Nagotane, Maharashtra blast in 1990---Bhopal, Madhyapradesh MIC leak in 1984---Doctors did not know how to treat the affected victims.Doctors practicing around industries in big cities and around sprawling industrial estates , find it difficult to give first-aid to the victims injured due to chemicals.

In our orientation trainings on occupational health (over the past 3 years), doctors asked us regarding immediate treatment of chemically injured patients- they are not covered in the MBBS syllabus.. Doctors around Lote industrial area (Maharashtra ) and Aurangabad too came with a similar request.

Dr Murlidhar has painstakingly put together the present monograph on emergenct first-aid and antidotal treatment for chemical injuries and Dr NK Mehrotra, Lucknow ,with his vast experience in toxicology has scrutinised the same and we are thankful to them for their efforts.

As with any monograph or write ups , this will need many additions in future and it is expected that the doctors would give such inputs in the future.

The present monograph does not deal with standard first aid treatments e.g. for shock, pulmonary edema etc..,because we have assumed that standard treatment in such cases are well known.

We will appreciate reader’s comments about the monograph. At a later date it will come out in a book form with improvements.

We hope that this monograph will prove to be useful in treating patients of industrial accidents.
 
 
 
 

Vijay Kanhere,

Consultant PRIA,

New Delhi.

July 1999.

Preface *

INTRODUCTION: *

First aid at the site of accident. *

PREPARATION *

TRIAGE *

PRIMARY SURVEY *

Airway maintenance *

Breathing and Ventilation *

Circulation with hemorrhage control *

Blood volume and cardiac output *

Level of consciousness *

Pulse *

Bleeding *

Disability (Neurologic Evaluation) *

Exposure *

Triage for chemical injuries *

Criteria to triage patients exposed to irritant gases *

Criteria to triage patients burnt with corrosives *

INITIAL SITE: *

DECONTAMINATION SITE: *

MAIN TRIAGE SITE: *

TREATMENT PRINCIPLES : *

RESUSCITATION *

AIRWAY *

BREATHING / VENTILATION / OXYGENATION *

CIRCULATION *

URINARY AND GASTRIC CATHETERS *

MONITORING *

CONSIDER NEED FOR TRANSFER *

General principles of treatment *

SKIN :- Chemical Burns *

INHALATION: *

EYE CONTACT : *

INGESTION : *

Chemicals where activated charcoal is ineffective: *

INITIAL TREATMENT: *

ANTIDOTES: *

Specific exposures and specific treatment : *

General Principles of treatment:[ For Gases like Ammonia, Chlorine, hydrofluoric acid, hydrogen sulphide, nitric acid, oxides of nitrogen ,sulphur dioxide and phosgene.] *

CARBON MONOXIDE ( CO ): *

Treatment *

Methaemoglobinaemia *

Causes: *

Methylene Blue(A1)(Reducing Agent) *

Dose: *

Cyano- compounds : *

Treatment: *

Organophosphorous pesticides : *

Additional first - aid measures : *

Antidote : *

Lab investigations: *

Carbamate Poisoning: *

Synthetic Pyrethreon and pesticides *

Organochlorine Compounds: *

Aluminium Phosphide: *

Methanol: *

Arsenic and its compounds: *

Arsene gas: *

Lead Compounds: *

Organic lead : *

Mercury and its compounds: *

Cadmium: *

Zinc Oxide: *

Manganese: *

Chromium: *

Treatment: *

Aluminium: *

Nickel carbonyl: *

Treatment: *

Classified lists of antidotes and other agents. *

Group 1.Antidotes *

Group 2.Agents used to prevent absorption of poisons,to enhance their elimination,or to treat symptomatically their effects on bodily functions *

Agents to prevent skin damage *

Group 3. Other therapeutic agents useful for the treatment of poisoning *

Group 4. List of antidotes and related agents now considered obsolete *

References: *

INTRODUCTION:

