Chemical, electrical & radiation burns: etiology, presentation & management.

1. CHEMICAL, ELECTRICAL &
RADIATION BURNS
Dr. Anam Saeed

2. CHEMICAL BURNS

3. 1/3rd
burn deaths.
Household chemicals:
• Ease of access,
• Wrong labelling
• Assault, suicide.
Face, eyes, arms & legs.
Deaths: ingestion

4. Pathophysiology
Denaturation of structural & functional proteins.
• Concentration
• Quantity
• Manner & duration of contact
• Extent of penetration
• Mechanism of action of agent
• Physical state
Severity:

5. Reduction: binding free electrons in tissue proteins, denaturation by reducing the amide link.
HCl, HNO3, alkyl mercuric compounds, ferrous iron, and sulfite compounds.
Oxidation: destruction by inserting oxygen, sulfur, or halogen atoms to proteins. By products toxic.
sodium hypochlorite, potassium permanganate, chromic acid, and peroxide.
Corrosive agents: denature tissue proteins on contact  eschar and a shallow ulcer.
phenols, cresols, white phosphorus, dichromate salts, sodium metals, lyes, H2SO4 & HCl.
Protoplasmic poisons: binding or inhibiting organic ion(Ca2+
) necessary for function. Form esters with
proteins and/or chelate Ca2+
or other ions.
“alkaloidal” acids; acetic acid; formic acid, oxalic acid, HF, and hydrazoic acid.
Vesicants: ischemia with necrosis at site of contact cytokine release and blister formation.
cantharides, dimethyl sulfoxide (DMSO), mustard gas (sulfur and nitrogen), and Lewisite.
Desiccants: dehydrating tissues and exothermic reactions, causing the release of heat into the tissue.
H2SO4 , muriatic acid, calcium sulfate, and silica gel.

6. • pH <2
• Coagulation necrosis precipitation of protein.
• Dry eschar.
Acids:
• pH >11.5
• Liquefactive necrosis deeper penetration.
Alkalis:

7. General principles
Stop the burn-remove offending agent:
• Remove clothing
• Irrigation
Neutralizing agent: exothermic reaction CONTRAINDICATED.
ATLS & ABLS.
URINE OUTPUT MONITORING.

8. ACIDS

9. Acetic Acid:
• Mild chelating agent
• Upper & lower airway tract irritation: cough, wheezing, tachypnea, nose & throat irritation,
pulmonary & pharyngeal edema.
• Tooth erosion, conjunctivitis, headache, nausea, vomiting, impaired vision, abdominal pain &
whitish discoloration of the skin.
• Initial treatment: irrigation
Carbolic acid/Phenol:
• Dermatitis, abnormal pigmentation and skin burns.
• Anaesthetic property deep burns.
• Ingestion >1000 mg: fatal.
• Systemic effects: ventricular arrythmia, pulmonary edema, stridor and tachypnea.
• Local effects: conjunctivitis, corneal edema or necrosis and skin necrosis.
• Acute poisoning: fatal
• Prompt irrigation, PEG
• Iv sodium bicarbonate

10. Chromic Acid
• Non painful but corrosive ulcers.
• Inhalation: septal ulcers & bronchospasm.
• Peak levels: 5 hours after exposure.
• Binds to Hb: spleen, liver, bones, brain.
• 1% TBSA- symptoms, >10% TBSA- fatal. 5-10g: lethal dose.
• Irrigation: dilute solution of sodium hyposulfite or water rinse in buffered
phosphate solution.
• Dimercaprol: 4 mg/kg im 4 hourly for 2 days 2–4 mg/kg/day for 7 days.
• Dialysis within 24 hours: remove chromium, correct electrolytes.
• Exchange transfusion.
• Ointments: 10% calcium EDTA or ascorbic acid for small superficial burns.
• Early excision of chromic acid burn: prevent systemic toxicity.

