Monday, June 9, 2008
Arsenic
The second most important pollutant for livestock.
Source:
v Inorganic form is used in paints.
v Pasture near smelters may be contaminated.
v Industrial effluents released into nearby water body.
v Insecticides (arsenic trioxide, lead arsenate).
v Herbicides (Sodium arsenite, lead arsenate)
v Rodenticides (arsenic trioxide) all can kill non-target species. (As arsenic is poisonous, all such products are being replaced with safer substances).
v Milk from affected dams poisons the calves.
v Arsenical preparations (Sodium thiacetarsamide for blood parasites, acetylarsan as a skin toxic) cause toxicity.
v Arsenic is used as a growth promoter in pigs and poultry. This form causes peripheral nerve demyelination that differs from inorganic arsenic toxicity.
Ex: - Roxarsone in poultry, Arsanilic acid in pigs.
Mechanism of action: Arsenic irrespective of route of absorption affects tissues rich in oxidative enzymes like intestine, liver and kidney. It crosses the placental barrier but does not seem to cross BBB. Excreted in faeces, bile, milk, saliva and sweat.
At cellular level Arsenic mainly causes relaxation of capillaries and increases capillary permeability. Increased capillary permeability causes oedema in gastric sub mucosa and overlying mucosa is disshelved.
At molecular level inhibits SH group of enzymes of lipoic acid, which is essential for glycolysis and citric acid cycle.
At local level Arsenic causes corrosion of the gastro intestinal mucosa.
Clinical Signs
Per acute cases – animal found dead or sudden and severe colic, staggering, collapse, paralysis and death are seen.
Acute cases - Severe colic, staggering, weakness, trembling, salivation, vomiting, thirst, projectile watery diarrhoea (rice water stools in humans), dysentery, rapid and weak pulse, prostration, normal or sub-normal temperature, death in 1-3 days.
Sub-acute cases - Same as acute toxicity except for partial paralysis of hind limbs, cold extremities, stupor, hematuria and convulsions.
Chronic cases - rare as the metalloid is excreted very fast. The symptoms could be wasting, poor condition, haemorrhagic dermatitis in buffaloes and humans as arsenic accumulates in skin, nails and hair. (tissues rich in thiol groups). Polyuria and anuria, haematuria, weak irregular pulse, brick red m.m.
Lesions are quite prominent except in per acute cases. Congestion and haemorrhages in abomasal or duodenal mucosa and sub mucosal oedema resulting in sloughing of the duodenal mucosa or perforation of gut wall. The intestinal contents are fluid; foul smelling, bloody with shreds of intestinal mucosa. Liver soft and yellow. Lungs oedematous and congested. Haemorahages on heart, peritoneum, kidneys and liver.
Swine: Inflamed and oedematous fauces, which extends to larynx and trachea causing asphyxia.
Poultry: Intense inflammation of proventriculus and gizzard, horny lining of gizzard may slough because of underlying gelatinous exudates. Duodenal mucosa is congested.
Differential Diagnosis: Pesticides, urea and lead show colic and other GI signs but watery diarrhoea with blood and mucous and foul smell, severity and the sudden onset, is only seen in arsenic.
Irritant plants, certain insects that harbour on plants too cause severe diarrhoea.
Rx
Arsenic binds to dithiol groups in the body; hence BAL (dimercaprol) is the drug of choice to revive inhibited enzyme activity. But caution is to be exercised and the treatment schedule be maintained strictly as BAL itself is toxic.
Large animals
1). BAL 3 mg/kg I/M 5% solution (in 10% of benzyl benzoate in peanut oil).
Repeat every 2 hours for first 2 days, every 6 hours 3rd day, 12 hours for the next 10 days till recovery.
2). Sodium thiosulfate
20-30 gm in 300 ml water orally. Also 8-10 gm. In 10-20% solution I/V.
Or
30-40 mg/kg. I/V 2-3 times a day until recovery.
60-80 mg/kg orally.
Small animals
1. BAL 2.5-5 mg/kg. 10% solution in arachis oil.
Dosage intervals same as for large animals. Use 5 mg/kg on the first day in acute cases only.
