General Approach to Treatment

Introduction

• Diagnosing poisoning can be challenging, as symptoms can vary widely depending on the type and amount of the toxic substance involved, as well as the individual's age, weight, and overall health. However, accurate and timely diagnosis is crucial for effective treatment and preventing serious or fatal outcomes.

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A confirmed toxicological diagnosis is based upon the appropriate findings and should account following points.

1. Physical examination
2. History
3. Clinical signs and symptoms
4. Pathological lesions
5. Analytical evidences
6. Experimental evidences
7. Response to treatment

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History

• Time of onset of clinical signs
• Number of affected cattle
• Duration of exposure
• Nature of the toxin
• Type of feed and water
• Changes in the environment
• Recent medications
• Past medical history
• Mortality rate.

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Clinical Signs and Symptoms

Observe the functional and structural abnormalities of following body system and organ respectively.

• Central nervous system
• Digestive system
• Respiratory system
• Skin, hair and nails
• Eyes
• Urogenital tract
• Body temperature
• Musculo-skeletal system

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Pathological Lesion

• Presence or lack of lesion should be closely observed.
• External examination of visceral organs should be studied.
• Histopathology of affected organ should be done to find out microscopic changes.

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Analytical Evidences

Detection of toxicant in the excreta and blood during life and in GI contents and tissues of the body after death may be done by various method available including chemical methods. Samples for toxicological analysis are taken during PM examination. Chemical analysis for toxicants is very important for the diagnosis of poisoning.

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Experimental Evidences

Experimental animals may be fed with the suspected food or toxicant after it is separated from the viscera and signs exhibited are closely observed.

Response to treatment

Response to a test dose of specific antidote in an intoxicated animal may confirm a clinical diagnosis. For example, clinical improvement (reduced salivation, dyspnoea, convulsions, etc) after administration of atropine is an evidence of oraganophosphorus and carbamate insecticide poisoning.

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LINE OF TREATMENT

1. GENERAL- MUST BE PROMPTLY

a. Symptomatic treatment accompanied by good care

b. maybe no specific antidote

c. may be residual effects such as liver damage and kidney damage

2. ELIMINATE THE SOURCE OF POISON�a. Feed and Water�b. Rubbish piles, old sheds etc�c. Change the environment

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3. INACTIVATION OF UNABSORBED POISON

• Potassium Permagnate( 1:5,000) : oxidizing agent for strychnine Tannic acid ( strong tea)
• Milk
• Tincture of iodine
• Raw egg white
• Bentonite����

4. REMOVE UNABSORBED POISON FROM THE BODY�a. wash with soap and cold water, clip hair and wool�b. removes poisons from gastrointestinal tract�c. emetic, lavage, surgery, cathartics�d. give gastric lavage to anaesthetized animal�e. Tannic acid- Alkaloid and glycosides�f. General detoxicants:� i. Calcium gluconate� ii. Dextrose� iii. Thiosulphate�

5. SYMPTOMATIC TREATMENT�Atropine sulfate: It is the pharmacological antidote for poisoning due to organic phosphorous and carbamate compounds�Oximes: Protopan chloride, 2-PAM and DAM act to reverse cholinesterase and are , therefore. Specific antidotes�a. Control Central Nervous signs�b. Keep respiratory tract open, oxygen, stimulants�c. Shock-fluids, blood. Oxygen. Warmth�d. control diarrhoea-intestinal protectants, astringents�e. Control vomition- sedation and soothe stomach �f. Maintain fluid and electrolyte balance�g. Antibiotic to control secondary infections�

6. INACTIVATION AND REMOVAL OF ABSORBED POISONS

�a. i. Diuresis- If the kidney is functioning well�ii. Oral fluids�iii. Dextrose

�b. Specific antidotes�i. Chloral hydrate or Barbiturates- Convulsions�ii. Atropine sulphate and protopam chlordies- organophosphorous pesticides�iii. BAL- Arsenic and other heavy metals�iv. Ca Ethyl Diamine Tetracetate (EDTA)- Lead�v. Dithizone- Thallium (with Caution)�vi. Amylnitrate- cyanide ( especially small animals)�vii. Methylene blue- Nitrate, sodium chlorate�viii. Sodium thiosulphate and sodium nitrate- cyanide�ix. Vit K or K1- Prothrombin deficiency, warfarin, pindome�

Oxalate Poisioning

Introduction

• Oxalate poisoning is caused by the ingestion of oxalate-containing plants.
• Principal oxalate-containing plants belong to the genera Halogeton, Sarcobatus, Oxalis, Rheum, and Beta.
• Halogeton glomeratus and Oxalis pescaprae are two important oxalate-producing plants of the world.