11. Epichlorhydrin acid:
• Rare, corrosive carcinogen.
• Colourless, garlic-like odour.
• Production of glue, plastic, glycerol & resin, paper reinforcement & water
purification.
• Rapid progression to a full thickness wound within hours.
• Management: copious irrigation and hemodynamic monitoring.
Formic Acid:
• Strong inorganic acid: glue makers and tanning workers.
• Creates an eschar, which does not prevent systemic absorption.
• Metabolic acidosis, intravascular hemolysis with hemoglobinuria, renal failure,
pulmonary complications, and abdominal pain with necrotizing pancreatitis.
• Most commonly used in assaults, easy availability.

12. Hydrochloric acid, Muriatic acid, Sulphuric Acid:
• HCl: common
• HCl & H2SO4: proton donors pH falls to 0.
• Coagulation necrosis and tissue ulceration consolidation of connective
tissue thrombosis of intramural vessels, ulceration, fibrosis, and hemolysis.
• Muriatic acid: commercial grade concentrated HCl denatures proteins into
chloride salts.
• Copious irrigation & early excision.
• HCl fumes: pulmonary edema.
• H2SO4: dehydration of tissues.
• White or grayish discoloration of the skin and exposed mucosa.
• Eye, mouth, throat, and abdominal pain and injuries.
• Hematemesis, vomiting, dizziness, headache, dyspnea, cough, tachypnea,
pneumonia, laryngospasm, and ultimately respiratory failure.

14. Hydroflouric acid:
• Corrosive: industrial application, computer processing, cleaning agent in
petroleum industry, production of high octane fuel, germicides, dyes,
tanning, fireproofing material, glass etching, rust removal.
• Acid & metabolic poison: LETHAL.
• Acid coagulation necrosis and cellular death.
• Fluoride ions chelates Ca2+
and Mg hypocalcemia & hypomagnesemia.
• Efflux of intracellular calcium cell death.
• Exceed body’s ability to mobilize Ca2+
and Mg: muscle contraction &
cellular dysfunction.
• Fluoride ion: metabolic poison by inhibiting Na-K ATPase efflux of
potassium shifts at nerve endings extreme pain associated with
hydrofluoric acid burns.

15. • Classified based on concentration of the exposure:
• >50%: immediate tissue destruction and pain
• 20–50%: burn becoming apparent within several hours of exposure
• <20%: up to 24 hours to become apparent.
• Symptoms: nausea, vomiting, fever, whitish tissue with surrounding
erythema, abdominal, mouth and throat pain, skin edema, ulcers and
necrosis, laryngeal edema, wheezing, tachypnea, tetany, and potentially fatal
cardiac arrhythmias.
• Death secondary to systemic complications.
• Symptoms due to acidosis, hypocalcaemia, hypomagnesemia,
hypokalaemia ventricular fibrillation.

16. • Monitor electrolytes & cardiac rhythm.
• Flouride: metabolic poison to myocardium Q-T prolongation.
• Copious irrigation.
• Topical, subcutaneous, or intraarterial mixtures of calcium gluconate.
• Topical gel: 3.5 g of 2.5% calcium gluconate+lubricant: 4-6 times/day for 3 to
4 days. Penetration into the dermis improved with the use of DMSO.
• Calcium gluconate injections into wound (0.5 mL/cm2
of 10% calcium
gluconate subcutaneously or intradermally).
• Intraarterial injections into the radial artery (10 mL of 10% calcium gluconate
and 40 mL of 5% dextrose over 2–4 hours): burns to the hand;
• Severe cases palmar fasciotomy.
• Injection: within 6 hours of exposure to prevent tissue necrosis and
minimize pain.

17. Nitric Acid:
• Oxidizing agents.
• Combines with organic proteins: organonitrates metabolic poison.
• Fertilizer management, casting iron and steel, and engraving.
• Skin contact: yellow-brown stain on skin and mucosa, with an eschar.
• Slow demarcation difficulty in discerning burn depth.
• Irrigation and the use of topical treatment.
• Whitish tinge of teeth, eye pain, oropharyngeal pain, or abdominal pain, dyspnea,
hematemesis, dizziness, cough, tachypnea, pneumonia and laryngospasm.
Oxalic Acid:
• Metabolic poison: combines with Ca2+
 limits muscle contraction.
• Industrially to remove rust and in bleaching products.
• Water irrigation and IV calcium, with continuous cardiopulmonary monitoring,
electrolytes and renal function tests.

