Jeetje Jolly, ik lees dit nu pas,
Hoe gaat het nu met Cissy?
Ik heb ook even gezocht en in het Merck handboek vond ik een tekst over metaldehyde-vergiftiging.
In die tekst vond ik wel dat de stof de darmen en de maag irriteert en dus braken op kan wekken, maar in de tekst staat inderdaad ook dat er vaak hyperthermie voorkomt en dat is naar mijn weten verhoging (denk maar aan hypernerveus, betekent erg nerveus) en niet verlaging van de lichaamstemperatuur.
Geef haar een hele dikke knuffel van me!!!
hier is de hele tekst:
Metaldehyde Poisoning: Introduction
------------------------------------------------------------------------
Metaldehyde is commonly used as a molluscicide in domestic gardens, especially during the wet season for slug and snail control. In certain locations, it is also used for rat control. Metaldehyde comes as a liquid or bait (3.5%) combined with bran, either as flakes or pellets, and is palatable to pets and farm animals. Some products also contain arsenic or carbamate insecticides, which are usually less toxic at the dosage used than the metaldehyde. All species are susceptible to metaldehyde poisoning (lethal dose 100-300 mg/kg); dogs are the species most frequently poisoned (3 oz of bait is toxic to a 30-lb dog). Metaldehyde is hydrolyzed in stomach acid to acetaldehyde polymers that readily enter the brain. Poisoning reduces levels of brain serotonin, norepinephrine, and the inhibitory neurotransmitter g-aminobutyric acid (GABA).
Clinical signs of toxicosis are similar in all mammals. Nervous signs are prominent and include severe muscle tremors, ataxia, hyperesthesia, nystagmus, and hyperpnea, followed by opisthotonos and continuous tonic convulsions. Nystagmus is most severe in cats. Nervous signs are more continuous and less exaggerated by stimulation than in strychnine poisoning ( Strychnine Poisoning: Introduction), which may appear clinically similar. Emesis, hypersalivation, dyspnea, tachycardia, and severe hyperthermia (profuse sweating in horses) are also seen. Severe acidosis develops due to acid metabolites and high muscle activity in all species. Cholinergic signs (especially pupillary constriction) may occur if the product contains a carbamate. In high-level exposure, death (4-24 hr) is from respiratory failure, while survivors may develop liver failure (3-4 days). Necropsy lesions are nonspecific and include congestion and edema of the liver, kidneys, and lungs, and intestinal hemorrhage. A mild formaldehyde-like odor may be present on opening the stomach or rumen. Stomach content, rapidly frozen, is the preferred sample for analysis due to the low levels and rapid loss of acetaldehyde from tissue (liver and urine).
An emetic (eg, apomorphine) in acute exposure may not be necessary because metaldehyde is a gastric irritant. However, gastric lavage with sodium bicarbonate is recommended. Diazepam (2-5 mg/kg, IV) to effect is preferred to reduce excitement and convulsions; acepromazine has been used successfully. Barbiturates (compete with acetaldehyde degradation) are indicated only if the animal doses not respond, and gas anesthesia is suggested to maintain severely affected animals. In large animals, activated carbon (preferred) or high doses of mineral oil reduce further absorption (metaldehyde is fat soluble). Aggressive fluid therapy with sodium lactate to reduce acidosis is required, and dextrose or calcium borogluconate is used to prevent possible liver damage. Cold water rinses are recommended when fever is severe. (See also Rodenticide Poisoning: Introduction.)
( ja ja blond 
)
, en je kan mij niet wijs maken dat al die slakekn zo snel alles op heben gevreten 
maar dat kwam er wel meteen na, braken 2 keer goed en daarna diarree en toen bleef ze persdrang houden.
