burns- chemical and pediatric by dr. sunil keswani, national burns centre, airoli

Chemical BurnsChemical Burns

Dr. Sunil Keswani, National Burns Centre, www.burns-india.com, [email protected]

Chemical BurnsChemical Burns

Epidemiology 60,000 patients/yr in US 2-6% of burn unit admissions


ClassificationClassification

Alkalis Sodium/potassium/ammonium/lithium/barium/

calcium: hydroxide or carbonate. Oven cleaners,drain cleaners, fertilizer (lime),

industrial cleaners, cement Mechanism:

Liquefactive necrosis & protein denaturization Promotes deeper spread of chemical and more severe

burns



Acids: Hydrochloric, Oxalic, Hydrofluoric, Muriatic, Sulfuric

acids Cleaners, rust removers, pool acidifiers, drain cleaners. Mechanism:

Coagulative necrosis and protein precipitation Limits depth of tissue damage (HF acid is an exception)



Organic compounds: Phenols, Creosote, petroleum products (gasoline,

diesel, varsol, turpentine) Mechanism:

Saponification of lipids and systemic toxicity due to lipophilicity

Cell membrane solvent action liver and kidney toxicity


Factors Determining SeverityFactors Determining Severity

Agent Concentration (depth) Volume (TBSA exposed) Duration of contact Mechanism of action of agent


TreatmentTreatment

Universal precautions Protect yourself first Gloves, gown, eye protection Remove offending agent

DO NOT ATTEMPT TO NEUTRALIZE pH

ABCDE, Primary and Secondary Surveys Identify active agent

Poison control centre


ALKALISALKALIS


AlkalisAlkalis

Slippery feel due to saponification of lipids in skin.

Liquefactive necrosis Treatment:

Irrigate copiously Supportive care ABC’s


Eye Injury Eye Injury

Frequently caused by alkali 2x more common than acid

injury to eye Young adults Occur at home, industrial

workplace, assault Swelling/spasm of eyelid Tx: flush with saline catheter

or Morgan lens until Opthalmologist arrives 10% potassium ascorbate drops Oral Ascorbic acid to ↓

inflammatory cell release and collagenase activityDr. Sunil Keswani, National Burns Centre, www.burns-india.com, [email protected]

Ammonia (gas or liquid)Ammonia (gas or liquid)

Fertilizer or industrial refrigerant Used in manufacture of illicit methamphetamine Strong base with penetrating odour Signs and symptoms of exposure:

Blistering of skin, pneumonitis, uveitis Eye injuries common

Tx: Copious irrigation with water Optho consult for eye wounds; may need

ventilator support for severe inhalation injuriesDr. Sunil Keswani, National Burns Centre, www.burns-india.com, [email protected]

Bleach (hypochlorite)Bleach (hypochlorite)

5% Na or Ca hypochlorite Strong base Common in suicidal

attempt May release chlorine gas

when mixed with acid Toxic to mucous

membranes Respiratory compromise


CementCement

Contains ~60% Ca02

Reacts with water to release CaOH (alkali)

pH >12 Short contact with irrigation may

cause contact dermatitis Prolonged contacts (2-6 hrs) can

cause full thickness burns May have solidified cement in

woundsDr. Sunil Keswani, National Burns Centre, www.burns-india.com, [email protected]

Sodium HydroxideSodium Hydroxide

Commonest cause of civilian burns Hydroxyl ion produces saponification & liquefaction

necrosis Insidious, full thickness injury Intense irritation of skin, mucous membranes, glottic

edema and rapid asphyxia; vomiting can cause rupture Tx: immediate copious irrigation with water for 12-24

hours Endpoint: Significant reduction in pain and normal pH

(test with pH paper)Dr. Sunil Keswani, National Burns Centre, www.burns-india.com, [email protected]

Sodium, Potassium, Magnesium MetalsSodium, Potassium, Magnesium Metals

Produce chemical and thermal injuries Highly reactive metals when in contact with air or

water Tx: fire extinguisher for flames; cover remaining

particles in oil to prevent water or air contact


ACIDSACIDS


Sulphuric AcidSulphuric Acid

Second commonest cause of chemical burns

Car batteries Very strong acid Severe injury Upper and lower airway

injury possible Irrigate x 2 h Graft when necessary


Hydrochloric AcidHydrochloric Acid

Immediate discomfort Slower and deeper reaction than sulfuric acid

More severe ulcers Muriatic acid = concentratedHydrochloric acid

Airway edema possible Tx: copious irrigation x 2h; sameas for sulfuric


Hydrofluoric AcidHydrofluoric Acid

Common in industry glass etching, chrome plating, making Teflon, cleaning semiconductors, rust removers.

