Australian Clinical Guidelines for Radiological Emergencies - September 2012

Internal Contamination

Page last updated: 07 December 2012

Internal contamination may occur when radioactive materials are accidentally or intentionally released into the environment, and inhaled, ingested or incorporated via wounds. The first priority for care is the stabilisation of any life-threatening injury, followed by decontamination of external contamination.

Assessment of internal contamination will be dependent on the history of the incident, consideration of potential routes of exposure, and information regarding the identification and chemical form of the radionuclide. There may be delays to obtaining confirmation of the nature of the radionuclide.

Treatment decisions need to be based on an understanding of the properties of the identified radionuclide including metabolic behaviour, the route of exposure and absorption characteristics, estimates of body burden, available treatments (including effectiveness, contraindications and risks) and individual patient status.

Treatment is maximally effective if commenced early. A clinical decision may need to be based on an estimation of whether exposure potential is low, medium or high and an understanding of the risks of treatment. Detailed dosimetry can be completed subsequently.

Radionuclide properties

The physical half-life is the time for half the amount of a substance to undergo radioactive decay.

The biological half-life is the time for half the amount of a substance to be eliminated from the body following absorption.

The effective half-life is the time taken for the radiological effect of the substance absorbed into the body to be reduced by half by biological elimination and radioactive decay.

Identifying potential intakes

The initial evaluation for potential internal contamination is directed at establishing whether or not there is alpha or beta / gamma radiation as this determines approach to detection in nasal swabs and wounds.
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Circumstances for potential inhalation of radionuclides may be identified by:
  • Sampling for air-borne contaminants
  • The presence of external contamination of the upper body, especially the face.
  • Activity on nasal smears. Nasal swabs are collected using separate moistened cotton swabs for each nostril as soon as the patient’s condition allows, then dried and counted.
Activity detected on nasal smears is usually an indication of an inhalation intake. Exceptions to this include:
  • Delay to obtaining nasal smears of 30 to 60 minutes from the time of exposure may be sufficient for nasal clearance.
  • Showering or washing the face may result in nose blowing and clearance of the nasal passages.
  • Mouth breathing may bypass the nasal passages for deposition.
  • Particle size also affects nasal deposition and clearance.
Counts in excess of 500 disintegrations per minute (dpm) of alpha emitters are considered significant exposures, whereas results less than 50 dpm suggest a low order exposure. A rule of thumb is that the combined activity of both nasal swabs approximates 5% of lung deposition. Substantial difference in the amount of activity between the two swabs suggests inadvertent contamination of one nare, rather than inhalation, and caution in interpreting the estimated results. It is unlikely that a patient will reach hospital in time for useful information to be obtained from the nasal swabs.

Wounds must be surveyed for the presence of contamination. The presence of dressings, soil, blood, or irrigation fluids is likely to interfere with the detection of alpha particles.

Confirmation of inhalation of radionuclides may be achieved by performing lung counts for retained substances. Ingestion may be confirmed by the presence of incompletely absorbed radionuclides in the faeces.
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Absorption of radionuclides may be confirmed with the appropriate detection technique or bioassay.

Assessment of dose

Following internal contamination, the radionuclide is distributed to various organs and tissues where it is retained until it decays or is excreted. The dose that is received this way from the radionuclide, from initial exposure until it is gone, is the committed dose. The calculated dose over 50 years is the committed effective dose equivalent (CEDE). The sum of the committed effective dose equivalent and any external dose received is the total effective dose equivalent (TEDE).

Dose may be assessed by:
  • physical reconstruction of events
  • the evolution of clinical symptoms
  • laboratory measurement of key clinical indicators (absolute lymphocyte count and dicentric assay)
  • contamination survey (including nasal swabs and wound dressings)
  • whole body and specific organ counts, and
  • bioassay of bodily fluids (urine, faeces, pulmonary lavage washings).
Some radioisotopes are widely prevalent in the environment, and are incorporated into the air that is breathed, and water, animal products and plants that are ingested. Uranium, radium, strontium and polonium are examples. Tiny amounts may be present on bioassay in otherwise unexposed persons.