18. Phosphoric Acid:
• Incendiary agent: hand grenades, artillery shells, fireworks, fertilizers.
• White phosphorus ignites in presence of air burns until entire
agent is oxidized/oxygen source is removed.
• Irrigated with water, easily identifiable pieces are removed.
• UV light: identify embedded particles through phosphorescence.
• 0.5% copper sulfate: impede oxidation and turn particles black: aid
in identification and removal.
• Hypocalcemia, hyperphosphatemia, and cardiac arrhythmias.
• Eye and respiratory tract irritation, blepharospasm, endophthalmitis,
foreign body sensation in eye, lacrimation, photophobia, cornea
perforation, blindness.

19. ALKALIS

20. • Strong alkalis: pH >=12.
• Wounds initially superficial but may often become full thickness in 2–3 days.
• Creates a soluble protein by binding with lipids and proteins passage of
hydroxyl ions into the tissue soft, brownish, gelatinous eschar is created.
• Corrosive, penetrate deeply.
• Eg: barium, sodium, ammonium, calcium, lithium, and potassium hydroxides.
• Household cleaning solutions.
• Ingested in suicide attempts: death secondary to airway occlusion.
• Management: immediate and copious irrigation.
• Dry residues of alkali (e.g., lime) must be brushed away copious irrigation.
• DO NOT NEUTRALIZE.
• Alkaline injury to eye: rapidly penetrate the cornea scarring and
opacification perforation.

21. Cement:
• Desiccant and an alkali.
• Calcium oxide calcium hydroxide upon exposure to water.
• Contains lime, sand, and other metal oxides.
• The dry powder is very hygroscopic desiccation injury if not washed away.
• Injury results from the action of the hydroxyl ion.
Metals:
• Occupational injuries: molten metal, such as elemental metals, sodium, lithium,
potassium, magnesium, aluminum, or calcium.
• Use of water: may result in an explosive exothermic reaction.
• Class D fire extinguishers or sand are ideal for management
• Mineral oil is also an option.

22. Hydrocarbons:
• Corrosive agents: plants, animal fats, and fuel oils.
• Prolonged contact with petroleum distillates  dissolution of lipid cell
membranes cell death.
• Superficial burns.
• Systemic toxicity: respiratory depression.
• Heat loss from rapid evaporation of gasoline: frostbite and dehydration.
• Early decontamination: soap and water.
Hypochlorite solutions:
• Potent oxidizers delivered in alkaline solution: bleaches & household cleaners.
• Exposure to 30 mL of 15% solution: fatal.
• Systemic manifestations: vomiting, confusion, dyspnea, airway edema,
cyanosis, cardiovascular collapse, and coma.
• Copious irrigation.

23. Alkyl mercuric compounds:
• Skin reaction releases free mercury: found in blister fluid.
• Mercury is absorbed systemic effects.
• After blisters are debrided, repeated washing to lavage the blister fluid.
Tar:
• Tar, crude oil, and asphalt: mineral products created from long-chain
petroleum and coal or fossil hydrocarbons.
• Removed from the skin immediately.
• After cooling, tar produces liquefaction: debrided from the skin, especially if
obvious burn, blister, or tissue loss is apparent.
• Antibiotic ointments, baby oil, mineral oil, mayonnaise, butter aid in
removal.

24. Vesicant chemical warfare agents
• Affect all epithelial tissues: skin, eyes, and respiratory epithelium.
• MUSTARD GAS:
• Burning eyes, burning throat, feeling of suffocation.
• Followed by erythema of skin (4 hours) & blister development (12-48 hours).
• Severe pruritus, particularly in moist areas: axilla and perineum.
• When the blisters rupture: shallow painful scar.
• Exposure to larger quantities: coagulative necrosis of skin, with either no
blistering or “doughnut blisters” surrounding a central necrotic zone.
• LEWISITE (2-chlorovinyl-dichloroarsine): best known arsine.
• It is more powerful than the mustards, and the symptoms occur sooner.

