This document provides guidance on the general principles and lines of treatment for poisoning cases. It outlines that the main goals of treatment are to prevent further absorption of toxins, counteract their effects, enhance detoxification and elimination. The key methods discussed are:
1. Removal of toxins from the stomach through gastric lavage or induced vomiting if ingestion was recent.
2. Hastening passage through the bowels using cathartics or laxatives to flush toxins through.
3. Neutralizing or binding toxins still in the gastrointestinal tract using adsorbents like activated charcoal or specific antidotes when available.
Supportive measures like fluid therapy, respiratory
This document provides guidance on the general principles and lines of treatment for poisoning cases. It outlines that the main goals of treatment are to prevent further absorption of toxins, counteract their effects, enhance detoxification and elimination. The key methods discussed are:
1. Removal of toxins from the stomach through gastric lavage or induced vomiting if ingestion was recent.
2. Hastening passage through the bowels using cathartics or laxatives to flush toxins through.
3. Neutralizing or binding toxins still in the gastrointestinal tract using adsorbents like activated charcoal or specific antidotes when available.
Supportive measures like fluid therapy, respiratory
Original Description:
GENERAL LINE Of treatment UREA AMMONIA SALT.poISONING
Original Title
GENERAL LINE Of treatment UREA AMMONIA SALT.poISONING
This document provides guidance on the general principles and lines of treatment for poisoning cases. It outlines that the main goals of treatment are to prevent further absorption of toxins, counteract their effects, enhance detoxification and elimination. The key methods discussed are:
1. Removal of toxins from the stomach through gastric lavage or induced vomiting if ingestion was recent.
2. Hastening passage through the bowels using cathartics or laxatives to flush toxins through.
3. Neutralizing or binding toxins still in the gastrointestinal tract using adsorbents like activated charcoal or specific antidotes when available.
Supportive measures like fluid therapy, respiratory
This document provides guidance on the general principles and lines of treatment for poisoning cases. It outlines that the main goals of treatment are to prevent further absorption of toxins, counteract their effects, enhance detoxification and elimination. The key methods discussed are:
1. Removal of toxins from the stomach through gastric lavage or induced vomiting if ingestion was recent.
2. Hastening passage through the bowels using cathartics or laxatives to flush toxins through.
3. Neutralizing or binding toxins still in the gastrointestinal tract using adsorbents like activated charcoal or specific antidotes when available.
Supportive measures like fluid therapy, respiratory
The key takeaways are that poisoning is always an emergency and needs to be managed immediately. Supportive care to maintain vital functions like respiration and circulation is important until specific treatment can be given. ABC (Airway, Breathing, Circulation) is important.
The general principles of treatment of poisoning include managing the emergency phases first to improve the animal's condition through supportive care. Prompt removal or neutralization of the poison while maintaining vital body functions is important until slow-acting specific treatment can be given.
Methods to remove poison from the stomach include gastric lavage and in ruminants, manual gastric emptying after emergency gastrotomy/ruminotomy. Gastric lavage should be done soon after ingestion and is indicated in small animals like dogs within 2-4 hours of ingestion.
TOXICOLOGY:
GENERAL LINE OF TREATMENT
OF POISONING
GENERAL PRINCIPLES OF TREATMENT OF POISONING Poisoning is always an emergency and need to be managed immediately with appropriate measures using specific antidotes whenever available. However, in majority of poisoning cases treatment with an antidote is not possible due to lack of confirmative diagnosis. In acute poisonings, first of all truly emergency phases should be managed to improve condition of the animal by providing appropriate supportive care to ensure its survival. For this, focus on prompt removal or the neutralization of poison whilst maintaining vital functions of the body by restoring respiration by giving artificial respiration and or drugs acting on cardiovascular system, CNS stimulants or depressants, emetics etc. depending on the clinical state of the patient/animal until slow acting and specific treatment is instituted. ABC- Airway, Breathing and Circulation
In order to treat the poisoning cases effectively, a clear understanding of some of the basic principles of toxicokinetics, toxicodynamics and specific therapeutic goals is essential e.g. absorption of the toxic substances be minimised antagonize the effects of absorbed toxicants metabolic biotransformation of poison with reduced toxicity be enhanced while biotransformation into toxic substances be inhibited/reduced elimination from the body be enhanced. These goals can be achieved generally by -general Line of treatment of poisoning. General Line of treatment of poisoning Gastrointestinal tract is an important site where from maximum absorption of toxicants takes place. Thus, prevention of gastrointestinal absorption is an important aspect in initial treatment of acute poisoning. It can be achieved by: Removal of the poison from the stomach; Hastening the passage through bowel; Neutralization of the poison within the gastrointestinal tract.
