Somatic injuries

General Somatic Injury. The literature is replete with descriptions of trace element-induced organ system injury. The most recent comprehensive review on this subject is by Louria, et al. (13). 

Psychological assessment and support skills are also important at this level of care, due to the inherent fear of chemical agents which could result in the worried well overloading any medical capacity to the detriment of casualties who have defined somatic injury. 

Compounds with moderate p-affinities are very potent in a variety of pain models in mice and rats. In addition to antinociceptive efficacy in models of acute pain (tail flick, writhing) these compounds inhibit acute and persistent inflammatory pain (Randall Selitto, formalin test). Furthermore, they show strong inhibition of acute visceral pain (colorectal distension) and of tactile and cold allodynia in models of neuropathic pain (spinal nerve ligation (Chung), chronic constriction injury (Bennett)). The data suggest these compounds to be potential candidates for the management of clinical pain indications. Somatic and visceral pain with and without inflammatory conditions as well as neuropathic pain might be addressed with this approach. 

Residents also report negative effects of sleep loss on their physical health. In one study of house officers in Scotland (71), both the number of hours worked and the number of hours slept while on call were associated with the number of somatic symptoms they reported experiencing over the previous year. In a recent resident survey study (72), sleep loss was associated with self-reported increased stress, accidents, and injuries, and alcohol and stimulant use sleep loss was correlated with stress and illness and injury levels, and with reported significant weight change and alcohol and medication use in a dose-dependent fashion. 

Substance P and the related tachykinins neurokinin A and neurokinin B are mainly found in neurons, particularly unmyelinated sensory somatic and visceral fibres, in enteric sensory neurons and in a number of pathways within the brain. The release of tachykinins from the peripheral ends of these neurons may play an important role in the neurogenic inflammatory responses to local injury and inflammation by promoting the release of histamine from mast cell degranulation, and the release of cytokines from invading white cells, as well as acting directly upon blood vessels to produce vasodilation and plasma extravasation. Neurogenic inflammation within... 

It is the philosophy of the International Commission on Radiological Protection (53) and of most scientists in this field, that the cautious assumption should be made that any exposure to radiation may carry some risk for the development of somatic effects, including leukemia and other malignancies, and of hereditary effects. The Commission and others recognize that this is a conservative assumption and that some effects may exhibit a minimum or threshold dose but most often, the simple pessimistic assumption is made that the chance of delayed radiation injury of this kind is directly proportional to the total dose accumulated by the organ in question (the whole body is included as a special case within this term). 

ICRP Publication 1 was adopted in 1958 and was available in the following year. This document gave background for a comprehensive protection system based on the knowledge that "Exposure to ionizing radiation can result in injuries that manifest themselves in an exposed individual and in his descendants these are called somatic and genetic injuries respectively". Essentially the recommended system comprised a dose limitation concept based on "maximum permissible doses" applied to different exposure categories. Probably the best known of diese recommendations is the formula D = 5(N-18), where D is the maximum allowable accumulated dose in rem units and N the age in years. 

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