While the incidence of venous thromboembolic (VTE) disease has been recently noted to be elevated among critically ill patients, the incidence among ambulatory and non-critically ill patients is not yet clearly defined. This is especially true among those progressing to severe pneumonia and multi-organ failure.
Additionally, many infected individuals were found to have coagulation markers abnormalities. Although a large proportion of infected individuals develop only mild symptoms or are asymptomatic, the spectrum of the disease among others has been widely variable in severity. The Coronavirus Disease 2019 (COVID 19) has been reported in almost every country in the world. Avoidance of thermal risk and early recognition of cold or heat stress are the cornerstones of preventive therapy. Ice water immersion has been shown to be superior to alternative cooling measures. Management requires the immediate reduction of core temperature. Mental status changes and core temperature distinguish potentially fatal heat stroke from heat exhaustion.
Hypothermia, defined as a core temperature of 40.5 ☌, may present with sweating, flushing, tachycardia, fatigue, lightheadedness, headache, and paresthesia, progressing to weakness, muscle cramps, oliguria, nausea, agitation, hypotension, syncope, confusion, delirium, seizures, and coma. Failure of neural thermoregulatory mechanisms or exposure to extreme or sustained temperatures that overwhelm the body's thermoregulatory capacity can also result in potentially life-threatening departures from normothermia. The clinical detection of thermoregulatory impairment provides important diagnostic and localizing information in the evaluation of disorders that impair thermoregulatory pathways, including autonomic neuropathies and ganglionopathies. Heat production and dissipation are dependent on a coordinated set of autonomic responses.
Thermoregulatory physiology sustains health by keeping body core temperature within a degree or two of 37 ☌, which enables normal cellular function. Thermoregulation is a vital function of the autonomic nervous system in response to cold and heat stress. Finally, adult cases appear to occur with this form of hand-foot-and-mouth disease, likely due to fecal-oral transmission in a household setting. These cases have caused extensive cutaneous disease variants, some of which are not previously recognized in Coxsackie infection, namely vesicobullous and erosive eruptions, extensive cutaneous involvement, periorificial lesions, localization in areas of atopic dermatitis or in children with atopic dermatitis (the so-called eczema coxsackium), Gianotti-Crosti–like lesions, petechial/purpuric eruptions, delayed onychomadesis, and palmoplantar desquamation. A recent outbreak of Coxsackie A6 infection has been seen worldwide with cases reported in the United States, Japan, Southeast Asia, and Europe. Other enteroviruses have recently been noted to cause severe neurologic illness and paralysis (enterovirus 68) with variable cutaneous features. Hand-foot-and-mouth disease is a viral exanthem caused, primarily by Coxsackie A16 and enterovirus 71 with typical clinical features of fever, painful papules and blisters over the extremities and genitalia and an enanthem involving ulceration of the mouth, palate, and pharynx.