1.Instructional Objectives:

The objective of this section is to acquaint the student with various emergency management techniques of toxicoses,as well as to provide information regarding the principles of diagnosis of toxicoses,general treatment of toxicoses and prevention of toxicoses.

After studying material presented in this section,the student should possess a basic knowledge of various procedures that can enable him to diagnose, manage and prevent cases of poisoning in animals. The students should also be familiar with antidotes and detoxifying agents for various types of toxicoses.

 

2.1. Emergency Management of Toxicoses

Animal toxicoses may be acute or chronic in nature. If it is acute,the veterinary physician must be prepared to institute emergency and supportive therapy necessary to maintain the animal alive. There is no magic antidote for individual toxicants. The so called"universal antidote" is not very good. Time is very important. A delay of 30 min is often fatal. The signs of poisoning should be treated symptomatically without wasting time on the diagnosis or looking for a specific antidote unless it is obvious.

If the physician is called by telephone, he must decide quickly if first aid treatment is necessary and give the following instructions to the client until the doctor is able to examine the case.

a. Protect the animal and the people

b. Give milk and/or egg white

c. Induce emesis (if appropriate) by teaspoon H2O2 or table salt

d. Cleanse the animal's skin

e. Do not waste time

f. Bring suspect materials with the animal

1. Vomitus

2. Suspected materials

3. Suspected containers

After the first-aid measures have been instituted the emergency measures should be started immediately. The emergency management of poisoning is aimed at preventing absorption of the poison beyond that amount which the body can likely detoxify or which can be effectively antagonized by antidotes. This can be accomplished by delaying absorption and by removing the poison from body to minimize further absorption and injury.

 

2.1.1 Ingested Poisons

1. Dilution, absorption, and delay of gastric emptying:

Water,milk or activated charcoal, flour or starch suspension should be given within the first few minutes after ingestion. The administration of milk or beaten eggs has the advantage of effectively delaying gastric emptying time and therefore reducing absorption in the intestine. Charcoal, flour or mashed potatoes in water adsorb the poison and prevent absorption. A number of poisons adsorb on activated charcoal very effectively. The procedure for administration of activated charcoal is as follows:

a. 1-4 gm/lb of body weight in 50-200 ml of water.

b. Administer by stomach tube.

c. Charcoal should be of vegetable origin and not be mineral or bone charcoal.

d. Charcoal only adsorbs and does not inactivate.

e. Twenty to 30 minutes following the administration of the charcoal,give either a laxative(mineral oil or osmotic cathartic) or a colonic lavage.

f. An emetic can be utilized following charcoal, but syrup of ipecac should not be utilized.

g. The "universal antidote" consisting of 2 parts activated charcoal, 1 part MgO and 1 part tannic acid is very inefficient.

h. Burned or charred toast is ineffective.

2. Induction of Emesis (no agent is ideal)

a. Syrup of Ipecac

dose = 1-2 ml/kg

Response should occur in 15-20 minutes

Do not use with activated charcoal

b. Apomorphine

Dose: 0.02 mg/lb i.v. or 0.04 mg/lb i.m. or subcu.

May cause respiratory depression and protracted emesis may develop. Effects can be controlled with narcotic antagonists such as naloxone

Contraindicated in respiratory depression

c. Contraindications for emetics:

Unconscious or severely depressed animals

Petroleum distillates

Acids

Alkalies

Other corrosive agents

After 30-60 minutes following ingestion of toxicant

d. Save vomitus for analysis

3. Gastric Lavage

Anesthetized or unconscious animals

Insert cuffed endotracheal tube

Insert a stomach tube

Use 2-5 ml of water per lb of body weight (small animals)

Attach aspirator bulb to the stomach tube

Repeat lavage as many times as possible

Not too effective after 30-60 minutes

The use of activated charcoal in the lavage solution will increase the effectiveness of the procedure

Use smaller volumes with possible weakened stomach

4. Cathartics

After gastric lavage or emesis for the removal of ingested poisons from the stomach, rapid catharsis is important not only for removing unabsorbed material from the intestines but also for removing material which has been excreted by the liver or intestines and not yet reabsorbed. Thus,in some types of poisoning by corrosives since administration of a cathartic may increase the extent of the intestinal injury.

Sodium sulfate is more efficient than magnesium sulfate

Mineral oil

Colonic lavage may help

 

 

2.1.2 Injected Poisons

 

Tourniquet: Apply a rubber band tourniquet close to the injection site. Tourniquet should not produce a throbbing sensation. Venous engorgement should occur, but must be relieved by loosening the tourniquet very often.

