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Co-use was relatively stable across the different periods. Writing in the journal of Addictive Behaviors, the researchers said that the evolving trends in use of the two substances could be evidence of a substitution effect amid changing harm perceptions, evolving legislation, and shifting norms. The rising cannabis-only use across groups parallels the expanding state-level recreational cannabis legalization, increasing accessibility and normalization, the paper says
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Other Causes of Reduced Pseudocholinesterase Activity Disease states Drugs (e.g., organophosphates, neostigmine , pyridostigmine) Effects: Prolonged paralysis , including diaphragm involvement Risk of respiratory failure Dibucaine Test Used to diagnose enzyme deficiency: Normal: ~80% inhibition Heterozygotes: 5060% Homozygotes: 2030% Management: Maintain sedation and mechanical ventilation Monitor recovery using train-of-four stimulation Other Contraindications History of malignant hyperthermia Conditions predisposing to hyperkalemia , including: Burns or major trauma (2472 hours post-injury) Neuromuscular disorders Myopathies Acute narrow-angle glaucoma or penetrating eye injury Side Effects Malignant hyperthermia (rare but fatal risk) Hyperkalemia (can be life-threatening) Risk of: Cardiac arrest Rhabdomyolysis Cardiac arrhythmias (bradycardia or tachycardia) Muscle pain (due to fasciculations) Increased intragastric pressure aspiration risk Increased intraocular pressure (contraindicated in glaucoma) Pharmacokinetics Routes: IV or IM Rapid metabolism by plasma pseudocholinesterase Not metabolized by acetylcholinesterase Key Parameters: Onset: 3060 seconds Duration: 610 minutes Half-life: 35 minutes Notes: Phase II block recovery may last 30 minutes or longer Duration depends on: Rate of receptor dissociation Plasma enzyme activity Drug Interactions Increase Duration of Action: Cholinesterase inhibitors (e.g., neostigmine , pyridostigmine) Administration of neostigmine & pyridostigmine to patients to reverse non-depolarizing skeletal muscle blockade has been shown to cause profound reductions of plasma pseudocholinesterase activity for several hours duration (Mirakhur et al, 1982), an effect that can mechanistically account for the observed prolongation of succinylcholine effect by these cholinesterase inhibitors (Sunew & Hicks, 1978
