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Pediatric Terrorism and Disaster Preparedness: A ... - PHE Home

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esponse. Precursor/stem cells are more sensitive than fully developed, mature cells.<br />

Similarly, cells that are actively replicating (going through mitosis) are also more<br />

responsive.<br />

After receiving a radiation dose, a progressive, chronic, <strong>and</strong> complex inflammatory<br />

process begins. The clinical course is a function of the following:<br />

• Type of radiation.<br />

• Inherent energy of the source.<br />

• Dose <strong>and</strong> the dose rate.<br />

• Length of exposure.<br />

• Tissue involved.<br />

• How the energy is distributed within that tissue.<br />

• Size <strong>and</strong> area of the body involved in the exposure.<br />

Although only a small superficial area may initially appear to be affected, because of the<br />

amount of energy involved, deeper tissues <strong>and</strong> organ systems may also be affected.<br />

Depending on the individual cells involved, onset of clinical symptoms will be variable.<br />

Perhaps the most pertinent rule of thumb in these types of injuries is that there is no<br />

pathognomonic sign or symptom of radiation injury. There is not always a specific linear<br />

relationship between the dose of radiation that a tissue receives <strong>and</strong> the subsequent<br />

somatic manifestations that result. Skin damage evolves over time according to the local<br />

dose with the tissue furthest from the direct local injury being the slowest to display<br />

damage. The extent of tissue damage or involvement is inversely proportional to the<br />

square of the distance from the source of radiation. There is no definite correlation<br />

between specific symptoms <strong>and</strong> cell types.<br />

CRS has been divided into five time-related stages: prodromal erythematous,<br />

manifestational, subacute, chronic, <strong>and</strong> late.<br />

Prodromal erythematous stage. This stage may last minutes to hours after exposure to<br />

doses >5–6 Gy. The time to onset, intensity, <strong>and</strong> duration are used to predict prognosis.<br />

The early erythema is likely due to release of vasoactive amines <strong>and</strong> secondary<br />

vasodilation. A clinically asymptomatic latent period may follow. At this stage, high-dose<br />

<strong>and</strong> low-dose casualties cannot be distinguished. If additional symptoms (e.g., nausea,<br />

vomiting, CNS changes) develop along with relevant patient history, then further<br />

assumptions or conclusions will be possible.<br />

Manifestational stage. After a latency period of 7–21 days, clinical signs develop that<br />

range from bright erythemas with a burning sensation to painful blisters <strong>and</strong> ulcers. These<br />

changes are due to injury to blood vessels <strong>and</strong> underlying connective tissue <strong>and</strong> death of<br />

skin stem cells. From 8 to 12 Gy, there is dry desquamation, <strong>and</strong> from 15 to 20 Gy, moist<br />

desquamation ensues. Moist desquamation occurs less commonly in children undergoing<br />

radiation therapy than in adults. This is probably because of the ability of the epithelium<br />

to recover more quickly in children than in adults. More changes are also observed in<br />

fair-skinned individuals <strong>and</strong> at the more radiosensitive areas of the body such as the<br />

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