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Page 1: ahma20.yolasite.comahma20.yolasite.com/resources/PHYSICAL INJURIES.docx · Web viewPathophysiology of burns: Local effects: The local effects are produced in part by accelerated metabolism

PHYSICAL INJURIESThis form of tissue injury is produced by the application of heat or

hot liquids or gases or solid heated substances to the surface of the body. It is also produced by the action of concentrated acids or alkalis and through contact with electrically charged conductors and exposure to sun rays, X-rays and radiation.

BURNSBurns are the commonest form of thermal injuries and are due to. the local effect of dry heat as a result of contact with a flame, heated objects or commonly follow the ignition of clothing which has come in contact with a coal gas or an electric fire.Pathophysiology of burns:Local effects:

The local effects are produced in part by accelerated metabolism of the cells, in part by inactivation of temperature critical enzymes and in part by inducing vascular injury.The severity of burn depends on the length of exposure and the temperature of the heat source.• Several classifications are put to describe these local effects:A. Dupuytren’s classification:It depends on the depth to which the tissue has been destroyed and the nature of the changes that have occurred in the burned tissue. It includes six degrees:First degree burn:It consists of erythema of the skin and it heals without scar. Second degree burn: It results in detachment of the epidermis from the dermis with the formation of vesicles.Third degree burn:It results in the destruction of the full thickness of the epidermis and the epj4ia1 lands and hair follicles. It is a shock degree due to stimulation of sensory nerve endings, it heals with elastic epithelial scar.Fourth degree burn:There is destruction of all the dermis down to the subcutaneous tissue.Fifth degree burn:it consists of total necrosis of soft tissue (including muscle) and bone.Sixth degree burn:There is complete carbonization of the burned part with charring of bones. It follows exposure to temperature of 300°C.

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B. Another classification of burns is based on the skin thickness and entails only two degrees:Partial thickness and full thickness bums.l- Full thickness burn:It denotes an open wound. It is not capable of self repair and must begrafted since there has been destruction of the dermal appendages from which re-epithelialization occurs.2. Partial thickness burn:it is produced by low intensity of heat. It comprises only erythema and vesicle formation. Some dermal epithelial elements have survived, so potential regenerative capacity is retained.This classification is important in skin grafting.Factors affecting prognosis of burns:I. Extent: .Involvement of a third or one half of the body surface will prove fatal due to associated hypovolaemic shock, hence fluid therapy is essential. To. assess the surface area affected we rely on (rule of nines”:head and neck and upper extremities each constitute 9% of the total body surface area, anterior trunk, posterior trunk and lower extremities each constitute 18% and the perineum makes .up the remaining 1%.2- Degree of burns:The third degree (Dupuytren) is the serious one due to associated neurogenic shock, so pain killer is indicated.3. Position of burns:When the bums involve the head and neck, trunk or the anterior abdominal wall, the patient’s condition is always grave. Deep burn of an arm or leg, although it may result in grave disability, is unlikely to he-fatal.4. Age of burned patient:In extremes of age the prognosis is guarded. In children, having thin skin, wide body surface area in relation to their body weight and increased oxygen need, all these factors endanger their lives. Burning among elderly persons are fatal due to pre-existing diseases which aggravate burns .and they are more vulnerable to infection and serious systemic effects of bums.Causes of death from burns:Early causes:1. Primary neurogenic shock.2. l-lypovolaemic shock due to fluid loss from the burnt area.3. Acute myocardial insufficiency and cardiac arrest (secondary to