25. • PHOSGENE OXIME:
• Common agent in chemical warfare.
• Most widely used halogenated oxime; immediate effect of stinging.
• Affected areas: swollen with blister formation, and eschars develop over a week.
• Wound healing is slow, typically over 2 months.
• Eye involvement is extremely painful and can result in permanent blindness.
• Inhalation leads to hypersecretion and pulmonary edema.

26. • Clothing must be removed and large volume lavage is undertaken. Eyes
are irrigated with water or “balanced salt solution.”
• Blisters: debrided and dressed with topical antimicrobials.
• Dimercaprol: chelating agent antidote for lewisite poisoning.
• No specific antidote for nitrogen mustard; sodium thiosulfate and N-
acetylcysteine helpful to reduce the effects if administered early.
• The blister fluid from nitrogen mustard injuries does not contain active
agent and is hence harmless.
• Agranulocytosis or aplastic anaemia can result from exposure.
• Bone marrow transplantation may be considered.

27. ELECTRICAL BURNS

28. • Direct damage to cell membranes, proteins.
• Indirect damage due to heat generation.
Electrical energy through tissues:
• voltage,
• current (amperage),
• type of current (alternating or direct),
• path of current flow,
• duration of contact,
• resistance at the point of contact,
• and individual susceptibility.
Severity:

30. Low voltage (<1000 V)
• Localized to the area of
the contact point.
• May penetrate deeper
structures but the zone
of injury is more limited.
High voltage (≥1000 V)
• Extension into deep
tissue as well as
spreading out
phenomenon to
surrounding structures.
• Resemble crush injuries:
“tip of the iceberg”
phenomenon.
• Urgent care.

31. Current (I) = Voltage (E)/Resistance (R)
Resistance varies continuously with time:
• initially dropping slowly then much more rapidly until arcing occurs at
the contact sites.
• Resistance then rises to infinity and current flow ceases.
Rate of temperature rise parallels changes in amperage.

32. The path of current: significant difference in outcome.
Current traversing the conduction system of the heart or central nervous
system: potential complications.
AC: tetanic muscle contractions- may either throw the victim away from the
source or draw him into a continued contact  “no-let-go” phenomenon.
Both forearm flexors and extensors stimulated: flexors overpower extensors:
unable to let go voluntarily.

33. True electrical injury
caused by the flow of
current
Arc injury from the
electric arc generated
as current passes from
the source to an object
Flame injury caused by
the ignition of
clothing/surroundings
Lightening strikes

34. • Damaging supraphysiological temperatures: affects proteins and cell
membranes.
• Joule’s law: amount of power (heat) delivered: J= I2
xR
• Tissue resistance: nerves<blood vessels<muscle<skin<bone.
• Body acts as a volume conductor: severity of injury inversely proportional
to cross-sectional area of body part.
• Deep periosseous tissues retain more heat: severe damage.
• Macro & microvascular injury:
●Necrosis of vascular walls
● Thrombosis with destruction of arterial endothelium
●Pyknosis of vascular smooth muscle
●Fibrinous exudates accompanying the thrombotic changes.
• Progressive muscle necrosis over 72 hours after injury more than a week.
• Serial debridement & delay definitive grafting.

35. Electroporation + electrochemical interactions + thermal interactions.
Plasma membrane: determines the rate and quantity of tissue injury
accumulation.
Electroporation:
• Formation of aqueous pores in lipid bilayers exposed to a supraphysiologic electrical field.
• Allows calcium influx into the cytoplasm and triggers a cascade leading to apoptosis.
• Long cells (skeletal muscle and nerve): more vulnerable to electroporation

36. Acute care
GOLDEN
HOUR
ECG
monitoring
Fluid
resuscitation
Compartment
syndrome

37. Electrocardiographic monitoring
Dysrhythmias & myocardial damage: both low & high voltage injuries.
Most frequent cause of death after electrical injury: cardiac.
MC ECG abnormality: nonspecific ST changes.
MC dysrhythmia: AF
MC cause of death: Vfib
Direct myocardial contusion: CK, CKMB, troponins, pro BNP.
Indications for cardiac monitoring:
• Loss of consciousness,
• ECG abnormality or evidence of ischemia
• Documented dysrhythmia either before or after admission
• CPR in the field.
24-48 hours monitoring.