2. Sodium thiosulfate 5-6 gm in 60 ml water orally,
2-2.5 gm in 10-20 % solution I/V.
Symptomatic Therapy
I/V fluids and electrolytes. Antibiotics, analgesics and demulcents.
Mercury
Source:
v Inorganic form is used in paints.
v Pasture near smelters may be contaminated.
v Industrial effluents released into nearby water body.
v Insecticides (arsenic trioxide, lead arsenate).
v Herbicides (Sodium arsenite, lead arsenate)
v Rodenticides (arsenic trioxide) all can kill non-target species. (As arsenic is poisonous, all such products are being replaced with safer substances).
v Milk from affected dams poisons the calves.
v Arsenical preparations (Sodium thiacetarsamide for blood parasites, acetylarsan as a skin toxic) cause toxicity.
v Arsenic is used as a growth promoter in pigs and poultry. This form causes peripheral nerve demyelination that differs from inorganic arsenic toxicity.
Ex: - Roxarsone in poultry, Arsanilic acid in pigs.
Mechanism of action: Arsenic irrespective of route of absorption affects tissues rich in oxidative enzymes like intestine, liver and kidney. It crosses the placental barrier but does not seem to cross BBB. Excreted in faeces, bile, milk, saliva and sweat.
At cellular level Arsenic mainly causes relaxation of capillaries and increases capillary permeability. Increased capillary permeability causes oedema in gastric sub mucosa and overlying mucosa is disshelved.
At molecular level inhibits SH group of enzymes of lipoic acid, which is essential for glycolysis and citric acid cycle.
At local level Arsenic causes corrosion of the gastro intestinal mucosa.
Clinical Signs
Per acute cases – animal found dead or sudden and severe colic, staggering, collapse, paralysis and death are seen.
Acute cases - Severe colic, staggering, weakness, trembling, salivation, vomiting, thirst, projectile watery diarrhoea (rice water stools in humans), dysentery, rapid and weak pulse, prostration, normal or sub-normal temperature, death in 1-3 days.
Sub-acute cases - Same as acute toxicity except for partial paralysis of hind limbs, cold extremities, stupor, hematuria and convulsions.
Chronic cases - rare as the metalloid is excreted very fast. The symptoms could be wasting, poor condition, haemorrhagic dermatitis in buffaloes and humans as arsenic accumulates in skin, nails and hair. (tissues rich in thiol groups). Polyuria and anuria, haematuria, weak irregular pulse, brick red m.m.
Lesions are quite prominent except in per acute cases. Congestion and haemorrhages in abomasal or duodenal mucosa and sub mucosal oedema resulting in sloughing of the duodenal mucosa or perforation of gut wall. The intestinal contents are fluid; foul smelling, bloody with shreds of intestinal mucosa. Liver soft and yellow. Lungs oedematous and congested. Haemorahages on heart, peritoneum, kidneys and liver.
Swine: Inflamed and oedematous fauces, which extends to larynx and trachea causing asphyxia.
Poultry: Intense inflammation of proventriculus and gizzard, horny lining of gizzard may slough because of underlying gelatinous exudates. Duodenal mucosa is congested.
Differential Diagnosis: Pesticides, urea and lead show colic and other GI signs but watery diarrhoea with blood and mucous and foul smell, severity and the sudden onset, is only seen in arsenic.
Irritant plants, certain insects that harbour on plants too cause severe diarrhoea.
Rx
Arsenic binds to dithiol groups in the body; hence BAL (dimercaprol) is the drug of choice to revive inhibited enzyme activity. But caution is to be exercised and the treatment schedule be maintained strictly as BAL itself is toxic.
Large animals
1). BAL 3 mg/kg I/M 5% solution (in 10% of benzyl benzoate in peanut oil).
Repeat every 2 hours for first 2 days, every 6 hours 3rd day, 12 hours for the next 10 days till recovery.
2). Sodium thiosulfate
20-30 gm in 300 ml water orally. Also 8-10 gm. In 10-20% solution I/V.