In 1990, a blast occurred in the IPCL factory in Nagothane (100 miles from Mumbai) and 60 acutely burnt workers came nearly 10 hours late to Sion Hospital (Mumbai) without First - Aid being given at the site of accident. Though such mishaps are highlighted in the press daily , many go unreported. Immediate relevant first-aid is rarely given at the site and there are no round the clock first aid centers in the vicinity of such industrial belts. In such a scenario, the doctor who is available nearby is called to give his services. This manual is for such doctors who reside and practice near chemical industrial belts, and who may be called upon to attend an emergency case following a chemical accident.It is necessary that doctors should be informed before hand about the chemicals that are used in the industry surrounding them.They can visit the factories and request for Material Safety Data Sheets (MSDS) and also procure the disaster management plan that is usually brought out by the Government.It is to be noted that usually the victim comes with exposure to a mixture of chemicals, hence if prior knowledge is lacking regarding the chemicals he is exposed to it is impossible to diagnose a specific chemical toxicity in the emergency setting.In most cases supportive treatment is the basic line of action.The manual is also useful in areas like Mumbai, New Delhi etc.. where patients come for treatment after being exposed to chemicals at the industries surrounding the cities and even from far away place,since at present there are very few first aid centers (equipped) surrounding the industrial belts in India.This manual would also dispel a common feeling among doctors that there is a magic antidote to many chemicals (the magic bullet like vaccines)--in reality there are very few antidotes,which are recognised worldwide.

The manual starts with common first aid treatments, followed by a brief information on specific chemicals, their relevant bio-chemical mechanisms (if known) and how they are countered by antidotes. Since ingestion of a chemical is rare in an industrial setting, it is given a cursory write-up. Ingestion as a mode of entry in an industrial settings can occur on swallowing sputum laden with chemicals (during the mechanism of removal of the substance from the lungs by the muco - ciliary escalator system). Ingestion can be an additional factor in the poisoning when workers eat using contaminated hands. Most of the acute poisonings are due to inhalation and dermal absorption. The manual covers acute injuries and some chronic injuries due to exposure to chemicals and their specific treatments (if any). There are controversies in the use of many antidotes. Hence, most of the antidotal treatments referred to in this manual are non-controversial ones, having been standardised in many centers around the world. All specific treatments are referenced. The antidotes are classified as follows (based on WHO guidelines)

The manual does not give details of standard supportive treatment (e.g. for pulmonary Edema, Shock etc.) unless it is specifically different for the chemical toxicants.Similarly signs and symptoms of the poisoning are not given in this manual,unless it is useful in understanding the biochemical action of the antidote.Biochemical mechanisms are mentioned as and where relevant to understanding of the actions of the antidote.

First aid at the site of accident.

It is unusual for the accident in the industrial setting to result in multiple casualties. Therefore, a MAJAX (Major accident) protocol needs to be a part of the routine safety drill in a all industries. It includes:

1. Preparation
2. Triage
3. Primary Survey (ABCs)
4. Resuscitation

An action plan chalking out the team of people who will constitute an "emergency squad" to be summoned in case of an accident, is a part of the preparation. Linking with an appropriate facility and discussing a transfer and transportation agreement, to minimize the transit time, (from accident to definitive care in a hospital) needs to be set up. Antidotes, first-aid equipment and resuscitation tools need to be checked on a regular basis and kept in optimal working condition.

TRIAGE

Triage is the sorting of patients based on the treatment and available resources to provide that treatment. Triage is rendered on the basis of ABC priorities as outlined below. Triage pertains to the sorting of patients in the field and the medical facility to which they are transported.

PRIMARY SURVEY

In the severely injured patient, logical sequential treatment priorities must be established based on overall patient assessment. The patient’s vital functions must be assessed quickly and efficiently. Patient management must consist of a rapid primary evaluation, resuscitation of vital functions, a more detailed secondary assessment, and finally, the initiation of definitive care.

A Airway maintenance

B Breathing and Ventilation

C Circulation with hemorrhage control

D Disability : Neurologic status

E Exposure

Airway maintenance

The airway should be assessed FIRST to ascertain patency. This rapid assessment for signs of airway obstruction should include inspection for foreign bodies and facial, mandibular, or tracheal fractures that may result in airway obstruction. Measures to establish a patent airway should protect the cervical spine. The chin lift or the jaw thrust maneuvers are recommended to achieve this task. The Pitfalls to watch out for are:

1. Foreign body in the airway.
2. Mandibular or maxillofacial fracture.
3. Tracheal or laryngeal disruption.
4. Cervical spine injury.

Breathing and Ventilation

Airway patency alone does not assure adequate ventilation. Adequate exchange of gases is mandatory to maximize oxygen transfer and carbon dioxide elimination. Ventilation involves adequate function of the lungs, chest wall and diaphragm. Each component should be examines rapidly.

The patient’s chest should be exposed to assess ventilatory exchange in the lungs. Percussion may reveal the presence of air or blood in the chest. Visual inspection and palpation may reveal injuries to the chest wall that might compromise ventilation.

