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Chemical Burns

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by

Anouk Bezuur

on 18 June 2013

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Transcript of Chemical Burns

Pathophysiology
Chemical Burns
Introduction
Chemical burns
* > 25000 chemicals
* 3% -> all burns
- 55% require surgery
* 30% of burns death
* Relevant loss of working time
* Long-term complications
Epidemiology
Carmen Blandin Tarleton
2007
2011
2013
* 6 : 1
* 40 Y/O

* Domestic violence
* Criminal use to assault
* Armed conflicts
- Syrian President
Bashar al-Assad
- Phosphorous
Jackson's Burn Model
Chemical burns vs. other burns
* Denaturation of proteins
* Relatively longer exposure
* May act systematically
&
Severity of chemical burn
Concentration
Quantity
Duration
Penetration
Mechanism of action
Chemical classes
Acids
Bases
Organic solutions
Inorganic solutions
Acids
Proton donors
Coagulation necrosis
Superficial
pH < 2
Bases
Proton acceptors
Liquefaction necrosis
Dissolving proteins
Fat saponification
Deeper tissue penetration

Organic solutions
Dissolving lipid membrane and disrupting protein structure

Inorganic solutions
Direct binding
Salt formation
Exothermic reaction
Mechanisms
of action
Oxidization
Reduction
Corrosion
Protoplasmic poisons
Vesicants
Desiccants
Chemicals
Specific agents
Cement
Hydrofluoric acid
Hydrochloric acid
Phosphorus
Sulfuric acid
Strong alkali
Dry lime
Chemical warfare agents
Cement
Most important component: CaO
CaO + H2O -> Ca(OH)2
Dermatitis, abrasions and burns
Hydrofluoric acid (HF)
Inorganic acid of fluorine
H+ -> superficial burns
F- -> penetrates the skin
Hypocalcaemia Hypomagnesaemia Nerve pain
Phosphorus (P)
Absorbed through the burned area -> liver-, heart- and renal failure

Used in both WW 1 and 2, Afghanistan, Gaza, Libya and many more

Sulfuric acid (H2SO4)
Burning through hydrolysis in the skin and dehydration
Fertilizer, glue, paint
Mustard Gas
Delayed symptoms after exposure
Used in WW 1
Lewisite and Sulphur Mustard
First Aid
Introduction
Symptoms
&
Complications

Patient
introduction
Complications are secondary symptoms
Differentiation
Dermal exposure
Ingestions/ inhalations
Ocular exposure
of
chemical burns
Dermal exposure
Prognosis
Age + % of body that is burned > 100:
Burn is likely to be fatal

Local effects
Tissue damage: thrombosed capillaries + increased permeability edema

Inflammatory response: cytokines + neutrophil _______phagocytosis of necrotic cells

Infection: within 24-48 hours microorganisms infect the burn may cause sepsis

Healing;
sometimes grafting is necessary
Scarring is unavoidable
Systemic effects
Cytokines + increased permeability  fluid loss
This may result in:
SHOCK
MULTIPLE ORGAN FAILURE
(toxaemia plays role as well)

RESPIRATORY DISTRESS

Hypovolemic shock
Curling’s ulcer
Differentiation: Inhalations/ Ingestions
Inhalation
Damage of bronchial tree and lungs
V/Q mismatch 
ARDS/ respiratory failure

Guidelines
Removal of chemical
Dilution
Examination of burn
Systemic toxicity
Ocular contact
Inhalation injury
Thorough history
Removal of the agent
Duration of chemical’s contact with the skin: determinant of injury severity
Removal of:
Agent
Affected clothing

Irrigation at scene
Dilution/ irrigation
Copious amounts of water
Scene of the accident
ER
Do NOT immerse patient!
Danger to unexposed tissues
Effects of water
Removal of agent
Correct hygroscopic effects of certain agents

Irrigation within 10 minutes:
5x decrease in full-thickness injuries
2x decrease in length of hospital stay
Exceptions to irrigation
Phenol: insoluble in water
Wiped off with 50% polyethylene glycol
Sulphuric acid and muriatic acids: produce extreme heat when combined with water
Neutralized with soap or lime
Dry lime: contains oxide which reacts with water to calcium hydroxide
Dusted off the skin
Chlorox
Milk, egg white or 1% sodium thiofusfate wash

Examine the wound
Exterior of wound may be deceiving
Damage may be bigger/ deeper than seems externally
Unusual tanning
Local anesthetic properties of some agents

Treat as typical burn patient: assess degree of burn
Fluid resuscitation
Complication prevention
Complications of lavage: hypothermia
Steady room temperature of 28-31 C
Lavage water as near as body temperature as possible
Fluid resuscitation
Calculate amount of fluid to be administered
Wounds < 20% of total body surface: oral treatment + IV fluids
Wounds > 20% of total body surface: Parkland formula
Hypertonic saline solution is not used
Replacement of lost protein
Catheterization and intubation (if necessary)

Systemic toxicity &
inhalation injury
Examples
Hydrofluoridic acid: hypocalcemia  ventricular fibrillation
Formic acid:
Intravascular haemolysis
Renal failure
Narcotizing pancreatitis
Other agents less likely to cause systemic toxicity: ALWAYS BE ALERT THOUGH

Nasal inhalation
Aerosolized chemical
Smoke
Respiratory injuries
Managed like smoke inhalation patients
Protection of airway
Oxygen therapy (mechanical ventilation): intubation?
Bronchoscopy: extent of damage
Oral ingestion
Gastric emptying contraindicated
Local sources of heat production minimized by moderate amounts of fluid (250-500 mL)
Neutralizing agent can cause more damage!

Ocular exposure
IRRIGATION!
Immediate removal of chemical agent from the eyes is essential
Goal in treatment: stabilize pH to 7.3-7.4
pH rechecked every 30 minutes
Can’t measure pH?
Decontamination with 2L of irrigation fluid for 30-60min
Diphoterine: water-soluble powder
Prevents or decreases severity of burns
Rapid decrease in pain
Less medical or surgical burn care (other than initial decontamination)

Dyspnea,
tachypnea,
wheezing,
stridor

Ingestion
Mouth: oral burns, patient can be drooling
Esophagus: tissue damage, stricture -> dysphagia
Abdomen: tenderness, guarding, ulcer->bleeding & perforation
Intestine: penetration, narrowing, hemorrhages
Rectum and colon: rare. Necrotizing lesions, often hidden by the absence of peritoneal inflammation signs->high mortality
Ocular Exposure
Alkalics vs Acids
Alkalics are lipophilic-> better penetration (within ±10 min in the anterior eye chamber) ->more damage

Acids cause protein coagulation->lesser penetration->only superficial burns

Hydrofluoric acid is the exception

Eye burns
Chemical burns are often bilateral and mostly cause complete vision loss

Other complications: cataract forming, glaucoma, corneal perforation, cornea scarring, retinal detachment, ulcerations etc.

Eye burns
Patient got caustic chemical in one eye

Patient was splashed with cement in one eye

4 grades of burns
What grade is this?
And this
Using chemicals
agents
Alkali
Industrial
& domestic
Cosmetic
Full transcript