Or
30-40 mg/kg. I/V 2-3 times a day until recovery.
60-80 mg/kg orally.
Small animals
1. BAL 2.5-5 mg/kg. 10% solution in arachis oil.
Dosage intervals same as for large animals. Use 5 mg/kg on the first day in acute cases only.
2. Sodium thiosulfate 5-6 gm in 60 ml water orally,
2-2.5 gm in 10-20 % solution I/V.
Symptomatic Therapy
I/V fluids and electrolytes. Antibiotics, analgesics and demulcents.
Mercury
Urea toxicity
Urea toxicity
Included in ruminant rations @ 3% of total concentration or 1% of total ration as a source of NPN. As a fertilizer and as a substitute for salts in melting of snow and ice in residential areas.
Sources:
Ø Excess in urea - molasses mixtures. (Salty in taste, hence animals relish)
Ø Improper mixing
Ø Spilling or improper storage of urea
Urea is acted upon by urease present in plants releasing ammonium ion, as the alkaline pH increases this is converted to ammonia. Ammonia is absorbed into the blood, enters CNS and inhibits citric acid cycle.
Only cattle are affected the reason is - urease in plants and alkaline pH of rumen. Monogastrics have acidic pH; even young ruminants whose rumen is not fully developed also are not susceptible. Degree of adaptation is important: Animal accustomed to ingestion of urea can ingest 1g/kg/day but in unaccustomed animals 0.3 - 0.5 g /kg/day may be toxic.
High body temperature, absence of water, rapid ingestion by starved / fasted animals, fibrous diet and feeds rich in urease all increase toxicity.
Physiological detoxification mechanism
In liver ammonia is converted into urea by urea cycle or incorporated into glutamic acid in the synthesis of glutamine. When the liberation of ammonia is more and the normal detoxification mechanisms fail, then ammonia crosses BBB, enters CNS (-) citric acid cycle causing decreased energy production, decreased cellular respiration, anoxia - convulsions that are tonic and elicitable like strychnine. (Ammonia decreases postsynaptic inhibition of cortical and spinal motoneurons, also seen in O.C. poisoning). Urine output also decreases. Death could be due to ventricular fibrillation / cardiac stoppage due to hyperkalemia. / respiratory paralysis
Signs: GI & CNS signs are prominent.
CNS signs:
Restlessness, dull / excited, hyperaesthesia, tremors, twitching and spasms of muscles progressing from head to tail, terminally tonic seizures with opisthotonus condition. Convulsions are elicitable by external stimuli and between the convulsions animal is rigid. In coordination and stumbling in the terminal stage.
Fever due to convulsive activity (Hot ears and skin) laboured breathing, (lung edema, fever), cardiac arrhythmias (direct effects of ammonia), frothing at the mouth, cyanosis. GI signs: Salivation, colic, atony, bloat (figure)
(tooth grinding, groaning, kicking at the abdomen, rolling on the ground, looking towards the abdomen - all colicky signs.) Absence of diarrhoea and aspiration of ruminal contents.
Diagnosis: history of, characteristic GI & CNS signs.
Severe colic (absence of diarrhoea), salivation, dyspnoea, strychnine like convulsions. Odour of ammonia in rumen. Ammonia is dissolved in ruminal liquor so collect ruminal liquor and freeze. Blood is refrigerated – if left at room temperature
ammonia increases in biologic samples due to decomposition. Suspected feed / molasses also should be frozen.
Differential diagnosis:
Caustic substances / arsenic - cause severe colic & bloody diarrhoea whereas in urea there is no diarrhoea.
OP compounds - atropinization is effective, in urea atropinization is ineffective.
Rx: In early stages
Cold water: acetic acid is helpful
In adult cow 19-38 L of cold water and 3.8 L of 5% vinegar (dil. acetic acid) are employed but after relieving bloat through puncture of rumen.
This treatment reduces alkaline pH (responsible for hydrolysis) and also dilutes ruminal contents therefore prevents further absorption of ammonia.