The most important conditions are:

1. Tension Pneumothorax
2. Flail chest
3. Open pneumothorax
4. Massive hemothorax

Pitfalls:

1. Intra-abdominal or intrathoracic injury
2. Fractures of the femur and/or pelvis
3. Penetrating injuries with arterial or venous involvement
4. External hemorrhage from any source

A rapid neurologic evaluation is performed at the end of the primary survey. It is done by the AVPU method:

A Alert

V Responds to Vocal stimuli

P Responds only to Painful stimuli

U Unresponsive

Pitfalls:

1. Head injury
2. Decreased oxygenation
3. Shock
4. Altered level of consciousness secondary to alcohol and/or other drugs.

Triage for chemical injuries

The fundamental principles of triage used for patients of trauma are also applicable to victims of chemical accidents.

The basic principle of paying immediate attention to airway ,breathing and circulation (ABC) of emergency care is followed and decisions are made regarding the need for admission accordingly.

DECONTAMINATION SITE:

Here the victim of exposure is transferred away from the initial site of exposure.Apart from isolation, the site requires the health personnel engaged in decontamination to wear protective appliances such as full masks, gloves, protective coats with hoods, and rubber boots.

Victims have to be undressed completely since clothes may harbour residual toxins.

MAIN TRIAGE SITE:

Depending upon the seriousness of the patients they are sent to any of the following definitive-care sites;

RESUSCITATION

If the patient is unconscious and has no gag reflex, an oropharyngeal airway may be helpful.

A Tension Pneumothorax compromises ventilation, and if suspected, chest decompression should be accomplished immediately. Also, every injured patient should receive supplemental oxygen therapy.

Gastric tubes reduce stomach distention and decrease the risk of aspiration.

General principles of treatment

General principles of treatment have been evolved by analysing the route through which the body is subjected to the toxic effects of chemicals. There are four main routes of exposure (1) Skin, (2) inhalation (3) Eye, (4) Ingestion.

SKIN :- Chemical Burns

3. Check for burns : Standard treatment is followed for burns (volumes of Ringerlactate solutions infused as per Parkland Formula).

1. Hydrofluoric Acid Burns :

• Solutions of 20% may not produce erythema upto 24 hours and concentrations of 20-505 produce effects within 1-8 hours.
• Inhalation burns should be assumed in burns:

1. Involving H.F. concentration of 50% or over.
2. Of head and neck
3. Of greater than 55 of body surface.
4. Where clothing is soaked and there is delay in removing clothing.
5. Occurring in confined spaces.

• Strong intravenous analgesia
• Trimming of nails / splitting of nails
• Locally 1% to 2% benzyalkorium Chloride (Zephiran) or iced 25% MgSO₄ or 10% Calcium gluconate gel is applied repeatedly. If pain persists local injection of 10% Ca gluconate. Dose = 0.5ml of 5% Ca gluconate per cm².

• (Note : Ca gluconate gel can be prepared by mixing K - Y jelly with 10% Ca gluconate solution).75 ml K-Y jelly plus 25 ml calcium gluconate (10%)
• surgical gloves filled with gel is useful for hand burns
• Areas covered with gel redressed every 4 hours.
• For conc. more than 20% to fingers:local infiltration ;Dose 0.5ml of 55 calcium gluconate per cm² using 27 or 30 gauge needle subcutaneously.
• Use of 1% calcium gluconate eye drops every 2-3 hours for eye injuries.
• Iv calcium treatment should not wait till blood tests are available.In case IV infusions are not available then tablets can be give orally.
• In case of extremity burns, if pain persists ,intra-arterial infusion can be tried ,if this also fails, then surgical excision.

1. Pre-Hospital give calcium Gluconate tabs every 2 hours.
2. 20 ml of 10% calcium Gluconate I.V before levels of Ca ⁺⁺ are known.
3. Monitor Ca ⁺⁺ levels and ECG
4. I.V infusion of 40 ml of 10 % calcium gluconate over 1 hour.
5. Serum Ca ⁺⁺ level ,if still not maintained, consider immediate burns excision and or haemodialysis.

2. In case of HF exposure use 1% Ca gluconate drops every 2 - 3 hours. Eye is to be padded.
3. If corneal injury is suspected homatropine drops are to used to relax the pupillary sphincter.

Activated Charcoal : A preparation of activated charcoal is available with LOCOST (Vadodara). It is mixed with water and the adult dose is 50 - 100 GMS. Emesis and gastric lavage decrease the effect of activated charcoal. A saline cathartic or sorbitol should accompany the administration of activated charcoal to enhance GI transit time and possibly drug elimination.

Alkali DDT

Boric Acid Malathion

Boron N - methyl Carbamate

INITIAL TREATMENT:

After first - aid, the initial treatment consists of clinical evaluation, administration of specific antidote if any and supportive treatment before shifting to a major tertiary care hospital.