Weak acid Fluoride ion ++ toxic Severe pain Variable presentation depending concentration

Low concentration may have delayed pain onset High concentration = immediate pain

Hypocalcemia → DEATHDr. Sunil Keswani, National Burns Centre, www.burns-india.com, [email protected]


Mechanism of action: H+ ion causes the acid burn F- ion causes extensive local and systemic necrosis by

chelating positively charged ions (e.g. Ca2+, Mg 2+) Efflux of intracellular Ca2+ with resultant cellular death

F- ion remains active until completely neutralized by the bivalent cations and penetrates bone

F- also inhibits Na-K ATPase and allows K+ efflux Electrolyte shifts at nerve endings thought to cause the

extreme pain associated with these burnsDr. Sunil Keswani, National Burns Centre, www.burns-india.com, [email protected]

Hydrofluoric AcidHydrofluoric Acid Treatment

Irrigate with water (1 minute) Topical Calcium gel

1 amp Ca gluconate in 100g MukoInvolved hand placed in glove containing Ca

gelDigital block and nail removal if nailbed

involved Injectable CaGluc 10%

0.5 ml/cm2 tissue injected intra/sub dermally Inta-arterial CaGluconate

Start invasive measures immediately if exposure to >40% HF



Monitor blood Ca2+, Mg2+ q2h Cardiac monitoring, ECG

Prolonged QT interval Refractory when dysrhythmia develops Important to stay ahead of this with Ca++ infusions

Calcium gluconate intravenous infusion for treatment of hypocalcemia

NEVER USE CaCl- CORRISIVE


ORGANICSORGANICS


Phenol (Carbolic Acid)Phenol (Carbolic Acid)

Acidic alcohol Coagulation necrosis of dermal proteins Paradoxical injury

Dilute penetrates deeper than concentrated DO NOT DILUTE WITH WATER

Copious irrigation with PEG or Etoh Dysrythmias, hepatitis, nephritis, cellular

respiratory inhibition, hypothermia


Petroleum injuriesPetroleum injuries

Primarily gasoline and diesel Delipidation injury Full thickness injury that appears only partial

thickness Systemic toxicity – liver, kidneys

Develops in 6-24 hours post-exposure Can occur concurrently with lead toxicity if gasoline

contains tetraethyl lead Supportive care, no specific antidotes


Halogenated hydrocarbonsHalogenated hydrocarbons

Solvent, paint strippers, cleaners Significant liver and kidney toxicity Defatting of skin may cause full thickness burns Methylene chloride metabolized to CO Dysrhythmias common


Tar BurnsTar Burns

Contact burns Bitumen compound not absorbed and is not toxic Cool molten material with cold water

Stops burning process Cover adherent tar with petroleum-based ointment

to emulsify tar White petroleum jelly Mayonnaise (Dr. Parkhill!)


Chemical Warfare AgentsChemical Warfare Agents

Vesicants Mustard gas – binds DNA & arrests cell function;

ARDS and bone marrow suppression Tx: clean skin with oil, then water, then SSD Intubate for airway compromise

Lewisite – organic arsenical, similar function to Mustard gas Tx: antidote – British Anti-Lewisite 2


Chemical Warfare AgentsChemical Warfare Agents

Nerve agents Organophosphate acetylcholinesterase inhibitors

Sarine, Tabun Inactivate enzymes by phosphorylation and cause

excessive ACh production Bronchoconstriction and parasympathetic overactivity Tx: Antidotes

Sarine → Palidoxime Tabun → Obidoxine


Chemical Warfare Agents - PhosphorusChemical Warfare Agents - Phosphorus

Used In Weapons Hand Grenades Mortar Bombs Artillery Shells Fireworks

Burns Seen Mainly In Military Personnel Ignites In The Presence Of Air


PhosphorusPhosphorus

Burns When In Contact With Skin Progresses Until Agent Is Oxidized Or Starved Of

Oxygen By Bathing In Water Wounds

Extremely Painful Necrotic

Characteristic Smell Garlic



Treatment Remove Clothing Irrigate With Saline or Water Transport To Specialized Unit

Cover Burns In Saline / Water Soaked Gauze

Specific Therapy Irrigate With 0.5% Copper Sulfate

• Forms Cupric Oxide - Impedes Oxidation

• Facilitates Location



Treatment Ultraviolet Light

Fluoresces Embedded Particles

Electrolyte Disturbances Even With Small Burn Hypocalcemia And Hyperphosphatemia Cardiac Arrythmias


THANK YOUTHANK YOUBurns Helpline 27793333Burns Helpline 27793333

[email protected]


burns- chemical and pediatric by dr. sunil keswani, national burns centre, airoli

Health & Medicine