et al., 2013; Yang et al., 2006). Accordingly, the higher values of AUC(0–t), MRT(0–t), AUC(0–∞) and MRT(0–∞), with decreased CL, in the MIRI model rats may have possibly resulted from a decrease in the elimination of quercitrin, astragalin, afzelin and taxifolin.