REMOVAL OF THE POISON FROM THE STOMACH: (i) Gastric lavage: It should be done as soon as possible after ingestion and its efficacy decreases with the passage of time. It is a rapid way of removing the poisons alongwith stomach contacts. However, its should not be attempted in unconscious or convulsing animals or in cases of ingestion of caustic substances or petroleum distillate hydrocarbons. It is useful only in small animals and is extensively used in dogs if ingestion has taken place in preceding 2-4 hours. It is indicated on the anaesthetized animals with endotracheal intubation For the purpose, an isotonic sodium chloride solution (occasionally sodium bicarbonate) occasionally @ 10 ml/ kg is indicated. Repeat the procedure until the washout stomach fluid is clear. However, in ruminants, manual gastric emptying after emergency gastrotomy/ruminotomy is the only satisfactory method of removing the rumen e.g. plant poisoning or for indigestible materials such as plastic, polyurethane foam ii) Emetics: In dogs, cats and swines, vomition may be induced to empty the stomach. Emetics may be used if ingestion has taken place within the preceding 2-3 hours. But vomition should not be induced if there are seizures (unless controlled) or the animal is in comatose state or there is severe respiratory distress or has ingested caustic substances (strong acid, alkali or cationic detergent) or petroleum distillate (gasoline, kerosene, paint thinner etc.) Emesis may be induced chemically by making used of hypertonic solutions of copper sulfate or sodium chloride, but not reliable Drugs like ipecac or apomorphine hydrochloride are used to induce vomition. However, there is a greater risk of aspiration pneumonitis due to aspiration of gastric contents into the trachea and lungs. a) Apomorphine hydrochloride is administered to dogs at the dose rate of 0.04- 0.07 mg/kg by I/V, I/M or S/C or subconjunctival routes. contraindicated in the presence of existing central depression. Do not give emetics to large animals. Apomorphine is contraindicated in cats and pigs.
b) Xylazine is used in dogs and cats. Emesis is produced within 10-20 min. Emesis in cats is more consistent compared to dogs. Dose for cats is I mg/kg by IM route. However, slightly higher dose is recommended for dogs.
(c) Syrup of ipecac (10%) is administered orally; 10-20 ml (1-2 ml/kg) for dogs and 2-5 ml (3.3 ml /kg) for cats. Emesis is produced within 20-30 minutes.
If none of these drugs are available, common salt (sodium chloride) 1-3 teaspoons in warm water or hydrogen peroxide (3% solution) 1 ml/kg may be administered orally. However, copper sulfate should not be used as it is an irritant and may hasten the absorption of poisons from the stomach.
HASTENING THE PASSAGE THROUGH BOWEL i) Cathartics may be of some value particularly if some slow acting poison is involved. Oily ones- no longer recommended in the management of orally ingested poisons as these may produce dehydration, hypernatremia, hypermagnesemia, hyperkalemia and hyperphosphatemia. Irritant purgatives or oil-based purgatives should never be used as these promote absorption of poison. However saline purgatives such as sodium sulphate, magnesium sulphate or magnesium citrate may be used either orally or as enema. Dose of sodium sulphate for dogs and cats is 1.0 g/kg (2-25 g) while 100-200 gm for large animals. Orally liquid paraffin is also recommended for inducing evacuation of the bowel. Doses for dogs are 5-15 ml, adult cattle and horses 0.5-2.0 litres,
ii) Urinary excretion of poisons may be hastened by increasing the flow of urine (diuresis).