38. Myoglobinuria
Pigmented urine: muscle damage & ischemia.
Risk of acute renal failure.
Titrating fluid to get double the goal rate of urine output or 100ml/hour.
Prevention of oliguria with loop diuretics.
Alkalisation with sodium bicarbonate.
Correct serum electrolytes.
Decompression of compartment.

39. Compartment Syndrome
High voltage injuries: keep watch
Damaged muscle and swelling in deep fascia increased pressure compromised blood flow metabolic
demand exceeds delivery.
Venous outflow reduces decreased arteriovenous pressure gradient arteriolar collapse.
Loss of pulsation: late sign.
Early decompression and aggressive surgical management in patients with markedly elevated CK levels.
Fasciotomy, escharatomy
Carpal tunnel release
Second look in 24 to 48 hours: serial debridement may follow.

41. Wound management
11.1% mafenidemacetate cream (Sulfamylon): excellent penetration and spectrum
of coverage.
Topical agents: silver sulfadiazine, bacitracin, silver containing dressings.
Surgical excision: 2 to 3 days postburn, either as a second-look after fasciotomy or as
first procedure.
Conservative tissue removal and wound closure with skin grafts or flaps.
VAC
Physical therapy and functional splinting.
Scalp & chest wall: difficult areas.

42. Lightning injury
Pathognomonic: dendritic, arborescent erythematous pattern  Lichtenburg figures/ keraunographic markings.
Extravasation of blood in the subcutaneous tissue.
Within an hour of injury and fades rapidly: wheal and flare reaction.
Full-thickness isolated burns on the tips of the toes: characteristic.
Respiratory and cardiac standstill: CPR.
10% strikes are fatal.
Ear: ruptured TM, middle ear damage, SNHL.
Ophthalmic: thermal keratopathy, anterior uveitis, subcapsular cataract, vitreous hemorrhage, RD, CRAO and VO,
cystoid macular edema, macular hole, and optic neuropathy.
Neurological: unconsciousness, seizures, paresthesias, and paralysis.
Charcot’s or temporary paralysis: vasomotor disorders- complete tetraplegia and loss of sensory awareness of
the trunk extremities; usually transient.

43. Low voltage injuries
<1000 V
Localized.
May extend deep but not much laterally.
Excision & cover.

44. Complications
Primary: renal, septic, cardiac, neurological, ocular.
Cataract: mc ocular complication.
Neurological: early or late
• Neuromuscular defects: paresis, paralysis, GBS, transverse myelitis, or amyotrophic lateral
sclerosis
• MC: numbness, weakness, memory problems, paraesthesia, chronic pain.
Psychological: anxiety, insomnia, nightmares, flashbacks.
Heterotopic ossification at cut ends of amputations: long bones.

45. RADIATION BURNS

46. Exposure to radiation:
Small-scale accidents/cumulative exposures: in lab or
from an X-ray in hospital setting.
Large industrial accidents: extra resources.
Detonation of nuclear device(military conflict):
resources overwhelmed/ unavailable; associated
multiple injuries.

47. Alpha Particles
• Helium nuclei: positively charged.
• Large mass, cant pass through a thin sheet of paper.
• Stopped by density of 2 to 9 cm of air.
• Radium and most of the radioactive isotopes emit alpha particles.
Beta Particles
• Negatively charged particles of electrons.
• Small mass, high speed: penetrate up to 1 cm of tissue but are easily stopped by thin sheets of metal.
• Used therapeutically in thin superficial lesions of the skin.
Gamma Rays
• Uncharged photons of high energy that travel at the speed of light.
• Penetrate deep layers of tissue.
• Product of the natural decay of radioactive materials, such as radium; used therapeutically for lesions in deeper tissue.
X-rays
• Similar to gamma rays but produced artificially by bombardment of electrons onto a tungsten target.
• The x-rays are filtered of their weaker energy, allowing higher energy particles to be directed toward tissue targets.

