There is a direct relationship between the degree of the neutropenia that emerges after exposure to radiation and the increased risk of developing infection. Since there are no controlled studies of therapeutic intervention in humans, most of the current recommendations are based on animal research.

The treatment of established or suspected infection following exposure to radiation (characterized by neutropenia and fever) is similar to the one used for other febrile neutropenic patients. However, important differences between the two conditions exist. Individuals that develop neutropenia after exposure to radiation are also susceptible to irradiation damage in other tissues, such as the gastrointestinal tract, lungs and central nervous system. These patients may require therapeutic interventions not needed in other types of neutropenic patients. The response of irradiated animals to antimicrobial therapy can be unpredictable, as was evident in experimental studies where metronidazole and pefloxacin therapies were detrimental.

Antimicrobials that reduce the number of the strict anaerobic component of the gut flora (i.e., metronidazole) generally should not be given because they may enhance systemic infection by aerobic or facultative bacteria, thus facilitating mortality after irradiation.

An empirical regimen of antimicrobials should be chosen based on the pattern of bacterial susceptibility and nosocomial infections in the affected area and medical center and the degree of neutropenia. Broad-spectrum empirical therapy (see below for choices) with high doses of one or more antibiotics should be initiated at the onset of fever. These antimicrobials should be directed at the eradication of Gram-negative aerobic bacilli ( i.e., Enterobacteriace, Pseudomonas ) that account for more than three quarters of the isolates causing sepsis. Because aerobic and facultative Gram-positive bacteria (mostly alpha-hemolytic streptococci) cause sepsis in about a quarter of the victims, coverage for these organisms may also be needed.

A standardized management plane of febrile, neutropenic patients must be devised in each institution or agency. Empirical regimens must contain antibiotics broadly active against Gram-negative aerobic bacteria (quinolones: i.e., ciprofloxacin, levofloxacin, a third- or fourth-generation cephalosporin with pseudomonal coverage: e.g., cefepime, ceftazidime, or an aminoglycoside: i.e. gentamicin, amikacin).

Where radioactive contamination is present, a gas mask, dust mask, or good hygiene practices may offer protection, depending on the nature of the contaminant. Potassium iodide (KI) tablets can reduce the risk of cancer in some situations due to slower uptake of ambient radioiodine. Although this does not protect any organ other than the thyroid gland, their effectiveness is still highly dependent on the time of ingestion which would protect the gland for the duration of a twenty-four-hour period. They do not prevent acute radiation syndrome as they provide no shielding from other environmental radionuclides.

In industrialized countries, Medical imaging contributes almost as much radiation dose to the public as natural background radiation. Collective dose to Americans from medical imaging grew by a factor of six from 1990 to 2006, mostly due to growing use of 3D scans that impart much more dose per procedure than traditional radiographs. CT scans alone, which account for half the medical imaging dose to the public, are estimated to be responsible for 0.4% of current cancers in the United States, and this may increase to as high as 1.5-2% with 2007 rates of CT usage; however, this estimate is disputed. Other nuclear medicine techniques involve the injection of radioactive pharmaceuticals directly into the bloodstream, and radiotherapy treatments deliberately deliver lethal doses (on a cellular level) to tumors and surrounding tissues.

It has been estimated that CT scans performed in the US in 2007 alone will result in 29,000 new cancer cases in future years. This estimate is criticized by the American College of Radiology (ACR), which maintains that the life expectancy of CT scanned patients is not that of the general population and that the model of calculating cancer is based on total-body radiation exposure and thus faulty.

In accordance with ICRP recommendations, most regulators permit nuclear energy workers to receive up to 20 times more radiation dose than is permitted for the general public. Higher doses are usually permitted when responding to an emergency. The majority of workers are routinely kept well within regulatory limits, while a few essential technicians will routinely approach their maximum each year. Accidental overexposures beyond regulatory limits happen globally several times a year. Astronauts on long missions are at higher risk of cancer, see cancer and spaceflight.