Initial (first 24 hours) urine and faecal samples may be of little value, as they may comprise residual bladder and bowel contents present prior to exposure or redistribution and excretion of absorbed radionuclide. Further, laboratory turnaround times may be several days. Variation in individual excretion rates and day-to-day variations may result in 3 to 4-fold errors in estimation of body burden using urine and faecal measurements. Use of chelation agents further complicates excretion patterns.

Lung burden can only be measured accurately by in vivo counting. Where this is not feasible because of deposition of an inhaled pure alpha emitter, the measured urinary and faecal excretion values and the assumed values from theoretical biokinetic models are used to estimate the residual lung burden. Considerable uncertainty is likely with such estimations. Measurement uncertainties for plutonium lung burdens have been estimated at +/- 100%.

Whole body counters are extremely sensitive and may detect residual external contamination that is unable to be detected by handheld detectors. This may result in over-estimation of lung or whole body burden in the first few days after a contamination event. The measurements are generally accurate to within 30% for gamma emitters.

Interpretation of whole body and organ counts and bioassays to determine dose will require the assistance of health physics experts.

Biokinetic models

The isotope and chemical forms of radionuclides are classified according to solubility and rate of transfer from the alveoli. Rate of transfer includes movement into the circulation and lymphatics, as well as mechanical clearance by ciliary action. These classes are described in ICRP 30 as inhalation classes D, W and Y (days, weeks, years). These were replaced in ICRP 66 with absorption types F, M and S (fast, medium, slow). Absorption rates apply only to the solubility of particles deposited in the alveoli.
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Expressed as approximate half-times for clearance, the assumed absorption rates are: type F 10 minutes (100%); type M 10 minutes (10%), 140 days (90%); type S 10 minutes (0.1%), 7000 days (99.9%).

Estimation of dose following internal contamination is dependent on understanding the nature and form of the radionuclide. Dose estimation is modelled using bioassay results and reference tables, manual and computer calculations. The tables and calculations utilise standard organ system models, such as the ICRP respiratory tract model.

Standard organ system models have limitations. It is difficult to determine precise aerosol aerodynamics, individual respiratory physiology and anatomy. Additionally, there is a range of variation within inhalation classes and absorption types.

The estimates produced need to be interpreted with regard to specific individual criteria such as age, pregnancy, and pre-existing medical conditions.

Toxicity

The biological effects of incorporated radionuclides are dependent on the dose, route of entry, chemical form, and distribution within the body. Susceptibility to the biological effects may be increased by host factors such as age and co-morbidities.

Pulmonary Injury

Radiological pulmonary injury may occur due to irradiation of a large volume (> 10%) of lung at high doses (daily dose >2.67 Gy, or high cumulative dose). Threshold and LD50 values for death due to radiation pneumonitis occur at dose rates of about 5 and 10 Gy respectively. Radiation pneumonitis may also develop following the deposition of sufficient radioactive particulates which are retained in the lung due to insolubility.

Alpha emitting radionuclides are especially concerning because their high linear energy transfer (LET) increases the local tissue damage twenty-fold compared to gamma emissions.

Aerosol size is a major determinant of retention of particles in the respiratory tract. Particles larger than 5 to 10 Ám are filtered by nasal hairs or deposited in the nasopharynx. Particles from 2 to 5 Ám deposit in bronchioles and bronchi, where they are removed by ciliary action to the nasopharynx. From the nasopharynx, they may be swallowed or expectorated. Swallowed particles contribute to ongoing gastrointestinal contamination. Particles < 3 Ám reach the alveoli.

Route of inhalation is another important determinant. Of particles larger than 10 Ám, 100% deposit in the nasopharynx during nasal breathing, and 65% during mouth breathing. Deeper penetration of larger particles occurs during mouth breathing.