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Properties

• Oxalates occur in plants primarily as calcium, sodium, ammonium, potassium, and magnesium salts.
• The calcium and magnesium oxalates are insoluble, so less absorbed from the GI tract.
• The sodium and potassium oxalates (more common in plants), being soluble, are free to be absorbed or to react with the calcium in the GI tract to form insoluble salts.

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Toxicity

• The toxicity of oxalate-producing plants depends on the species of animal, type of plant, form of oxalate, and duration of exposure.
• Ruminants, especially cattle, are more effective in producing insoluble calcium oxalate from free oxalate than simple stomach animals.
• Toxicity in ruminants mostly occurs when large quantities of soluble potassium and sodium oxalates are eaten which overwhelms the rumen's ability to metabolize the oxalates.
• Toxicity is commonest in sheep and also occurs in cattle and horses. Pregnant and lactating animals are more susceptible than others.

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Toxicokinetics:

• Oxalate may undergo different pathways when consumed by a ruminant.
• Once absorbed from the GI tract, soluble oxalates readily combine with blood calcium and magnesium to produce hypocalcemia and hypomagnesaemia, respectively.
• Insoluble oxalate salts may accumulate in various tissues, especially the rumen wall and kidneys.

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Mechanism of Action

• Soluble oxalate combines with serum calcium to form calcium oxalate, depleting ionized calcium and causing hypocalcemia.
• Oxalate interferes with cellular energy metabolism that contributes to the acute death of affected animals.
• Insoluble oxalate crystals accumulate in various organs and produce direct organ damage in renal tubules, rumen, blood vessels.
• Continued low-level dosing of oxalate in sheep may cause ruminal dysfunctions due to changes in pH and interference with cellulose digestion.
• Oxalic acid is corrosive and may cause skin and gastrointestinal irritation.

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Clinical Signs

• Early clinical signs include dullness, reluctance to move, slobbering, lowering of the head, loss of appetite, stasis of rumen motility, and bloat.
• In acute poisoning, there is salivation, progressive weakness, incoordination, prostration, labored respiration, dilatation of the pupil, twitching of muscles, tetany, convulsions, and coma. (due to hypocalcaemia)
• Death occurs due to shock
• Azotemia, Oliguria, hyperkalemia, and cardiac failure may occur due to renal tubular necrosis.
• In subacute poisoning, there are stiff gait, frequent attempts to urinate, and recumbency.
• Chronic poisoning primarily results in renal damage resulting in uremia.

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PM Findings

• Edema and hemorrhages of the rumen wall and GI Haemorrhages in swine.
• In acute poisoning, edematous and dark color Kidney, whereas in chronic poisoning the Pale and smaller kidney. On examination of the cut surface of kidneys, oxalate crystals can be seen in the renal tubules
• Calculi may be found in the urethral Process of ram and sigmoid flexure of bull and ram
• Lungs may be filled with blood and are of dark red or purplish color.
• Cyanosis in various tissue

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Diagnosis

• History of feeding, clinical signs
• Hypocalcaemic Syndrome and lesions.
• Demonstration of calcium Oxalate crystals in the kidneys and rumen epithelium histologically is diagnostic of oxalate Poisoning.
• Suspected plants should be analyzed for Oxalate content.
• PCV decreases but BUN and blood K+ level may increase.

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Prevention and control

• Identification of oxalate-containing plants in pastures and removal or avoidance of such plants.
• Supplementation with calcium and magnesium in the diet of animals grazing on oxalate-containing plants.
• Provision of adequate water to dilute the effects of oxalates in the rumen.
• Administration of limewater.

Prognosis

• Prognosis is poor if advanced signs of oxalate intoxication have occurred.

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