Some occupations are exposed to radiation without being classed as nuclear energy workers. Airline crews receive occupational exposures from cosmic radiation because of reduced atmospheric shielding at altitude. Mine workers receive occupational exposures to radon, especially in uranium mines. Anyone working in a granite building, such as the US Capitol, is likely to receive a dose from natural uranium in the granite.

Chronic radiation syndrome is a constellation of health effects that occur after months or years of chronic exposure to high amounts of ionizing radiation. Chronic radiation syndrome develops with a speed and severity proportional to the radiation dose received, i.e., it is a deterministic effect of radiation exposure, unlike radiation-induced cancer. It is distinct from acute radiation syndrome in that it occurs at dose rates low enough to permit natural repair mechanisms to compete with the radiation damage during the exposure period. Dose rates high enough to cause the acute form (> ~0.1 Gy/h) are fatal long before onset of the chronic form. The lower threshold for chronic radiation syndrome is between 0.7 and 1.5 Gy, at dose rates above 0.1 Gy/yr. This condition is primarily known from the Kyshtym disaster, where 66 cases were diagnosed, and has received little mention in Western literature. A future ICRP publication, currently in draft, may recognize the condition but with higher thresholds.

In 2013, Alexander V. Akleyev described the chronology of the clinical course or CRS while presenting at ConRad in Munich, Germany. In his presentation, he defined the latent period as being 1-5 years, and the formation coinciding with the period of maximum radiation dose. The recovery period was described as being 3-12 months after exposure ceased. He concluded that "CRS represents a systemic response of the body as a whole to the chronic total body exposure in man." In 2014, Akleyev's book "Comprehensive analysis of chronic radiation syndrome, covering epidemiology, pathogenesis, pathoanatomy, diagnosis and treatment" was published by Springer.

Radiation burns are caused by exposure to high levels of radiation. Levels high enough to cause burn are generally lethal if received as a whole-body dose, whereas they may be treatable if received as a shallow or local dose.

If the status of the source patient is unknown, their blood should be tested for HIV as soon as possible following exposure. The injured person can start antiretroviral drugs for PEP as soon as possible, preferably within three days of exposure. There is no vaccine for HIV. When the source of blood is known to be HIV positive, a 3-drug regimen is recommended by the CDC; those exposed to blood with a low viral load or otherwise low risk can use a 2-drug protocol. The antivirals are taken for 4 weeks and can include nucleoside reverse transcriptase inhibitors (NRTIs), nucleotide reverse transcriptase inhibitors (NtRTIs), Non-nucleoside reverse transcriptase inhibitors (NNRTIs), protease inhibitors (PIs), or fusion inhibitors. All of these drugs can have severe side effects. PEP may be discontinued if the source of blood tests HIV-negative. Follow-up of all exposed individuals includes counseling and HIV testing for at least six months after exposure. Such tests are done at baseline, 6 weeks, 12 weeks, and 6 months and longer in specific circumstances, such as co-infection with HCV.

Immunoglobulin and antivirals are not recommended for hepatitis C PEP. There is no vaccine for HCV; therefore, post-exposure treatment consists of monitoring for seroconversion. There is limited evidence for the use of antivirals in acute hepatitis C infection.

Fluoroscopy may cause burns if performed repeatedly or for too long.

Similarly, Computed Tomography and traditional Projectional Radiography have the potential to cause radiation burns if the exposure factors and exposure time are not appropriately controlled by the operator.

A study of radiation induced skin injuries has been performed by the Food and Drug Administration (FDA) based on results from 1994, followed by an advisory to minimize further fluoroscopy-induced injuries. The problem of radiation injuries due to fluoroscopy has been further investigated in review articles in 2000, 2001, 2009 and 2010.

Ionizing radiation is classified as a neurotoxicant. A 2004 cohort study concluded that irradiation of the brain with dose levels overlapping those imparted by computed tomography can, in at least some instances, adversely affect intellectual development. Prenatal exposure to ionizing radiation at the 8-15 and 16–25 weeks after ovulation was found to induce severe mental retardation as well as variation in intelligence quotient (IQ) and school performance. It is uncertain, if there exist a threshold, under which one or more of these effects, of prenatal exposure to ionizing radiation, do not exist. Cumulative equivalent doses above 500 mSv of ionizing radiation to the head were proven with epidemiological evidences to cause cerebro-vascular atherosclerotic damage. The equivalent dose of 500 mGy x-rays is 500 mSv.