Once in the alveoli, the chemical form of the radionuclide determines its solubility. Soluble forms are absorbed into the alveolar capillaries. The rate of transfer is dependent on the precise chemical form. Insoluble forms may be retained for many years. Small amounts may be phagocytosed, move into lymphatics and drain to regional lymph nodes.

Following phagocytosis by alveolar macrophages, inhaled particulates may trigger a chronic inflammatory response with release of cytokines and leukotrienes, and proliferation of inflammatory cells. Stimulation of fibroblasts and deposition of extracellular collagen lead to pulmonary fibrosis.

The development of acute radiation pneumonia follows a latent period of 1 week to 7 months after radiation exposure. The onset may be insidious with non-productive cough dyspnoea, fever, pleuritic pain, malaise and weight loss. Auscultation may be normal. Chest x-ray demonstrates peri-vascular or alveolar opacities in 45% of patients. Atypical pneumonia and malignant change must be excluded.

Fibrosis may follow radiation pneumonia or develop gradually without other clinical manifestations. There is no proven therapy for radiation fibrosis. Prolonged treatment with corticosteroids is advised to mitigate against the chronic inflammatory reaction.
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Elevated risk of lung cancer is associated with the biological effects of ionising radiation as well as the chemical activity of the particular substance inducing free radicals, reactive oxygen species, mobilisation of intracellular iron, and chronic inflammatory reaction. The spectrum of radionuclide-induced cancers, in decreasing frequency of occurrence, is adenocarcinoma, bronchiolo-alveolar carcinoma, and combined epidermoid and adenocarcinoma. Mesothelioma and fibrosarcoma have been observed in some animal models.

Gastrointestinal injury

Many radionuclides are not absorbed from the gastrointestinal tract. Injury is limited to the combination of the amount ingested, the specific activity of the radionuclide, and the gastrointestinal transit time. If the amount is significant or the activity of the substance is high, there is a likelihood of mucosal damage to the GIT, or whole body irradiation.

Ingestion in pelletised form or as a solid metal, such as iridium, may lead to localised gastrointestinal burns, with consequent perforation or stricture formation.

Polonium has a propensity to form colloids, and will deposit on the mucosal surface of the intestine. On autoradiographs, the polonium accumulates at the tips of villi but the alpha radiation does not reach the basal stem cells in the crypts. It is thought that this contributes to the earlier development of the gastrointestinal syndrome following polonium ingestion, than is accounted for by the whole body irradiation effect.

Target organ injury

Some radionuclides are isotopes of essential elements normally absorbed by the body, such as iodine and cobalt. Others behave as analogues or substitutes for other elements. Strontium, radium and plutonium follow calcium metabolism pathways, and caesium behaves like potassium.

The distribution of radionuclides following absorption into the bloodstream relates to the normal or analogous behaviour of that element. Hence, the thyroid takes up radioiodine preferentially, leading to eventual hypothyroidism and thyroid tumours. The calcium analogues are distributed to the skeleton where they affect haematopoiesis (bone marrow hypoplasia and aplasia, and leukaemia), bone turnover (osteonecrosis and osteosarcoma) and local soft tissue (rhabdomyosarcoma).

Radionuclides that are deposited in the reticuloendothelial system (americium, polonium) may cause local injury due to the biological effects of ionising radiation to the liver, spleen and kidneys manifesting as organ failure.

Uranium damages the kidneys where it precipitates in the renal tubules in acid urine, because of its chemical, rather than its radiological properties.

Whole body irradiation

Because of wide intracellular distribution, radioactive potassium analogues such as caesium cause whole body irradiation. This is also seen with any other radionuclide with distribution throughout the body, such as tritium, cobalt and polonium.

Contaminated wounds

Intact skin is a barrier to most radionuclides.

