Theobromine poisoning

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Structural formula of theobromine

The theobromine poisoning or chocolate poisoning is an intoxication with the Purinalkaloid theobromine , which is particularly dogs and cats can fall victim if they Chocolate eat. Such poisoning can be fatal.

Occurrence

Dark chocolate contains more theobromine than milk chocolate and can therefore cause poisoning in dogs and cats even in small quantities.

Theobromine poisoning is most common in dogs, but also in other animal species . It is mostly a result of consuming chocolate ; However, other products of the cocoa tree also contain enough theobromine to cause poisoning: Poisoning through the shell of the cocoa bean has also been described, which is occasionally used as garden litter and which dogs like to eat because of its attractive aroma. Cats are less likely to be poisoned with theobromine than dogs because they usually avoid chocolate. Cases in cattle and other livestock have also been described and occur when by-products of cocoa production are fed. Bears can also poison themselves in chocolate because of its theobromine content.

product Theobromine content
Dried cocoa powder 28.5 mg / g
bitter chocolate 16 mg / g
Shell of the cocoa bean 9.1 mg / g
Dark chocolate 5.7 mg / g
milk chocolate 2.3 mg / g
Drinking chocolate (liquid) 0.4 mg / g
White chocolate 0.009 mg / g

Symptoms

The combined neurological effects of theobromine lead to an increase in blood pressure and pulse rate , constriction of blood vessels, especially in the brain , a reduced stimulus threshold of the nervous system and thus to restlessness, tremors and hyperreflexia up to seizures . In addition, vomiting often occurs ; also diarrhea occurs. In fatal poisoning, the immediate cause of death is usually either cardiac arrhythmia, hyperthermia, or respiratory failure .

Depending on the dose taken, different symptoms can appear to different degrees:

Dose (dog) Symptoms
20 mg / kg Vomiting, diarrhea, increased thirst
40-50 mg / kg Additionally effects on the circulatory system : tachycardia , arrhythmias
≥60 mg / kg Additional effects on the CNS : seizures, impaired consciousness

The first symptoms usually appear within 2 to 4, in exceptional cases up to 12 hours after ingestion and consist of increased thirst, accompanied by diarrhea, vomiting and occasionally a swollen stomach. In the further course of the poisoning, depending on the dose, they can also spread to the circulatory system and the central nervous system and, if left untreated, lead to death within 12 to 36 hours.

Mechanism of action

Theobromine is almost completely absorbed by the dog after ingestion , is subject to the enterohepatic cycle and has a bioavailability of 77 ± 12%. The maximum blood level is reached two to four hours after intake. The plasma half-life in dogs is around 17.5 hours after oral intake and is therefore very long compared to the other xanthines caffeine and theophylline . In addition to theobromine, chocolate often also contains small amounts of caffeine, which can also contribute to poisoning. Its plasma half-life in dogs is, however, at 2.5 to 4.5 hours, much shorter than that of theobromine.

Theobromine acts directly as an inhibitor of the adenosine receptors and also as a non-specific phosphodiesterase inhibitor , which in turn increases the release of catecholamines via cAMP . As a result, it has a strong sympathomimetic effect, which, together with its slow degradation in dogs, is responsible for its effect as a poison. In addition, it leads to an increased uptake of calcium by the cells and prevents its encapsulation in the sarcoplasmic reticulum of the muscle cells , which increases their contractility .

Various information can be found in the literature on the fatal effects of theobromine: A range of 100–500 mg per kilogram of body weight is mentioned for the oral LD 50 in dogs. Symptoms of severe poisoning can occur at much lower doses. A dog's individual sensitivity can also differ from these mean values.

In contrast to dogs, cats, horses , cattle and many other animal species, humans (like rats and mice ) are not very sensitive to theobromine. This depends, among other things, the enzyme equipment in the cytochrome P450 complex (particularly CYP1A2 and CYP2E1 ) together: These enzymes have a higher activity in humans and thus contribute to a much faster reduction of the substance at.

treatment

Treatment for fresh theobromine poisoning consists of first inducing vomiting, which removes unabsorbed theobromine from the stomach. By administering activated charcoal , theobromine that has already been absorbed can be removed from the enterohepatic circulation and excreted with the feces . By infusions existing in blood plasma theobromine can be diluted and its excretion by the kidneys are favored. The reabsorption by the bladder wall can by a urinary catheter be prevented. In addition, the effects of theobromine are symptomatically suppressed as far as possible by appropriate drugs. Because of the long plasma half-life, repeated doses are usually necessary.

If treatment begins within two to four hours of admission, the prognosis is good. If central nervous disorders are present, the prognosis is less good. Theobromine itself does not cause permanent damage; however, some of the complications of poisoning (such as severe hyperthermia ) can cause permanent damage.

See also

Individual evidence

  1. ^ R. Drolet, TD Arendt, CM Stowe: Cacao bean shell poisoning in a dog. In: Journal of the American Veterinary Medical Association. Volume 185, Number 8, October 1984, pp. 902, ISSN  0003-1488 . PMID 6501051 .
  2. Four animals died of a chocolate overdose. In: Tagesspiegel. January 23, 2015 on the basis of a dpa report.
  3. ^ GD Osweiler: Chocolate Toxicity . In: LP Tilley, FWK Smith (Eds.): The 5-Minute Veterinary Consult - Canine and Feline . 3. Edition. Lippincott, Williams & Williams, Baltimore, MD, USA 2004, ISBN 0-7817-4038-X , pp. 216 f .
  4. ^ Food Hazards: Chocolate. In: CM Kahn (Ed.): The Merck Veterinary Manual. 9th edition. Merial, Whitehouse Station, NJ, USA 2005, ISBN 0-911910-50-6 , pp. 2362-2364.
  5. a b B. Loeffler, Katharina Kluge, FR Ungemach, M. Kietzmann: Plasma and urine concentrations of caffeine, theophylline and theobromine after the application of coffee, tea and chocolate in dogs and their relevance to doping in greyhound races. ( Memento of the original from July 14, 2014 in the Internet Archive ) Info: The archive link was inserted automatically and has not yet been checked. Please check the original and archive link according to the instructions and then remove this notice. In: Tierärztl. Practice. 2000; 28 (K), pp. 79-85. @1@ 2Template: Webachiv / IABot / pharmakologie.vetmed.uni-leipzig.de
  6. Poisoning by theobromine and other methylxanthines on the veterinary pharmacology page of the University of Zurich
  7. B. Loeffler, Katharina Kluge, FR Ungemach, M. Kietzmann: Studies on the pharmacokinetics of caffeine, theophylline and theobromine in dogs. ( Memento of the original from March 4, 2016 in the Internet Archive ) Info: The @1@ 2Template: Webachiv / IABot / pharmakologie.vetmed.uni-leipzig.de archive link was inserted automatically and has not yet been checked. Please check the original and archive link according to the instructions and then remove this notice. In: Tierärztl. Practice. 2000; 28 (K), pp. 71-78.
  8. S. Gates et al: Cytochrome P450 isoform selectivity in human hepatic theobromine metabolism. In: Br J Clin Pharmacol . 47 (3) (1999), pp. 299-305. doi: 10.1046 / j.1365-2125.1999.00890.x . PMID 10215755 .

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