Download - Hazardous Material Medical Care Corrosives and Oxidizing Agents Methemoglobin forming agents น. พ. สัมมน โฉมฉาย สาขาพิษวิทยาคลินิค

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

Corrosives, Oxidizing & MetHb forming Agents

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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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Download - Hazardous Material Medical Care Corrosives and Oxidizing Agents Methemoglobin forming agents น. พ. สัมมน โฉมฉาย สาขาพิษวิทยาคลินิค

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