 

Ice Pack: If possible immerse the injection site in ice or apply a plastic sack filled with ice. Application of cold, slows capillary flow and thus limits absorption to some extent.

 

Cross Incision: Although this is sometimes useful,it does not remove enough of the injected poisons or snake venoms significantly to prevent fatalities.

 

Specific Antidote: If a specific antidote is available, such as snake venom antiserum, give according to the directions included with the package.

 

 

 

 

2.1.3 Skin Contamination

Flood the contaminated area with copious amounts of water from a hose, shower, or pour from a bucket to dilute and remove the poison. The rapidity and volume of washing is extremely important in reducing the extent of injury from corrosives or other agents. DO NOT USE CHEMICAL ANTIDOTES. The heat liberated by a chemical reaction may increase the extent of injury.

 

 

2.1.4 Eye Injury Due to Chemical Irritants

Use eye-wash fountains or if it is not available, the victim should be taken to a hose or sink where the eye can be flooded with water under low pressure. Washing must begin immediately, since a delay of a few seconds will greatly increase the extent of injury. DO NOT USE CHEMICAL ANTIDOTES. Next, wash the eyes with sterile normal saline solution or sterile water. Then take the patient to the ophthalmologist.

 

 

2.1.5Inhaled Poisons

Remove from exposure, establish an adequate airway and give oxygen and artificial respiration. Determine blood pressure frequently and maintain the body temperature. Use a specific antidote when available, e.g., amylnitrite for cyanide poisoning.

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2..2 Principles of Diagnosis of Toxicoses

Any case of sudden illness or death from no apparent cause is commonly held to be one of poisoning. But, this is not always true. Cases of poisoning generally fall into three categories:

A. exposure to a known poison

B. exposure to an unknown substance which may be a poison

C. disease of undetermined etiology in which poisoning must be considered as part of the differential diagnosis.

 

2.2.1. Exposure to known Poisons

Inmost cases of poisoning, the agent responsible is known and the physician's only problem is to determine whether it will require more than emergency treatment.

 

2.2.1. Exposure to Substances which may be Poisonous

Call manufacturer or his local representative

Call poison information center. These centers are in most cases able to identify the ingredients of trade-named mixtures, give some estimate of their toxicity and suggest the necessary treatment.

Useful reference books. Modern drug encyclopedia or physicians desk reference (PDR) may be of help.

 

2.2.3 Differential Diagnosis of Disease which may be the result of poisoning

In any disease state of questionable etiology, poisoning must be considered as a part of the differential diagnosis. Then an accurate diagnosis becomes the single-most important factor in dealing with animal toxicoses.

Prior to that time, however, the veterinarian is limited to supportive and symptomatic therapeutic measures. The toxicologic diagnosis is based upon certain diagnostic criteria, detection of the toxicant in proper specimens and of course, clinician's own judgment.

The accurate diagnosis of toxicosis is made by five types of criteria.These include complete history,clinical signs, post mortem findings,laboratory animal tests,and chemical analysis.

 

2.2.3.1. History

The presence of poisons such as pesticides, drugs, paints, etc., on the premises, or a history of their having been used or available for animal exposure should be ascertained. The type of pasture, the feed, the clinical signs etc. should be described.

 

2.2.3. 2. Clinical Signs

Vomiting,diarrhea and abdominal pain can be due to heavy metal salts,strong acids and alkalis and many plants.

Vomiting in ruminants is seen following poisoning with rhododendrons and related plants.

Convulsions are caused by many poisons, e.g.,ammonium salts, lead, phenols, opium alkaloids, etc.

Coma is seen in poisoning by bromides,CO,nicotine, anesthetics and sedatives.

Muscle in coordination can be due to ammonium salts, CO, cyanides, and plants including bracken, lupins, ragwort.

Respiratory failure may be caused by CO, cyanides, yew and strychnine.

Dilatation of pupils is a sign of atropine poisoning.

Contraction of pupils is a toxicity sign of morphine and its derivatives.

Photosensitization is a syndrome which occurs in poisoning by phenothiozine, algae, grasses and buckwheat.

Other symptoms - Lameness is caused by fluoride, selenium poisoning. The odor of the breath is also characteristic of a poison, e.g., phosphorus breath smells like garlic.