ANTIDOTES:

Antidotes are therapeutic substances that in a specific way can prevent, eliminate or at least reduce the harmful effects of certain poisons. Some have intrinsic activity and may cause adverse reactions. They should be given as early as possible during the course of poisoning and in an adequate dose.

**In most poisoning cases, symptomatic and supportive care is the mainstay of treatment. Without a history of occupational exposure, it is nearly impossible to identify the chemical toxin by symptoms alone e.g. cyanosis can be due to respiratory failure or due to methaemoglobinemia. Also many clinical signs (like miosis in organophosphorous poisoning) occur later and immediate treatment would be delayed. Hence, occupational history and prior knowledge of workplace, working atmosphere and the list of hazardous chemicals is extremely important when giving antidotal treatment.**The occupational physician should visit the workplace!

Antidotes can be classified as:

1. Immediately available,


available within 2 hours or

2. available within 4 - 6 hours.

1. In the GI treat : e.g. : activated charcoal.
2. Formation of chelates :e.g. demercaprol (BAL) for Arsenic.
3. Formations of other complexes :e.g. hydroxycobalamine for cyanide.

General Principles of treatment:[ For Gases like Ammonia, Chlorine, hydrofluoric acid, hydrogen sulphide, nitric acid, oxides of nitrogen ,sulphur dioxide and phosgene.]

1. The agents inhaled cannot be washed away or otherwise removed, unless, when only the skin is involved.
2. Arterial blood gases are of primary importance in determining the extent of the damage.
3. Supportive measures include suctioning (intubation may be required), volume cycle ventilator (positive end expiratory pressure (PEEP), steroids and antibiotics.

1. Phosgene may cause pulmonary edema often seen several hours after exposure. Treatment is similar to that for irritant gases except PEEP is extremely useful.
2. A unique property of hydrogen sulphide (H₂S) is that it can kill by directly paralyzing the respiratory center within seconds of heavy exposure. It also causes olfactory fatigue, making its presence undetectable by persons exposed to smaller amounts. Here too delayed pulmonary edema can occur. Hyperbaric oxygen is valuable in cases of H₂S poisoning.
3. Oxides of nitrogen (nitrogen dioxide and nitrogen tetroxide) also have a delayed action on the lungs. A worker may be exposed for 8 hours during the day with no ill effects and later while at home may lapse into pulmonary edema.

CARBON MONOXIDE ( CO ):

CO is readily absorbed by the lungs. It combines with haemoglobin,myoglobin and cytochrome oxidase system and affects cellular respiration. The affinity of CO for haemoglobin is 250 times that of oxygen.

Methaemoglobinaemia

The haem ion is oxidised into ferric state ,which is called methemoglobin. -Normal 1%

1. Inherited defect
2. Nitrites and Nitrates ( nitrates are converted to nitrites in the GI tract )
3. Aniline
4. Acetanilide and phenacetin
5. Aromatic nitro compounds
6. Cyanogen
7. Chlorates
8. Toluidine

In addition to causing methaemoglobinaemia most of the above chemicals cause a Heinz- body haemolytic anaemia. This process is characterized by oxidative denaturation of haemoglobin, leading to the formation of punctate membrane-bound red cell inclusions known as Heinz bodies. Oxidative damage to the red cell membrane also occurs. Haemolysis will be most prominent part of the clinical picture in individuals with Glucose-6-Phosphate dehydrogenase(G6PD) deficiency.

1. Do not use in case of amyl nitrite treatment after CN poisoning.
2. Haemolysis will occur in patients having G6PD deficiency.
3. Higher concentration of methylene blue can itself cause methaemoglobinaemia.
4. Methaemoglobinaemia caused due to chlorates does not respond to methylene blue.

Inorganic cyanides are readily hydrolysed by water and decomposed by mineral acids and carbondioxide to form hydrocyanic acid.

Hydroxy cobalamine (A1) or dicobalt edetate (A1) are also good antidotes.

Dose of Hydroxy cobalamine: 4 gm I.V. in 5% dextrose. Repeat in case of massive poisoning. 4 - 8 g. of thiosulphate is co-administered.

Dose of Dicobalt edetate: Adults:- 1 -2 ampoules (300 - 600 mg.) I.V. over 1 - 5 min. A third ampoule can be injected I.V. over 1 - 5 min. A third ampoule can be injected I.V. if there is no sufficient clinical improvement.

*Note: Di cobalt edetate is not to be given in mild cases.

