hazardous material medical care corrosives and oxidizing agents methemoglobin forming agents น....
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Hazardous Material Medical CareCorrosives and Oxidizing AgentsMethemoglobin forming agentsน.พ . สั�มมน โฉมฉาย
สาขาพิ�ษวิ�ทยาคลิ�นิ�ค อาชี�วิเวิชีศาสตร์� แลิะ เวิชีศาสตร์�ส��งแวิดลิ�อม
ภาควิ�ชีาเวิชีศาสตร์�ป้�องกั นิแลิะส งคมคณะแพิทยศาสตร์�ศ�ร์�ร์าชีพิยาบาลิ
มหาวิ�ทยาลิ ย มห�ดลิ
[email protected]@hotmail.com
October 28, 2003
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Outline:
• Corrosives & Oxidizing agents• Phosphorus • Corrosives with systemic effects
– Hydrofluoric acid– Phenol and related agents
• Methemoglobinemia
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Corrosive
• Corrosives: Any chemical with corrosive effects and can cause chemical burns
• Acids• Bases• Oxidizers• white phosphorus
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Acid, Base and Oxidizing Agents• Arrhenious system, following a swedish
chemist• Acid: A substance that dissolves and ionizes
in water to produce hydrogen ion, H+
• Base: A substance that dissolves and ionizes in water to produce hydroxide ion, OH-
• Oxidizing agents: A substance that reacts with other substances by taking an electrons.
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Common industrial and house bases• Sodium and potassium hydroxide:
cleaning• Calcium hydroxide: concrete• Lithium hydroxide: photographic industry• Ammonium hydroxide: fertilizers• Ammonium compounds: glass, tub, tile
cleaner• Sodium hypochlorite: bleach
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• Hydrochloric and sulfuric acid: cleaning• Hydroflouoric acid: glass and metal
cleaning• Phosphoric acid: Fertilizers, detergents• Acetic acid: Polymer, rayon, plastic and
rubber production• Chromic acid: metal plating• Formic acid: leather tanning, rust remover• Sulfuric acid: automobile batteries
Common industrial and house acids
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Common oxidizing agents
• Chlorine dioxide: Bleaching, water treatment
• Hydrogen peroxide: rocket fuel, bleaching food, denture cleaner
• Sodium chlorate: Dye production, leather tanning
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Alkali burns
• Contact with tissue: ‘Liquefaction necrosis’– Protein dissolution– Collagen destruction– Fat saponification
• Penetration of alkali until the excess OH- are consumed
• Heat generation from reaction with tissue• Determinants: Strength of alkali (pKa 14
or more is strong), concentration
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Acid burns
• Protein denaturation and precipitation
• Eschar formation• Most acid burns are limited to
superficial layer• Determinants:
– pH less than 2.5– volume of acid solution
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Oxidizing agent injury
• Oxidizing agents react quickly with tissue– Oxidation of tissue – Free oxygen radical production– Heat production
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Exposure to corrosives
• Inhalation: – The commonest route of exposure– Fume of concentrated acid or base– Aerosols of sprayed acid or base
• Skin or mucous membranes:The second commonest route of exposure
• Ingestion
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Corrosive injury: clinical manifestations
• With skin and mucosal exposure, respiratory involvement should always be considered.
• Skin: pain, reddening and inflammation, swelling
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• Ingestion:
– Oropharyngeal pain, dysphagia, throat and
chest pain, abdominal pain
– Absence of oral lesion does not preclude
esophageal and gastric lesion
– Upper airway obstruction, respiratory
distress
– GI tract performation
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– Systemic effects after ingestion– Alkali only cause local contact injury.– acid absorption with acute metabolic
acidosis•Anion gap: sulfuric acid•Non-anion gap: hydrochloric acid
– Oxidizing agents may be absorbed and cause methemoglobinemia
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• Airway management• Decontamination
– Gastric lavage and induction of emesis is contraindicated:•Repeated corrosive exposure•Perforation risks
– Activated charcoal is relatively contraindicated•No proven benefit•Worsen endoscopic visibility
Corrosive Ingestion: treatment
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• Dilution may be done with drinking 1 cup (250 mL) of water or milk in patients– Ingestion within 30 minutes– No vomiting– No signs of perforation
• Neutralization is contraindicated
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• Endoscopy:– Flexible fiberoptic endoscopy– Indicated in all intentional patients and
symptomatic patients– Determine: Location and severity of the injury– Treatment plans and prognosis– A delay of 4-6 hours after ingestion to prevent
underestimation of the lesion– Perform no later than 24 hours after the
ingestion to minimize risk of perforation
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• Thorough decontamination with water or saline
• Alkali burns may need longer irrigation and soft soap
• Chemical blisters should be broken and irrigated because corrosive substances may be collected within the blister
Corrosive skin burn: Management
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• Irrigate affected eye with large amount of water or saline
• Nitrazine (pH) paper checked
• Irrigate until pH 7.5-8• Complete
ophthalmologic examination after the irrigation
Ocular corrosive injury: Management
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Yellow or white phosphorus• Colorless or yellow wax-like
crystalline solid • Garlic-like odor• Insoluble in water• Industries:
– Fireworks– Fertilizers
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Phosphorus: Skin exposure
• Spontaneous combustion when exposed to oxygen in air
• Releases phosphorus oxide: – Upper and lower respiratory system
irritation– Non-cardiogenic pulmonary edema
• Severe skin burns
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Phosphorus: Ingestion
• Severe GI tract burns• fluid and electrolyte loss & shock• Hyperphosphatemia and hypocalcemia• Tetany• QT-interval prolongation and cardiac
arrhythmias• Diarrhea with smoking stool• Acute hepatitis and renal failure on day 2-
3
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Phosphorus: Treatment
• Decontamination• If solid embedded in tissue: keep the area
submerged in water before surgical debridement
• Identification of embedded phosphorus is often difficult
• Paint with 1-3% copper sulfate solution: blue solids of copper phosphide
• Removed phosphorus placed under water
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• Fluid replacement• Calcium replacement for
hypocalcemia
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Corrosives with systemic involvement
• Hydrogen fluoride• Phenol
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Hydrofluoric acid
• An acid with industrial and household applications– Glass and ceramic – Cleaning sand stone and marble– Semiconductor
• Exposure– Topical skin and mucosal exposure– inhalation of fume– Ingestion
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• Ionize after penetration into tissue• H+ release like other acids• F- ion binds calcium and magnesium• Insoluble calcium fluoride and
magnesium salt in tissue• Deplete intracellular calcium and
magnesium
Hydrofluoric acid
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• Household agents: • concentration less than 20% may not
result in immediate pain and delay up to 24 hours
• concentration 20-50 % may not result in immediate pain and delay up to 8 hours
• Concentration >50% causes immediate pain and rapid onset of hypocalcemia
Hydrofluoric acid: skin exposure
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• Tissue burns may progress gradually over a week
• Facial exposure may be very susceptible for systemic toxicity
• Lesion starts with mild erythematous area that progresses to second or third degree burns in low concentration
• Immediate pale and blanched area with surrounding erythema for high concentration
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• Commonly exposed area is hand.• Nail involvement
– needs aggressive management– nail bed necrosis and distal
phalanx demineralization
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• Severe pain in mouth and throat, esophagus
• Inflammation, necrosis and perforation of esophagus
• Gastrointestinal hemorrhage• Systemic toxicity usually occur after GI
symptoms• Onset of systemic toxicity within 6 hours
(mostly within 1 hour)
Hydrofluoric acid: Ingestion
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• Industrial setting: HF concentration of 50% or more
• Indicators for suspicion– Burn with > 50% BSA– Burn in head and neck– Confined space burn– Delayed removal of soaked
clothing• Upper and lower respiratory irritation• Possible systemic toxicity
Hydrofluoric acid: inhalation
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• The eye is very sensitive to HF fume in the air: severe irritation
• Severe conjunctival injection and chemosis
• Keratitis and corneal opacity• These pathology may be delayed
for up to 24 hours
Hydrofluoric acid: ocular injury
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• Hypocalcemia• Muscle weakness and tetany• Fatigue• Prolonged QT interval • Refractory torsade de pointes and
ventricular fibrillation• Seizures and alteration of
consciousness
Hydrofluoric acid: systemic toxicity
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• Decontaminate with large amount of water (at least 20 minutes)
• Patients with burn should be treated with topical calcium gluconate therapy
• Cover burned areas with 2.5% calcium gluconate gel
• Gel may be applied using surgical glove• Pain should be relieved within 45 minutes• Change gel when pain recurs or every 4
hours• In small, severe burns, surgical debridement
may facilitate topical treatment
Hydrofluoric acid skin burn: management
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• Preparation of calcium Preparation of calcium gluconate gelgluconate gel
• Mix 10 ml of 10% calcium gluconate in 60 mL of KY gel
• Mix 10 tablets of 10 g calcium carbonate (crushed) in 60 mL of KY gel
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• Tissue infiltrationTissue infiltration• Indications
– 1. Failure to respond to 30 minutes of topical treatment
– 2. Severe burns
• 5% calcium gluconate not more than 0.5 mL per cm2
• Gauge 27 or 30 needle• Normal tissue 0.5 cm away from necrotic margin• Calcium chloride should not be used
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• Recurrence or persistence of pain indicates on-going tissue damage
• and more aggressive treatment is indicated
• Limitations of tissue infiltration– 1. Pain due to calcium– 2. Nail involvement needs nail
extraction
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• Intravenous regional infusion ‘Bier Block technique’
• Indicated if tissue infiltration is ineffective• 1. An IV cannula place on dorsum of affected
hand• 2. Elevated the extremity for 5 minutes• 3. Apply pneumatic cuff tourniquet just proximal
to the elbow• 4. Apply pressure to 100 mmHg above systolic BP• 5. 10 ml of 10% calcium gluconate in 30 mL of
D5W is infused into the cannula• 6. Release tourniquet at 25 minutes by gradually
decrease cuff pressure over 3-5 minutes
