Hashish Poisoning

Hashish Poisoning

Marijuana refers to a mixture of cut, dried, and ground flowers, leaves, and stems of the leafy green hemp plant Cannabis sativa . The plant grows in most tropical and temperate regions of the world. Marijuana is the principal drug produced from the hemp plant. There are several cannabinoids present in the plant resin but delta-9-tetrahydro-cannabinol (THC) is considered the most active and main psychoactive agent. The concentration of THC in marijuana varies between 1-8%. Hashish is the resin extracted from the top of the flowering plant and is higher in THC concentration than marijuana. Street names for marijuana include pot, Mary Jane, hashish, weed, grass, THC, ganja, bhang, and charas. Pure THC is available by prescription under the generic name dronabinol. A synthetic cannabinoid, nabilone, is also available. Marijuana or hashish sold on the streets may be contaminated with phencyclidine, LSD, or other drugs.
Marijuana is a schedule I controlled substance mostly used by people as a recreational drug. It is also used as an antiemetic for chemotherapy patients and to decrease intraocular pressure in glaucoma patients. Some clinicians advocate the use of dronabinol as an appetite stimulant, but the dysphoric effects of this drug outweigh any benefit of appetite stimulation.
Pharmacokinetics and Toxicity:
The most common route of exposure is oral. After ingestion, THC goes through a substantial first pass effect. It is metabolized by liver microsomal hydroxylation and nonmicrosomal oxidation. In dogs, the onset of clinical signs occurs within 30-90 min and can last up to 72 hr. THC is highly lipophilic and readily distributes to the brain and other fatty tissues following absorption. The oral LD50 of pure THC in rats and mice is 666 mg/kg and 482 mg/kg, respectively. However, clinical effects of marijuana are seen at much lower doses than this.

Pathogenesis:
THC is believed to act on a unique receptor in the brain that is selective for cannabinoids and is responsible for the CNS effects. Cannabinoids can enhance the formation of norepinephrine, dopamine, and serotonin. They can also stimulate release of dopamine and enhance γ-aminobutyric acid turnover.

Clinical Findings and Diagnosis:
The most common signs of marijuana toxicosis are depression, ataxia, bradycardia, hypothermia, vocalization, hypersalivation, vomiting, diarrhea, urinary incontinence, seizures, and coma.
Diagnosis is based on a history of exposure and typical clinical signs. THC is difficult to detect in body fluids because of the low levels found in the plasma. Urine testing in the early course of exposure may help confirm the diagnosis. Marijuana toxicosis can be confused with ethylene glycol (antifreeze, Ethylene Glycol Toxicity: Introduction) or ivermectin toxicosis; hypoglycemia; or benzodiazepine, barbiturate, or opioid overdose.

Treatment:
Treatment consists of supportive care. The animal should be decontaminated if the exposure is recent and there are no contraindications. Comatose animals should be given IV fluids, treated for hypothermia, and rotated frequently to prevent dependent edema or decubital ulceration. Diazepam can be given for sedation or to control seizures. Treatment and monitoring should be maintained until all clinical signs have resolved (up to 72 hr in dogs).