Organophosphorous pesticides :

70 - 80% of the poisoning is accidental and is common in agricultural and industrial workers. The mode of entry is inhalational and dermal and occasionally ingestional in workers. It crosses the blood - brain barrier. They are potent inhibitors of acetylcholinesterase and pseudocholinesterase. The inhibiton of these enzymes is due to irreversible binding of phosphate radicals of organophosphates to active sites of enzymes. In case of carbarmates this binding is irreversible. The toxicological effects are due to accumulation of acetylcholine at synapses resulting in initial stimulation followed by paralysis of neurotransmission at cholinergic synapses. The cholinergic synapses are present in CNS, somatic nerves, autonomic ganglion, parasympathetic nerve endings and some sympathetic nerve endings like in sweat glands.

The signs and symptoms which are due to muscarinic and nicotinic effects appear within a few minutes to a few hours (av.: 6-8 hrs.). The crucial period is the first 24 hrs.

2] Cardiac monitoring

(b)Oximes (cholinesterase enzymes reactivators.)

Pralidoxime (A1) is given to all patients with severe toxicity (muscle weakness and respiratory depression). It rapidly ameliorates muscle weakness, fasiculations and coma.

Dose:1-2 GMS in adults or 25-50 mg/kg in children over 5-10 minutes I.V. The dose may be repeated after 1 hour.

Drugs contraindicated : Opiates, phenothiazines , parasympathomimetic drugs.

1. Latent poisoning (Serum Cholinesterase activity 50-90% of normal value;)-- No treatment.
2. Mild (20-50% of normal value); --Needs treatment.
3. Moderate (10-20% of normal value)
4. Severe (Serum Cholinesterase less than 10% of normal)

Atropine - (A1) is a specific antidote. Do not give PAM in carbamate poisoning except in case of combined organophosphate and carbamate poisoning.

Organochlorine Compounds:

There is no specific antidote. Convulsions can be treated by diazepam (5-10 mg I.V. over 2-3 minutes) - Max dose : Adults: 30 mg, Children: 10 mg.

If seizures are uncontrolled Phenobarbitone (loading dose 10mg/ kg) can be given. Drugs Contraindicated: Adenaline, Atropine as they can induce arrythmias.

Aluminium Phosphide:

No specific antidote is available. Since phosphine is excreted through breath and urine, adequate hydration and renal perfusion by low dose dopamine 4-6 m g/kg/ min is to be used. Shock and pulmonary edema are treated by standard measures.

Magnesium Sulphate can be used as an antioxident and is also useful as an anti-arrythimic and antihypoxic agent.

A dose of 1 gm of MgSO₄ I. V, stat is given followed by 1g for next 2 hours and finally 1.0 -1.5g after 4-6 hours for 3-5 days or final outcome of these patients.

Methanol:

It is well absorbed following inhalation. The metabolism is principally in the liver, by the metalloenzyme alcohol dehydrogenase to produce formaldehyde. Thereafter formaldehyde is converted to formate by enzyme systems like aldehyde dehydrogenase. Formic acid formed is associated with metabolic acidosis and retinal toxicity. It also inhibits cytochrome oxidases and causes optic neuritis.

Treatment measures:

1.Correction of acidosis by IV sodium bicarbonate (preferably with ABG monitoring)

1. Folinic acid (5-formyl tetrahydrofolic Acid) (B1) enhances the elimination of formic Acid. Intravenous folate (Folinic or folic acid) at 50 -70 mg. every 4 hours for at least 24 hours can be given.
2. 4-methypyrazole (A1) which inhibits alcohol dehydrogenases is a suitable adjunct to ethanol,.Also depression, which is common with ethanol will not be a problem.

Arsenic and its compounds:

Arsenic trioxide gets into the body through inhalation. Over 23% of the particles are larger than 4m m. Particles of this size get deposited in the upper ciliary tract, cleared by the muco-ciliary system and swallowed ,thus entering by GI route.

Arsenic acts through the formation of covalent bonds with the sulphur atom of mercapto-groups (also called sulfhydryl or thiol) in the body. This is the only biological pathway that arsenic can enter a physiological reaction. It blocks the pyruvate oxidase and a glutarate oxidase systems.

Treatment:

Children: 3 - 5 mg / kg /dose by deep IM injection.

Note:

1. Do not give BAL to patients allergic to peanuts.
2. Persistent hyperpyrexia can occur.
3. Maintain the urinary pH alkaline to prevent dissociation of metal - BAL complex.
4. BAL may cause haemolysis in patients with G6PD deficiency.
5. *In cases of Arsine poisoning BAL is not effective. Treat with exchange transfusion.