a). Increase glomerular filtration: Use of potent diuretics is contraindicated. Administer 10% glucose or 10% mannitol or sterile saline solution by slow IV infusion. Large animals: 1-2 ml/kg/24 h;Small animals: 1-2 ml/kg/24 h b). Reduce tubular reabsorption: Changing pH of the urine by Urinary Acidifiers (ammonium chloride, ascorbic acid, sodium acid phosphate) or Alkalizers (sodium bicarbonate, sodium acetate, sodium citrate) in an attempt to ionize the offending toxic substance will promote diuresis and urinary excretion of poisons-weak bases and weak acids, respectively (c) Dialysis: Haemo-or peritoneal dialysis NEUTRALIZATION OF THE POISON WITHIN THE GASTROINTESTINAL TRACT 1) Specific antidotal treatment of poisoning is highly desirable and most effective. An antidote may be defined as a specific remedy used for countering the action of a particular poison Very few antidotes are available for a limited number of toxicants. Thus, these are being employed rather rare under such circumstances. Depending on the mechanism of action, the antidotes may be classified as Competitive antagonism: e.g. nalorphine for morphine poisoning. Non-competitive antagonism: e.g. atropine for carbamate poisoning. Chemical neutralization: e.g. sodium nitrite and sodium thiosulfate for cyanide poisoning. Metabolic inhibition: e.g. ethanol for methanol poisoning. Oxidative reduction: e.g. methylene blue for nitrite poisoning. Chelation: e.g. dimercaprol (BAL) for arsenic, CaEDTA for lead, deferoxamine for iron poisoning etc 2) Use of adsorbing agents like activated charcoal or neutralizing agents like acids, alkalies, chelating agents e.g. dimercaprol (British antilewisite, BAL), calcium EDTA or tannic acid, magnesium oxide, aluminium hydroxide gel etc. is recommended for various poisons,. Activated vegetable charcoal is inert, non-absorbale, odourless and tasteless and binds or adsorbs organic material to form stable complex (es) which is not absorbed, currently, it is the single most effective and useful agent employed for prevention of absorption of ingested poisons. dose rate of 250-500 g in large animals and 5-50 gm in small animals, preferably as a suspension in water several minutes to 24 hrs after ingestion and before emetics, if possible. An important ingredient of the universal antidote in combination with kaolin, tannic acid and magnesium oxide. The universal antidote contains vegetable charcoal 10 g, magnesium oxide 5g, kaolin 5 g, tannic acid 5 g and water added upto 200 ml. TOXICITY OF Non Metals: Ammonia/urea, acids, alkalies, sulphur, phosphorous, salt, Fluorosis, Nitrate/nitrite etc Metals: As, Bi, Hg, Pb,Cu,Se etc Plants: Cyanogenetic Glycosides, Alkaloid, NO3 rich etc Ricinus communis (Castor); Lantana camera (Lantana), photosensitization Drugs: NSAIDS, Antibiotics- aminoglycosides, tetracyclines, fluoroquinolone, feed additives , vitamins etc Insecticides, herbicides, weedicide, agrochemicals etc Mycotoxins, bacterial toxins Venoms/Bites/Stings Zootoxins : snake, scorpion, wasp, spider etc Radiation hazards, environmental pollutants UREA AND AMMONIA TOXICITY Urea is used as a fertilizer on crop and pasture fields a cheap source of non-proteinous nitrogen (NPN) in ruminants ration better tolerated when mixed with sufficient amounts of other feeds. About 1-2 per cent of total ration (dry weight basis)-SAFER, but larger amounts are likely to produce poisoning. Ruminal microflora possesses urease activity which hydrolyse urea into ammonia and water. Ammonia is assimilated for amino acids and microbial protein synthesis. Therefore, dietary requirement of proteins is decreased IF NPN source is added to the ration of ruminants. For proper utilization of ammonia (NH3)' within certain limits, readily and sufficiently available soluble carbohydrates in the form of starch and glucose are essential. However, production of ammonia beyond handling capacity of liver results in urea poisoning.