 

2.2.3. 3. Postmortem

Upon opening the abdominal cavity a typical odor maybe noted. The nature of the stomach content may be of interest. Suspicious traces of poisonous plants may be recovered. Metal salts impart characteristic color. Inflammation or corrosion of GI tract is common in acute poisoning.

Lesions in the liver and kidney are also seen. Hepatic lesions are found in metal poisoning and renal damage occurs whenever an irritant poison is absorbed and excreted in the urine.

 

2.2.3.4. Laboratory Animal Tests

It involves an administration of suspected toxic material to a susceptible animal (such as frog) and observing the effects. It is also known as bioassay.

 

2.2.3.5. Chemical Analysis

Final proof of poisoning lies in the detection of a significant quantity of the toxic agent in the body of the animal.

It should be noted that to test for a single poison or a group of poisons is practicable but to make a general search for poison is not. The function of a chemical analysis is to provide evidence to confirm a tentative diagnosis.

When submitting specimens to a diagnostic toxicology laboratory for analysis following considerations should be made.

Supply complete account of history,symptoms,and lesions with specimens.

Specimens should not be contaminated.

All specimens should be properly labeled.

Tissue specimens should be frozen while serum and blood refrigerated.

Never add preservative unless there is specific reason to do so.

Always send more material than you think necessary.

Always try to remove serum from the clot within two hrs.

Specimens that should be submitted from a live animal should include at least 5 ml of serum, 10 ml of whole blood, 50 ml of urine, and 200 gm of stomach contents

Specimens that should be submitted from a dead animal include at least 10 ml of serum, 50 ml of urine,100 gm of liver, 100 gm of kidney, 100 gm of body fat, entire brain and 500 gm of stomach contents.

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3.3. General Treatment of Toxicoses

In general,antidotal treatment of poisoning can be divided into the following four categories.

 

 

3.3.1. Nonspecific (Emergency) Treatment

This should be started immediately after knowing the incidence of poisoning. Main purpose of this treatment is to delay further absorption of poison and to remove it from the body. Measures include emesis, gastric lavage and catharsis. Tannic acid precipitates certain metals and alkaloids. Lime water and magnetia neutralize acids whereas vinegar and tartaric acid neutralize alkalis. Irritation may be allayed by using demulcents. Ion trapping involves ionization of toxicant to prevent its absorption from GI tract.

 

3.3.2 Supportive Management

Supportive measures depend on the severity of clinical signs in the animal. These include the following:

3.3.2 .1. Control of Body Temperature

Hypothermia, especially during anesthesia

a. Circulating warm water pads

b. Infrared lamps Use with caution

c. Heating pads

Hyperthermia

a. Ice bags

b. Cold baths

2. Respiration

Endotracheal tube

Tracheostomy

Mechanical respirator

Do not use 100% oxygen unless absolutely necessary

Analeptic drugs-questionable

3. Central Nervous System

CNS Depression

 

 

a. Analeptics (if absolutely essential)

Doxapram - 2.5-5 mg/lb

Mikedimide - 5-10 mg/lb

Metrazol - 3-5 mg/lb

b. Artificial respiration

CNS Hyperactivity

a. Barbiturates

b. Inhalant anesthetics

c. Central acting skeletal muscle relaxants

1. Robaxin - 50 mg./lb., i.v.

2. Glyceryl Guaiacolate - 50 mg./lb.

4. Cardiovascular System

Acid-base imbalances

a. Acidosis

1/6M sodium lactate, 8-6 ml/lb

Lactate ringers solution, 60 ml/lb

5% sodium bicarbonate, 1-3 ml/lb

THAM buffer, 300 mg/kg

b. Alkalosis

NH4Cl

Arginine HCl

Hypovolemia

a. Whole blood-sufficient to raise PCV up to

75% of normal

b. Lactated Ringers

c. Plasma expanders

d. Monitor central venous pressure

 

 

2.3.3 Specific Antidotes or Detoxifying Agents

The antidotes render poisons harmless once they have been absorbed in to the body. There are not too many specific anti- dotes. The various available antidotes and their mechanisms of action are listed below:

Mechanism 1. Antidote complexes with poison rendering it inert. Examples are the heavy metals which are chelated by EDTA, and arsenic which complexes with dimercaprol (BAL).

Mechanism 2. Antidote accelerates biotransformation of toxicant to a nontoxic product. For example, antidotes nitrite and thiosulfate complex with cyanide to form cyanmethemoglobin and thiocyanate, respectively. Thiocyanate is 200 times less toxic than cyanide.