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hyperkalaemia from hydrolyzed erythrocytes).4. Biochemical disturbance secondary to the electrolyte loss anddestruction of red blood cells and tissues.5. Toxemia following absorption of various metabolites and burntoxins.6. Poisoning by inhaling smoke and irritating gasses e.g. carbonmonoxide, carbon dioxide, sulphur dioxide, nitrogen dioxide andhydrocyanic acid, following burning of organic matters, silky and woolymaterials as well as artificial leatherette and .plastic materials..7. Glottic or pulmonary edema caused by smoke or flame in burning ofPace and neck regions.8. Pulmonary fat embolism if burns affect fatty area.9. Associated trauma e.g. head injury or traumatic asphyxia followingcollapse of a building.Delayed causes:I. Infection: local and systemic especially of the respiratory system.2. Acute renal failure.3. Gastrointestinal hemorrhage by perforating 9jjn’sjgcers (in the duodenum)Jt is due to tissue hypoxia, elevated catecholamines and acid peptic mucosal digestion.4. Suprarenal hemorrhage and failure.5. Brain herniation due to edema and increased intracranial pressure.Healing of burns:First & second degrees burn: The erythema will disappear within J.3 days. Vesicles may resolve by absorption of fluid but the raised epidermis is later shed and replaced by new epithelial growth from the periphery of the bum and from the hair follicles within two weeks. Repair is normally complete without scar formation.Third & fourth degrees burn:Third degree burn heals with epithelial elastic scar within a month. Fourth degree burns always heal with scar formation because the true skin is damaged and the repair is by growth of new tissue, Within a week the necrotic tissue separates to leave an ulcer which in turns, heals slowly with a disfiguring scar and often requires correction by plastic surgery. Ungrafted burn may be seen still unhealed, for years.Fifth & sixth degrees burn:These are deep burns and devitaliation of tissues in the burnt area renders them prone to infection and slow to repair.

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The age of burn scar depends on the extent and depth of the burn. If not extensive it may remain red and sensitive for about two months, then itattains a coppery colour up to six months then the colour fades away.Post mortem artifacts caused by heat:In addition to burns, damage may be produced by the action of heat on the body and must be distinguished from injuries caused by other means due to violence.1. Heat ruptures:They are produced by a splitting of the soft parts. They may resemble lacerations or incised wounds.A distinction between heat rupture and incised wound is by the absence of bleeding in heat rupture as heat coagulates the blood in the vessels. Also the demonstration of nerves in the floor of the heat rupture is an important differentiating point.A distinction from lacerations is made by the absence of bruising or other signs of vital reaction in the margins of heat rupture.2. Heat contractures or pugilistic attitude:The posture of a body which has been exposed to fire is often characteristic and the so-called “pugilistic attitude” or heat rigor is a well known feature of the effects of heat. Coagulation and contraction of the mus often occur, thus the limbs, the arms in particular, are fixed in an attitude commonly adopted by boxers. This position may give a false impression that the victim was engaged in a fight at the moment of death.3. Heat hematoma:It follows the exposure of the head to intense heat sufficient to cause charring of the skull. The blood in the hematoma is converted into a soft friable clot of light chocolate color, may be pinkish if the victim’s bloodcontains carbon monoxide. Heat haematoma may be mistaken with anextradural hemorrhage, but it is unaccompanied by any signs of injury by blunt force and it follows the distribution of the charring of the outer table of the skull.4. Thermal fractures:Fractures of the skull are often found in charred bodies. They are of two types: The first one results from rapid increase in intracranial pressure and he fragments are displaced outwards. In the other type the fracture is produced by rapid desiccation of the bone and only involves the outer table of the skull. There is no displacement and the lines of the fracture are frequently stellate. Thermal fractures may simulate ante-mortem fractures due to violence.

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Differentiation between both could be done by the following table:

Traumatic fracture Thermal fracture

Signs of ante-mortem burn

Absent .

Present and extensive and may .be charring

Associated scalp injuries

Common (due to blunt force)

Absent, if present, they are heat ruptures

Skull fracture

Related to the scalp injUry appears as localized depression with shelving of bone

Unrelated to the scalp injury usually stellate fissure -

fracture and follows the suture lines

Haematoma • .

Extensive, related to the fracture, firm adherent and red in colour .

It follows the distribution of the charring of bone, soft, friable and chocolate brown in colour

Brain .

Oedematous, fills the cranial cavity may show contusion or laceration,

Desiccated, shrinks to a third of its normal size with no signs of injury

Evidence of ante-mortem violence

Present .

Absent - .

NB: Thermal fractures should be differentiated also from postmortem fracture following rough handling of the dead body.Antemortem and postmortem burns:The differentiation between antemortem and postmortem burns is very important to confirm that the victim was alive at the time. the fire reached him, as it frequently happens that bodies are burnt after death in order to conceal the presence of other crimes.An antemortem burn is characterized by:1. Redness of the parts.2. Vesicles are surrounded by a thin bright red area of inflammation. They are filled with fluid rich in albumin and chloride. After removal of the vesicle, they may be present and it indicates a survival of at least 36 hours.