Ruminants/ Animals should be accustomed to urea feeding by gradually increasing its level in the ration/feed Tolerance and adaptation to urea feeding is lost rapidly. If the animals receive no urea for three days, they become susceptible to urea poisoning. Higher Susceptibility Factors : starvation and low protein diet., insufficient availability of soluble carbohydrate sources in the feed/diet, adaptation of the animals, abrupt change in the diet, lack of water, ruminal pH (alkaline pH- predispose for toxicity) Food/ rations based on concentrates reduce severity of intoxication Simultaneous feeding of soyabean meal potentiates urea toxicity due to liberation of excess of ammonia as soyabean meal contains urease enzyme..
Ruminants are most sensitive speciessusceptible to ammonia poisoning Higher capacity of ruminants than non-ruminants to handle absorbed ammonia as the former have a greater hepatic urea synthesizing ability or a high glutamine synthetase activity in the spleen, liver and brain.
Equines appear to be tolerant to relatively large.doses of urea where its hydrolysis takes place in the caecum. Pigs are quite resistant to even very large doses of urea.
Oral LDso value of urea in cattle and sheep is 1.0-1.5 glkg and horse is 4.0 glkg while toxic dose in cattle and sheep is 0.3 - 0.5 glkg Sources of Urea poisoning Accidental ingestion of solid or liquid form of urea due to improper storage or spilage Feeding of large quantities of NPN urea- mollases feeds to unaccustomed animals Improperly mixed feed- excess urea in ration etc.
Mechanism of toxicity: Hydrolysis of urea occurs in the rumen. The rate of ammonia production depends primarily on the amount of ration ingested, the amount of urease present in the ruminal contents or the diet and pH of the ruminal contents. Toxicity of urea is due to ammonia absorbed from the stomach /rumen which depends on ruminal pH. Urea + water > CO 2 + NH 3
At rumen pH of < 6.2, majority of the released ammonia is in the form of ammonium ions (NH4) which are highly water soluble and absorbed poorly i.e. low pH favours production of NH4 If absorption of ammonia into blood is up to certain limits, body detoxifies ammonia as absorbed ammonia is normally incorporated into the urea cycle and excreted as urea in urine Conversion of ammonia (NH3) to urea occurs in the liver. Ruminants have a higher capacity to handle absorbed NH3 than the non-ruminants- greater hepatic urea - synthesizing ability When concentration of NH3 in rumen exceeds 80 mgldl, NH3 appears in the peripheral blood and high NH3 concentrations are built up in blood stream and thus NH3 accumulates in tissue cells. When blood NH3 nitrogen reaches 0.80 - 1.30 mg/dl, clinical signs of poisoning become apparent. Ammonia inhibits the citric acid cycle, exact mechanism -not known. Saturation of glutamine-synthesizing system causes a backing up in the citric acid cycle and decrease in its. Intermediates. As a result there is decrease in energy production and cellular respiration and thus cells begin to malfunction. CNS is the first to 'be affected as it has a large requirement for energy Impairment of TCA cycle results in cellular energy and respiration deficits and ultrastructural degenerative changes. An increase in anaerobic glycolysis, blood glucose and blood lactate. Liver dysfunction increases susceptibility to poisoning Clinical signs: Onset- fast or delayed- on the production of ammonia in the rumen and its absorption into the blood stream But signs are most acute in nature and death generally occurs within half to four hours of ingestion. Characteristic signs : weakness, initial restlessness, salivation, prominent frothing at the mouth and nose, grinding of teeth, abdominal pain(Colic), bradycardia, marked jugular pulse dyspnoea, bloat, forced rapid breathing, pulse and respiration progressIvely become weak and slow. Later severe groaning, shivering, twitching of eye lids, lips, taiL, ataxia, terminal toniC convulsions and death, generally when the blood ammonia concentration are> 5 mgldl. Animals appear rigid rather than depressed between the convulsions. Post -mortem lesions: No characteristic post-mortem lesions are present in urea poisoning Strong odour of ammonia in the rumen. Generalized haemorrhages, congestion and vascular injuries. Hydrothorax and hydropericardium. Haemorrhagic enteritis with oedema and ulceration of intestinal mucous membrane. Liver is enlarged, pale and friable., Fatty degenerations of liver and kidneys Haemorrhagic degenerative changes in brain. Pulmonary oedema and acute catarrhal bronchitis, peribronchial and intraalveolar haemorrhages.