Absorption of contamination from wounds is dependent on the physicochemical properties of the radionuclide such as solubility, pH, reactivity and particle size. Solubility may be altered by prolonged contact with body fluids. The contaminant may:
  • absorb into the bloodstream
  • transfer to regional lymph nodes
  • migrate along fascial planes, potentially making it difficult to localise
  • incorporate into coagulated tissue following acid or caustic exposure
  • incorporate into the eschar following full thickness burns
  • incorporate into the scab over an abrasion
  • remain in the wound causing local irradiation, and development of fibrotic nodules

Treatment Options

The clinical decision to undertake any specific treatment must consider the risks and benefits of the therapy in the specific clinical scenario. Ideally, this is informed by evidence of effectiveness.

Gastrointestinal decontamination

The amount of a substance able to be removed from the stomach by emesis or gastric lavage is unreliable, and negligible if performed more than one hour after ingestion. The risks of pulmonary aspiration or physical injury with emesis or lavage are considerable. The benefit of these procedures for gastrointestinal decontamination of radionuclides is unproven.
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Whole bowel irrigation is occasionally considered for life-threatening ingestions of metals such as lead and iron prior to established severe toxicity, where supportive care and antidotes alone may not result in good clinical outcome. However, there are significant contraindications (uncooperative patient, uncontrolled vomiting, inability to place a nasogastric tube, ileus or bowel obstruction, and potential impairment of conscious state or development of seizures) and complications of therapy (nausea, vomiting, abdominal distension, pulmonary aspiration, and metabolic acidosis). It is unlikely to be tolerated by patients with injury or significant illness. The efficacy of whole bowel irrigation for radionuclide ingestions is unknown.

Catharsis is an ineffective means of reducing gastrointestinal transit time and not used in current clinical toxicological practice.

Enhanced Elimination

Metals are poorly bound to activated charcoal. Therefore charcoal is not likely to be effective in reducing absorption of radionuclides. Alginates and antacids complex with a number of radionuclides (polonium, radium, strontium, uranium) and are relatively non-toxic, if oral therapy is not contraindicated.

137Cs is secreted and reabsorbed via the enterohepatic circulation. Prussian blue acts as an ion exchange resin to form non-absorbable complexes with 137Cs which are excreted in the faeces.

Urinary alkalinisation promotes the ionisation of uranium, preventing reabsorption across the renal tubular epithelium and promoting urinary excretion. The resultant metabolic alkalosis is usually well tolerated, however serum potassium may be lowered.

Urinary acidification promotes the ionisation of strontium, preventing reabsorption across the renal tubular epithelium and promoting urinary excretion. However, acidification of urine cannot be achieved without metabolic acidosis, which may not be desirable in the context of intercurrent illness or injury. The associated metabolic acidosis has seen this form of therapy fall into disuse for any other indication.

Extracorporeal techniques are invasive with significant complications. No controlled clinical trials have been undertaken in poisoned patients. Efficacy and optimal application are unknown. Dialysis may be useful to remove a substance with a small volume of distribution, particularly in the presence of renal failure.

Methods to reduce lung burden include:
  • Nebulised DTPA is comparable in effectiveness to parenteral therapy with the same chelation agent.
  • Pulmonary lavage is described in the literature, but limitations include lack of pre-existing respiratory disease, and a recommendation that the procedure be limited to those under 30 years of age. It is not a suitable procedure for casualties with potential blast lung injury. The effectiveness in humans is based on a single case report in which 13% of inhaled plutonium was removed with repeated bronchopulmonary lavage, however studies in beagles demonstrated efficacy of 25 to 50% and in baboons 60 to 90% with repeated treatments. It is suggested where large amounts (> 100 ALI, see section on antidotes) of insoluble radionuclides with long retention times, chiefly plutonium, are deposited in the lungs and may result in major pulmonary compromise. It is described in the following section.