Radiation therapy was found to cause cognitive decline. Cognitive decline was especially apparent in young children, between the ages of 5 to 11. Studies found, for example, that the IQ of 5-year-old children declined each year after treatment by additional several IQ points, thereby the child's IQ decreased and decreased while growing older.

Injury is damage to the body caused by external force. This may be caused by accidents, falls, hits, weapons, and other causes. Major trauma is injury that has the potential to cause prolonged disability or death.

In 2013, 4.8 million people died from injuries, up from 4.3 million in 1990. More than 30% of these deaths were transport-related injuries. In 2013, 367,000 children under the age of five died from injuries, down from 766,000 in 1990. Injuries are the cause of 9% of all deaths, and are the sixth-leading cause of death in the world.

Measures to reduce facial trauma include laws enforcing seat belt use and public education to increase awareness about the importance of seat belts and motorcycle helmets. Efforts to reduce drunk driving are other preventative measures; changes to laws and their enforcement have been proposed, as well as changes to societal attitudes toward the activity. Information obtained from biomechanics studies can be used to design automobiles with a view toward preventing facial injuries. While seat belts reduce the number and severity of facial injuries that occur in crashes, airbags alone are not very effective at preventing the injuries. In sports, safety devices including helmets have been found to reduce the risk of severe facial injury. Additional attachments such as face guards may be added to sports helmets to prevent orofacial injury (injury to the mouth or face); mouth guards also used.

The role of chemotherapy in DIPG remains unclear. Studies have shown little improvement in survival, although efforts (see below) through the Children's Oncology Group (COG), Paediatric Brain Tumour Consortium (PBTC), and others are underway to explore further the use of chemotherapy and other drugs. Drugs that increase the effect of radiotherapy (radiosensitizers) have shown no added benefit, but promising new agents are under investigation. Immunotherapy with beta-interferon and other drugs has also had little effect in trials. Intensive or high-dose chemotherapy with autologous bone marrow transplantation or peripheral blood stem cell rescue has not demonstrated any effectiveness in brain stem gliomas. Future clinical trials may involve medicines designed to interfere with cellular pathways (signal transfer inhibitors), or other approaches that alter the tumor or its environment.

Most head injuries are of a benign nature and require no treatment beyond analgesics and close monitoring for potential complications such as intracranial bleeding. If the brain has been severely damaged by trauma, neurosurgical evaluation may be useful. Treatments may involve controlling elevated intracranial pressure. This can include sedation, paralytics, cerebrospinal fluid diversion. Second line alternatives include decompressive craniectomy (Jagannathan et al. found a net 65% favorable outcomes rate in pediatric patients), barbiturate coma, hypertonic saline and hypothermia. Although all of these methods have potential benefits, there has been no randomized study that has shown unequivocal benefit.

Clinicians will often consult clinical decision support rules such as the Canadian CT Head Rule or the New Orleans/Charity Head injury/Trauma Rule to decide if the patient needs further imaging studies or observation only. Rules like these are usually studied in depth by multiple research groups with large patient cohorts to ensure accuracy given the risk of adverse events in this area.

Conventional radiotherapy, limited to the involved area of tumour, is the mainstay of treatment for DIPG. A total radiation dosage ranging from 5400 to 6000 cGy, administered in daily fractions of 150 to 200 cGy over 6 weeks, is standard. Hyperfractionated (twice-daily) radiotherapy was used previously to deliver higher radiation dosages, but did not lead to improved survival. Radiosurgery (e.g., gamma knife or cyberknife) has no role in the treatment of DIPG.

Pharmacotherapy is the utilization of drugs to treat an illness. There are several different drugs that have been used to alleviate symptoms experienced after a head injury including anti-depressants such as amitriptyline and sertraline. Use of these drugs has been associated with a decrease in depression and increased functioning in social and work environments. An antidiuretic called Desmopressin Acetate (DDAVP) has also been shown to improve memory performance in patients

Recent studies have examined the preventative effects of progesterone on brain injuries. Phase III trials are currently being conducted at 17 medical centers across the United States. Preliminary results have shown a 50% reduction in mortality in those treated with progesterone and showed an improved functional outcome.

