Radiation injury natural history, complications and prognosis

Jump to: navigation, search

Radiation injury Microchapters

Home

Patient Information

Overview

Classification

Pathophysiology

Causes

Differentiating Radiation injury from other Diseases

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

History and Symptoms

Physical Examination

Laboratory Findings

MRI

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Radiation injury natural history, complications and prognosis On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Radiation injury natural history, complications and prognosis

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Radiation injury natural history, complications and prognosis

CDC on Radiation injury natural history, complications and prognosis

Radiation injury natural history, complications and prognosis in the news

Blogs on Radiation injury natural history, complications and prognosis

Directions to Hospitals Treating Radiation injury

Risk calculators and risk factors for Radiation injury natural history, complications and prognosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Please help WikiDoc by adding more content here. It's easy! Click here to learn about editing.

Natural History, Complications and Prognosis

Natural History

Responses of the Skin to Radiation

  • Acute epidermal necrosis (time of onset: < 10 days postexposure; threshold dose: ~550 Gy or 55,000 rads)— Interphase death of postmitotic keratinocytes in the upper visible layers of the epidermis (may occur with high-dose, low-energy beta irradiation)
  • Acute ulceration (time of onset: < 14 days postexposure; threshold dose: ~20 Gy or 2000 rads)—Early loss of the epidermis— and to a varying degree, deeper dermal tissue—that results from the death of fibroblasts and endothelial cells in interphase
  • Dermal atrophy (time of onset: > 26 weeks postexposure; threshold dose: ~10 Gy or 1000 rads)— Thinning of the dermal tissues associated with the contraction of the previously irradiated area
  • Dermal necrosis (time of onset > 10 weeks postexposure; threshold dose: ~20 Gy or 2000 rads)— Necrosis of the dermal tissues as a consequence of vascular insufficiency
  • Dry desquamation (time of onset: 3–6 weeks postexposure; threshold dose: ~8 Gy or 800 rads)— Atypical keratinization of the skin caused by the reduction in the number of clonogenic cells within the basal layer of the epidermis
  • Early transient erythema (time of onset: within hours of exposure; threshold dose: ~2 Gray [Gy] or 200 rads)— Inflammation of the skin caused by activation of a proteolytic enzyme that increases the permeability of the capillaries
  • Epilation (time of onset: 14–21 days; threshold dose: ~3 Gy or 300 rads)— Hair loss caused by the depletion of matrix cells in the hair follicles
  • Late erythema (time of onset: 8–20 weeks postexposure; threshold dose: ~20 Gy or 2000 rads)— Inflammation of the skin caused by injury of blood vessels. Edema and impaired lymphatic clearance precede a measured reduction in blood flow.
  • Invasive fibrosis (time of onset: months to years postexposure; threshold dose: ~20 Gy or 2000 rads)— Method of healing associated with acute ulceration, secondary ulceration, and dermal necrosis that leads to scar tissue formation
  • Main erythema (time of onset: days to weeks postexposure; threshold dose: ~3 Gy or 300 rads)— Inflammation of the skin caused by hyperaemia of the basal cells and subsequent epidermal hypoplasia (see photos 1 and 2)
  • Moist desquamation (time of onset: 4–6 weeks postexposure; threshold dose: ~15 Gy or 1500 rads)— Loss of the epidermis caused by sterilization of a high proportion of clonogenic cells within the basal layer of the epidermis
  • Secondary ulceration (time of onset: > 6 weeks postexposure; threshold dose: ~15 Gy or 1500 rads)— Secondary damage to the dermis as a consequence of dehydration and infection when moist desquamation is severe and protracted because of reproductive sterilization of the vast majority of the clonogenic cells in the irradiated area
  • Telangiectasia (time of onset: > 52 weeks postexposure; threshold dose for moderate severity at 5 years: ~40 Gy or 4000 rads)— Atypical dilation of the superficial dermal capillaries.

Complications

Acute (short-term) vs chronic (long-term) effects

Radiation sickness is generally associated with acute exposure and has a characteristic set of symptoms that appear in an orderly fashion. The symptoms of radiation sickness become more serious (and the chance of survival decreases) as the dosage of radiation increases. These effects are described as the deterministic effects of radiation.

Longer term exposure to radiation, at doses less than that which produces serious radiation sickness, can induce cancer as cell-cycle genes are mutated. If a cancer is radiation-induced, then the disease, the speed at which the condition advances, the prognosis, the degree of pain, and every other feature of the disease are not functions of the radiation dose to which the sufferer is exposed.

Since tumors grow by abnormally rapid cell division, the ability of radiation to disturb cell division is also used to treat cancer (see radiotherapy), and low levels of ionizing radiation have been claimed to lower one's risk of cancer (see hormesis).

References



Linked-in.jpg