Rumenotomy or Gastric lavage is aimed at removing the ruminal liquor.
Included in ruminant rations @ 3% of total concentration or 1% of total ration as a source of NPN. As a fertilizer and as a substitute for salts in melting of snow and ice in residential areas.
Sources:
Ø Excess in urea - molasses mixtures. (Salty in taste, hence animals relish)
Ø Improper mixing
Ø Spilling or improper storage of urea
Urea is acted upon by urease present in plants releasing ammonium ion, as the alkaline pH increases this is converted to ammonia. Ammonia is absorbed into the blood, enters CNS and inhibits citric acid cycle.
Only cattle are affected the reason is - urease in plants and alkaline pH of rumen. Monogastrics have acidic pH; even young ruminants whose rumen is not fully developed also are not susceptible. Degree of adaptation is important: Animal accustomed to ingestion of urea can ingest 1g/kg/day but in unaccustomed animals 0.3 - 0.5 g /kg/day may be toxic.
High body temperature, absence of water, rapid ingestion by starved / fasted animals, fibrous diet and feeds rich in urease all increase toxicity.
Physiological detoxification mechanism
In liver ammonia is converted into urea by urea cycle or incorporated into glutamic acid in the synthesis of glutamine. When the liberation of ammonia is more and the normal detoxification mechanisms fail, then ammonia crosses BBB, enters CNS (-) citric acid cycle causing decreased energy production, decreased cellular respiration, anoxia - convulsions that are tonic and elicitable like strychnine. (Ammonia decreases postsynaptic inhibition of cortical and spinal motoneurons, also seen in O.C. poisoning). Urine output also decreases. Death could be due to ventricular fibrillation / cardiac stoppage due to hyperkalemia. / respiratory paralysis
Signs: GI & CNS signs are prominent.
CNS signs:
Restlessness, dull / excited, hyperaesthesia, tremors, twitching and spasms of muscles progressing from head to tail, terminally tonic seizures with opisthotonus condition. Convulsions are elicitable by external stimuli and between the convulsions animal is rigid. In coordination and stumbling in the terminal stage.
Fever due to convulsive activity (Hot ears and skin) laboured breathing, (lung edema, fever), cardiac arrhythmias (direct effects of ammonia), frothing at the mouth, cyanosis. GI signs: Salivation, colic, atony, bloat (figure)
(tooth grinding, groaning, kicking at the abdomen, rolling on the ground, looking towards the abdomen - all colicky signs.) Absence of diarrhoea and aspiration of ruminal contents.
Diagnosis: history of, characteristic GI & CNS signs.
Severe colic (absence of diarrhoea), salivation, dyspnoea, strychnine like convulsions. Odour of ammonia in rumen. Ammonia is dissolved in ruminal liquor so collect ruminal liquor and freeze. Blood is refrigerated – if left at room temperature
ammonia increases in biologic samples due to decomposition. Suspected feed / molasses also should be frozen.
Differential diagnosis:
Caustic substances / arsenic - cause severe colic & bloody diarrhoea whereas in urea there is no diarrhoea.
OP compounds - atropinization is effective, in urea atropinization is ineffective.
Rx: In early stages
Cold water: acetic acid is helpful
In adult cow 19-38 L of cold water and 3.8 L of 5% vinegar (dil. acetic acid) are employed but after relieving bloat through puncture of rumen.
This treatment reduces alkaline pH (responsible for hydrolysis) and also dilutes ruminal contents therefore prevents further absorption of ammonia.
Rumenotomy or Gastric lavage is aimed at removing the ruminal liquor.
General line of treatment of Poisoning
General line of treatment of poisoning
I. General non-specific measures
(a) Stop giving contaminated feed (selenium, nitrate, cyanide, oxalate, lead, alfalfa, molybdenum and ergot) and water (fluorine, nitrate, heavy metals like lead etc.).
Provide feed and water from known source.
(b) Elimination of toxicant from its region of absorption
(Eyes, skin, stomach, intestinal tract)
If the exposure is through ocular route - never rub the eyes: irrigate eyes with clean water.