Overall, the efficacy of pharmacotherapuetic treatments is dependent on the treatment being used and the symptoms being targeted by the treatment.

Many closed-head injuries can be prevented by proper use of safety equipment during dangerous activities. Common safety features that can reduce the likelihood of experiencing a brain injury include helmets, hard hats, car seats, and safety belts. Another safety precaution that can decrease a person's risk for brain injury is "not" to drink and drive or allow oneself to be driven by a person who has been drinking or who is otherwise impaired.

Helmets can be used to decrease closed-head injuries acquired during athletic activities, and are considered necessary for sports such as American "tackle" football, where frequent head impacts are a normal part of the game. However, recent studies have questioned the effectiveness of even American football helmets, where the assumed protection of helmets promotes far more head impacts, a behavior known as risk compensation. The net result seems to have been an increase, not decrease, in TBI. The similar sports of Australian-rules football and rugby are always played helmetless, and see far fewer traumatic brain injuries. (See Australian rules football injuries.)

Bicycle helmets are perhaps the most promoted variety of helmet, based on the assumption that cycling without a helmet is a dangerous activity, with a large risk of serious brain injury. However, available data clearly shows that to be false. Cycling (with approximately 700 American fatalities per year from all medical causes) is a very minor source of fatal traumatic brain injury, whose American total is approximately 52,000 per year. Similarly, bicycling causes only 3% of America's non-fatal TBI.

Still, bicycle-helmet promotion campaigns are common, and many U.S jurisdictions have enacted mandatory bicycle-helmet laws for children. A few such jurisdictions, a few Canadian provinces, plus Australia and New Zealand mandate bicycle helmets even for adults. A bicycle-helmet educational campaign directed toward children claimed an increase in helmet use from 5.5% to 40.2% leading to a claimed decrease in bicycle-related head injuries by nearly 67%. However, other sources have shown that bicycle-helmet promotion reduces cycling, often with no per-cyclist reduction in TBI.

Estimates of bicycle-helmet use by American adults vary. One study found that only 25-30% of American adults wear helmets while riding bicycles, despite decades of promotion and despite sport cyclists' adoption of helmets as part of their uniform. It would appear that the typical American adult correctly recognizes ordinary cycling as a very minor risk.

Following the commercial (as opposed to public-health) success of bicycle helmets, there have been successful attempts to promote the sale of ski helmets. Again, results have been less than impressive, with great increases in helmet use yielding no reduction in fatalities, and with most injury reduction confined to lacerations, contusions, and minor concussions, as opposed to more serious head injuries.

There have been rare campaigns for motoring helmets. Unfortunately, just as people greatly overestimate the TBI danger of bicycling, they greatly underestimate the risk of motoring, which remains the largest source of TBI in the developed world, despite the protective effects of seatbelts and airbags.

An occupational injury is bodily damage resulting from working. The most common organs involved are the spine, hands, the head, lungs, eyes, skeleton, and skin. Occupational injuries can result from exposure to occupational hazards (physical, chemical, biological, or psychosocial), such as temperature, noise, insect or animal bites, blood-borne pathogens, aerosols, hazardous chemicals, radiation, and occupational burnout.

While many prevention methods are set in place, injuries may still occur due to poor ergonomics, manual handling of heavy loads, misuse or failure of equipment, exposure to general hazards, and inadequate safety training.

While less studies have been completed examining deintensification in this setting, than in primary radical radiation for this cancer (see below), it is an area of active investigation. In one single institution study, a decision was made to reduce the radiation dose in high risk patients with HPV+OPC from 66 to 60 Gy, corresponding to the actual evidence, and follow up has shown no decrease in cancer control. Current trials, both in North America and Europe (such as ECOG 3311 and PATHOS) use 50 Gy as the comparison arm. The comparator of 50 Gy was chosen on the grounds of (i) the exquisite sensitivity of HPV+OPC to radiation, both "in vitro" and "in vivo"; ECOG 1308 showing excellent disease control at 54 Gy; and data suggesting that 50 Gy in 1.43 Gy (iso-effective dose 43 Gy in 2.0 Gy was sufficient to electively treat the neck. Other studies are evaluating doses as low as 30 Gy in high risk cases.