Diagnosis: History of access to urea. Clinical signs. Post mortem lesions. Laboratory investigations indicating high ruminal fluid and blood ammonia concentrations, rumina I pH of more than 7.5 and increase in blood urea nitrogen. Feed analysis for urea, ammonium salts etc. Stomach / ruminal contents for urea or ammonical fertilization.
Differential diagnosis:
(i) Arsenic poisoning. (ii) Strong caustics poisoning. (iii) Lead poisoning. (iv) Organochlorine pesticides. (v) Organophosphates toxicity. (vi) Nitrate and cyanide poisoning. (vii) Encephaletic disease, enterotoxaemia, brain engorgement.
TREATMENT: No specific antidote for urea poisoning and generally the treatment is ineffective. Aimed at reducing the concentration of ammonia in the blood either by reducing the production of ammonia and hastening the conversion of ammonia to urea. Weak acids, generally vinegar or 5% acetic acid in sufficient quantity of cold water is administered. for sheep is 0.5-1.0 litre and cattle are 4.0 liters. It not only dilutes the ruminal contents but also reduces the production of ammonia by lowering pH of the rumen and slowing the rate of hydrolysis of urea by reducing urease activity and also promotes diuresis. Excessive gas accumulated in the rumen is removed by trocar and canula. stomach tube or ruminotomy.
CORROSIVES TOXICITY/ POISONING
ACIDS AND ALKALIES Definition of Corrosive A corrosive poison is one that causes tissue injury by a chemical reaction
Most commonly: Strong acids & alkalis Concentrated weak acids & alkalis Oxidizers (with neutral pH) Alkylating agents Dehydrating agents Halogens & organic halides Other organic chemicals (phenol) Common Agents Acids: automobile batteries, gun barrel cleaning fluid and swimming pool cleaning agents. Car battery fluid : H 2 SO 4 toilet bowl cleanersDe-scalers: HCl Metal cleaners: HNO 3 Rust removers: HF Disinfectants: Phenol Alkali: More Dangerous than acids Alkaline (NaOH, KOH,Na2CO3, NH4OH,KMnO4) products drain cleaners, washing products, liquid cleansers and toilet bowl products Household cleaners: Ammonia- based Disinfectants; Bleach (hypochlorite) Drain cleaners; NaOH Factors Determining Corrosiveness Solid particulate: deep local burns Liquids; diffuse/ circumferential
Food may buffer
Pyloric spasm from acid J transit time
Titrable acid/alkali reserve (TAR) (amount needed to normalize pH of corrosive) Mechanism of Injury Aci d Coagulation (desiccate / denature protein)
Eschar formed
Delayed eschar loss (> 3 days): perforation / bleeding Fibrosis & cicatrization is subsequently seen Alkali Liquefaction (saponify fat / solubilize protein)
Collagen swelling
Small vessel thrombosis
Heat CORROSIVES On dermal and ocular exposure: serious burns, extremely painful, corneal/conjuctival necrosis, perforation and opacity which may not be evident immediately. On ingestion corrosive burns of mucosal membranes appear firstly as milky white or grey, which later turns to wrinkled black. Animal may vocalize or depressed; manifest pain by panting inability to swallow. Haematemesis abdominal pain, polydypsia, respiratory distress, shock, secondary pneumonia from aspiration of vapours gastrointestinal bleeding, perforation and fistula are the other signs observed depending on the severity. Clinical Approach Identify immediate life threats Mortality ~10-15% reported in hospitalized patients
Mainly due to: Airway injury: Mucosal edema obstruction Inhalation ALI / ARDS Gastro-esophageal injury: Perforation sepsis Haemorrhage
Treatment Oral dilution with egg white , milk or water Skin and eyes thourghly flushed with copious water and sterile saline respectively Therapy for shock: IV fluids, steroids within 48 hours, which reduce the fibroblastic activity and inflammation, reduce the stricture from circumferential alkaline burns. Analgesics and antibiotics prophylactically in animals with perforations. Contraindications: 1. Attempts to neutralize burns chemically, as exothermic reactions produce elevated local heat and thermal burns.. 2. Gastric lavage and induction of emesis 3. Charcoal is ineffective in binding to caustics Decontamination- X? Almost any attempt to gastric emptying / dilution is CONTRAINDICATED in corrosive poisoning
NO emetics (ipecac): injury & perforation risk NO Nasogastric (NG) tube: Esophageal perf. ; aspiration NO Activated charcoal; No adsorption / interferes