Skin:
Wash the skin with copious amounts of water and scrub gently the area of exposure.
In pesticide poisoning, do not apply soap as it enhances absorption of pesticide.
Mercurial ointments (dermally toxic) if applied to be cleaned.
In acid / alkali poisoning wash the external parts of mouth with large quantity of water.
Stomach: Empty the contents by,
Gastric lavage: in dogs with 10 ml/kg of an isotonic solution of sodium chloride (or sodium bicarbonate). Proper precaution is to be taken by passing a rubber tube with a cuff attached to prevent aspiration. Repeat the procedure till clear fluid comes out from the stomach.
Rumenotomy - in ruminants in cases of plant poisons (now a days plastic bags are commonly ingested). Replace rumen contents by suitable feeds and micro flora through cuds.
Emetics:
Apomorphine in dogs - 0.05 - 0.1 mg / kg S/C or I/M.
Causes arrhythmias and CNS depression. Vomition in 3-5 min.
Not to be used in pigs and cats.
Xylazine in cats and dogs - 0.25 - 0.5 ml of 2% solution S/C.
Vomition in 10-20 min.
Tr. Ipecacaunha (10% syrup) - 10-20 ml/dog: 2-5 ml / cat.
Vomition in 20-30 min.
Alternatively,
Large crystal of NaCl / Sod. carb. (washing soda) on the posterior side of pharynx.
Salt (1-3 tsp) in warm water.
o Copper sulphate is preferred in pigs only (4% solution, 60 ml orally)
Hydrogen peroxide orally, 1 ml/kg.
Emesis is contra - indicated in poisoning by volatile oils, hydrocarbons and petroleum products, old animals, unconscious and semi-comatose patients the problem being aspiration. In acid / alkali poisoning - further damage to oesophageal lining is the disadvantage.
Purgation:
Sodium / Magnesium sulphate by mouth or as enema (up to 20% solution)
Small animals - 2-2.5 gm.
Large animals - 100 - 200 gm (max 400 g)
Liquid paraffin (Mineral oil) - orally
Dogs 5 - 15 ml
Cats - 2-6 ml
(2) Reduce the rate of absorption and resorption.
By administering suitable chemical antidotes.
· Tannic acid (general antidote) ppts. - Al, Pb, Ag, Alkaloids, Co, Cu, Hg, Ni, Zn apomorphine, strychnine, cocaine, nicotine and pilocarpine.
Tannic acid is of no value in - Arsenic, antimony and atropine.
Universal antidote - Powdered charcoal - 2 parts (adsorbent)
Tannic acid - 1 part (precipitant)
Mg oxide - 1 part (Purgative)
Mix with water - make slurry and administer
Tr. iodine solution - 15 drops of Tr.iodine in 1/2 glass of water. ppts. Pb, Hg & Ag. and alkaloids like strychnine & quinine.
Neutralization for Acids / Alkalis is best through large amount of water / milk as this dilutes the acid / alkali.
Administration of weak alkali like lime water and magnesium or weak acids like vinegar (5% acetic acid), lemon juice, citric acid (5-10 % sol.) tartaric acid (5-10% sol.) in acid / alkali poisoning respectively has the potential to release energy and gas resulting in perforation of stomach.
Milk & Egg white neutralize heavy metals & phenols, but milk is contraindicated in lipophilic poisons.
· To neutralize irritant mucosa - demulcents like – raw white of an egg, milk, gruel and sugar solution can be administered.
Activated charcoal is the best bet,
for large animals 250-500 g.
small animals 5- 50 g.
charcoal is not effective for cyanide and absorbs vitamins and minerals.
cholestyramine resin is used to break the enterohepatic cycle.
(3) Blockade of actions with non-specific antidote and specific antidote. (list appended).
(4) Hastening of metabolic inactivation and excretion of the toxin.
(a) Metabolic inactivation through enzyme inducers - phenobarbitone.
(b) Excretion – through diuresis.
Increasing diuresis by giving osmotic diuretics.
5% glucose slow I/V. 10% glucose slow I/V.