48. Ionizing radiation energy transfer tissue damage.
• Electromagnetic radiation: x-rays, gamma rays
• Particulate radiation: alpha and beta particles, neutrons
Severity: energy deposited per unit track length LINEAR ENERGY TRANSFER(LET).
The biological effect of ionizing radiation is measured by radiation absorbed dose (rad).
SI unit of absorbed dose is gray (1 Gy = 100 rad).
Unit of dose equivalence: to compare radiations with different LET.
• REM: dose in rads x quality factor (QF).
• QF takes into account the LET, different values; for X-rays: 1.0 and for neutrons: 10.
Widely used international unit: Sievert (Sv)
• 1 Seivert= 100 rem.

49. • UVA: 315-400 nm
• UVB: 280-315 nm
• UVC: 10-280nm
Sun: source of electromagnetic rays:
First & second degree burns to skin.
Pyrimidine dimers in DNA malignancies.

50. Significant radiation accident is one
which exceeds at least one of the
following:
Whole-body doses ≥ 25 rem (0.25 Sv)
Skin doses equal ≥ 600 rem (6 Sv)
Absorbed dose ≥ 75 rem (0.75 Sv) to other tissues or organs from an external source
Internal contamination ≥ one-half the maximum permissible body burden (MPBB) as
defined by the International Commission on Radiological Protection.
Medical misadministration resulting in a dose ≥ criteria listed above.

51. Radiation
accidents:
Radioactive sources used for industrial radiography.
Radioisotope accidents: unsealed radioactive materials,
such as tritium, fission products, radium, and free
isotopes used for diagnosis and therapy.
Enough fissionable material (enriched uranium) is
brought together to produce a neutron flux nuclear
reaction.

52. Pathophysiology
Detonation of nuclear device extremely hot, luminous fireball
emits intense thermal radiation capable of causing burns and
starting fires.
Accompanied by a destructive blast wave moving away from the
fireball at supersonic speed + emission of irradiation (gamma rays
and neutrons).
Thermal + radiation injuries: synergistic effect on the outcome.

53. THERMAL EFFECTS
• Range from erythema to charring of the superficial layers of the skin.
• Secondary flame burns: ignition of clothing/environment.
• Flame burns may heal & relapse:
• greyish coating, granulation tissue disorder, infection,
thrombocytopenia bleeding.
• Agranulocytosis & bacterial invasion.
RADIATION EFFECTS
• Free radicals: damage cellular & nuclear membranes, DNA.
• Morbidity: dose, dose rate, sensitivity of cells.
• Cells in mitosis- bone marrow, skin, GIT
• Overall effect: duration, body surface area exposed, homogeneity of field.
• Long term: cancer, wound healing defects: damage to p53.
• Children more susceptible.

54. LOCALIZED INJURY
Small area exposed, less systemic effects.
• Low energy radiation: skin & subcutaneous tissue.
• High energy radiation: deeper tissues.
Skin: progressive features depending on dose:
• Erythema(first degree burn)- 2 stages
• Mild erythema: minutes or hours after initial exposure; subsides in 2–3 days.
• Second onset of erythema: 2–3 weeks after exposure + dry desquamation of epidermal keratinocytes.
• Loss of hair: 7 days after injury; temporary <5 Gy, may be permanent with higher doses.
• Moist desquamation(second degree burn)
• Latent period of 3 weeks (12–20 Gy); shorter with higher doses.
• Blisters form, which are susceptible to infection.
• Full-thickness skin ulceration and necrosis: > 25 Gy.
• Weeks to few months after exposure.
• Obliterating endarteritis: fibrosis, atrophy, and necrosis.
• Skin cancers after months or years.

55. Radiation therapy
Ionizing radiation: propagation of energy necessary to displace >= 1 orbital
electrons.
Direct ionization: charged particle of sufficient energy can directly disrupt the
atomic structure of the absorbing material, such as DNA.
Indirect ionization: ionization of an intermediary(water) free radicals-
hydroxyl radical (OH−) damage DNA, cell membranes cell injury or death.

56. Can affect both tumor and normal tissue.
Important to increase tumor control and decrease the normal
tissue complication.
Dose-response relationship between tumor control & normal
tissue complication: therapeutic ratio.
Upto 5% compication risk is acceptable.