NG tube aspiration may be considered early (<90 minutes) in large volume ingestions Dilution & Neutralization? Dilution of ingestants by NasoGastric Tube lavage generates heat & increases risk of aspiration No proven benefit
Attempts at neutralization have similar effects Small volume dilution with water may be rarely considered early (<30 minutes) with particulate agents DISINFECTANTS QACs, phenol, pine oil, bleaches, alcohols; are more toxic than soaps and detergent compounds Phenols Highly reactive and corrosive contact poisons; denatures and precipitates cellular proteins of all contacting cells. Nephrotoxic, hepatotoxic and neurotoxic; rapidly absorbed through ingestion, inhalation or skin. Cats are highly sensitive to phenolic compounds. S Sources of phenolic compounds include flooring materials, coal tar, creosote, tar paper. Dermal exposure : in intense pain, areas of coagulative necrosis; treated by glycerol, polyethylene glycol washing, thorough rinsing with water , dressings soaked in 0.5% soda bica. Ocular exposure : corrosive burns of mouth, oropharynx, oesophagus. vomition, salivation, hyperactivity, ataxia, panting, weakness, tremor, coma, seizures, methhaemoglobinaemia, respiratory alkalosis, severe liver and kidney damage.
Treatment : Demulcents-milk, egg white, gastric lavage Emesis(contraindicated if severe damage) Activated charcoal, saline cathartic, 1% methylene blue, 4mg/kg;IV; ascorbic acid 20mg/kg,PO; N-acetyl cysteine 140mg/kgIV, 70mg/kg PO. q,id for 3 days. Ocular exposure is treated by sterile saline wash. Bleaches sodium hypochlorite. Calcium hypochlorite and trichloroisocyanuric acid in industrial strength bleaching solutions ,swimming pool chlorine products and chlorine laundry bleaches. Non chlorine bleach preparations or colorfast bleaches contain sodium peroxide, sodium perborate or enzymatic detergents. Toxicity is of lower degree Irritation of oropharynx, salivation, vomition and abdominal pain. Bleaching of hairs, pulmonary irritation- coughing , dyspnoea and retching on inhalation Nonchlorine bleach products, (sodium perborate, sodium peroxide) are alkaline and severe gastric irritatants causing renal damage and CNS excitation. Treatment Milk and water orally Washing with soap and rinsing with abundant water/sterile saline on dermal/ocular exposure. Induction of emesis and orogastric lavage is contraindicated to avoid the risk of causing further oesophageal irritation. Milk of magnesia (2-3ml/kg) can be administered symptomatically Boric acid ingredient in ant and roach killers Vomition(blue-green vomitus), renal damage, CNS excitation and depression. Gastric decontamination with emesis induction Gastroprotectants ( activated charcoal is ineffective) Cathartics, IVfluid therapy and antiemetics COMMON SALT (SODIUM CHLORIDE) TOXICITY
An essential nutrient and added to the feed and ration of animals but it is the quantity consumed which makes it toxic. Excessive ingestion of sodium chloride causes toxicity and the condition is also termed as water deprivation syndrome. All species of animals including human beings and poultry are poisoned but poultry and pigs are most susceptible to salt poisoning. In poultry- young chicks are most susceptible due to indiscriminate feeding behaviour, poor sense of taste, low plasma proteins in chicks and decreased glomerular filtration area in the kidneys of chicks compared to mammals.
Sources of poisoning: Feeds containing high quantities of common Salt Accidental over ingestion of common salt or excessive licking of salt licks kept on the premises particularly when the animals have been on restricted salt supply After a period of salt deprivation for quite some time then the animals may develop cravmg for salt or salt hunger Excessive consumption of salty meat or meat flavoured brines by carnivores, swill feeding to pigs (residues from bakeries, brine from butcher's shop, salt whey from cheese factories ) or salted fish waste, oil fields as salt water is an effluent from oil production. Change from low salt ration to high salt ration, low vitamin E and sulphur containing aminoacids. Overdosing of animals with sodium sulphate or some other sodium salts also results in salt poisoning. However, - over-consumption of salt can be tolerated by the animals if sufficient quantity of water is made available to the animals immediately after ingestion 0fsalt.