Large animals 2-5 ml Kg/24 hrs. Large animals 0.5%-1 ml /Kg/24 hrs.
Small animals 5-20 ml/Kg/24hrs. Small animals 1-2 ml / Kg/ 24 hrs.
10% Mannitol solution. Frusemide I/M / I/V.
Large animals 1-2 ml/ Kg/24 hrs. Large animals (LA) 0.5 - 1 mg/Kg.
Small animals 2 ml / Kg/ 24 hrs. Small animals (SA) 2.5 - 5 mg/Kg.
Acidification of urine to eliminate weak bases by
Ammonium chloride - orally LA - 20 - 40 gm. SA - 2 -5 gm.
Arginine chloride - I/M or I/V. LA - 7-10 g. SA 0.1 - 0.2 g/Kg.
Ascorbic acid (IV): all sps . 40 mg/Kg.
Alkalinize the urine to eliminate weak acids.
Sodium bicarbnate 1.4% solution I/V. LA - 2-4 ml /Kg/24 hrs.
Ringers lactate I/V. All species. 5 - 10 ml /Kg/ hr.
Heamodialysis & charcoal haemoperfusion if no specific antidotes are available.
(5) Symptomatic therapy - To revive cardiac & respiratory functions, analeptics to be administered. Doxapramine: Dog / Cat 2mg/Kg I/V. repeat if necessary.
Caffeine and Theophylline (cardiac and respiratory stimulants.)
Dose 100 - 250 mg / kg. I/M or S/C.
· Nikethamide: Dog 22 - 44 mg /kg. I/M or S/C.
(respiratory stimulant)
Astringents, Anti-histamines, sedatives, etc,
(6) Supportive therapy.
Ø I/V fluids
Ø liver tonics
Ø vitamins
Ø minerals
Ø herbal immunomodulators.
I. General non-specific measures
(a) Stop giving contaminated feed (selenium, nitrate, cyanide, oxalate, lead, alfalfa, molybdenum and ergot) and water (fluorine, nitrate, heavy metals like lead etc.).
Provide feed and water from known source.
(b) Elimination of toxicant from its region of absorption
(Eyes, skin, stomach, intestinal tract)
If the exposure is through ocular route - never rub the eyes: irrigate eyes with clean water.
Skin:
Wash the skin with copious amounts of water and scrub gently the area of exposure.
In pesticide poisoning, do not apply soap as it enhances absorption of pesticide.
Mercurial ointments (dermally toxic) if applied to be cleaned.
In acid / alkali poisoning wash the external parts of mouth with large quantity of water.
Stomach: Empty the contents by,
Gastric lavage: in dogs with 10 ml/kg of an isotonic solution of sodium chloride (or sodium bicarbonate). Proper precaution is to be taken by passing a rubber tube with a cuff attached to prevent aspiration. Repeat the procedure till clear fluid comes out from the stomach.
Rumenotomy - in ruminants in cases of plant poisons (now a days plastic bags are commonly ingested). Replace rumen contents by suitable feeds and micro flora through cuds.
Emetics:
Apomorphine in dogs - 0.05 - 0.1 mg / kg S/C or I/M.
Causes arrhythmias and CNS depression. Vomition in 3-5 min.
Not to be used in pigs and cats.
Xylazine in cats and dogs - 0.25 - 0.5 ml of 2% solution S/C.
Vomition in 10-20 min.
Tr. Ipecacaunha (10% syrup) - 10-20 ml/dog: 2-5 ml / cat.
Vomition in 20-30 min.
Alternatively,
Large crystal of NaCl / Sod. carb. (washing soda) on the posterior side of pharynx.
Salt (1-3 tsp) in warm water.
o Copper sulphate is preferred in pigs only (4% solution, 60 ml orally)
Hydrogen peroxide orally, 1 ml/kg.
Emesis is contra - indicated in poisoning by volatile oils, hydrocarbons and petroleum products, old animals, unconscious and semi-comatose patients the problem being aspiration. In acid / alkali poisoning - further damage to oesophageal lining is the disadvantage.