Wound care

Irrigation and surgical debridement of contaminated wounds reduces the direct-to-bloodstream absorption and transfer of the contaminant to regional lymph nodes. Wound decontamination should not take precedence over resuscitation and stabilisation of life-threatening injuries. Specially designed probes may be required to assist in localising the contaminant within the wound.

Irrigation using decorporation agents such as DTPA has been proven to be ineffective in increasing the amount of radionuclide removed from the wound. Sterile water or saline are adequate. The criteria for surgical excision must have regard to the location and nature of the wound and quantity of contaminant in the wound.
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Removal of radioactive shrapnel should only be undertaken using long-handled instruments. Such fragments should never be directly touched or handled because of the risk to the fingers or hand of the surgeon, and should be placed into a lead pot, which should be obtainable from the hospital nuclear medicine department.

Where contamination is associated with full thickness burns, the radionuclide will be fixed in the eschar and mostly removed with excision of the eschar.

As surgical instruments, swabs and dressings become contaminated, they should be replaced. Excised tissue should be retained for radiological survey. Systemically absorbed radionuclide should be managed with the relevant decorporation therapy.

Annual follow up of wounds with residual contamination is required to detect and excise nodules. Pathology and radiochemistry analysis of excised nodules is recommended.

Blocking Agents

The metabolic behaviour of selected radionuclides provides opportunity for decreasing uptake with the appropriate stable isotope (iodine) or relevant analogue (calcium for radium and strontium) by saturating the target organ and diluting the radionuclide proportionately. For maximal effectiveness, these agents need to be given without delay.

Antidotes

The decision to use decorporation agents is dependent on:
  • The chemical form of the radionuclide and the route of exposure, as both affect the biokinetics of absorption and distribution throughout the body.
  • Assays including nasal smears, whole body or specific organ counts, and 24 hour urine and faeces collections.
  • An estimation of the amount of retained radionuclide. This requires expert interpretation and advice from a nuclear medicine physician or health physicist following bioassay.
  • The advice is usually expressed relative to the annual limit of intake (ALI) for occupational exposure. One ALI is the maximum permissible exposure each year, without detectable health risk. One ALI corresponds to a committed effective dose equivalent of 0.05 Sv, or a committed effective dose equivalent of 0.5 Sv to any individual organ or tissue, whichever is the more limiting.
  • The age of the patient, as the relative biological effect for children is increased.
  • The contraindications to, and side effects from, decorporation agents. Use of the decorporation agent itself must be weighed against the clinical scenario and projected health risk from the estimated burden of radionuclide.
  • The rationing of resources in a mass casualty scenario may influence treatment rationale.
  • In general, decorporation treatment is not required for < 1 ALI, but should be considered for 2 to 10 ALI dependent on clinical circumstances and resource availability, and is recommended for > 10 ALI.
Treatment effectiveness is likely to be greatest when commenced as soon as possible. The immediate decision to treat is likely to be based on incomplete information, as bioassay results are likely to be unavailable initially, or even for days. An evaluation of the incident details, especially the presence of air-borne contaminants, the identity and nature of the radionuclide, and the amount of contamination on the face and nares, may be all that is available to inform the initial decision to treat.

Following initial treatment, more accurate assessment of internal contamination can be made with repeated bioassay and physical measurements. This will allow more considered treatment decisions to be made, based on the probability of radiation-induced disease occurring in the patient’s lifetime.
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References:

  1. Alexander GA, Swartz HM, Amundsen SA, Blakely WF, Buddemeier B, et al. BiodosEPR-2006 meeting: acute dosimetry consensus committee recommendations on biodosimetry applications in events involving uses of radiation by terrorists and radiation accidents. Radiation Measurements. 2007; 42: 972-996.
  2. Armed Forces Radiobiology Research Institute. Medical management of radiological casualties handbook, military medical operations. 2nd ed. Bethesda: Armed Forces Radiobiology Research Institute; 2003.
  3. Crawford SW. Diagnosis and management of pulmonary problems associated with radiation injury. In: Ricks RC, Berger ME, O’Hara Jnr FM, editors. The medical basis for radiation-accident preparedness. The Parthenon Publishing Group. 2002: 131-8.
  4. Dagle GE, Sanders CL. Radionuclide injury to the lung. Environmental Health Perspectives 1984; 55: 129-137.
  5. Dart RC, editor. Medical toxicology. 3rd ed. Lippincott, Williams & Wilkins; 2004.
  6. Gerber GB, Thomas RG, editors. Internal contamination guidebook, Radiation Protection Dosimetry 1992; 41 (1): 1-49.
  7. Goans RE. Update on the treatment of internal contamination. In: Ricks RC, Berger ME, O’Hara Jnr FM, editors. The medical basis for radiation-accident preparedness. The Parthenon Publishing Group; 2002: 201-16.
  8. Guilmette RA, Muggenburg BA, Cambron BL. Bronchoalveolar lavage: a new bioassay tool for plutonium inhalation exposures. Journal of Occupational Medicine. 1986; 28: 492 – 496.
  9. Harrison J, Leggett R, Lloyd D, Phipps A, Scott B. Polonium-210 as a poison. J Radiol Prot. 2007; 27: 17-40
  10. Inchiosa MA. Toxicokinetics: deposition, absorption, distribution, and excretion. In: Salem H, Katz SA, editors. Inhalation toxicology, 2nd ed. Taylor & Francis Group, CRC Press; 2006: 405-38.
  11. International Atomic Energy Agency. Methods for assessing occupational radiation doses due to intakes of radionuclides, safety reports series, no. 37. Vienna: IAEA; 2004.
  12. Marcus CS, California Disaster Medical Assistance Team-9, Western National Medical Response Team, Los Angeles County Department of Health Services Emergency Medical Services Agency. Administration of decorporation drugs to treat internal radionuclide contamination: medical emergency response to radiologic incidents. UCLA and Los Angeles County Department of Health Services.
  13. Marcus CS, Siegel JA, Sparks RB. Medical management of internally radiocontaminated patients. Los Angeles County Department of Health Services, Emergency Medical Services Agency; 2006.
  14. Medical Preparedness and Response Sub-Group, Department of Homeland Security Working Group on Radiological Dispersal Device (RDD) Preparedness. Medical guidelines. United States Department of Homeland Security; 2003
  15. Methods of Treatment. In Radiation Protection Dosimetry. Nuclear Technology Publishing; 1992; 41(1): 27-36
  16. Murray L, Daly F, Little M, Cadogan M, editors. Toxicology handbook. Elsevier Australia; 2007.
  17. National Council on Radiation Protection and Measurements. Management of persons accidentally contaminated with radionuclides, NCRP Report No. 65. Bethesda: National Council on Radiation Protection and Measurements; 1980.
  18. O’Connell KP, Salem H. Health Aspects of Bioaerosols. In: Salem H, Katz SA, editors. Inhalation toxicology, 2nd ed. Taylor & Francis Group, CRC Press; 2006: 913-32.
  19. Pacific Northwest National Laboratory. Methods and models of the Hanford internal dosimetry program, radiation and health technology. Richland, Washington: Pacific Northwest National Laboratory; 2003. Available from Pacific Northwest National Laboratory website.
  20. Smith H. Assessment of and therapy following contamination through the lungs or gastrointestinal tract. J Soc Radiol Prot; 1985; 5 (1): 15-20.
  21. Smith JM, Spano MA. Interim guidelines for hospital response to mass casualties from a radiological incident. United States Department of Health and Human Services, Centers for Disease Control and Prevention; 2003.
  22. Voelz GL. Assessment and Treatment of Internal Contamination: General Principles. In: Gusev IA, Guskova AK, Mettler FA, editors. Medical management of radiation accidents, 2nd ed. CRC Press; 2001: 319-36.

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