Lead Compounds:

Lead dust and compounds are absorbed after inhalation. Deposition in the lungs is maximal (63%) at particle size 1 m m and minimal (39%) at 0.1 m m for resting persons. Larger particles are deposited in the upper respiratory tract and cleared or swallowed. A crude estimate of the percentage of inhaled lead reaching the blood stream would be about 30 - 40%.

All enzyme systems are potentially susceptible to heavy metals. The biochemical interactions of Lead with sulfhydryl groups are of great toxicological importance. Lead also has a high affinity for amines and simple amino acids.

During haem synthesis lead inhibits ALA dehydrogenases initially and coproporphyrinogen decardoxylase later. Basophillic stippling of the erythrocytes is probably made up of fragments of deranged mitochondria, microsomal remnants and RNA.

Treatment:

1. Convulsions can be controlled by diazepam.
2. In lead encephalopathy, combined chelation with BAL (C2) and CaNa₂ EDTA (C2) for 5 - 7 days. This is followed by a course of oral penicilamine.

Children: 20 mg / kg / day in 2 divided doses before meals. Maximum: 1 gm / day.

DMSA (2,3 dimercaptosuccinic acid) (B3) has advanced therapeutic options in lead poisoning. It is less toxic and does not cause depletion of body stores of essential cations such as zinc, copper and iron.

Dose: Adults: 30 mg / kg / day in 3 divided doses for 5 days followed by 20 mg / kg / day in 2 divided doses for 14 days.

Children: Initial dose is 10 mg / kg or 350 mg / m2 every 8 hours for 5 days, then every 12 hours for next 14 days.

Note:

1. Monitor liver function.
2. DMSA can be mixed with food.
3. DMSA can be given after a course of BAL / EDTA after an interval of 4 weeks.

Alkyl lead (Tetra-ethyl lead) poisoning: Only symptomatic treatment, chelating agents have no proved role.

Mercury and its compounds:

Elemental mercury and mercurous compounds are readily absorbed from the alveoli of the lungs and are oxidised to mercuric salts. Inhalation results in 80% deposition and retention.

Treatment of inorganic mercury poisoning:

D-acetyl penicilamine(C3):

Dose: Adults: 250 - 500 mg. orally, 4 times a day for 6 - 10 days, totaling 20 - 30 mg / kg. In case of prolonged therapy give for 1 - 2 weeks intermittently.

D-Penicillamme (C2):

Dose: Adults: 250mg., orally 4 times a day half an hour before meals for 5 days or 20 - 40 days depending on severity.

Children: 20 mg / kg / day orally in 2 divided doses.

Note:

1. In patients, not able to take oral chelators, give BAL (except in associated liver failure).
2. *There is no specific antidote for poisoning due to organic mercury compounds.

Cadmium:

Depending upon the size of the particles, 10% to 50% of the inhaled cadmium is deposited in the alveoli.

The absorption of the retained Cadmium depends on its chemical form. For CdO it is 60%. Acute inhalational injury due to freshly generated cadmium fumes may be caused after several hours. Symptoms are similar to metal fume fever and a significant decrease in PFT.

Cadmium accumulates in the renal cortex giving rise to a functional lesion involving the proximal tubule giving rise to tubular type of proteinuria ( b 2 –microglobulin, retinal binding protein etc.).

Sometimes even high molecular weight proteins (suggesting glomerular dysfunction) like albumin, transferrin, IgG etc..are excreted.

This may be associated with amino-aciduria, glycosuria and calcuria.

Treatment:

1. Symptomatic.
2. Vitamin D in cases of osteomalacia
3. Unithol (DMPS) (C3)

Children: Max: 1gm. (75 mg / kg / kg for encephalopathy)

Dilute 1 ampoule (1 g) in 250 - 500 ml of isotonic saline or 5% dextrose. Infuse I.V. slowly over 15 - 20 min or by continuous infusion over 4 - 6 hours.

Zinc Oxide:

Inhalation causes metal fume fever with severe respiratory irritation. Malaise, chills and fever (101 - 102 F) may occur 4 - 6 hours after exposure. It can also lead to pulmonary edema.

Treatment:

1. Supportive treatment

Manganese:

Inhalation of dust or fumes is the major route of entry. The term manganism is usually referred to the chronic neurological disorder caused by inhalation of manganese laden dust.

Manganese neurotoxicity results from the enhanced auto-oxidation of dopamine by a higher valency Mn 3+ ion with increased generation of cytotoxic free radicals. Mn 3+ complexes are formed in the brain and catecholamines are destroyed.