Chemotherapy has been used concurrently with radiation in this setting, as in primary treatment with radical radiation, particularly where pathological features indicated a higher risk of cancer recurrence. a number of studies have suggested that this does not improve local control, although adding toxicity.

Minimizing exposure to sources of ultraviolet radiation (the sun and sunbeds), following sun protection measures and wearing sun protective clothing (long-sleeved shirts, long trousers, and broad-brimmed hats) can offer protection.

Using artificial light for tanning was once believed to help prevent skin cancers, but it can actually lead to an increased incidence of melanomas.

The body uses UV light to generate vitamin D so there is a need to balance getting enough sunlight to maintain healthy vitamin D levels and reducing the risk of melanoma; it takes around a half hour of sunlight for the body to generate its vitamin D for the day and this is about the same amount of time it takes for fair-skinned people to get a sunburn. Exposure to sunlight can be intermittent instead of all at one time.

The World Health Organization (WHO) developed the International Classification of External Causes of Injury (ICECI). Under this system, injuries are classified by

- mechanism of injury;

- objects/substances producing injury;

- place of occurrence;

- activity when injured;

- the role of human intent;

and additional modules. These codes allow the identification of distributions of injuries in specific populations and case identification for more detailed research on causes and preventive efforts.

The United States Bureau of Labor Statistics developed the Occupational Injury and Illness Classification System (OIICS). Under this system injuries are classified by

- nature,

- part of body affected,

- source and secondary source, and

- event or exposure.

The OIICS was first published in 1992 and has been updated several times since.

The Orchard Sports Injury Classification System (OSICS) is used to classify injuries to enable research into specific sports injuries.

In children with uncomplicated minor head injuries the risk of intra cranial bleeding over the next year is rare at 2 cases per 1 million. In some cases transient neurological disturbances may occur, lasting minutes to hours. Malignant post traumatic cerebral swelling can develop unexpectedly in stable patients after an injury, as can post traumatic seizures. Recovery in children with neurologic deficits will vary. Children with neurologic deficits who improve daily are more likely to recover, while those who are vegetative for months are less likely to improve. Most patients without deficits have full recovery. However, persons who sustain head trauma resulting in unconsciousness for an hour or more have twice the risk of developing Alzheimer's disease later in life.

Head injury may be associated with a neck injury. Bruises on the back or neck, neck pain, or pain radiating to the arms are signs of cervical spine injury and merit spinal immobilization via application of a cervical collar and possibly a long board.If the neurological exam is normal this is reassuring. Reassessment is needed if there is a worsening headache, seizure, one sided weakness, or has persistent vomiting.

To combat overuse of Head CT Scans yielding negative intracranial hemorrhage, which unnecessarily expose patients to radiation and increase time in the hospital and cost of the visit, multiple clinical decision support rules have been developed to help clinicians weigh the option to scan a patient with a head injury. Among these are the Canadian Head CT rule, the PECARN Head Injury/Trauma Algorithm, and the New Orleans/Charity Head Injury/Trauma Rule all help clinicians make these decisions using easily obtained information and noninvasive practices.