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• Muscle cramping may develop– Diazepam 5-10 mg IV
• Repeat the treatment if pain recurs
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• Irrigation with water or saline, if avai lable Lactated Ringer’s solution is pr
eferable.• Irrigate with calcium gluconate solut
ion: 10% calcium gluconate solution 50 ml in normal saline 500 ml
• Apply 1% calcium gluconate as eye drops every 2-3 hours
Hydrofluoric acid ocular burn: management
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• Monitor Calcium level hourly in first 6 hours
• Monitor ECG • Patients should be monitored for at
least 24 hours
Hydrofluoric acid: management
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Hydrofluoric acid: Treatment of systemic toxicity• Prolonged QT syndrome• 10 ml of 10% calcium gluconate
over 5 minutes (bolus if in emergency)
• 20 mL of 20% magnesium over 20 minutes
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Phenol• White crystalline, pink, red
• Exposure
– Disinfectant
– Pharmaceuticals
– Lab. Reagent
– Wood preservatives
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• Low concentration (5%) can kill
• Well absorbed through skin and mucosa
• Skin burn: white layer of precipitated protein (keratocagulation)
• Ingestion: GI irritation, nausea & vomiting
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• Systemic effects onset of 15-60 minutes: – excitation
– CNS depression
– hypotension: vasodilation and negative inotropic effects
– respiratory depression
– convulsion
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Phenol: Management
• Removal of soaked cloth• Initial decontamination with dry
decontamination and large amount of water ASAP
• Then: further decontamination– If skin area less than 5% BSA use
70% isopropyl alcohol or polyethylene glycol
– If skin area larger than 5% BSA use polyethylene glycol (Colyte) or olive oil, mineral oil, vegetable oil
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• For ingestion: – Gastric lavage if present within 1
hours– Activated charcoal if presented
after 1 hour• Supportive and symptomatic care• Observe for 6 hours for
asymptomatic patients
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Methemoglobinemia• Hemoglobin binding to oxygen needed
heme iron in ferrous state (Fe2+)• Methemoglobinemia
– Oxidized Hb (1 electron taken)– Heme iron in ferric state (Fe3+)– Do not bind oxygen & impaired oxygen
release to tissue• In normal human body less than 1%
metHb: maintained by reduction system
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• Regular pathway in human body
• High energy compound (NADH) from glycolysis
• NADH reduces (donates 1 electron) cytochrome B5
• Reduced cytochrome B5 reduces MetHb to Hb2+
Methemoglobin reduction system
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Methemoglobin-forming agents• Industrial agents
– Aniline: Dye, pharmaceuticals, resin, perfume, rubber
– Nitrobenzene: Dye, shoe polish– Nitroglycerine: Explosive– Sodium nitrite: Meat preservatives, fiber
bleaching: silk, linen, flax• Most are liquid• Dermal exposure
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• Central cyanosis• Brownish discoloration, blue-gray or
brown-gray discoloration of lips, skin, nail beds
• Unresponsive to oxygen• Malaise, fatigue, headache, dyspnea,
tachycardia• Impaired consciousness• Inclusion body hemolysis
Methemoglobinemia: clinical presentation
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Methemoglobinemia: Diagnosis• Chocolate brown blood discoloration• Blood does not become red with exposure
to air– test on filter paper or white paper towel
• Saturation gap from arterial blood gas (>5)– = Oxygen saturation from calculation
methods (from PaO2)- Oxygen saturation from direct measurement
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Left (MetHb) Right (Normal)
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• Pulse oximetry is not a reliable test– underestimate oxygen saturation
with mild methemoglobinemia– overestimate oxygen saturation
with severe methemoglobinemia• Multiple wave length co-oximetry
to measure methemoglobin level
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MetHb levels and clinical correlation
<3% No symptoms
10-15% Skin discoloration, low PaO2 frompulse oximetry
15-20% Cyanosis, Chocolate brown blood
20-50% Dyspnea, fatigue, headache,dizziness
50-70% Tachypnea, metabolic acidosis,arrhythmias, CNS depression
>70% Death
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Methemoglobinemia: Treatment• Removal of exposure• Decontamination of skin• 100% oxygen• Definitive treatment: methylene
blue: indications– Symptoms of tissue hypoxia: alteration
of consciousness, hypotension– methemoglobin level > 30%
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Therapeutic Methemoglobin reduction
pathway:• No active role in
physiologic condition• Activated into action by
administration of methylene blue
• NADPH from hexose monophosphate pathway (G6PD)
• NADPH reduces methylene blue
• Reduced methylene blue (Leucomethylene blue) reduces metHB to Hb2+
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Methemoglobinemia: Methylene blue• 1-2 mg/kg of 1% methylene blue
solution (10 mg/mL) over 5 minutes• Reduction of metHb within 15-30
minutes• Repeat at 30-60 minutes interval• Maximum dose 7 mg/kg• Without any response after 2 doses,
do not repeat doses.
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• Contraindications– G6PD or metHb reductase deficiency– Renal insufficiency
• Adverse effects– Headache, nausea, vomiting, GI upset– Methemoglobinemia at dose > 7 mg/ kg – Local tissue necrosis with extravasation
Methemoglobinemia: Methylene blue
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Thank you•Do you have any question?