Purgation:
Sodium / Magnesium sulphate by mouth or as enema (up to 20% solution)
Small animals - 2-2.5 gm.
Large animals - 100 - 200 gm (max 400 g)
Liquid paraffin (Mineral oil) - orally
Dogs 5 - 15 ml
Cats - 2-6 ml
(2) Reduce the rate of absorption and resorption.
By administering suitable chemical antidotes.
· Tannic acid (general antidote) ppts. - Al, Pb, Ag, Alkaloids, Co, Cu, Hg, Ni, Zn apomorphine, strychnine, cocaine, nicotine and pilocarpine.
Tannic acid is of no value in - Arsenic, antimony and atropine.
Universal antidote - Powdered charcoal - 2 parts (adsorbent)
Tannic acid - 1 part (precipitant)
Mg oxide - 1 part (Purgative)
Mix with water - make slurry and administer
Tr. iodine solution - 15 drops of Tr.iodine in 1/2 glass of water. ppts. Pb, Hg & Ag. and alkaloids like strychnine & quinine.
Neutralization for Acids / Alkalis is best through large amount of water / milk as this dilutes the acid / alkali.
Administration of weak alkali like lime water and magnesium or weak acids like vinegar (5% acetic acid), lemon juice, citric acid (5-10 % sol.) tartaric acid (5-10% sol.) in acid / alkali poisoning respectively has the potential to release energy and gas resulting in perforation of stomach.
Milk & Egg white neutralize heavy metals & phenols, but milk is contraindicated in lipophilic poisons.
· To neutralize irritant mucosa - demulcents like – raw white of an egg, milk, gruel and sugar solution can be administered.
Activated charcoal is the best bet,
for large animals 250-500 g.
small animals 5- 50 g.
charcoal is not effective for cyanide and absorbs vitamins and minerals.
cholestyramine resin is used to break the enterohepatic cycle.
(3) Blockade of actions with non-specific antidote and specific antidote. (list appended).
(4) Hastening of metabolic inactivation and excretion of the toxin.
(a) Metabolic inactivation through enzyme inducers - phenobarbitone.
(b) Excretion – through diuresis.
Increasing diuresis by giving osmotic diuretics.
5% glucose slow I/V. 10% glucose slow I/V.
Large animals 2-5 ml Kg/24 hrs. Large animals 0.5%-1 ml /Kg/24 hrs.
Small animals 5-20 ml/Kg/24hrs. Small animals 1-2 ml / Kg/ 24 hrs.
10% Mannitol solution. Frusemide I/M / I/V.
Large animals 1-2 ml/ Kg/24 hrs. Large animals (LA) 0.5 - 1 mg/Kg.
Small animals 2 ml / Kg/ 24 hrs. Small animals (SA) 2.5 - 5 mg/Kg.
Acidification of urine to eliminate weak bases by
Ammonium chloride - orally LA - 20 - 40 gm. SA - 2 -5 gm.
Arginine chloride - I/M or I/V. LA - 7-10 g. SA 0.1 - 0.2 g/Kg.
Ascorbic acid (IV): all sps . 40 mg/Kg.
Alkalinize the urine to eliminate weak acids.
Sodium bicarbnate 1.4% solution I/V. LA - 2-4 ml /Kg/24 hrs.
Ringers lactate I/V. All species. 5 - 10 ml /Kg/ hr.
Heamodialysis & charcoal haemoperfusion if no specific antidotes are available.
(5) Symptomatic therapy - To revive cardiac & respiratory functions, analeptics to be administered. Doxapramine: Dog / Cat 2mg/Kg I/V. repeat if necessary.
Caffeine and Theophylline (cardiac and respiratory stimulants.)
Dose 100 - 250 mg / kg. I/M or S/C.
· Nikethamide: Dog 22 - 44 mg /kg. I/M or S/C.
(respiratory stimulant)
Astringents, Anti-histamines, sedatives, etc,
(6) Supportive therapy.
Ø I/V fluids
Ø liver tonics
Ø vitamins
Ø minerals
Ø herbal immunomodulators.
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