57. Therapeutic x rays: kilovoltage
• Superficial therapy (50 to 150 kV): lesions up to 5 mm in depth,
delivery of 90% of dose to skin surface skin cancers, as radiation
does not penetrate deep and is focused to the treatment zone.
• Deep therapy(orthovoltage): 150 to 500 kV penetration depth of 4
to 6 cm.
• Increased penetration, MV therapy is used for improved skin sparing
and dose homogeneity:
• Cobalt-60 units: generate gamma rays with an average energy of
1.3 MV
• Linear accelerator units (Linac), with photon energies of 4 to 18
MV.

58. EBRT
Particle therapy.
Heavy particle therapy: protons, neutrons, or other positive ions such as
carbon.
Maximal deposition of energy at the end of their intended path, with minimal
dose deposition along the path: Bragg peak.
Less toxicity to surrounding normal tissue with greater effect on the target
tissue.

59. Brachytherapy
Interstitial: source is directly implanted into the target tissue,
Intracavitary: sealed source is inserted into the cavity of an organ (e.g., a
cylindrical rod inserted into the cervix),
Surface application: an applicator can be used to directly deliver a radiation
dose to the surface of a tumor (e.g., eye plaque for uveal melanoma).

60. • ACUTE TOXICITY:
• Free radicals and irreversible breaks in DNA  local inflammatory cascade of cytokines,
chemokines recruit an eosinophil and neutrophil response.
• In the skin, injury can also affect the epidermal permeability barrier entrance of toxins and
antigens to aggravate dermal inflammation infections.
• 2 to 4 weeks after the initiation of therapy, is dependent on dose of radiation, volume of
tissue irradiated, or concurrent chemotherapy.
• Reversible with healing beginning at about 2 weeks after the completion.
• Presents with skin erythema, edema, pigmentary changes, depilation, wet and dry
desquamation, mucositis, and esophagitis

62. • ACUTE DELAYED TOXICITY:
• Acute radiation pneumonitis: 8 to 16 weeks following the initiation of radiation to the lung.
• Endothelial & epithelial cell death, microvascular thrombosis, type II pneumocyte
desquamation.
• Lhermitte syndrome: temporary demyelination of the posterior columns during spinal
irradiation, presenting 2 to 6 months following RT.
• DELAYED TOXICITY:
• 6 months to years following the completion of RT.
• Not reversible.
• Stromal tissue fibrosis, parenchymal tissue atrophy.
• Damage to vessel endothelium, particularly capillaries telangiectasia and tissue
ischemia.
• Poor vascularity tissue becomes fragile & poor wound healing with minor trauma

64. Delay RT at least seven or more days after surgery to allow
adequate time for healing.
Surgery should be delayed 3 to 10 weeks after completion of
RT for optimal wound healing  effects of acute radiation
toxicity resolved & before the onset of delayed tissue toxicity.

66. Complications
• Osteonadionecrosis:
• chronically exposed devitalized irradiated bone for 3 to 6 months without the recurrence of
tumor.
• Generally within first 3 years after RT.
• maxilla, sternum, pelvis, temporal bone, and vertebrae, MC: mandible after irradiation of HNC.
• Due to microvascular thrombosis and decreased vascularity, abnormal fibroblastic activity, and
fibroblastic remodeling leading to bone fibrosis and loss of osteocytes in the bone.
• Prevention with dental care before the initiation of RT.
• Improved oral hygiene, saline irrigation, antibiotic therapy, hyperbaric oxygen therapy, and
newer medical modalities including pentoxifylline and tocopherol.
• Late stage ORN: wound debridement, sequestrectomy, decortication & resection of necrotic
bone, and free flap reconstruction.
• Lymphedema
• Lymph node dissection.
• Depletion of lymphatic vessels and endothelial cells as well as increased fibrosis.