Mechanism 3. Antidote blocks formation of a toxic metabolite from a less toxic parent compound. Conversion of methanol to formic acid,and ethylene glycol to oxalic acid, respectively, by alcohol dehydrogenase is blocked by ethanol as an antidote.

Mechanism 4. Antidote specifically accelerate the excretion of toxicant. The presence of chloride in bromide poisoning or calcium in strontium poisoning aids in rapid elimination of the toxicants bromide and strontium, respectively.

Mechanism 5. Antidote compete with toxicant for essential receptors. For example, vitamin K competes with coumarin anticoagulants (e.g., warfarin) for receptors involved in formation of prothrombin.

Mechanism 6. Antidote blocks receptors that are responsible for toxic effect. Example includes organophosphate poisoning treated with atropine as an antidote.

Mechanism 7. Antidote restores normal function by repairing or bypassing effect of poison. This mechanism is illustrated by the use of methylene blue in the treatment of nitrite poisoning.

 

 

2.3.4. Special Methods used in Poisoning to Hasten Elimination of Absorbed Toxicants primarily through the Kidney

1. Diuretics

Mannitol: 1mg/lb/hr with adequate hydration

Furosemide: Lasix 2 mg/lb

2. Alter Urine pH

a. Alkalinize

Sodium bicarbonate

Tham

Carbonic anhydrase inhibitors

b. Acidify

Ammonium chloride

Arginine HCl

3. Peritoneal Dialysis

Peritoneal dialysis may be an alternative to consider especially if renal function does not allow for effective urinary manipulation.

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2.4. Prevention of Toxicoses

Living organisms can come in contact with man-madeor naturally occurring toxicants through accidental or intentional exposure. For example, poisoning may occur through improper storage of chemicals or entering sprayed areas, by eating sprayed or contaminated foods and because of the exposure to several poisons in various ways. Poisoning may be prevented by attention to the following:

 

 

2.4.1. Storage of poisons: Poisons must be stored in well-marked containers. Mixtures of poisons with flour or cereals must not be stored near food. Emptied containers must be burned immediately to destroy residual poisons.

 

2.4.2. Protective Measures: Masks and exhaust ventilation should be used during dry mixing of poisons. Other suggestions include avoiding poisoning by dilution, selective, grazing, improved pasture,selective methods of decontamination, e.g.,public water supply. Excessive use of argicultural chemicals should be avoided, because some of the mare persistent and may enter in food chain. People should be educated to the dangers present in the natural toxicants and pesticides. Ultimate responsibility for the control of the use of toxicants is in the hands of man who uses them on plants, soils, or animals.

 

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Review Questions

1. List various types of emergency management techniques of poisoning and briefly discuss how they are performed on on an acutely poisoned animal.

2. List 5 types of criteria that are used to make a differential diagnosis of a suspected case of poisoning. Which criterion can be used alone to make accurate diagnosis?

3. What is supportive management of poisoning? How will you control body temperature, respiration, CNS and cardiovascular system of a poisoned animal?

4. List various mechanisms of specific antidot at actions and give at least one example of an antidote for each mechanism.

5. What measures are necessary to prevent accidental exposure to poisons?

References

Aronson, A.L. 1972. Chemical Poisonings in Small Animal Practice.

Veterinary Clinics of North America, 2:379-395.

Fane, L.R., Combs, H.F. and Decker, W.J. 1971. Physical Parameters

in Gastric Lavage. Clinical Toxicology, 4:389-395.

Simon, N.M. and Krumlovsky, F.A. 1971. The Role of Dialysis in the

Treatment of Poisoning. Rational Drug Therapy 5(3). 7 pages.

Szabuniewicz, M.,Bailey, E.M. and Wiersig, D.O. 1971. Treatment of

some Common Poisoning in Animals. VM/SAC., 66:1197-1205.

Thoman, M.E. 1970. The Use of Emetics in Poison Ingestion. Clinical

Toxicology, 3:185-188.

Wilkinson,G.R. 1970. Treatment of Drug Intoxication: A review of

some Scientific Principles. Clinical Toxicology, 3:249-265.

Bailey,E.M., 1979. Management and Treatment of Toxicoses in Cattle

VM/SAC., pp 1650-1657, (November) and pp 1775-1784, (December).

Mathew, H. and Lawson, A.A.Treatment of Common Acute Poisoning,

4th ed., 1980. Churchill Pub. New York.

Buck, W. B. and Bratich,P.M.1986. Activated charcoal: Preventing unnecessary death by poisoning. Vet. Med. 81:73-77.