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3. lea! examination of an antemortem burn is reliable evidence. It will reveal tissue reaction.4. Fine carbon particles in the ha and bronchi are often mixed with mucous following inhalation of smoke . 5. The blood contains carboxyhaemoglobin in a significant amount i.e.60.70%. I is an evidence of antemortem burns, as carbon monoxide is not absorbed by a body after death. The increased amount of carboxyhaemoglobin in the blood may explain why the victim was unable to escape.Postmortem examination of a case of burn:Examination is directed to ascertaining the position and depth of burns whether they were sustained in life or not, and whether their situationgives any indication of the position of the body when the fire started.Externally:1-The clothes are burnt.2-The hairs are singed (in burns of hairy area).3. Soot is present in the nostrils, face and clothes.4. Any degree of burn could be found.5. The rate of cooling is diminished as the body temperature is raised atthe moment of death,6. In aseptic burns putrefactive changes are delayed.7. Heat rigor or pugilistic attitude is present.Internally:The internal signs depend on the site of burns, the time passed sincebums, the systemic effects of burns and the cause, of death.’in rapid death, there will be:1-Congestion of internal organs which may be cherry red in colour(carboxyhacmoglobin). 2-The blood in the blood vessels and heart may be viscid and coagulated (hypovolaemia and haemoconcentration) or dark and fluid (asphyxia )3-The tongue, larynx or trachea are inflamed and coated by a layer of soot adherent to the mucous.4-The larynx may be blistered and edematous (in burns of the neck). 5-Fat embolism (in bums of fatty areas).6. Thermal fracture (in severe burns of the head).In delayed death the internal signs may reveal:1- infection, local and systemic.2- Suprarenal hemorrhage.3-Rupture of Curling’s ulcers.4- Renal and hepatic necrosis.

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Circumstances of burns:Accidental:it is the commonest form of burns and are seen most frequently in infants, children and old persons. Also in persons who are unable to escape when a fire breaks out, being under the influence of drugs or alcohol. Accidental bums may also associate motor car and aeroplane accidents.Suicidal:It is also common especially amongkerosene then fire is set to them.Homicidal:It is uncommon where kerosene or other inflammable material is thrown over the victim and his clothing, and then a fire is lit. Another form. of a deliberately inflicted burn may be encountered among children in the course of the “battered baby syndrome”. Patterned burns are found, which correspond to a particular hot object which was applied to the skin.Postmortem burns:They are quite common to conceal the real crime as throttling, strangulation, firearm injuries, stab wounds, etc... The signs of antemortem burns will be absent.

SCALDSThese are tissue damage produced by the application of moist at asBoiling water or oils or steam. The injuries do not penetrate deeply. They consist of erythema and vesicles. They may be dangerous because of the extent of the body surface affected, or when affecting the upper air passages. They heal without leaving a scar. Scalds are usually caused by accidents, as. when steam-pipes burst, or a child is dropped into a hot bath or overturns a tea-pot. Very rarely the damage is produced deliberately as a mean of killing a child. The scald may show the course taken by the hot liquid trickling over the skin, and so indicate the position of the body at the time of injury.

CORROSIVE BURNSThese are burns produced by concentrated acj4..and alkalis. They

are seen in industrial, laboratory, and domestic accidents. Deliberate criminal assaults also occur. The injury is due to both thermal and chemical changes in the tissues and clothes.

Due to corrosive nature of these chemicals, there is no vesication of the affected skin and damage may be deep. Injuries produced by

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corrosive acids may be recognized by certain colour changes. Sulphuric acid: being hygroscopic acid will produce brownish, later black discoloration. Nitric agj: it combines with organic material, whether skin or fabric, to produce yellow discoloration due to the production of xanthoproteic or picric acid. hydrochloric acid: produces brownish red discoloration due to production of acid hematin.Corrosive alkali burn will colour the skin white with a soapy feel to the touch. Due to the penetrating nature of corrosive burns they heal by a disfiguring scar.