67. Radiation induced malignancy
• Cahan criteria:
1. Malignancy arising in an irradiated field,
2. Sufficient latency between the initial RT and new malignancy (generally >4 years),
3. New malignancy of different histology to the primary cancer,
4. Tissue of the new malignancy is genetically & metabolically normal prior to the radiation
exposure.
• Sarcomas are most common.
• RT for HNC: SCC> Sarcome
• RT for breast cancer: Ca lung, c/l breast, esophagus, and sarcoma.
• Mantle field RT for Hodgkin disease: breast, lung, and thyroid RIM.
• Craniospinal RT and total body irradiation: meningioma, glioma, leukemia, and lymphomas.

68. ACUTE RADIATION SYNDROME
• Physiological effects of whole body radiation.
• Hours after exposure:
• Nausea, vomiting, diarrhoea, fatigue, fever,
headache.
• Latent period- dose dependant.
• Hematopoietic & GI complications.

69. Hematopoietic Neurovascular Gastrointestinal

70. Hematopoietic Syndrome
• 1-4 Gy
• Bone marrow:
pancytopenia.
• Opportunistic
infections.
• Bleeding.
• May be fatal.
Gastrointestinal
Syndrome
• 10-12 Gy.
• Nausea, vomiting,
cramps, watery
diarrhoea.
• Bowel epithelial loss.
• Bacterial translocation:
septicaemia, bowel
ischemia, bloody
diarrhoea.
• Fluid loss:
hypovolemia, acute
renal failure &
anaemia.
• Fatal.
Neurovascular Syndrome
• >15-30 Gy.
• Collapse of vascular
system.
• Caused by massive
release of mediator
substances, NO
abnormalities, or
destruction of
endothelium.
• Variable neurological
symptoms, respiratory
distress, cardiovascular
collapse & death.

71. Treatment
FIRST AID
• Evacuate from source.
• Remove clothing.
• Copious irrigation with water/saline: until Geiger counter indicates steady state or
minimum radiation count.
• Follow resuscitative protocol.
• Second scrub: soap/detergent.
• Povidone-iodine solution or hexachlorophene soap & rinse for 2–3 minutes and dried.
• Exposure:
• < 1Sv/Gy: outpatient treatment.
• >1Sv/Gy: full evaluation
• > 2 Sv/Gy or symptoms of ARS: specialist centre.

72. ASSESSMENT
• Clinically by symptoms of ARS.
• CBC immediately & after 12-14 hours.
• If lymphocyte count falls by 50% in 48 hours:
moderate exposure.
• History: age, comorbidities, smoke inhalation,
trauma.
• Examine to exclude injuries.

73. Management
Analgesia: opiates- iv
Antiemetics: Ondensetron
Resuscitation same as thermal burns.
Monitor & titrate as per urine output.
Replace fluid losses due to diarrhoea & vomiting.
In mass casualties, iv fluids may be limited: oral resuscitation.

74. Wound care
Ascertain extent of burn.
Mild erythema: prevent sun exposure
Dry desquamation: lotion
Deeper burns with moist desquamation: like thermal burns
Dehydration & immunosuppression: bacterial invasion & sepsis.
Early tangential excision & grafting.
Severely injured tissue: excision & reconstruction.

75. Complications
HEMATOLOGICAL
• Blood & platelet transfusion.
• Total body irradiation: bone marrow transplant; 3-5 days post-exposure.
• Stimulation of hematopoietic stem cells:
• Antiapoptotic cytokines: stem cell factor, flt-3 ligand, thrombopoietin,
and IL-3.
• Hematopoietic growth factors: granulocyte colony-stimulating factor
(G-CSF) and granulocyte– macrophage colony-stimulating factor (GM-
CSF).

76. INFECTIO
N
• Immunosuppression: endogenous & exogenous
pathogens.
• Aseptic technique & sterile environment.
• Empirical antibiotics as per nosocomial infection pattern.
• Broad-spectrum antibiotics: imipenem, ceftazidime, and
ciprofloxacin.
• If Gram positive infection: vancomycin or teicoplanin.
• Antifungal agent if inadequate response.

77. References
• Total Burn Care: David N. Herndon
• Plastic Surgery 4th
Volume : Peter C Neligan, 4th
edition
• Plastic surgery 1st
volume: Stephen J Mathes
• Grabb and Smith’s Plastic Surgery, 8th
edition

78. THANK YOU!