Cats with thermal burn injuries from California wildfires show echocardiographic evidence of myocardial thickening and intracardiac thrombi

Ashley N Sharpe,Ronald H L Li,Catherine T Gunther-Harrington,Joshua A Stern,Steven E Epstein

doi:10.1038/s41598-020-59497-z

Ashley N Sharpe, Ronald H L Li + Show 3 more

Open Access

https://doi.org/10.1038/s41598-020-59497-z

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Abstract

Recent increases in the prevalence and severity of wildfires in some regions have resulted in an increased frequency of veterinary burn patients. Few studies exist regarding diagnostics and management of burn wounds in veterinary patients and current knowledge is extrapolated from human literature and research models. Post-burn cardiac injury is a common finding and predictor of mortality in human patients and echocardiography is an important tool in monitoring response to therapy and predicting outcome. We describe the notable findings from cats naturally exposed to California wildfires in 2017 and 2018. Domestic cats (n = 51) sustaining burn injuries from the Tubbs (2017) and Camp (2018) wildfires were prospectively enrolled and serial echocardiograms and cardiac troponin I evaluations were performed. Echocardiograms of affected cats revealed a high prevalence of myocardial thickening (18/51) and spontaneous echocardiographic contrast and thrombi formation (16/51). Forty-two cats survived to discharge and 6 died or were euthanized due to a possible cardiac cause. For the first time, we describe cardiovascular and coagulation effects of thermal burn and smoke inhalation in cats. Further studies in veterinary burn victims are warranted and serve as a translational research opportunity for uncovering novel disease mechanisms and therapies.

Highlights

Recent increases in the prevalence and severity of wildfires in some regions have resulted in an increased frequency of veterinary burn patients
Our study demonstrates the characteristic echocardiographic findings in cats with naturally-occurring thermal burn injury and smoke inhalation from California wildfires
Significant systolic dysfunction was not appreciated in our patient population which may be explained by the elapsed time from initial injury to evaluation as the hypodynamic phase of cardiac dysfunction is only present for approximately the initial 48–72 hours in thermal burn injury animal models and human studies[1,35,36]

Summary

Introduction

Recent increases in the prevalence and severity of wildfires in some regions have resulted in an increased frequency of veterinary burn patients. Significant cardiovascular effects secondary to thermal burn injury and accompanying smoke inhalation have been demonstrated in human populations and experimental animal models[9,10,11,12]. A prospective experimental study of severe burn injury and smoke inhalation injury in sheep suggested triphasic dysregulation of coagulation culminating with hypercoagulability evidenced by platelet activation with increased fibrinogen and depressed anti-thrombin III levels at 96 hours following injury[22]. A study in mice demonstrated that acrolein, an aldehyde present in high concentrations in smoke from wood fire, results in direct platelet activation[23] These findings demonstrate the widespread effects of smoke inhalation and burn injury on various body systems that should be considered when determining appropriate therapy. Current recommended therapy includes oxygen support, fluid resuscitation, wound management performed under heavy sedation, pain management, and treatment for ophthalmic and neurologic complications secondary to wildfire exposure[1,2,6]

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