The following table differentiates between burns due to dry heat, moist heat and corrosives:

ELETRIC TRAUMAThe passage of electrical current through the tissue can cause skin lesions, organ damage and death. This injury is called Electrocution. Fatalities are usually accidental but suicides from electricity have increased in recent years.

ElectrocutionSymptomsAt the moment, of contact, there may be generalized muscular spasm which may cause the victim to grip the conductor firmly or may throw the individual some distance away. Sudden death may occur. If death does not occur and recovery takes place, the patient may. suffer from late effects of the electric injury.Causes of death:I. Immediate or electric death due to:1-Ventricular fibrillation.2-Tetanic asphyxia due to titanic contraction of the extrinsic muscles of respiration.3-Respiratory arrest due to paralysis of the respiratory centre,4- Cerebral anoxia: prolonged ventricular fibrillation may cause brain damage due to an inadequate blood supply.5- Neurological damage by the passage of the current through the head.II. Delayed death: from complications of electrical injury e.g. renal failure.III. Associated mechanical injury e.g. skull injury following fall from a height.Treatment:Although the victim may appear to be dead, immediate and energetic treatment may revive the individual. The victim should not be pulled

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away with bare hands. The current should be disconnected or the victim should be removed from the sour of contact by means of a wooden stick or by hands using rubber gloves or wrapped in several thickness of dry cloth. Artificial respiration should be continued till recovery oi the appearance of rigor mortis. Cardiac and res irato stimulants should be given. In the hospital defibrillator and mechanical respirator could be used.Effects of electrical injury:I. Skin:

The skin is a relatively thin layer but highly resistant to the passage of electric current. If this tissue resistance is diminished, the current can penetrate the skin and gives rise to the following effects:a. Current marks:They vary from superficial circumscribed lesions to severe burns with full thickness tissue necrosis. Current marks are found at the site of entrance and exit of the electric current. At the entrance the mark appears as a grayish white ulcer like opening with everted and corrugated exploded margins and necroses tissue. At the exit, the tissues are frequently split in the form of punctured or lacerated wounds. These marks are caused by the explosive electric force. Current mark is of the same size and sha e as the conductor with which the victim comes in contact. It gives useful information on the path of the current inside the body and it resists putrefaction.b. Electric burns:They follow prolonged contact with the electric source. They are produced by the electric heat generated within the tissue itself i.e. endothermic heat. They differ from common bums (flame burn) by being less uniform i.e. between the damaged areas; intact areas may still be found.c. Flash burns:They are caused by exogenous thermal heat, following contact with high voltage current. They are deep and may involve underlying bone andare associated with progressive vascular injury which may require repeated amputations.d. Flame burns:They are related to the ignition of clothing by electrical spark.e-Skin metallization:Penetration of metal of the conductor into the skin may occur at the point of entry of the current especially with high voltage current. The colour of the imprint left by the metal depends on the composition of

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the electrode; that of iron is brownish black, that of copper is reddish brown and that of aluminum is silvery. Skin metallization may help to identify the kind of the electrode with which the skin was in contact.H. Muscles and tendons:Violent and uncoordinated muscular contraction induced by the current may cause alterations in the affected muscles. A sensation of pain in the muscles is a common complaint among surviving victims. Muscular damage is also produced by the local elevation in temperature. Large amounts of myoglobin are released from the injured muscles and may lead to obstruction of renal tubules resulting in acute renal failure.III. Bones and joints:The violent muscular contractions may lead to fracture of bones. Osteonecrosis and even melting of bone by the eleetrothermic effect may follow high voltage aceidents producing the so called “osseous pearls”.IV. Heart and circulatory system:

Brief exposure to low voltage current may cause momentary stoppage of the heart while exposure to a current of greater intensity and for a longer duration may cause ventricular fibrillation or cardiacarrest.Late manifestations:

Pericardial pains similar to those occurring in pec!of S (called angina pectoris electrica ) may happen. The angina attacks usually fade away within weeks but may persist and proceed to coronary thrombosis and myocardial infarction. Fatal cases reveal dilatation of the auricle and petechial hemorrhages on the endocardium, pericardium and myocardium.V. Nervous system:immediate effects are: Temporary loss of consciousness, persistent headache, somnolence, nausea, vomiting and convulsions, painful muscular spasm, loss of hearing and distorted feelings.Late effects .which lasts for days or weeks. Psychic reactions such as a feeling of phobia against electric current or equipment also occur. Fatal cases:Scattered hemorrhages, degeneration of ganglion cell, demyelination of neuro- axons, may be seen.Spinal cord:

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There may be spinal atrophy due to vascular insufficiency, and manifested a few weeks to several months later by weakness and parathesia of the extremities.VI. Sympathetic and endocrine systems:Cerpetiform skin eruptions, graying and loss of hair, disorders in the menstrual cycle, glycosuria, polyuria, and rapid loss or gain in weight may occur. All these manifestations reflect the reaction to stress.VII. Blood:in fatal cases; the blood is dark and fluid. in survived cases, blood hemolysis, anemia and elevation in the serum bilirubin are found.VIII. Lungs:in fatal cases, pulmonary edema and petechial hemorrhage are usually seen. in surviving victims, aggravation of pre-existing pulmonary conditions will occur.IX. Alimentary tract: Petechial hemorrhages are seen.X, Kidneys: Renal failure is a common complication of high voltage accidents associated with extensive body burns. Following extensive burning of muscle, myoglobin is released through the kidney.Myoglobinuria is usually associated with renal tubular necrosis with resulting oliguria and even anuria.Xl. Organs of sense:Ear:Whenever the ear is in the path of the current, hemorrhages in the tympanic membrane, middle ear and secondary infection e.g. mastoiditis, sinus thrombosis, meningitis and brain abscess may complicate the electric injury.Eye:Early effects:Early electrothermal effects are in the form of burns of the eyelids, eyebrows, eyelashes, conjunct.iva and cornea. Ptosis, paralysis of ocularmuscles, disturbances in accommodation and .scotoma may occur.Late effects:Optic atrophy and cataracts formation which are unilateral, may follow the passage of the current through the eye or through the head.XII. Electrical shock and pregnancy:Electric shock in pregnancy can lead to death of the fetus and $ion.Post mortem examinationExternally: Electric marks and other skin effects diagnostic for electric, injury are found.

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Intern ally:It is usually the picture of asphyxia. It may be absent if the causes of death was due to cardiac arrest. Other systemic changes may be found which depends on the type of the current, the path of the current and the time passed between electric injury and death.Circumstances of electrocution:I. Accidental electrocution:It is the commonest form of electric injury. Accidents may occur for reasons related to the individual such as inattention carelessness, ignorance, alcoholic intoxication or because of malfunction of appliances, inefficient insulation lack protection grounding ,faulty or inadequate instruments.2. Suicidal electrocution:Uncommon. Persons using electricity as a mean of suicide will befound with wires and apparatus in position e.g. connecting the wrists to a wall plug-socket.3. Homicidal electrocution: It is rare.4. Legal electrocution:It is the method of execution in USA. . The condemned. person is strapped to a chair and metal electrodes are placed over his shaved scalp and around one leg. An impulse of 2000 V is. transmitted through the body for sixty seconds with alternating current of 7 Amperes.

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RADIATION INJURYIonizing radiation is widely used in medicine and industry, so large numbers of persons are exposed to its injurious effects.Sources of ionizing radiation:Natural causes:Cosmic rays from the sunRadium-thorium series in granitic rocks and sands.\c Naturally occurring radio-active material e.g. C14 and K4° in our body, food, air and waterMan-made sources -1. Diagnostic X-ray equipments.2. Therapeutic radiation apparatus.3. Clinical nuclear pharmaceutical agents.4. Radiation sources used in industry.Nuclear sources:1. Nuclear power generating reactors.2. Fallout from nuclear weapons tests.Radiation energy:Ionizing radiation is characterized by its ability to create energy in the irradiated material. This energy is not absorbed uniformly throughout the tissue or even throughout a single cell and thus radiation injury results.Types of ionizing radiation:I. Electromagnetic waves; infra-red, ultraviolet, X-rays, gamma rays and cosmic rays.2. Particulate radiation includes: beta and alpha particles, protons and neutrons.Measurement of radiation:Rad: It represents the radiation absorbed dose.RBE: It is the amount of cellular damage caused by a specific amount of radiant energy (RBE = Relative biological effectiveness).Rem: Equal to RBE x rad.Factors affecting radiation injury:The dose:

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A sufficiently high dose may kill the cells immediately. There is a threshold dose for every effect.a. Tue maxim urn permissible dose:

For irradiation of the whole body or critical organs as the haemopoietic system or the gonads, the dose should not exceed 3 rem in any period of 13 consecutive weeks.b. The permissible occupational dose:It is equal to N - 18 x 5 rem., where, N is the age in years.II. Fractionation of the dose:One single dose is more serious than small repeated doses. lIt III-Dose rate:At a relatively slow dose rat the cells may recover from their radiant injury and repair-will occur.IV. Body surface area irradiated:Whole body exposure is more serious than localized exposure. V. Cell sensitivity to radiation: .Less differentiated, rapidly dividing, cells are more sensitive to radiation damage e.g. erythroblasts, gonads and endothelial lining of blood vessels and gastro-intestinal tract.VT. Type of radiation:Electromagnetic waves are highly penetrating than particulate radiation.Biological effects of radiation:The radiation effects can be divided into:1-Somatic cells effects.2-Germ cells effects.L Somatic effects of radiation:They include:A) Degenerative disorders.B) Proliferative disorders.C) Developmental disorders.A. Degenerative disorders: result in:1- Acute radiation syndrome: Three syndromes may develop:i. Cerebral.ii. Gastro-intestinal.

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iii. Haemopoietic.2. Delayed radiation manifestations.1. Acute radiation syndromes:i. Cerebra! syndromeIt is produced by very high doses of radiation (>3 000 rad). It is fatal within hours. It starts by nausea and vomiting, followed by agitation; apathy, tremors, convulsion, ataxia and death.iii- Gastro-intestinal! syndrome:It is produced by 600 rad. It is characterized by nausea, vomiting, diarrhea, leading to severe dehydration shock and death occurs within two weeks.iiL Haemopoietic syndrome:It follows a radiation dose of 200 rad. It starts by anorexia, nausea and vomiting which subside after 1-2 days, followed by leucopenia, anemia and thrombocytopenia in 3-4 weeks, with increased susceptibility to infection and hemorrhage. Death occurs within two months.2- Delayed radiation manifestations:Following prolonged or repeated exposure to radiation or extensive radiotherapy, the following late radiation effects may occur:• Eyes: radiation cataract may develop after a latent period of 2-3 years. it is more common in y1owinjen.• Bone marrow: There will be anemia, leucopenia andthrombocytopenia. Chest: Radiation penumonitis, pericarditis and endocarditis

may follow radio-diagnosis or radiotherapy.• Gastro-intestinal tract: chronic ulceration , fibrosis, perforation with fistulae, adhesions and strictures formation may complicate radiotherapy.•Kidneys: Radiation glomerulofibrosis may happen.• Reproductive system: in female; permanent sterility may occur, whereas the sterility in male is temporary.• Bone: radiation osteonecrosis will occur.• Life span: Life shortening may occur due to low immunity and

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premature ageing of the cells,• Skin and hair:. Loss of hair follicles, erythema, vesication followed by dry then moist desquamation, necrosis and ulceration. These changes are accompanied by itching or pain. Hyperpigmentation or depigmentation may be permanent.B. Proliferative disorders:Irradiation may cause impairment of the proliferative control of the body cells, result in cancer. Increased incidence of cancer has been observed among radium dial painters, uranium miners and atomic bomb survivors.C. Developmental disorders:Irradiation in utero during the period of differentiation and organ formation by a dose over 200 rem results in repeated miscarriages, neonatal deaths and congenital anomalies. It is absolutely contraindicated to expose a pregnant female to X-ray during theIL GERM cell effects of radiation:Chromosomal and chromatid mutations are induced by radiation, including deletions, breaks, translocation. and fragmentations When the mutant germ cell is subsequently involved in reproduction the mutation may be expressed in the offspring or in later generations.Radiation protection measures:1-Avoid over exposure.2- Proper shielding of the body and of the radioactive source. 3- Proper handling and disposal of radioactive materials.4. Appropriate alarms, barriers, radiation monitors and pocket dosimeter should be used.