Treatment:

1. Supportive.
2. Levadopa (controversial) (C3)
3. Vitamin E (Not proven yet) (C3)
4. For acute exposure, Ca- EDTA can be used. (C3)

Chromium:

1. Inhalation of aluminium fumes (bauxite) cause both obstructive and restrictive pulmonary disease,hence will need both lung physiotherapy as well as bronchodilators.
2. Systemic toxicity causing neurological syndrome will have to be treated with chelating agent desferoxxamine (C 1)
3. Vitamin D and calcium to treat osteomalacia
4. Iron defeciency to be treated.

Nickel carbonyl:

After acute exposure initial symptoms can be mild nausea,chest pain and dyspnoea.These symptoms disappear after a few hours.After 12 to 36 hours and occasionally as long as 5 days after exposure,severe pulmonary symptoms develop.Human fatalities have occurred 4 to 13 days after exposure from diffuse interstitial pneumonitis and cerebral edema.

• Oxygen (preferably humidified)
• Rest
• Corticosteroids and prophylactic antibiotics
• Sodium Diethyldithiocarbamate (A3) has been suggested as an antidote-further research needs to be done.

Classified lists of antidotes and other agents.

Group 1 List of antidotes

Group 2 Agents used to prevent the absorption of poisons,to enhance their elimination,or to treat symptomatically their effects on bodily functions.

Group 3 Other useful therapeutic agents for the treatment of poisonings.

Group 4 List of antidotes and therapeutic agents considered obsolete.

The antidotes listed in groups 1 and 2 are considered useful in the treatment of acute human poisoning and their availability in terms of urgency of use may be classified as follows:

A required to be available immediately (within 30 minutes)

B required to be available within 2 hours.

C required to be available within 6 hours.

Their effectiveness in practice can be classified as follows:
 

1	effectiveness well documented,e.g reduction of lethality in animal experiments and reduction of lethality or of severe complications in human poisoning.
2	Widely used but not yet universally accepted as effective,owing to lack of research data,and requiring further investigations concerning effectiveness or indications for use.
3	Questionable usefulness;as many data as possible regarding effectiveness should be collected.

The classification in terms of urgency of availability (A,B,C) or proven effectiveness (1,2,3) is given next to the main indication for the antidote.The classification is also given in the right-hand column of Group 1 list when an antidote has other possible applications.If there is doubt as to the classification of the antidote,the lower score is always given,e.g B2 instead of A1.

Group 1.Antidotes
 

Antidote	main indication or pathological condition	Other possible applications
Acetylcystine N-acetyl penicillamine amyl nitrite atropine     benzyl penicillin b -blockers (b 1 and b 2,preferably short acting) calcium gluconate or other soluble calcium salts dantrolene deferoxamine diazepam cobalt edetate digoxin-specific antibodies  dimercaprol 4-dimethyl amino phenol edetate calcium disodium ethanol flumazenil folinic acid glucagon glucose (hypertonic) hydroxycobalamine isoprenaline methionine 4-methlypyrazole methylthionium chloride (Methylene Blue) naloxone neostigmine obidoxime oxygen oxygen,hyperbaric	paracetamol (B1) mercury (inorganic and vapour) (C3) cyanide (A2) organophosphorous compounds And carbamates (A1) amanitins (B3) b -adrenergic agonists(A1)     HF,fluorides and oxalates drug-induced hyperthermia iron (B1) organophosphates (A2) cyanide (A1) digoxin/digitoxin (A1) arsenic (B3) cyanide (A1) lead (C2) methanol,ethylene glycol (A1) benzodiazepenes (B1) folinic acid antagonists (B1) b -blockers (A1) insulin (A1) cyanide (A1) b -blockers (A1) paracetamol (B1) ethylene glycol (A1) methamoglobinemia (A1) opiates (A1) curare type agents (B2) organophosphorous insecticides (B2) cyanide,carbon-monoxide hydrogen sulphide (A1) carbon monoxide	theophyline (B1) calcium antagonists (B3) malignant-neuroleptic syndrome aluminium (C2) chloroquine (A2)     gold (C3),mercury inorganic (C3)             methanol (B3)                 Methanol,disulfiram (B2)                             Cyanide,hydrogen sulfide,carbon tetrachloride.