The probability of xerostomia at one year increases by 5% for every 1Gy increase in dose to the parotid gland. Doses above 25–30 Gy are associated with moderate to severe xerostomia. Similar considerations apply to the submandibular gland, but xerostomia is less common if only one parotid gland is included in the radiated field and the contralateral submandibular gland is spared (less than 39 Gy) In the same manner, radiation dose to the pharyngeal constrictor muscles, larynx, and cricopharyngeal inlet determine the risk of dysphagia (and hence dependence on gastrostomy tube feeds). The threshold for this toxicity is volume-dependent at 55–60 Gy, with moderate to severe impairment of swallowing, including aspiration, stricture and feeding tube dependence above a mean dose of 47 Gy, with a recommended dose to the inferior constrictor of less than 41 Gy. Dose-toxicity relationships for the superior and middle constrictors are steep, with a 20% increase in the probability of dysphagia for each 10 Gy. For late dysphagia, threshold mean total constrictor doses, to limit rates of greater than or equal to grade 2 and 3 below 5% were 58 and 61 Gy respectively. For grade 2 dysphagia, the rate increased by 3.4% per Gy. Doses above 30 Gy to the thyroid are associated with moderate to severe hypothyroidism. Subjective, patient-reported outcomes of quality of life also correlate with radiation dose received.

Altered fractionation schemes, such as RTOG 9003 and RTOG 0129 have not conferred additional benefit. Radiation dose recommendations were largely determined empirically in clinical studies with few HPV+OPC patients, and have remained unchanged for half a century, making it difficult to determine the optimum dose for this subgroup. A common approach uses 70 Gy bilaterally and anteriorly, such as RTOG 9003 (1991–1997) and RTOG 0129 (2002–2005). For lateralized tonsil cancer unilateral neck radiation is usually prescribed, but for tongue base primaries bilateral neck radiation is more common, but unilateral radiation may be used where tongue base lesions are lateralised.

Sunscreen appears to be effective in preventing melanoma. In the past, use of sunscreens with a sun protection factor (SPF) rating of 50 or higher on exposed areas were recommended; as older sunscreens more effectively blocked UVA with higher SPF. Currently, newer sunscreen ingredients (avobenzone, zinc oxide, and titanium dioxide) effectively block both UVA and UVB even at lower SPFs. Sunscreen also protects against squamous cell carcinoma, another skin cancer.

Concerns have been raised that sunscreen might create a false sense of security against sun damage.

Radiation-induced cognitive decline describes the possible correlation between radiation therapy and mild cognitive impairment. Radiation therapy is used mainly in the treatment of cancer. Radiation therapy can be used to cure care or shrink tumors that are interfering with quality of life. Sometimes radiation therapy is used alone; other times it is used in conjunction with chemotherapy and surgery. For people with brain tumors, radiation can be an effective treatment because chemotherapy is often less effective due to the blood–brain barrier. Unfortunately for some patients, as time passes, people who received radiation therapy may begin experiencing deficits in their learning, memory, and spatial information processing abilities. The learning, memory, and spatial information processing abilities are dependent on proper hippocampus functionality. Therefore, any hippocampus dysfunction will result in deficits in learning, memory, and spatial information processing ability.

The hippocampus is one of two structures of the central nervous system where neurogenesis continues after birth. The other structure that undergoes neurogenesis is the olfactory bulb. Therefore, it has been proposed that neurogenesis plays some role in the proper functionality of the hippocampus and the olfactory bulb. To test this proposal, a group of rats with normal hippocampal neurogenesis (control) were subjected to a placement recognition exercise that required proper hippocampus function to complete. Afterwards a second group of rats (experimental) were subjected to the same exercise but in that trial their neurogenesis in the hippocampus was arrested. It was found that the experimental group was not able to distinguish between its familiar and unexplored territory. The experimental group spent more time exploring the familiar territory, while the control group spent more time exploring the new territory. The results indicate that neurogenesis in the hippocampus is important for memory and proper hippocampal functionality. Therefore, if radiation therapy inhibits neurogenesis in the hippocampus it would lead to the cognitive decline observed in patients who have received this radiation therapy.

In animal studies discussed by Monje and Palmer in "Radiation Injury and Neurogenesis", it has been proven that radiation does indeed decrease or arrest neurogenesis altogether in the hippocampus. This decrease in neurogenesis is due to apoptosis of the neurons which usually occurs after irradiation. However it has not been proven whether the apoptosis is a direct result of the radiation itself or if there are other factors that cause neuronal apoptosis, namely changes in the hippocampus micro-environment or damage to the precursor pool. Determining the exact cause of the cell apoptosis is important because then it may be possible to inhibit the apoptosis and reverse the effects of the arrested neurogenesis.