Mechanism of toxicity: Sodium ions and water balance are mainly disturbed. Excess of sodium ions in gastrointestinal tract cause mild irritation and secretion of water into the lumen of intestine and thus diarrhoea further resulting into dehydration. Absorption of Na + results in hypertonicity of blood and hypernatremia, shrinkage of kidney tubules, deposition of sodium crystals in the tubules, anuria and uremia etc. following transient polyuria due to initial excretion of Na+ in the urine. Decreased ability of sodium pumps to remove Na+ from the cells set up an osmotic gradient. Excess of Na+ in blood stream (extracellular hyperosmolarity) results in shrinkage of capillary vascular endothelial cells in the brain and meninges which in turn stimulate the capillary permeability and escape of water from blood to interstitial spaces (intracellular dehydration) and development of brain or cerebral oedema. Cerebral oedema in pigs is also associated with the accumulation of eosinophils in the brain tissue. As a result of cerebral oedema, there is increased cerebrospinal fluid pressure and reduced blood flow to the brain and thus hypoxia.
Clinical signs: General signs- anorexia, excessive thirst, salivation, initially diarrhoea followed by constipation, polyuria followed by anuria, (Vomiting in dogs, ) Nasal discharge and weak pulse. Body temperature is normal but ear and skin are cold. Rigidity of muscles, hyper-irritability, blindness, stumbling, walking backwards or in circles, pedalling of limbs, recurrent convulsive seizures, recumbency, coma and death -hrs to days. profuse watery diarrhoea with colic in ruminants, diarrhoea with colic, mucus in faeces, knuckling of fetlocks, dehydration and prostration in lactating animals Pruritis, ataxia, dog sitting posture, blindness, convulsions, comatose and paddling in pigs Intense thirst, respiratory distress, fluid discharge from beak, weakness, wet faeces and limb paralysis in poultry .
Post mortem lesions: Congestion and inflammation of gastrointestinal tract. Faeces are fluidy and dark or dry. Hydropericardium Severe acute inflammation of gastric and intestinal lining Oedema of tissues and body cavities. Renal congestion. Oedema of the cerebral cortex (polioencephalomalacia in cattle, eosinophilic Meningoencephalitis in pigs). Microscopically : large number of eosinophils in the distended perivascular space and meninges are almost pathognomonic hl pigs but not in poultry. Other changes are degeneration of neurons and slight general gliosis, vacuolization, disruption of the area between cortex and white matter. Polultry: Congestion of liver in chicks, hyperaemia of the organs and deposits of uric acid in kidneys. ureters and droppings in mature birds.
Diagnosis: History of salt ingestion. Clinical signs of poisoning including excessive thirst. Post-mortem lesions. Species involved. Circumstantial evidences of relatively restricted water or salt supply. Laboratory investigations indicating plasma sodium levels of exceeding 150 mEq/L in live animals and CSF sodium level of> 145 mEq/L and brain sodium > 1800 ppm in dead animals.
Differential diagnosis: Chlorinated hydrocarbons(OCC) toxicity: ( no thirst and hyperthermia.) organophosphate compounds (OPC)- hypothermia. Drugs or plants causing central symptoms of stimulation. Lead or other metals toxicity where gastric symptoms are more severe. Injury to CNS., Pseudorabies, Encephalitis Treatment: No specific antidote is available. Remove the toxic feed/ or water. Salt free fresh water be made available, however, initially access of the animal to Water should be restricted as large intake of water will kill the animal by aggravating cerebral oedema. Small quantities of water frequently Isotonic or hypotonic salt solution intraperitoneally daily for 2- 3 days. Gastrointestinal tract sedatives. Sedatives to counter the CNS stimulation.
SINTESIS SURFAKTAN METIL ESTER SULFONAT DARI METIL ESTER MINYAK BIJI KARET (Havea Brasiliensis) MELALUI REAKSI SULFONASI DENGAN PENGARUH VARIASI KATALIS