 
 

Antidote	main indication or pathological condition	Other possible applications
penicillamine pentatic acid phentolamine physostigmine     vitamin K prussian blue pralidoxime prenalterol protamine sulfate pyridoxine     silibin sodium nitrite sodium nitroprusside sodium thiosulfate succimer (DMSA)         trintine unithiol (DMPS)	copper (C1) cobalt (C3) a -adrenergic poisoning (A1) central anti-cholinergic syndrome (from atropine) coumarin derivatives (C1) thallium (B2) organophosphorous (A2) b -blockers (A1) heparin (A1) isoniziad,hydrazines (A2) amanitin (B2) cyanide  ergotism (A1) cyanide (A1)     antimony,arsenic,bismuth,cadmium,cobalt,copper,gold,lead mercury (organic and inorganic )(B2) copper (Wilson’s disease) (C2) cobalt,gold,lead,mercury (inorganic,nickel (C2)	Lead ,mercury (inorganic))c2) radio-active metals                                 ethylene glycol (C3),gyrometrine (B2)                     bromate,chlorate,iodates (C2)     mercury (elemental),platinum,silver (c3)     cadmium,mercury (organic ) (C3)

Group 2.Agents used to prevent absorption of poisons,to enhance their elimination,or to treat symptomatically their effects on bodily functions

Emetics

Listed below are certain therapeutic agents that are not antidotes according to the accepted definition;however,because of their established value and sometimes specific role in the management of poisoning,they border on the concept of antidotes.In practice, these agents are used frequently in cases of poisoning and in other medical circumstances.Most of them are considered essential drugs and therefore are required to be available for immediate use.
 

Agent

Indications/Symptoms arising from poisoning

benztropine chlorpromazine corticosteroids     diazepam diphenhydramine dobutamine dopamine adrenaline furesamide glucose haloperidol heparin magnesium sulfate mannitol oxygen pancuronium promethazine salbutamol sodium bicarbonate

Dystonia psychotic states with severe agitation acute allergic reactions,laryngeal oedema (systemic/topical),bronchoconstriction,mucosal oedema (Inhaled) convulsions,excitation,anxiety,muscular hypertonia dystonia myocardial depression myocardial depression,vascular relaxation anaphylactic shock,cardiac arrest fluid retention,left ventricular failure hypoglycemia hallucinatory and psychotic states hypercoagulability states cardiac arrhythmia's cerebral oedema,fluid retention hypoxia muscular rigidity,convulsions allergic reactions bronchoconstriction (systemic/inhaled) acidosis

Group 4. List of antidotes and related agents now considered obsolete
 

Antidote	Indicated for
acetazolamide ascorbic acid aurintricarboxilic acid b -aminopropiononitrile castor oil copper sulfate cyclophosphamide cysteamine diethydithiocarbamate fructose guanidine precursers levallorphan nalorphine potassium permanganate sodium chloride sodium salicylate strychnine sulfadimidine tannins thioctic acid vitamin E tolonium chloride universal antidote	modification of urinary pH methamoglobinemia berrylium caustics as cathartic as emetic gold-paraquat paracetamol thallium ethanol botulism opiates opiates fluorides as emetic berrylium CNS depressants amanitidine alkhloids amanitidine paraquat methamoglobinemia ingested poisons

 

References:

1. Essentials of clinical toxicology.S.B.Lal;Narosa publishers,New Delhi,1998.
2. Occupational medicine 3^rd edition;ed:Carl Zenz:Published:Mosby,1994.
3. NIOH-Poison information cards (Poison information centre) -National Institute of Occupational Health,Meghani Nagar,Ahemedabad.

1. chemicals and methamoglobinemia
2. organophosphorous pesticides
3. aluminium phosphide
4. synthetic pyrethroid pesticides
5. organochlorine pesticides
6. Inorganic acids

4. IPCS :Guidelines for poison control;WHO,UN environmental programme,ILO-WHO,Geneva,1997
5. WHO,Geneva,United nations environmental programme,International labour organisation,Environmental health criteria series:

1. Ammonia (54,1986)
2. Cadmium (134,1992)
3. Carbon Monoxide (13,1979)
4. Chlorine and Hydrogen Chloride (21,1982)
5. Hydrogen sulphide (19,1981)
6. Lead (3,1977)
7. Mercury (1,1976)
8. Mercury inorganic (118,1991)
9. Nitrogen,oxides of (4,1991)
10. Organophosphorous pesticides (63,1986)
11. Tricresyl Phosphate (110,1990)

6. ILO encyclopedia 4^th ed. Volumes III and IV,International labour Organisation,Geneva.
7. Harrison’s Principles of internal medicine;14^th ed;Mcgraw-Hill Book company New york
8. Diagnosis of Occupational Diseases;Murlidhar V,Vijay Kanhere;PRIA,42 Tughlakabad Institutional Area,New Delhi-62.
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